The High-risk Surgical Patient 3031172728, 9783031172724

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The High-risk Surgical Patient Paolo Aseni Antonino Massimiliano Grande Ari Leppäniemi Osvaldo Chiara Editors

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The High-risk Surgical Patient

Paolo Aseni  •  Antonino Massimiliano Grande • Ari Leppäniemi • Osvaldo Chiara Editors

The High-risk Surgical Patient

Editors Paolo Aseni Dipartimento di Emergenza Urgenza ASST Grande Ospedale Metropolitano Niguarda Milan, Italy Ari Leppäniemi Div. of Emerg. Surg., Abdominal Center Helsinki University Hospital Meilahti Helsinki, Finland

Antonino Massimiliano Grande Divisione di Cardiochirurgia IRCCS Fondazione Policlinico San Matteo Pavia, Pavia, Italy Osvaldo Chiara Department of Pathophysiology and Transplantation General Surgery and Trauma Team University of Milano ASST Grande Ospedale Metropolitano Niguarda Milan, Italy

ISBN 978-3-031-17272-4    ISBN 978-3-031-17273-1 (eBook) https://doi.org/10.1007/978-3-031-17273-1 © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Foreword

Fifty years ago, general surgeons cared for pathology in every body cavity. Subspecialization came later as surgical care became more complicated. Treatment options became far more numerous. It was no longer possible for a surgeon to be an expert in all of these areas. Surgical residency no longer provided sufficient training in all of these areas. Fellowship training was necessary to attain sufficient expertise in these various specialties. Minimally invasive techniques revolutionized surgical care. While the average general surgeon was certainly capable of learning to perform the standard procedures, advanced laparoscopic training was necessary to do the more sophisticated procedures. Most surgical residents chose to pursue fellowship training after residency. Once they finished their fellowship, many surgeons limited their practice to their area of specialization. There were very few people competent and willing to care for the myriad of complex general surgery emergencies. Acute Care Surgery was the specialty created to fill this need. Acute Care Surgery practice differs in various parts of the world. In the United States, Acute Care Surgery embraces Surgical Critical Care, Emergency General Surgery (EGS), and Trauma. Outside of the United States, critical care is more commonly provided by intensivists and Acute Care Surgery is Trauma and EGS. Regardless of the specifics of how practice is organized, it seemed likely that there would be two kinds of physicians, those that cared for those acutely ill and those who had more elective practices. Acute Care Surgeons care for those patients who are acutely ill, regardless of the etiology of the pathology. This book is a resource for anyone caring for high-risk surgical patients. The editors have amassed a set of worldwide authors, all of whom are recognized experts in the care of the acutely ill, high-risk surgical patient. The subject matter covered is wide ranging and includes surgical technique, pre- and post-op assessment, and complications in high-risk patients. The editors wisely recognized the techniques from other specialties, such as minimally invasive surgery can sometimes be quite useful in caring for high-risk patients. This is covered in the book. The artwork is of the highest quality and should illustrate the principles discussed in the text beautifully. The editors have recognized that sometimes “over the top” support is necessary in these acutely ill patients, like the use of ECMO. This is also covered in the book. The topics are not restricted to general surgery subjects. The editors have realized that it is necessary to understand the principles of Anesthesiology, Orthopedics, Maxillofacial Surgery, and Transplantation in order to be truly well versed; these are covered as well. We were honored to be included in those invited to contribute to this impressive textbook. This should be a great resource to all who provide emergency and critical care to those at highest risk. We believe this will be useful and hope that you, the readers, enjoy it as much as those of us who contributed enjoyed writing it. Baltimore, MD, USA Baltimore, MD, USA

Sharon M. Henry, MD Thomas M. Scalea, MD

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Preface

The emerging paradigm of the “High-Risk Surgical Patient” is increasingly providing grounds for discussion and debate in the surgical community. This book tries to coherently organize the currently available information by describing how to identify high-risk patients undergoing surgery and how to treat them to improve their outcomes. Surgery is a team-based discipline. We believe that improving surgical patient outcomes largely depends on the preoperative identification of these high-risk patients and their multidisciplinary treatment. This work was partly inspired by an old book entitled The Aged and High-Risk Surgical Patient. Medical Surgical and Anaesthetic Management by J. H. Siegel and P. Chodoff, published in 1976 by Grune and Stratton; our aim was to reproduce it in a more complete and up-to-date format including the latest scientific evidence. Siegel’s textbook, at that time, was probably the first systematic attempt to identify those patients undergoing surgery with a reduced functional reserve, who were at a higher risk of morbidity and mortality. This book is divided into five different sections; (a) identification and characterization of the high-risk surgical patients, (b) strategies to improve outcomes in high-risk surgical patients, (c) new trends in the acute care of high-risk surgical patients, (d) improvement of patient “safety and prevention of major complications”, (e) identification of the high-risk trauma patient. First, we tried to select all relevant issues of the high-risk patients identifying those patients who, for different reasons, may face a failure in the oxygen transport and an imbalance of cardiac and respiratory reserve during and after surgery. The infinite number of issues potentially involved in identifying and managing high-risk surgical patients has made it challenging to select and describe all the critical ones encountered in surgical practice. However, we have highlighted some special and unique critical settings where several experts had considerable experience despite robust evidence is still limited. The textbook includes 82 chapters written by an exceptional group of experts in different areas of intensive care, anesthesiology, and acute and trauma care surgery. We are very fortunate to have these expert colleagues and friends and want to congratulate them for their extraordinary commitment and hard work. We want to dedicate this book to all our young colleagues, intensivists, anesthesiologists, and surgeons worldwide, and, last but not least, to our patients from whom we have learned so much. The Editors. Milan, Italy Pavia, Italy  Helsinki, Finland  Milan, Italy 

Paolo Aseni Antonino Massimiliano Grande Ari Leppäniemi Osvaldo Chiara

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Contents

Part I Identification and Characterisation of High-Risk Surgical Patients 1 Defining  the High-Risk Surgical Patient�������������������������������������������������������������������   3 Lucrezia Rovati, Sergio Arlati, and Paolo Aseni 2 The  Frail Patient in the Operating Room: Practical Steps to Reduce the Operative Risk �����������������������������������������������������������������������������������������������������   9 Andrea De Gasperi, Elena Roselli, and Ombretta Amici 3 The  High Risk Surgical Patients: The Pathophysiologic Perspective �������������������  19 Sergio Arlati 4 Monitoring  and Interpretation of Vital Signs in the High-Risk Surgical Patients���������������������������������������������������������������������������������������������������������  41 Sergio Arlati 5 Evaluation  and Critical Care Management of the Burn Patient���������������������������  65 Franz W. Baruffaldi Preis and Antonella M. Citterio 6 Acid–Base  Abnormalities in Surgical Patients Admitted to Intensive Care Unit���������������������������������������������������������������������������������������������������������������������  77 Fabio Daniel Masevicius and Arnaldo Dubin 7 Pre-operative  Cardiovascular Risk Assessment in Non-cardiac General Surgery ���������������������������������������������������������������������������������������������������������  95 Andrea Farina, Mauro Zago, and Stefano Savonitto 8 Post-operative  Liver Failure and Pre-­operative Evaluation of the Risk of Surgery in Patients with Liver Disease����������������������������������������������������������������� 107 Federico Tomassini, Anna Mariani, Paolo Aseni, and Roberto Ivan Troisi 9 Radiology  for Surgeons: Improving the Diagnostic Accuracy in the High-­Risk Surgical Patient ����������������������������������������������������������������������������� 117 Diana Artioli, Francesco Rizzetto, and Angelo Vanzulli 10 Oncologic  Emergencies in Patients Undergoing Major Surgery��������������������������� 125 Annabella Curaba, Pietro Di Masi, Katia B. Bencardino, Andrea Sartore-­Bianchi, and Salvatore Siena 11 The  High-Risk Pediatric Surgical Patient ��������������������������������������������������������������� 135 Carine Foz, James A. DiNardo, and Viviane G. Nasr 12 Difficult  Intubation in the High-Risk Surgical Patient������������������������������������������� 151 Michal Barak, Daniel Braunold, and Aeyal Raz 13 Recognition  and Early Management of Sepsis in Frail Patients ��������������������������� 163 Andrea Beltrame and Marco Anselmo

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14 Preoperative  Evaluation for Complex Pulmonary Surgery: How Can We Balance the Risk?������������������������������������������������������������������������������������������������� 169 Alessandro Rinaldo, Luca Pogliani, and Massimo Torre 15 Assessment  of Pre-operative Risk in Complex Cardiac Surgery��������������������������� 179 Antonino Massimiliano Grande, Antonio Fiore, and Antonio Salsano Part II Strategies to Improve the Outcome in High-Risk Surgical Patients 16 Patient  Safety in Surgery: Strategies to Achieve the Best Outcome in the High-Risk Surgical Patient ����������������������������������������������������������������������������� 197 Robyn Clay-Williams and John Cartmill 17 Strategies  to Reduce the Risk of Post-­operative Pulmonary Complications��������� 203 Andrew B. Lumb and Victoria Boardman 18 Prevention  and Management of Perioperative Neurological Complications in High-Risk Surgical Patients����������������������������������������������������������������������������������� 213 Rachele Tortorella 19 Acute  Aortic Syndrome (AAS): A High-­Risk Missed Diagnosis in the Emergency Department����������������������������������������������������������������������������������� 221 Paola Tracanelli and Paolo Aseni 20 Trans-Catheter  Interventional Treatment of Structural Heart Diseases��������������� 239 Giuseppe Bruschi, Bruno Merlanti, Aldo Cannata, and Claudio F. Russo 21 New  Technologies in Urologic Surgery: Robotic and Minimally Invasive Procedures������������������������������������������������������������������������������������������������������������������� 249 Francesca Ambrosini, Paolo Dell’Oglio, Aldo Massimo Bocciardi, and Antonio Galfano 22 New  Trends in Vascular Surgery: Less Open and More Endovascular Procedures������������������������������������������������������������������������������������������� 257 Maria Teresa Occhiuto, Nicola Monzio Compagnoni, Antonietta Cuccì, Erika De Febis, Matteo Cazzaniga, and Valerio Stefano Tolva 23 New  Trends in Laparoscopic Procedures in the Emergency Abdominal Surgery����������������������������������������������������������������������������������������������������� 269 Chiara Maria Ranucci, Quirino Lai, Silvia Quaresima, Alessandro Maria Paganini, Serena Celani, Massimo Rossi, Giovanni Domenico Tebala, and Salomone Di Saverio 24 New  Trends in the Treatment of Severe Acute Pancreatitis ����������������������������������� 279 Ari Leppäniemi and Matti Tolonen 25 Point-of-Care  Ultrasound in the Preoperative Evaluation of the High-Risk Surgical Patient Requiring Urgent Non-cardiac Surgery��������������������������������������� 287 Enrico Storti and Michele Introna 26 Perioperative  Monitoring in High-Risk Surgical Patients: A Step-by-Step Approach��������������������������������������������������������������������������������������������������������������������� 301 Agostino Roasio 27 High-Risk  Pancreatic Anastomosis: Prediction, Mitigation, and Management of Postoperative Pancreatic Fistula��������������������������������������������������������������������������� 311 Andrea Caravati, Giampaolo Perri, Giovanni Marchegiani, and Claudio Bassi

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Part III New Trends in Acute Care of High-Risk Surgical Patients 28 Anesthesia  in High-Risk Surgical Patients with Uncommon Disease ������������������� 323 Andrew K. Gold, Tam Mandelbaum, and Lee A. Fleisher 29 Perioperative  Management and Surgical Challenges in Patients with Spinal Cord Dysfunction����������������������������������������������������������������������������������� 345 Gianluca Sampogna, Antonello Forgione, Giorgio Chevallard, and Michele Spinelli 30 Non-invasive  Ventilation in the High-­Risk Surgical Patients��������������������������������� 355 Massimo Zacchino, Andrea Bellone, and Giampaolo Casella 31 Extracorporeal  Life Support (ECLS) for Critically Ill Patients in the Emergency Department����������������������������������������������������������������������������������� 361 Fabio Sangalli, Silvia Mariani, and Roberto Fumagalli 32 Perioperative  Management of Severe Bleeding and Coagulopathy in High-­Risk Surgical Patients����������������������������������������������������������������������������������� 369 Sibylle A. Kietaibl 33 Endovascular  Management of Post-­Operative Bleeding����������������������������������������� 379 Fabiane Barbosa, Francesco Morelli, Angea Alfonsi, Pietro Brambillasca, Alcide Alessando Azzena, Pietro Gemma, and Antonio Rampoldi 34 Evaluation  and Management of Malnutrition in the High-Risk Surgical Patient����������������������������������������������������������������������������������������������������������� 385 Biljana Andonovska and Alan Andonovski 35 The  Role of Selective Drug Therapy in Reducing Mortality in the High-risk Surgical Patients (Tranexamic Acid, Selective Bowel Tract Decontamination, Levosimendan, Beta-blockers, Insulin, Aprotinin, and Statins)����������������������������� 395 Giovanni Landoni, Martina Baiardo Redaelli, and Alberto Zangrillo 36 Strategies  for Advanced Mechanical Circulatory Support in Refractory Cardiogenic Shock ����������������������������������������������������������������������������������������������������� 405 Aldo Cannata, Massimiliano Carrozzini, Alessandro Costetti, Marco Lanfranconi, and Claudio Francesco Russo 37 Evaluation  and Management of Patients with Left Ventricular Assist Device (LVAD) Requiring Noncardiac SurgicalProcedures ����������������������������������������������� 415 Michele G. Mondino, Emanuela Paradiso, and Sandra Nonini 38 Rescue  Surgery and Failure to Rescue��������������������������������������������������������������������� 425 Ari Leppäniemi and Matti Tolonen 39 Endoscopic  Submucosal Dissection for Early Malignant Epithelial Neoplasms of the Digestive Tract in Frail and Elderly Patients����������������������������� 429 Pietro Gambitta, Camilla Ciscato, Venerina Imbesi, Antonio Armellino, and Paolo Aseni 40 Advanced  Therapeutic Endoscopy for Acute Pancreatic and Biliary Diseases in Frail Patients����������������������������������������������������������������������������������������������������������� 437 Massimiliano Mutignani and Lorenzo Dioscoridi 41 Appropriate  Perioperative Therapy in Patients with Chronic Heart Failure Undergoing Surgery��������������������������������������������������������������������������������������������������� 447 Boris Cox, Valerie Smit-Fun, and Wolfgang F. Buhre

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42 Robot-Assisted  Pancreatic Surgery: Safety and Feasibility����������������������������������� 453 Lapo Bencini, Irene Urciuoli, and Luca Moraldi 43 Safety  of Minimally Invasive Laparoscopic Approach in Major Liver Surgery��������������������������������������������������������������������������������������������������������������� 465 Mariano Cesare Giglio, Gianluca Cassese, and Roberto Ivan Troisi Part IV Improving Patients’ Safety and Prevention of Major Complications 44 Major  Complications in Hepatobiliary and Pancreatic Surgery��������������������������� 475 Anna Mariani, Matteo Tripepi, Iacopo Mangoni, and Paolo Aseni 45 Major  Complications After Esophageal, Gastric, and Bariatric Surgery������������� 491 Monica Gualtierotti 46 Major  Complications of Vascular Surgery��������������������������������������������������������������� 499 Pierantonio Rimoldi, Alfredo Lista, Maria Teresa Occhiuto, Antonietta Cuccì, Ilenia D’Alessio, and Valerio Stefano Tolva 47 Major  Complications of Urologic Surgery��������������������������������������������������������������� 511 Angelo Naselli, Isabella Oliva, and Pierpaolo Graziotti 48 Major  Complications of Thoracic Surgery��������������������������������������������������������������� 527 Joseph Seitlinger, Antonio Fiore, Antonino Massimiliano Grande, and Stéphane Renaud 49 Major  Complications of Cardiac Surgery ��������������������������������������������������������������� 537 Antonio Fiore, Antonino Massimiliano Grande, and Giuseppe Gatti 50 Major  Complications of Abdominal Organ Transplantation Surgery������������������� 551 Anna Mariani, Matteo Tripepi, Iacopo Mangoni, and Paolo Aseni 51 Corticosteroid  Insufficiency in High-­Risk Surgical Patients ��������������������������������� 567 Djillali Annane and Karim Asehnoun 52 The  Rationale Use of Antimicrobials in Septic Surgical Patients��������������������������� 579 Sandro Luigi Di Domenico, Paolo Aseni, Elena Clerici, and Carloandrea Orcese 53 Major  Complications of Heart Transplant Surgery ����������������������������������������������� 595 Antonino Massimiliano Grande and Antonio Fiore 54 Major  Complications of Lung Transplant Surgery������������������������������������������������� 609 Antonino Massimiliano Grande, Alessia Alloni, and Antonio Fiore 55 3D  Printing Technology in Medicine: A Personalised Approach Towards a Safer Surgical Practice ������������������������������������������������������������������������������������������� 621 Giulia Mazzoleni, Tommaso Santaniello, Federico Pezzotta, Fabio Acocella, Francesco Cavaliere, Nicolò Castelli, Alessandro Perin, and Paolo Milani 56 Multiorgan  Procurement for Transplantation as a Way to Improve Surgical Education��������������������������������������������������������������������������������������������������������������������� 639 Paolo Aseni and Alessandro Giacomoni 57 From  “See One, Do One, Teach One” to Hands-On Simulation and Objective Assessment in Surgical Training������������������������������������������������������������������������������� 647 Antonello Forgione and Gianluca Sampogna 58 New  Trends in Surgical Education and Mentoring by Immersive Virtual Reality: An Innovative Tool for Patient’s Safety ������������������������������������������������������������������� 657 Francesco Rizzetto, Sofia Rantas, Federico Vezzulli, Simone Cassin, Paolo Aseni, and Maurizio Vertemati

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59 Artificial  Intelligence in the Management of Difficult Decisions in Surgery and Operating Room Optimization��������������������������������������������������������������������������� 669 Elena Bignami, Valentina Bellini, and Emanuele Paolo Rafano Carnà Part V Identifying the High-Risk Trauma Patient 60 Trauma Surgeons Training Programs����������������������������������������������������������������������� 679 Stefania Cimbanassi, Roberto Bini, and Osvaldo Chiara 61 Telemedicine  for Prehospital Trauma Care: A Promising Approach��������������������� 683 Patrick Andreas Eder and Asarnusch Rashid 62 New  Trends in Critical Care Assessment and Management of the Trauma Patient������������������������������������������������������������������������������������������������� 691 Melike N. Harfouche and Thomas M. Scalea 63 Potentially  Preventable Trauma Deaths: A Challenge for Trauma Care Systems��������������������������������������������������������������������������������������������������������������� 699 Stefania Cimbanassi, Roberto Bini, and Osvaldo Chiara 64 Updates  in the Management of Complex Pancreatic Trauma ������������������������������� 703 Ari Leppäniemi and Matti Tolonen 65 Updates  in the Management of Complex Liver Trauma����������������������������������������� 709 Federico Coccolini, Dario Tartaglia, Riccardo Guelfi, Camilla Cremonini, Enrico Cicuttin, and Massimo Chiarugi 66 Updates  in the Management of Complex Renal Trauma ��������������������������������������� 715 Paul Gravestock, Arjun Nambiar, Rajan Veeratterapillay, Phil Haslam, and Andrew Thorpe 67 Updates  in the Management of Complex Chest Trauma ��������������������������������������� 727 Aris Koryllos, Klaus-Marius Bastian, and Corinna Ludwig 68 Updates  in the Management of Complex Cardiac Injuries ����������������������������������� 737 Riyad Karmy-Jones, Megan R. Lundeberg, and William B. Long III 69 The  Ongoing Dilemma of Thoracoabdominal Injuries: Which Cavity and When?������������������������������������������������������������������������������������������������������� 755 Juan A. Asensio, John J. Kessler, Parinaz J. Dabestani, and Miguel A. Cubano 70 Subclavian  Vessel Injuries: An Anatomic and Surgical Challenge to the Surgeon������������������������������������������������������������������������������������������������������������� 767 Juan A. Asensio, John J. Kessler, Parinaz J. Dabestani, and Miguel A. Cubano 71 Management  of Complex Laryngotracheal Injuries: A Challenging Surgical Emergency������������������������������������������������������������������������������������������������������������������� 783 Raja Kalaiarasi, Kushwaha Akshat, and Ramasamy Karthikeyan 72 Complex Duodenal Injuries��������������������������������������������������������������������������������������� 795 Areg Grigorian, Kazuhide Matsushima, and Demetrios Demetriades 73 Abdominal  and Peripheral Vascular Injuries: Critical Decisions in Trauma������� 803 Alfredo Lista, Pierantonio Rimoldi, Erika De Febis, Nicola Monzio Compagnoni, Giulia Lerva, and Valerio Tolva 74 Updates  in the Management of Complex Craniofacial Injuries����������������������������� 815 Gabriele Canzi, Giorgio Novelli, Giuseppe Talamonti, and Davide Sozzi

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75 Non-Operative  Management of Blunt Traumatic Injuries������������������������������������� 839 Stefania Cimbanassi, Roberto Bini, and Osvaldo Chiara 76 Recent  Advances in Minimally Invasive Surgery for Spinal Trauma ������������������� 845 Daniel Cavanaugh, Ivan Ye, Alexandra E. Thomson, and Steven Ludwig 77 Current  Perspectives of Interventional Radiology in Trauma������������������������������� 853 Francesco Morelli, Fabiane Barbosa, Marco Solcia, Angela Alfonsi, Pietro Brambillasca, Pietro Gemma, and Antonio Rampoldi 78 Strategies  to Control Hemorrhage in the Trauma Patient������������������������������������� 867 Joshua Dilday and John B. Holcomb 79 Selective  Use of Anesthetics in Patients with Major Trauma��������������������������������� 883 Christopher R. Parrino, Justin E. Richards, and Bianca M. Conti 80 Lifesaving  and Emergency Surgical Procedures in Trauma Patients ������������������� 901 Paolo Aseni, Sharon Henry, Antonino Massimiliano Grande, Antonio Fiore, and Thomas M. Scalea 81 Extracorporeal  Membrane Oxygenation (ECMO) in Trauma Patients ��������������� 947 Silvia Mariani, Anne Willers, Roberto Fumagalli, and Fabio Sangalli 82 The  Role of Trauma Surgeon in Mass Casualties ��������������������������������������������������� 957 Nikolaos Pararas, Andreas Pikoulis, Panagis M. Lykoudis, and Emmanouil Pikoulis

Contents

Contributors

Fabio  Acocella Department of Health, Animal Science and Food Safety “Carlo Cantoni” (VESPA), University of Milan, Milan, Italy Interdisciplinary Centre for Nanostructured Materials and Interfaces (CIMAINA), Physics Department, University of Milan, Milan, Italy Kushwaha Akshat  Department of Otorhinolaryngology, Jawaharlal Institute of Postgraduate Medical Education & Research (JIPMER), Pondicherry, India Angela Alfonsi  Interventional Radiology, AAST GOM Niguarda, Milan, Italy Alessia  Alloni, MD Department of Cardiac Surgery, IRCCS Fondazione Policlinico San Matteo, Pavia, Italy Francesca  Ambrosini Department of Urology, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Department of Urology, Policlinico San Martino, Genoa, Italy Ombretta Amici  Service Anesthesia and Critical Care Medicine, Niguarda Hospital, Milan, Italy Biljana  Andonovska, PhD University Clinic for Traumatology, Orthopedic Diseases, Anesthesia, Reanimation, Intensive Care and Emergency Center, Medical Faculty, University “St. Cyril and Methodius”, Skopje, North Macedonia Alan Andonovski, PhD  University Clinic for Traumatology, Orthopedic Diseases, Anesthesia, Reanimation, Intensive Care and Emergency Center, Medical Faculty, University “St. Cyril and Methodius”, Skopje, North Macedonia Djillali  Annane General Intensive Care Unit, FHU SEPSIS, Raymond Poincaré Hospital (AP-HP), School of Medicine Simone Veil Santé, University of Versailles SQY, University Paris Saclay, Garches, France Marco Anselmo  SC Malattie Infettive ASL 2 Savonese Ospedale S. Paolo, Savona, Italy Sergio  Arlati Intensive Care Unit “G.  Bozza”, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Antonio Armellino  Endoscopy Division, Ospedale San Leopoldo Mandic di Merate, ASST Lecco, Lecco, Italy Diana  Artioli  Department of Radiology, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Paolo  Aseni  Dipartimento di Emergenza Urgenza, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Department of Biomedical and Clinical Sciences, Università degli Studi di Milano, Milan, Italy

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Karim Asehnoun  CHU Nantes, Université de Nantes, Pôle Anesthésie-Réanimation, Service d’Anesthésie Réanimation Chirurgicale, Hôtel Dieu, Nantes, France Juan A. Asensio  Division of Trauma Surgery and Surgical Critical Care, Trauma Center and Trauma Program, Department of Surgery, Creighton University School of Medicine, Omaha, NE, USA Department of Translational Science, Creighton University School of Medicine, Omaha, NE, USA Uniformed Services University of the Health Sciences, F. Edward Hébert School of Medicine, Walter Reed National Military Medical Center, Bethesda, MD, USA Creighton University Medical Center, Omaha, NE, USA Alcide Alessando Azzena  Interventional Radiology, AAST GOM Niguarda, Milan, Italy Martina  Baiardo  Redaelli Department of Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy Michal  Barak Department of Anesthesiology, Rambam Health Care Campus, Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel Fabiane Barbosa  Interventional Radiology, AAST GOM Niguarda, Milan, Italy Franz  W.  Baruffaldi  Preis Burn Unit and Plastic Surgical Department, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Claudio  Bassi  General and Pancreatic Surgery Unit, University of Verona Hospital Trust, Verona, Italy Klaus-Marius  Bastian Department of Thoracic Surgery, Florence Nightingale Hospital, Düsseldorf, Germany Valentina Bellini  Anesthesiology, Critical Care and Pain Medicine Division, Department of Medicine and Surgery, University of Parma, Parma, Italy Andrea Bellone  Emergency Department, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Andrea Beltrame  SC Malattie Infettive ASL 2 Savonese Ospedale S. Paolo, Savona, Italy Katia  B.  Bencardino Department of Hematology, Oncology and Molecular Medicine, Grande Ospedale Metropolitano Niguarda, Niguarda Cancer Center, Milan, Italy Lapo  Bencini Division of Oncologic Surgery and Robotics, Department of Oncology, Azienda Ospedaliero Universitaria di Careggi, Florence, Italy Elena  Bignami Anesthesiology, Critical Care and Pain Medicine Division, Department of Medicine and Surgery, University of Parma, Parma, Italy Roberto  Bini General Surgery and Trauma Team, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Victoria Boardman  St. James’s University Hospital, Leeds, UK Aldo  Massimo  Bocciardi  Department of Urology, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Pietro  Brambillasca Interventional Radiology, AAST Grande Ospedale Metropolitano Niguarda, Milan, Italy Daniel Braunold  Department of Anesthesiology, Rambam Health Care Campus, Haifa, Israel

Contributors

Contributors

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Giuseppe  Bruschi  Department of Cardiac Surgery, ASST Grande Ospedale Metropolitano Niguarda, Niguarda Hospital, Milan, Italy Wolfgang  F.  Buhre Division of Anesthesiology, Perioperative Medicine, Emergency- and Critical Care Medicine, Department of Anesthesiology and Pain Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands Aldo  Cannata Department of Cardiac Surgery and Heart Transplantation, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Gabriele Canzi  Maxillofacial Surgery Unit, Emergency Department, ASST-GOM Niguarda, Niguarda Hospital, Milan, Italy Andrea Caravati  General and Pancreatic Surgery Unit, University of Verona Hospital Trust, Verona, Italy Emanuele Paolo Rafano Carnà  Anesthesiology, Critical Care and Pain Medicine Division, Department of Medicine and Surgery, University of Parma, Parma, Italy Massimiliano Carrozzini  Department of Cardiac Surgery and Heart Transplantation, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy John  Cartmill Faculty of Medicine, Health and Human Sciences, Macquarie University, Macquarie Park, NSW, Australia Giampaolo Casella  Giampaolo Casella Department of Anesthesia and Intensive Care, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Gianluca Cassese  Department of Clinical Medicine and Surgery, Division of HPB, Minimally Invasive and Robotic Surgery, Transplantation Service, Federico II University Hospital, Naples, Italy Simone Cassin  Department of Biomedical and Clinical Sciences “L. Sacco”, Università degli Studi di Milano, Milan, Italy Francesco  Cavaliere  Interdisciplinary Centre for Nanostructured Materials and Interfaces (CIMAINA), Physics Department, University of Milan, Milan, Italy Daniel  Cavanaugh  Division of Spine Surgery, Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD, USA Matteo Cazzaniga  Vascular Surgery Unit, ASST Grande Ospedale Metropolitano Niguarda Hospital, Milan, Italy Serena Celani  Università degli studi di Roma La Sapienza, Rome, Italy Giorgio  Chevallard Neurointensive Care Unit, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Osvaldo Chiara  Department of Pathophysiology and Transplantation, General Surgery and Trauma Team, University of Milano, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy General Surgery and Trauma Team, ASST Grande Ospeale Metropolitano Niguarda, Milan, Italy Massimo  Chiarugi  General, Emergency and Trauma Surgery Department, Pisa University Hospital, Pisa, Italy Enrico  Cicuttin General, Emergency and Trauma Surgery Department, Pisa University Hospital, Pisa, Italy

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Stefania Cimbanassi  Department of Pathophysiology and Transplantation, General Surgery and Trauma Team, University of Milano, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy General Surgery and Trauma Team, ASST Grande Ospeale Metropolitano Niguarda, Milan, Italy Camilla Ciscato  Department of Gastroenterology, ASST Ovest Milanese, Legnano, Italy Antonella M. Citterio  Burn Unit and Plastic Surgical Department, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Robyn Clay-Williams  Australian Institute of Health Innovation, Faculty of Medicine, Health and Human Sciences, Macquarie University, Macquarie Park, NSW, Australia Federico  Coccolini  General, Emergency and Trauma Surgery Department, Pisa University Hospital, Pisa, Italy Bianca M. Conti  R Adams Cowley Shock Trauma Center, Division of Trauma Anesthesiology, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD, USA Alessandro  Costetti Department of Cardiac Surgery and Heart Transplantation, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Boris Cox  Division of Anesthesiology, Perioperative Medicine, Emergency- and Critical Care Medicine, Department of Anesthesiology and Pain Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands Camilla Cremonini  General, Emergency and Trauma Surgery Department, Pisa University Hospital, Pisa, Italy Miguel A. Cubano  United States Navy Medical Corp., Navy Medical Center, San Diego, CA, USA Uniformed Services University of the Health Sciences, F. Edward Hébert School of Medicine, Walter Reed National Military Medical Center, Bethesda, MD, USA Antonietta Cuccì  Vascular Surgery Unit, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Annabella Curaba  Department of Hematology, Oncology and Molecular Medicine, ASST Grande Ospedale Metropolitano, Niguarda Cancer Center, Milan, Italy Department of Oncology and Hemato-Oncology, Università degli Studi di Milano (La Statale), Milan, Italy Elena Clerici  Università degli Studi di Milano-Bicocca, Milan, Italy Ilenia D’Alessio  Università degli Studi di Milano, Milan, Italy Parinaz  J.  Dabestani Department of Surgery, Creighton University, Medical School, Bethesda, MD, USA Erika  De  Febis Vascular Surgery Unit, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy S.C.  Chirurgia Vascolare, Dipartimento Cardiotoracovascolare, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Paolo Dell’Oglio  Department of Urology, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy

Contributors

Contributors

xix

Demetrios  Demetriades Division of Trauma, Emergency Surgery, and Surgical Critical, LAC+USC Medical Center, University of Southern California, Los Angeles, CA, USA Joshua Dilday  University of Southern California+Los Angeles Medical Center, Los Angeles, CA, USA Sandro Luigi Di Domenico  Department of Emergency Medicine, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy James A. DiNardo  Department of Anesthesiology, Critical Care and Pain Medicine, Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA Lorenzo Dioscoridi  Digestive and Interventional Endoscopy Unit, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Arnaldo  Dubin Sanatorio Otamendi, Buenos Aires, Argentina Cátedras de Farmacología Aplicada y Terapia Intensiva, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, La Plata, Argentina Patrick Andreas Eder  Zentrum für Telemedizin Bad Kissingen, Bad Kissingen, Germany Andrea Farina  Division of Cardiology, Manzoni Hospital, Lecco, Italy Antonio Fiore , MD  Department of Cardiac Surgery, Hôpitaux Universitaires Henri Mondor, Assistance Publique-Hôpitaux de Paris, Créteil, France Department of Cardiac Surgery, APHP, Mondor, France Sapienza University of Rome, Roma, France Department of Cardiothoracic Surgery, Henry Modor University Hospital. AP-HP, Paris-Est University, Créteil, Italy Lee A. Fleisher  Department of Anesthesiology & Critical Care, Hospital of the University of Pennsylvania, Philadelphia, PA, USA Antonello Forgione  Unit of Division of Oncologic and Mini-invasive General Surgery, ASST Grande Ospedale Metropolitano, Niguarda Hospital, Milan, Italy Carine  Foz Department of Anesthesiology, Critical Care and Pain Medicine, Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA Roberto Fumagalli  University of Milano-Bicocca, Milan, Italy Department of Anesthesia and Intensive Care, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy School of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy Antonio Galfano  Department of Urology, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Pietro Gambitta  Department of Gastroenterology, ASST Ovest Milanese, Legnano, Italy Andrea De Gasperi, MD  Service Anesthesia and Critical Care Medicine, Niguarda Hospital, Milan, Italy Giuseppe  Gatti Division of Cardiac Surgery, Cardio-Thoracic and Vascular Department, Trieste University Hospital, Trieste, Italy Pietro Gemma  Diagnostic Radiology, ASST GOM Niguarda, Milan, Italy Alessandro Giacomoni  General Surgery and Transplantation Unit, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy

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Mariano  Cesare  Giglio  Department of Clinical Medicine and Surgery, Division of HPB, Minimally Invasive and Robotic Surgery, Transplantation Service, Federico II University Hospital, Naples, Italy Andrew K. Gold  Department of Anesthesiology & Critical Care, Hospital of the University of Pennsylvania, Philadelphia, PA, USA Antonino Massimiliano Grande , MD  Department of Cardiac Surgery, IRCCS Fondazione Policlinico San Matteo, Pavia, Italy Paul  Gravestock Department of Urology, Freeman Hospital, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK Pierpaolo Graziotti  San Giuseppe Hospital, MultiMedica Group, Milan, Italy Areg  Grigorian Division of Trauma, Burns and Surgical Critical Care, University of California, Irvine, Orange, CA, USA Monica  Gualtierotti Oncological and Miniinvasive Surgery Department, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Riccardo  Guelfi General, Emergency and Trauma Surgery Department, Pisa University Hospital, Pisa, Italy Melike  N.  Harfouche R Adams Cowley Shock Trauma Center, University of Maryland Medical Center, Baltimore, MD, USA Phil  Haslam Department of Radiology, Freeman Hospital, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK Sharon Henry  University of Maryland School of Medicine, University of Maryland Medical Center R Adams Cowley Shock Trauma Center, Baltimore, MD, USA John B. Holcomb  Division of Acute Care Surgery, Department of Surgery, Center for Injury Science, University of Alabama at Birmingham, Birmingham, AL, USA Venerina Imbesi  Department of Gastroenterology, ASST Ovest Milanese, Legnano, Italy Michele  Introna Department of Anesthesiology and Intensive Care Medicine, Cremona Hospital, Cremona, Italy Raja  Kalaiarasi  Department of Otorhinolaryngology, Jawaharlal Institute of Postgraduate Medical Education & Research (JIPMER), Pondicherry, India Riyad  Karmy-Jones  Divisions of Thoracic and Vascular Surgery, PeaceHealth Southwest Washington Medical Center, Vancouver, WA, USA Trauma/Critical Care, Legacy Emanuel Medical Center, Portland, OR, USA Ramasamy Karthikeyan  Department of ENT, Jawaharlal Institute of Postgraduate Medical Education & Research (JIPMER), Karaikal, India John  J.  Kessler  Department of Surgery, Creighton University, Medical School, Bethesda, MD, USA Sibylle  A.  Kietaibl Department of Anesthesia and Intensive Care, Evangelical Hospital Vienna, Vienna, Austria Sigmund Freud Private University, Campus Prater, Medical Faculty, Vienna, Austria Aris Koryllos  Department of Thoracic Surgery, Florence Nightingale Hospital, Düsseldorf, Germany Quirino Lai  Università degli studi di Roma La Sapienza, Rome, Italy

Contributors

Contributors

xxi

Giovanni  Landoni Department of Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy Vita-Salute San Raffaele University, Milan, Italy Marco  Lanfranconi Department of Cardiac Surgery and Heart Transplantation, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Ari  Leppäniemi Division of Emergency Surgery, Abdominal Center, Helsinki University Hospital Meilahti, Helsinki, Finland Giulia Lerva  Università degli Studi di Milano, Milan, Italy Alfredo  Lista Dipartimento Cardio-Toraco-Vascolare, S.C.  Chirurgia Vascolare, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy William B. Long III  Trauma/Critical Care, Legacy Emanuel Medical Center, Portland, OR, USA Corinna Ludwig  Department of Thoracic Surgery, Florence Nightingale Hospital, Düsseldorf, Germany Steven  Ludwig Division of Spine Surgery, Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD, USA Andrew B. Lumb  Department of Anaesthesia, St. James’s University Hospital, Leeds, UK Megan R. Lundeberg  Trauma/Critical Care, Legacy Emanuel Medical Center, Portland, OR, USA Panagis M. Lykoudis  3rd Department of Surgery, “Attikon” University Hospital, National & Kapodistrian University of Athens, Athens, Greece Division of Surgery & Interventional Science, University College London (UCL), London, UK Tam Mandelbaum  Department of Anesthesiology & Critical Care, Hospital of the University of Pennsylvania, Philadelphia, PA, USA Iacopo  Mangoni Department of General Surgery and Transplantation, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Giovanni Marchegiani  General and Pancreatic Surgery Unit, University of Verona Hospital Trust, Verona, Italy Anna Mariani  Department of General Surgery and Transplantation, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Silvia Mariani  Cardio-Thoracic Surgery Department, Maastricht University Medical Centre (MUMC+), Maastricht, The Netherlands Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands Fabio Daniel Masevicius  Sanatorio Otamendi, Buenos Aires, Argentina Pietro  Di Masi Department of Hematology, Oncology and Molecular Medicine, Grande Ospedale Metropolitano Niguarda, Niguarda Cancer Center, Milan, Italy Department of Oncology and Hemato-Oncology, Università degli Studi di Milano (La Statale), Milan, Italy Kazuhide  Matsushima Division of Trauma, Emergency Surgery, and Surgical Critical, LAC+USC Medical Center, University of Southern California, Los Angeles, CA, USA

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Giulia  Mazzoleni Interdisciplinary Centre for Nanostructured Materials and Interfaces (CIMAINA), Physics Department, University of Milan, Milan, Italy Nicolò  Castelli  NeuroSim Center and First Division of Neurosurgery, IRCCS Foundation Carlo Besta Neurological Institute, Milan, Italy Bruno Merlanti  Department of Cardiac Surgery, Niguarda Hospital, Milan, Italy Paolo  Milani Interdisciplinary Centre for Nanostructured Materials and Interfaces (CIMAINA), Physics Department, University of Milan, Milan, Italy Nicola Monzio Compagnoni  Vascular Surgery Unit, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy S.C.  Chirurgia Vascolare, Dipartimento Cardiotoracovascolare, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Michele  G.  Mondino Cardiovascular and Thoracic Intensive Care Unit and Anaesthesia, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Luca Moraldi  Division of Oncologic Surgery and Robotics, Departmet of Oncology, Azienda Ospedaliero Universitaria di Reggi, Florence, Italy Francesco Morelli  Interventional Radiology, AAST GOM Niguarda, Milan, Italy Massimiliano  Mutignani Digestive and Interventional Endoscopy Unit, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Arjun  Nambiar Department of Urology, Freeman Hospital, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK Angelo Naselli  San Giuseppe Hospital, MultiMedica Group, Milan, Italy Viviane  G.  Nasr  Department of Anesthesiology, Critical Care and Pain Medicine, Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA Sandra  Nonini Cardiovascular and Thoracic Intensive Care Unit and Anaesthesia, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Giorgio Novelli  O.U. Maxillofacial Surgery, Department of Medicine and Surgery, School of Medicine, ASST-Monza, San Gerardo Hospital-University of Milano-Bicocca, Monza, Italy Maria  Teresa  Occhiuto Vascular Surgery Unit, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Dipartimento Cardio-Toraco-Vascolare, S.C.  Chirurgia Vascolare, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Isabella Oliva  San Giuseppe Hospital, MultiMedica Group, Milan, Italy Caroloandrea  Orcese Department of Infectious Diseases, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Alessandro Maria Paganini  Università degli studi di Roma La Sapienza, Rome, Italy Emanuela  Paradiso Cardiovascular and Thoracic Intensive Care Unit and Anaesthesia, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Nikolaos  Pararas 3rd Department of Surgery, “Attikon” University Hospital, National & Kapodistrian University of Athens, Athens, Greece Dr Sulaiman Al-Habib Medical Group, Riyadh, Saudi Arabia

Contributors

Contributors

xxiii

Christopher  R.  Parrino R Adams Cowley Shock Trauma Center, Division of Trauma Anesthesiology, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD, USA Alessandro Perin  NeuroSim Center and First Division of Neurosurgery, IRCCS Foundation Carlo Besta Neurological Institute, Milan, Italy Giampaolo Perri  General and Pancreatic Surgery Unit, University of Verona Hospital Trust, Verona, Italy Federico  Pezzotta Interdisciplinary Centre for Nanostructured Materials and Interfaces (CIMAINA), Physics Department, University of Milan, Milan, Italy Andreas Pikoulis  3rd “Attikon” University Hospital, National & Kapodistrian University of Athens, Athens, Greece Emmanouil Pikoulis  3rd Department of Surgery, “Attikon” University Hospital, National & Kapodistrian University of Athens, Athens, Greece Luca  Pogliani Thoracic Surgery Department, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Silvia Quaresima  Università degli studi di Roma La Sapienza, Rome, Italy Antonio  Rampoldi Interventional Radiology, AAST Grande Ospedale Metropolitano Niguarda, Milan, Italy Sofia Rantas  Department of Biomedical and Clinical Sciences “L. Sacco”, Università degli Studi di Milano, Milan, Italy Chiara  Maria  Ranucci  Department of Digestive and Emergency Surgery, Hospital Santat Maria di Terni, Università degli studi di Perugia, Perugia, Italy Asarnusch Rashid  Zentrum für Telemedizin Bad Kissingen, Bad Kissingen, Germany Aeyal Raz  Department of Anesthesiology, Rambam Health Care Campus, Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel The Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel Stéphane  Renaud Department of Thoracic Surgery, Nancy Regional University Hospital, Nancy, France Justin  E.  Richards R Adams Cowley Shock Trauma Center, Division of Trauma Anesthesiology, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD, USA Pierantonio Rimoldi  S.C. Chirurgia Vascolare, Dipartimento Cardiotoracovascolare, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Alessandro Rinaldo  Thoracic Surgery Department, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Francesco  Rizzetto Department of Radiology, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Postgraduate School of Diagnostic and Interventional Radiology, Università degli Studi di Milano, Milan, Italy Agostino Roasio  Anaesthesia and Intensive Care Service, Cardinal Massaia Hospital, Asti, Italy Elena Roselli  Service Anesthesia and Critical Care Medicine, Niguarda Hospital, Milan, Italy

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Massimo Rossi  Università degli studi di Roma La Sapienza, Rome, Italy UOC Chirurgia epatobiliare e Trapianti d’Organo, Rome, Italy Lucrezia  Rovati  School of Medicine and Surgery, University of Milano-Bicocca, Milano, Italy Emergency Department, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Claudio F. Russo  Department of Cardiac Surgery, Niguarda Hospital, Milan, Italy Department of Cardiac Surgery and Heart Transplantation, Milan, Italy Antonio Salsano , MD  Department of Surgical Sciences and Integrated Diagnostics (DISC), University of Genova, Genoa, Italy Gianluca Sampogna  Neuro-Urology Service, Unipolar Spinal Unit, ASST Grande Ospedale Metropolitano Niguarda, University of Milan, Milan, Italy ASST Grande Ospedale Metropolitano Niguarda, Unicersità degli Studi di Milano, Milan, Italy Fabio Sangalli  University of Milano-Bicocca, Milan, Italy Department of Anesthesia and Intensive Care, ASST Valtellina e Alto Lario, Sondrio, Italy School of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy Tommaso Santaniello  Interdisciplinary Centre for Nanostructured Materials and Interfaces (CIMAINA), Physics Department, University of Milan, Milan, Italy Andrea  Sartore-Bianchi  Department of Hematology, Oncology and Molecular Medicine, Grande Ospedale Metropolitano Niguarda, Niguarda Cancer Center, Milan, Italy Salomone Di Saverio  Università degli studi di Roma La Sapienza, UOC General Surgery, Hospital Madonna Del Soccorso, San Benedetto del Tronto, Italy Stefano Savonitto  Division of Cardiology, Manzoni Hospital, Lecco, Italy Thomas  M.  Scalea University of Maryland School of Medicine, University of Maryland Medical Center R Adams Cowley Shock Trauma Center, Baltimore, MD, USA Joseph  Seitlinger Department of Thoracic Surgery, Nancy Regional University Hospital, Nancy, France Salvatore  Siena Department of Hematology, Oncology and Molecular Medicine, Grande Ospedale Metropolitano Niguarda, Niguarda Cancer Center, Milan, Italy Department of Oncology and Hemato-Oncology, Università degli Studi di Milano (La Statale), Milan, Italy Valerie  Smit-Fun Division of Anesthesiology, Perioperative Medicine, Emergency- and Critical Care Medicine, Department of Anesthesiology and Pain Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands Marco Solcia  Interventional Radiology, AAST GOM Niguarda, Milan, Italy Davide Sozzi  O.U. Maxillofacial Surgery, Department of Medicine and Surgery, School of Medicine, ASST-Monza, San Gerardo Hospital-University of Milano-Bicocca, Monza, Italy Michele  Spinelli Neuro-Urology Service, Unipolar Spinal Unit, ASST Grande Ospedale Metropolitano Niguarda, University of Milan, Milan, Italy Enrico Storti  Department of Anesthesiology and Intensive Care Medicine, Cremona Hospital, Cremona, Italy

Contributors

Contributors

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Giuseppe  Talamonti Department of Neurosurgery, ASST-GOM Niguarda, Niguarda Hospital, Milan, Italy Dario  Tartaglia General, Emergency and Trauma Surgery Department, Pisa University Hospital, Pisa, Italy Giovanni Domenico Tebala  UOC Chirurgia digestiva e D’Urgenza Terni, Rome, Italy Alexandra E. Thomson  Division of Spine Surgery, Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD, USA Andrew  Thorpe Department of Urology, Freeman Hospital, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK Matti  Tolonen Division of Emergency Surgery, Abdominal Center, Helsinki University Hospital and University of Meilahti, Helsinki, Finland Valerio Tolva  S.C. Chirurgia Vascolare, Dipartimento Cardiotoracovascolare, ASST Grande Ospedale Metropolitano Niguarda, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Valerio  Stefano  Tolva Vascular Surgery Unit, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Federico Tomassini  General and Emergency Surgery Unit, GB Grassi Hospital, Rome, Italy Postdoc II Level Master Federico II University, Naples, Italy Massimo  Torre Thoracic Surgery Department, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Rachele  Tortorella S C Neurologia e Stroke Unit, Dipartimento di Neuroscienze, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Paola  Tracanelli S.C.  Chirurgia Vascolare, Dipartimento Cardiotoraco-vascolare, ASST Grande Ospedale Metropolitano Niguarda, Vimercate, Italy Vascular Surgery, ASST Vimercate, Vimercate, Italy Matteo Tripepi  Department of General Surgery and Transplantation, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Roberto Ivan Troisi  Division of HPB, Minimally Invasive and Robotic Surgery, Federico II University Hospital, Naples, Italy Department of Clinical Medicine and Surgery, Division of HPB, Minimally Invasive and Robotic Surgery, Transplantation Service, Federico II University Hospital, Naples, Italy Irene Urciuoli  Surgical Oncology and Robotics, Careggi University Hospital, Florence, Italy Angelo Vanzulli  Department of Radiology, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Department of Oncology and Hemato-Oncology, Università degli Studi di Milano, Milan, Italy Rajan  Veeratterapillay Department of Urology, Freeman Hospital, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK Maurizio Vertemati  Department of Biomedical and Clinical Sciences “L. Sacco”, Università degli Studi di Milano, Milan, Italy CIMaINa (Interdisciplinary Centre for Nanostructured Materials and Interfaces), Università degli Studi di Milano, Milan, Italy Federico Vezzulli  Department of Biomedical and Clinical Sciences “L. Sacco”, Università degli Studi di Milano, Milan, Italy

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Anne Willers  Cardio-Thoracic Surgery Department, Maastricht University Medical Centre (MUMC+), Maastricht, The Netherlands Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands Ivan  Ye Division of Spine Surgery, Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD, USA Massimo  Zacchino Emergency Department, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Mauro Zago  Division of Surgery, Manzoni Hospital, Lecco, Italy Alberto  Zangrillo Department of Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy Vita-Salute San Raffaele University, Milan, Italy

Contributors

Part I Identification and Characterisation of High-Risk Surgical Patients

1

Defining the High-Risk Surgical Patient Lucrezia Rovati, Sergio Arlati, and Paolo Aseni

Key Points • The high-risk surgical patient is defined as a patient presenting a risk of mortality or morbidity that is higher than the reference population based on epidemiological data. • Perioperative risk stratification is a complex task and depends on interactions between surgical and patient-­ specific factors. • An accurate estimation of surgical risk is important in communication with patients and their families, helping them to make informed decisions regarding the best possible care and preparing them for the possibility of adverse events. • Early recognition of high-risk patients can aid in surgical decision-making, preoperative optimization, and tailored intraoperative and postoperative management, all factors that can potentially improve patient outcomes. • Several studies have shown how the hospital volume can influence the operative mortality only for some types of interventions, such as surgery of the pancreas, the aorta, the oesophagus, and the bladder. • Multiple studies have recently demonstrated that patients undergoing emergency surgery, in particular major gastrointestinal operations, have higher rates of postoperative morbidity and mortality compared to patients undergoing elective surgery. L. Rovati (*) School of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy Emergency Department, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy e-mail: [email protected] S. Arlati Intensive Care Unit “G. Bozza”, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy e-mail: [email protected] P. Aseni Dipartimento di Emergenza Urgenza, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy Department of Biomedical and Clinical Sciences “L. Sacco”, Università degli Studi di Milano, Milan, Italy

• Patient-specific risk factors might impact morbidity and mortality differently in emergency versus elective surgery. • The simplest and most widely used method to assess perioperative risk is the American Society of Anesthesiologists Physical Status (ASA-PS) classification. • Haemodynamic instability can trigger vital organ hypoperfusion and dysfunction, leading to several serious consequences, mainly due to cellular oxygen debt; for these reasons haemodynamic optimization before and during surgery with the use of goal-directed fluid therapy and vasoactive drugs to improve tissue perfusion can be crucial in decreasing surgical risk. Surgical risk perception in clinical practice is often based on subjective impressions regarding the probability that a specific surgical procedure will be successful and that the patient will be able to return to his baseline daily activities. However, the patient, his family, the surgeon, the anaesthesiologist, the intensivist, and the hospital administrator are all likely to perceive risk in entirely different ways, leading to communication difficulties and profound misunderstandings. The importance of an objective assessment of surgical risk derives from the fact that perioperative morbidity and mortality remain largely clustered in a relatively small group of high-risk surgical patients [1]. Early recognition of high-­ risk patients can aid surgical decision-making, preoperative optimization, and tailored intraoperative and postoperative management, which can potentially improve outcomes [2]. In addition, estimation of risk is important in communication with patients and their families, helping them to make informed decisions regarding their care and preparing them for the possibility of adverse events [3]. At an institutional level, the assessment of risk can be used to guide the allocation of resources, both financially and in terms of personnel and facilities. Finally, risk assessment can be used as part of a standardization tool to allow the comparison of outcomes between different hospitals that are undertaking similar procedures [4].

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 P. Aseni et al. (eds.), The High-risk Surgical Patient, https://doi.org/10.1007/978-3-031-17273-1_1

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We will define at ‘high risk’ any surgical patient that presents a risk of mortality or morbidity, particularly with regard to organ failure, that is higher than the reference population based on epidemiological data. In practical terms, according to the Royal College of Surgeons (RCS) of England, high-­ risk patients can be defined by predicted hospital mortality of ≥5% [5]. The RCS 2018 guidelines recommend that where any of the recognized appropriate risk prediction tools, frailty assessment, or clinical judgement results in an ­assessment of predicted hospital mortality of ≥5% the patient should be managed as high risk [6]. Perioperative risk stratification is complex and depends on interactions between surgical and patient-specific factors [7]. Risk factors related to the surgery include the type of surgical procedure, whether that procedure is undertaken in an elective or an emergency fashion, and the experience of the centre and surgeon performing the procedure. Regarding this last point, different studies have shown how the hospital volume can influence the operative mortality only for some types of interventions, such as surgery of the pancreas, the aorta, the oesophagus, and the bladder [8]. Far more critical when evaluating operative risk is the distinction between emergency and elective procedures. In general, emergency surgery is widely recognized as inherently riskier than non-­ emergency surgery because of the acuity of illness and the associated time sensitivity that prevents patient preoperative optimization [9]. Multiple studies have recently demonstrated that patients undergoing emergency surgery, in particular major gastrointestinal operations, have higher rates of postoperative morbidity and mortality compared to patients undergoing elective surgery [10–15]; as an example, mortality rates following emergency laparotomy are reported in a range of 13–18% at 30 days, compared to an average 90-day mortality of 1.8% for elective colon cancer resection [16– 19]. Therefore, emergency surgery remains an independent risk factor for perioperative adverse outcomes even after adjusting for relevant preoperative and intraoperative risk factors. Moreover, individual risk factors might impact morbidity and mortality differently in emergency versus elective surgery [9]. Patient-specific risk factors comprise age, comorbidities, physiologic reserve, and primary diagnosis. The history and physical exam are key components in identifying these risk factors. Patients who are at high risk for surgery comprise those who are older than 65 years, those who had a previous severe cardio-respiratory illness, dialysis-dependent patients, insulin-dependent diabetes mellitus patients, immunosuppressed patients, cirrhotic patients, class 2 and 3 obese patients (BMI ≥ 35 kg/m2), and pregnant patients. Moreover, it is of crucial importance to evaluate the presence of sepsis,

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acute organ dysfunction, or shock with elevated lactate levels at the time of surgery, since these factors carry a very high burden on patient outcomes [5]. Different tools can be used for perioperative general risk stratification; however, the simplest and most widely used is the American Society of Anesthesiologists Physical Status (ASA-PS) classification. This score was originally introduced in 1941 and was modified in 1963 when the number of grades was reduced from seven to five [20, 21]. More recently, a sixth category and an additional suffix, ‘E’ for emergency operations, have been added. Class assignment is independent of the type of surgical procedure and is based solely on subjective assessment by the anaesthesiologist of a patient’s overall health status. This subjectivity leads to significant inter-operator variability in ASA-PS scoring; in addition, this classification does not incorporate surgery-­ specific risks and has diminished accuracy in settings with high overall mortality rates [22]. Despite its limitations, ASA-PS scoring remains useful, and it has been shown to be predictive of both postoperative complications and mortality after non-cardiac surgery; in particular, an ASA-PS score of IV and V will independently identify high-risk patients [23]. Other more complex scoring systems, freely available on the internet, have shown a greater prognostic accuracy compared to the ASA-PS classification, both for the prediction of overall operative morbidity and mortality and for the estimation of the risk of major adverse cardiovascular events [24]. Some of these scores include operative details and can be updated at the end of surgery. Some examples comprise the Physiological and Operative Severity Score for the Enumeration of Mortality and Morbidity (POSSUM) and its modification P-POSSUM, the Surgical Apgar Score, the Revised Cardiac Risk Index, and the American College of Surgeons’ National Surgical Quality Improvement Program Risk Calculators [3, 25–27]. There are no prospective trials directly comparing these perioperative risk assessment tools, but their strengths and weaknesses have been shown in different observational studies. The choice of the scoring system mainly depends on hospital practices; however, we must consider that these scores suffer from many limitations when applied to a single patient for individualized preoperative prediction of outcomes. Perioperative risk in elective patients can be further assessed by the measurement of physiological reserve. International societies recommend a cut-off below four metabolic equivalents to guide specialized preoperative cardiac testing for intermediate-to-high-risk surgeries [28]. Evaluation of functional capacity can be done by asking the patient to self-report his functional status, using the Duke Activity Status Index questionnaire, or performing a cardiopulmonary exercise test, which is considered the gold stan-

1  Defining the High-Risk Surgical Patient

dard [29, 30]. Finally, it is recommended to monitor natriuretic peptides and troponins pre- and postoperatively to enhance cardiac risk estimation [31]. Increasingly more important with population aging, is the evaluation of frailty level through a recognized assessment tool, such as the Clinical Frailty Scale and modified Frailty Index. Frailty has been recognized as a prognostic indicator of postoperative outcomes and discharge destination, complementing perioperative risk assessment by capturing functional domains that are missed by traditional risk assessment tools [32]. In addition, all patients aged over 65 years undergoing inpatient elective or emergency surgery should be screened for the risk of perioperative neurocognitive ­disorders using a tool such as the AWOL score for delirium (a mnemonic standing for Age ≥ 80 years, failure to spell “World” backwards, disOrientation to place, and higher nurse-rated iLlness severity) or the 4AT, a screening instrument designed for rapid initial assessment of delirium and cognitive impairment using four test domains. Evidence-­based approaches should be instituted to reduce the incidence of acute postoperative delirium, to minimize its severity, and to reduce the risk of longer term consequences [6]. In summary, it is recommended that surgical patients have their risk of morbidity and mortality assessed and documented in the medical records using appropriate risk prediction tools and clinical judgement. Frailty, the likelihood of perioperative neurocognitive disorders, and the type and urgency of surgery should be taken into account during this assessment, as these may not be adequately reflected in existing risk prediction tools. The risk should be reassessed and recorded again after operative interventions and after any patient deterioration; any change should prompt an appropriate adjustment in patient care [6]. Indeed, accurate and timely identification of high-risk surgical patients is required for optimizing their care through improved preoperative evaluation and perioperative management. Many observational cohort and quality improvement studies involving high-risk surgical patients are available in the literature; however, no randomized trials comparing the results of different standards of care have been performed so far. Key components in the management of high-risk surgical patients include the use of specialized investigations and referral to medical specialists before elective surgery to reduce the impact of medical comorbidities [33]. In addition, screening for sepsis and managing it according to updated guidelines remain crucial in emergency surgery [34]. Since perioperative management of high-risk surgical patients is a complex process, these patients should receive adequate peri- and postoperative monitoring with a possibility to be admitted to the intensive care unit [35]. Haemodynamic optimization before and during surgery with

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the use of goal-directed fluid therapy and vasoactive drugs to improve tissue perfusion is crucial in decreasing surgical risk [36]. Indeed, haemodynamic instability can trigger vital organ hypoperfusion and dysfunction, leading to several serious consequences, mainly due to cellular oxygen debt. Any alteration that impacts macrocirculation should be followed by therapeutic measures that improve microcirculatory perfusion and ensure adequate oxygen delivery to the cells. Therefore, adequate monitoring-guided early interventions are necessary to avoid severe postoperative complications. Conventional indices, including heart rate, blood pressure, skin temperature, and urine output, have limited value in diagnosing compensated shock, and advanced haemodynamic monitoring may sometimes become necessary in high-risk patients undergoing major or emergency surgical procedures. Clinical observations and physiological considerations support the view that oxygen debt is the major determinant of perioperative morbidity and mortality. After Shoemaker’s ground-breaking trial in 1988 using pulmonary artery catheter to monitor cardiac index, a new concept was introduced [37]. A goal-directed management to optimize oxygen delivery by monitoring cardiac index and guiding interventions to supra-normal values during major surgery was adopted. Several trials have been conducted using this strategy on different patient populations evaluating mortality, morbidity, length of stay, and specific postoperative complications. Some meta-analyses showed that this perioperative goal-­ directed therapy was effective in reducing postoperative complications in high-risk surgical patients in cardiac and non-cardiac surgery, but failed to show the same benefit in vascular surgery and did not show any significant benefit in reducing rates of complications and mortality in the lower risk population among the high-risk surgical patients [38, 39]. However, putting the puzzle of haemodynamic stabilization together requires a complex approach. The challenge of the future is to provide clinicians with better tools to select the appropriate level of monitoring for high-risk patients with several alternatives, from simple, non-invasive continuous monitoring to advanced, invasive haemodynamic assessment [40]. In conclusion, the definition of the high-risk surgical patient is a complex but essential process in modern clinical practice. Risk assessment allows easier communication within the multidisciplinary team and in discussion with the patient and his family; moreover, it is fundamental to optimize perioperative care of high-risk patients. In the future, the development of more accurate methods to assess and predict risk and the conduct of clinical trials to compare different standards of care will be needed to further improve patient outcomes.

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References 1. Pearse RM, Harrison DA, James P, Watson D, Hinds C, Rhodes A, Grounds RM, Bennett ED. Identification and characterisation of the high-risk surgical population in the United Kingdom. Crit Care. 2006;10(3):R81. 2. Moonesinghe SR, Mythen MG, Das P, Rowan KM, Grocott MP. Risk stratification tools for predicting morbidity and mortality in adult patients undergoing major surgery: qualitative systematic review. Anesthesiology. 2013;119(4):959–81. 3. Bilimoria KY, Liu Y, Paruch JL, Zhou L, Kmiecik TE, Ko CY, Cohen ME.  Development and evaluation of the universal ACS NSQIP surgical risk calculator: a decision aid and informed consent tool for patients and surgeons. J Am Coll Surg. 2013;217(5):833– 42. e831–3. 4. Boyd O, Jackson N. Clinical review: how is risk defined in high-­ risk surgical patient management? Crit Care. 2005;9(4):390. 5. Royal College of Surgeons of England, Department of Health. The higher risk general surgical patient: towards improved care for a forgotten group. London: RCSE; 2011. 6. Royal College of Surgeons of England. The high-risk general surgical patient: raising the standard. London: RCSE; 2018. 7. Sankar A, Beattie WS, Wijeysundera DN. How can we identify the high-risk patient? Curr Opin Crit Care. 2015;21(4):328–35. 8. Finks JF, Osborne NH, Birkmeyer JD.  Trends in hospital volume and operative mortality for high-risk surgery. N Engl J Med. 2011;364(22):2128–37. 9. Bohnen JD, Ramly EP, Sangji NF, de Moya M, Yeh DD, Lee J, Velmahos GC, Chang DC, Kaafarani HM. Perioperative risk factors impact outcomes in emergency versus nonemergency surgery differently: time to separate our national risk-adjustment models? J Trauma Acute Care Surg. 2016;81(1):122–30. 10. Ingraham AM, Cohen ME, Bilimoria KY, Raval MV, Ko CY, Nathens AB, Hall BL. Comparison of 30-day outcomes after emergency general surgery procedures: potential for targeted improvement. Surgery. 2010;148(2):217–38. 11. Ingraham AM, Cohen ME, Bilimoria KY, Feinglass JM, Richards KE, Hall BL, Ko CY. Comparison of hospital performance in nonemergency versus emergency colorectal operations at 142 hospitals. J Am Coll Surg. 2010;210(2):155–65. 12. Becher RD, Hoth JJ, Miller PR, Mowery NT, Chang MC, Meredith JW. A critical assessment of outcomes in emergency versus nonemergency general surgery using the American College of Surgeons National Surgical Quality Improvement Program database. Am Surg. 2011;77(7):951–9. 13. Akinbami F, Askari R, Steinberg J, Panizales M, Rogers SO Jr. Factors affecting morbidity in emergency general surgery. Am J Surg. 2011;201(4):456–62. 14. Havens JM, Peetz AB, Do WS, Cooper Z, Kelly E, Askari R, Reznor G, Salim A. The excess morbidity and mortality of emergency general surgery. J Trauma Acute Care Surg. 2015;78(2): 306–11. 15. Saunders DI, Murray D, Pichel AC, Varley S, Peden CJ, Network UKEL. Variations in mortality after emergency laparotomy: the first report of the UK emergency laparotomy Network. Br J Anaesth. 2012;109(3):368–75. 16. Vester-Andersen M, Lundstrom LH, Moller MH, Waldau T, Rosenberg J, Moller AM, Danish Anaesthesia D.  Mortality and postoperative care pathways after emergency gastrointestinal surgery in 2904 patients: a population-based cohort study. Br J Anaesth. 2014;112(5):860–70. 17. Al-Temimi MH, Griffee M, Enniss TM, Preston R, Vargo D, Overton S, Kimball E, Barton R, Nirula R. When is death inevitable after emergency laparotomy? Analysis of the American College of Surgeons National Surgical Quality Improvement Program database. J Am Coll Surg. 2012;215(4):503–11.

L. Rovati et al. 18. Symons NR, Moorthy K, Almoudaris AM, Bottle A, Aylin P, Vincent CA, Faiz OD.  Mortality in high-risk emergency general surgical admissions. Br J Surg. 2013;100(10):1318–25. 19. Association of Coloproctology of Great Britain and Ireland, Royal College of Surgeons of England, Health and Social Care Information Centre. National Bowel Cancer Audit annual report 2017, version 2. London: Health and Social Care Information Centre; 2017. 20. Saklad M.  Grading of patients for surgical procedures. Anesthesiology. 1941;2(3):281–4. 21. Horvath B, Kloesel B, Todd MM, Cole DJ, Prielipp RC.  The evolution, current value, and future of the American Society of Anesthesiologists Physical Status Classification System. Anesthesiology. 2021;135(5):904–19. 22. Knuf KM, Maani CV, Cummings AK.  Clinical agreement in the American Society of Anesthesiologists physical status classification. Perioper Med (Lond). 2018;7:14. 23. Koo CY, Hyder JA, Wanderer JP, Eikermann M, Ramachandran SK.  A meta-analysis of the predictive accuracy of postoperative mortality using the American Society of Anesthesiologists’ physical status classification system. World J Surg. 2015;39(1):88–103. 24. Bose S, Talmor D. Who is a high-risk surgical patient? Curr Opin Crit Care. 2018;24(6):547–53. 25. Prytherch DR, Whiteley MS, Higgins B, Weaver PC, Prout WG, Powell SJ. POSSUM and Portsmouth POSSUM for predicting mortality. Physiological and operative severity score for the enumeration of mortality and morbidity. Br J Surg. 1998;85(9):1217–20. 26. Gawande AA, Kwaan MR, Regenbogen SE, Lipsitz SA, Zinner MJ.  An Apgar score for surgery. J Am Coll Surg. 2007;204(2):201–8. 27. Lee TH, Marcantonio ER, Mangione CM, Thomas EJ, Polanczyk CA, Cook EF, Sugarbaker DJ, Donaldson MC, Poss R, Ho KK, Ludwig LE, Pedan A, Goldman L. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation. 1999;100(10):1043–9. 28. Fleisher LA, Fleischmann KE, Auerbach AD, Barnason SA, Beckman JA, Bozkurt B, Davila-Roman VG, Gerhard-Herman MD, Holly TA, Kane GC, Marine JE, Nelson MT, Spencer CC, Thompson A, Ting HH, Uretsky BF, Wijeysundera DN, American College of Cardiology/American Heart Association. 2014 ACC/ AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association task force on practice guidelines. J Am Coll Cardiol. 2014;64(22):e77–137. 29. Wijeysundera DN, Pearse RM, Shulman MA, Abbott TEF, Torres E, Ambosta A, Croal BL, Granton JT, Thorpe KE, Grocott MPW, Farrington C, Myles PS, Cuthbertson BH. Assessment of functional capacity before major non-cardiac surgery: an international, prospective cohort study. Lancet. 2018;391(10140):2631–40. 30. Levett DZH, Jack S, Swart M, Carlisle J, Wilson J, Snowden C, Riley M, Danjoux G, Ward SA, Older P, Grocott MPW, Perioperative Exercise T, Training S.  Perioperative cardiopulmonary exercise testing (CPET): consensus clinical guidelines on indications, organization, conduct, and physiological interpretation. Br J Anaesth. 2018;120(3):484–500. 31. Biccard BM, Devereaux PJ, Rodseth RN. Cardiac biomarkers in the prediction of risk in the non-cardiac surgery setting. Anaesthesia. 2014;69(5):484–93. 32. Beggs T, Sepehri A, Szwajcer A, Tangri N, Arora RC.  Frailty and perioperative outcomes: a narrative review. Can J Anaesth. 2015;62(2):143–57. 33. Bierle DM, Raslau D, Regan DW, Sundsted KK, Mauck KF. Preoperative evaluation before noncardiac surgery. Mayo Clin Proc. 2020;95(4):807–22. 34. Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, Kumar A, Sevransky JE, Sprung CL, Nunnally ME, Rochwerg

1  Defining the High-Risk Surgical Patient B, Rubenfeld GD, Angus DC, Annane D, Beale RJ, Bellinghan GJ, Bernard GR, Chiche JD, Coopersmith C, De Backer DP, French CJ, Fujishima S, Gerlach H, Hidalgo JL, Hollenberg SM, Jones AE, Karnad DR, Kleinpell RM, Koh Y, Lisboa TC, Machado FR, Marini JJ, Marshall JC, Mazuski JE, McIntyre LA, McLean AS, Mehta S, Moreno RP, Myburgh J, Navalesi P, Nishida O, Osborn TM, Perner A, Plunkett CM, Ranieri M, Schorr CA, Seckel MA, Seymour CW, Shieh L, Shukri KA, Simpson SQ, Singer M, Thompson BT, Townsend SR, Van der Poll T, Vincent JL, Wiersinga WJ, Zimmerman JL, Dellinger RP.  Surviving sepsis campaign: international guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;43(3):304–77. 35. Aseni P, Orsenigo S, Storti E, Pulici M, Arlati S. Current concepts of perioperative monitoring in high-risk surgical patients: a review. Patient Saf Surg. 2019;13:32. 36. Futier E, Lefrant JY, Guinot PG, Godet T, Lorne E, Cuvillon P, Bertran S, Leone M, Pastene B, Piriou V, Molliex S, Albanese J, Julia JM, Tavernier B, Imhoff E, Bazin JE, Constantin JM, Pereira

7 B, Jaber S. Effect of individualized vs standard blood pressure management strategies on postoperative organ dysfunction among high-­ risk patients undergoing major surgery: a randomized clinical trial. JAMA. 2017;318(14):1346–57. 37. Shoemaker WC, Appel PL, Kram HB, Waxman K, Lee TS. Prospective trial of supranormal values of survivors as therapeutic goals in high-risk surgical patients. Chest. 1988;94(6):1176–86. 38. Giglio M, Dalfino L, Puntillo F, Rubino G, Marucci M, Brienza N.  Haemodynamic goal-directed therapy in cardiac and vascular surgery. A systematic review and meta-analysis. Interact Cardiovasc Thorac Surg. 2012;15(5):878–87. 39. Cecconi M, Corredor C, Arulkumaran N, Abuella G, Ball J, Grounds RM, Hamilton M, Rhodes A.  Clinical review: goaldirected therapy-­what is the evidence in surgical patients? The effect on different risk groups. Crit Care. 2013;17(2):209. 40. Leiner T, Tánczos K, Molnar Z.  Avoiding perioperative oxygen debt. J Emerg Crit Care Med. 2019;4:6.

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The Frail Patient in the Operating Room: Practical Steps to Reduce the Operative Risk Andrea De Gasperi, Elena Roselli, and Ombretta Amici

Key Points • Frailty is an ageing-related multidimensional syndrome associated with physiological decline, loss of homeostatic mechanisms, marked vulnerability, and reduced resistance to stressors. Frailty is more and more recognised in the older surgical patients and in candidates to solid organ transplant (SOT) surgery. • Frailty is associated, more frequently if compared to chronological age or comorbidities, with poorer outcomes in terms of morbidity, mortality, prolonged hospital stay, and increased postoperative complications. Feasible and reliable frailty assessment tools are to be implemented in the preoperative evaluation. • Clinical Frailty Scale (CFS) seems to be the most reliable, feasible, and easy-to-use instrument for the preoperative frailty assessment. Frail phenotype (FP), the most often used instrument, is as reliable as CFS but less feasible, being time consuming and relying upon extra tools to complete the score. • Identification of frailty components (physical dysfunction, malnutrition, and cognitive dysfunction) should allow perioperative optimization via a specific multimodal prehabilitation. • Prehabilitation should include exercise to improve cardiorespiratory fitness and muscle strength, appropriate nutritional support and measures able to improve attention, and cognition and mental health to reduce postoperative delirium. • Expected benefits coming from perioperative frailty management should be better outcomes, reduced hospital stay, safer discharge planning, and reduce hospital readmission.

A. De Gasperi (*) · E. Roselli · O. Amici Anesthesia and Critical Care Medicine, ASST Grande Ospedale Metropolitano, Niguarda Hospital, Milan, Italy e-mail: [email protected]; [email protected]; [email protected]

• Ongoing clinical trials in the older frail surgical patients should provide definitive and robust evidences to support these multidisciplinary interventions.

2.1 Introduction Frailty is defined as” an ageing-related multidimensional syndrome associated with a physiological decline not compensated by homeostatic mechanisms and characterized by marked vulnerability to adverse health outcome (AHO)” [1–5]. Although a consensus exists on the deficits included in the broadest definitions (reduced physical performance, poor nutritional status, impaired mental health, and impaired cognition), a consensus has not been reached, so far, on the way to “clinically” assess frailty (so-called “operationalization of measurements”). Frailty, reported in 4–16% of men and women aged 65 and older, and up to 43% of older patients with cancer, could be considered a sort of continuum, whom end-stage is often considered the “failure to thrive”, with the so-called pre-frailty status (patients at risk for frailty fulfilling some, not all, frailty criteria) ranging from 28% to 44% in individuals>65 years [1–5]. According to Veld et  al. [6], there are many ways to conceptualize frailty, but three seem to be the main approaches. Fried et al. [7] described the “frailty phenotype” (FP), addressing the decline in physical functioning: they identified five criteria widely and frequently used in clinical practice (weight loss, exhaustion, low physical activity, slowness, and weakness). Rockwood et al. [8] developed the Frailty Index (FI), a multidomain set of non-fixed clinical conditions and deficits (cognition, physical functioning, self-rated health, smoking history, and laboratory results). A simplified version of FI is the Edmonton Frail Scale [1]. The third, developed by the Groningen group, is the Groningen frailty indicator [9], again using a multiple domains approach (physical, social, and psychological) and considering a predefined set of questions to characterize the concept of frailty for each domain. As evident, the state of overall reduced functional capacity— and not comorbidities or altered laboratory or diagnostic

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 P. Aseni et al. (eds.), The High-risk Surgical Patient, https://doi.org/10.1007/978-3-031-17273-1_2

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imaging values—is crucial to make the single “frail” individual vulnerable to internal and external noxae (the surgical stress is an example). In fact, Veld et al., challenging FP in cross-sectional comparison of three frailty stages on various health domains in a cohort of 8684 community-dwelling older people (>65 years), found true frailty in close to 10% of the individuals and a “prefrailty” condition in 28% [6]. Veld et al. concluded FP criteria were to be considered, in general, helpful to identify and treat frail older people in an efficient way, being able to provide indications for risk stratification and problems resolution in other domains [6].

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2.3 Frail Assessment Tools: In Need for Feasibility to Expand the Recognition

All persons aged over 70 years and adults with chronic disease or weight loss exceeding 5% over a year should be screened for frailty using the available tools. Unfortunately, the number of the proposed instruments/scales/scores to assess preoperative frailty in the current literature is too large, and, due to frequent suboptimal feasibility (“how practical is the use of the tool in everyday clinical practice”) of part of the instruments, frailty assessment is seldom implemented in the preoperative evaluation routine 2.2 Frailty and Surgery: The Game [10]. To shed light into this specific item, very recently, Changer Aucoin et al. evaluated outcomes at the individual instrument level or specific to clinical assessment of frailty, tryFrailty in the perioperative period is gaining a relevant inter- ing to combine accuracy (how well outcomes are predicted est and an ever-greater importance, as older patients are by the tool) with feasibility to support (and possibly confiprone to surgical pathologies and more and more frequently dently expand) their use in clinical practice [1]. Aims of proposed for surgical solutions. Frailty is since long recog- this systematic review and meta-analysis of 70 studies (all nised a strong predictor of morbidity and mortality after sur- prospectively assessing preoperative frailty conditions) gery, particularly when compared to chronological age or were: (i) to perform a comparison between the different comorbidities, and is becoming a strong and reliable marker instruments; (ii) to provide the instruments with the best of severe postoperative disability and poor outcome [5]. predictive accuracy for relevant postoperative outcomes; Translating the most common definitions into the periopera- and (iii) to provide reliable, feasible, and easy-to-use instrutive setting, frailty should be considered “an aggregate ments for the clinical practice [1]. According to this expression of risk resulting from the accumulation of age-­ research, the Clinical Frailty Scale (CFS, Dalhousie and disease-related deficits across multiple domains” [5]. University, Fig. 2.1) seems to be the most reliable, feasible, The prevalence of frailty in the surgical population is as high and easy-to-use instrument for the preoperative frailty as 40% (higher if compared to the general population). Such assessment. It is easily available in the internet (i.e., in the a figure is mainly correlated with: (i) the instruments used MEDCALC app, free of charge the download, and the use) for the assessment; (ii) the type of surgery (oncologic vs. and provides, when used, the most reliable predictions of non-oncologic surgery); and (iii) urgency or emergency pro- postoperative mortality [1]. cedures [10]. Interestingly enough, odds of complications FP, the most often used instrument reported in the availfor the frail patient are greater also after “minor surgery” able literature is, according to Aucoin et  al., as reliable as (hernia, breast, and thyroid surgery). In fact, the elderly frail CFS but unfortunately less feasible, being quite time concandidate to surgery is more prone to longer hospitalization suming and relying upon extra tools to complete the score and multiple complications. Physical decline, cognitive dys- [1]. The most recent systematic review and meta-analysis on function, and reduced muscle strength can further worsen an this specific item was proposed by the same Canadian group already delicate equilibrium. According to Olutu, elderly [2]. The authors analysed 90 studies using 22 unique frailty frail patients have up to a fivefold increase in mortality and instruments derived from electronic databases and concluded an unacceptably high risk of postoperative complications, that the electronic assessment used to identify preoperative equal or above 50% [4]. Among postoperative complica- frailty might improve preoperative risk stratification and tions, delirium, a feared and not uncommon acute complica- could reliably predict postoperative outcomes. The strongest tion of the elderly surgical patient, is reported in as high as message provided by the study conclusions—if and when 50% of the frail individuals. New or relevant worsened dis- multidimensional data are applied to multidimensional abilities have a severe impact on the quality of life and auton- frailty instruments—is to confidently adhere to the most omy within the first 3  months after surgery. It is also comprehensive and broad clinical pathways utilized in the important to distinguish between absolute 30-day mortality preoperative assessment of the older surgical patients [2]. A risk (close to 5% after major, non-cardiac elective surgery) word of caution, however, was wisely provided by the and the 1-year mortality rate, which can reach 40% in case of authors, due to the need of further insights into feasibility of cancer surgery, due to the oncologic nature of the disease. the routine electronic assessment, and an eagerly awaited

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Fig. 2.1  Clinical Frailty Scale—Dalhousie University (downloaded from www.Dal.Ca, Geriatric Medicine Research). With permission of Geriatric Medicine Research https://www.dal.ca/sites/gmr/our-­tools/permission-­for-­use/thank-­you.html?status=200

head-to-head comparison of the different multidimensional instruments. Rapid screening tools are key to implement in the clinical practice frailty screening assessment and to provide alternative care plans based on the frailty profile. Among the rapid instruments to be included in the history-taking, an interesting tool is the modified “mnemonic” FRAIL scale (see below), with a binary option (0/1, NO/YES) and a score ranging from 0 to 5 (0 = best, 5 = worst) with scores of 3–5 indicating frailty, 1–2 pre-frailty, and 0 robust health status [11]:

• Illnesses (“Do you have any of these illnesses: hypertension, diabetes, cancer (other than a minor skin cancer), chronic lung disease, heart attack, congestive heart failure, angina, asthma, arthritis, stroke, and kidney disease?”) Five or > = 1; < 5 = 0. • Loss of weight (“Have you lost more than 5% of your weight in the past year?”) Yes = 1, No = 0.

• Fatigue (“Have you felt fatigued? Most or all of the time over the past month?”) Yes = 1; No = 0. • Resistance (“Do you have difficulty climbing a flight of stairs?”) Yes = 1; No = 0. • Ambulation (“Do you have difficulty walking one block?”) Yes = 1; No = 0.

Recently, Spies et al., discussing anaesthesia in the high-risk surgical patients, defined frailty as a “multidimensional syndrome”, including relevant physiological derangements, and organ system(s) dysfunction [3]. Risk is a situation or condition able to expose the individual to damage, injury, or adverse event(s): it depends on the patient state, comorbidi-

2.4 Frailty, Ageing, and the High-Risk Surgical Patient

12

ties, type, duration and context of surgery, or a combination of all [10]. The frail patient, due to the reduced functional reserve, is unable to match surgical or medical stressors, opening up the way to an heavy impact on the short- and long-term perioperative outcomes (morbidity and mortality) [3]. Frailty also predicts adverse outcomes related to renal transplantation, general surgery (elective and emergency), and cardiac surgery interventions [11]. Invasive procedures and surgery are poorly tolerated by the frail patient, due to weakness, fatigue, and sarcopenia, a multidimensional condition well beyond the profile provided by traditional medical complexities usually associated with comorbidities. This profile, independently from the single organ derangement, put the frail patient at “high risk” during the perioperative period. Interestingly, during surgery, due to an increase in oxygen demand up to 40%, patients who develop a prolonged oxygen debt die significantly more often than patients able to pay back oxygen debt within 24 (albeit developing complications) or 6  h (with no complications) [12, 13]. Patients with the frailty profile are exposed to the additional risk associated with a reduced functional reserve, with a limited, if at all, ability to match the increased physiological demand [1–5, 12, 13]. However, advanced age is not necessarily associated with frailty and/or a poor outcome [10, 14]. Despite the intrinsic risk associated with ageing, large part of the older patients survive surgery with no serious complication (>95% survival and >75% without a major complication) [10]. A reliable and comprehensive risk stratification is then eagerly awaited to further improve postoperative outcomes. The frail surgical patients have many domains in which the word “reduced” is key, making perioperative consequences relevant. Reduction of neurons and synapses, reduced basal metabolic rate, reduced muscle mass and strength (sarcopenia, the physical frailty due to muscle waisting) (respiratory muscles included), reduced renal, hepatic, cardiac and cerebral blood flow, reduced response to infections together with an increased catabolism (particularly evident in the oncologic patients), all decrease the physiological response to stress, the regenerative capacity, and the “buffer potential” able to limit the injury [3]. In a large systematic review, the prevalence of frailty in individuals over 65 years was close to 11% (confirming the figures proposed by Veld et al.) [6], but reaches 50% in subjects above 85  years [5]. More, frailty, when present, increases the chance of requiring a surgical solution to solve health problems, making quite common to propose a surgical approach in elderly and very elderly patients, but potentially starting a vicious circle (the most risky solution for the most exposed individual) [14, 15]. However, half of all the surgical procedures can now be safely performed in patients over 65 years due to reduced contraindications, technical surgical refinements and improved capacity of anaesthesiologists and intensivists to manage complex perioperative situations.

A. De Gasperi et al.

Experts in the field and evidences from the clinical practice strongly suggest that in the surgical setting improved awareness of frailty in both patients and health care providers and an appropriate “enlarged” risk stratification might favourably impact on AHOs using dedicated perioperative interventions [1–5, 10, 14, 15]. The same message is emphasized in the last update of the preoperative assessment guidelines issued by the European Society of Anaesthesiology [16]. To improve the postoperative results, a timely and correct identification of the truly high-risk patients is crucial, making mandatory not only more “usual” objective parameters (comorbidities and invasiveness of surgery), but, as early as possible in the preoperative period, also the functional reserve capacity assessment and the dedicated prehabilitation pathways, with the broadest sense prehabilitation deserves [17]. As a matter of fact, the role of preoperative frailty assessment might be more than relevant, due to the important reflexes it might have on the entire perioperative period [14, 15, 17]. According to a modern vision of the perioperative period, the main aim of the perioperative physicians (and anaesthesiologists are) should become a personalized perioperative strategy able to prepare the index patient to meet the specific stress(es) associated with the proposed surgical intervention, including all its multiple components with the goal of reducing postoperative complications and improving outcomes.

2.5 Frailty and Surgery in Elderly Patients: The New Comprehensive Paradigm As mentioned before, surgery is performed at an ever-­ increasing rate in elderly patients [10, 14, 15]. Availability of reliable, comprehensive, feasible predictors of postoperative complications (both morbidity and mortality) is mandatory to favourably impact on the outcomes. Frailty is one of the main targets of the comprehensive geriatric assessment for hospitalized older patients to determine medical, psychological, and functional capacities and their limitations [18, 19]. From a practical point of view, feasibility of this tool is, however, suboptimal, since a single evaluation takes 60–90 min and the presence of a skilled geriatrician is mandatory. As already alluded to, feasibility is key to implementing and easing this program. In the case of the elderly surgical patient, the main aim is a multidisciplinary, multitasking, comprehensive, feasible, and reliable preoperative assessment [5] to: (i) make an appropriate and personalized surgical indication, including the use of more commonly utilised indicators or markers; (ii) implement the often reported, but less often applied “prehabilitation” program(s) [17]; and (iii) define personalized perioperative pathways which must include (a) preoperative finalized specific interventions (car-

2  The Frail Patient in the Operating Room: Practical Steps to Reduce the Operative Risk

diac, biliary or intrahepatic stents if and when clinically indicated, to ease the perioperative course, anticipating possible complications); (b) pharmacological, nutritional and “mental optimization” interventions; (c) tailored surgical strategies (type and/or surgical approach); (d) intraoperative monitoring and drugs choice(s), the main duty of the anaesthesiologist; (e) level and intensity of postoperative care (ICU vs. high dependency units vs. wards); and (f) a palliative care consultation, whose main aims are to alleviate symptoms of related medical conditions and to help in considering of the appropriateness of potential medical and surgical interventions (such as chemotherapy or major surgery) and their impact on mortality and quality of life. This last point is crucial to make the care plan more transparent and clearer [20]. Subramanian et  al. [5] and Schwarze et  al. [21] recently underlined the relevance of “aligning surgical quality with outcomes, considered value(s) by the patients and their families”. According to Taylor et al., it is necessary to improve the surgeon ability to communicate with the patients and their relatives when proposing problematic surgical decisions [22]. In our opinion, this should also be a main task the of the anaesthesiologists involved in the care of the fragile patients. A framework, the best case/worst case, might promote better shared, comprehensive, inclusive decisions, discussing in a multidisciplinary setting every single problematic case, with the appropriate, wise and empathic involvement of patients and families [22]. According to Subramanian et al. [5], the multidisciplinary team should include surgeons, anaesthesiologists, geriatricians, critical care physicians, nurses, health therapists, and pharmacists. Many recent multidisciplinary programs running dedicated perioperative co-­ management of older frail surgical patients demonstrated improved outcomes with reduced functional decline, reduced delirium, reduced hospital stay, and reduced mortality [5]. However, relevant in this setting is the balance between the person’s goals and the choice of surgery: choosing wisely and with shared empathic decisions is always key.

2.6 How to Improve the Outcomes of the Older Frail Surgical Patients The identification of the frailty condition in the older (>75 years) surgical patients is the prerequisite to start a process in which rather homogeneous and high-risk patients are included in dedicated, finalized programs, and managed by a multidisciplinary team aiming at perioperative outcomes improvements. As recently underlined by McIsaac et al. [10] and Subramanian et al. [5], and as we have alluded to, frailty, being a multidimensional status with several relevant contributors, deserves different, reliable, and feasible screening tools able to define the impact every single component of frailty (physical performance, nutrition, cognition, and men-

13

tal health) might have on the patient condition [17]. The problem of comorbidities and the associated multiple drugs therapy is beyond the scope of this chapter; however, non-­ essential medications, often inappropriate if not inadequate, should be withheld, as they could constitute a potential perioperative risk for the older patients [4].

2.7 Physical Performance Pre-existing physical vulnerability, surgical stress, and postoperative reduced physical activity/immobility are responsible for a consistent loss of muscle mass (sarcopenia), even in healthy older adults undergoing surgery, even if guidelines to protect muscle mass (particularly lower limbs function during bed rest) have been proposed since long, but are not always implemented [23]. Quite recently, the American College of Surgeon National Surgical Quality Improvement Program Surgical Risk Calculator has incorporated in the calculator basic geriatric assessment measures and the level of functional dependency to predict postoperative complications, postoperative delirium, functional decline, the use of mobility aid, and the probability to be discharged to a nursing or rehabilitation facility (https://riskcalculator.facs.org/ RiskCalculator/) [12, 16, 17]. Implementing this in the preoperative assessment measures of functional capacity provides the opportunity to identify high-risk frail surgical patients and to improve their surgical recovery using multimodal prehabilitation programs [17]. Many are the instruments to quantify physical performance before surgery. Suggested in the guidelines for preoperative cardiological evaluation before non-cardiac surgery [16], the functional capacity estimating metabolic equivalents (METs) is the most used subjective assessment. METs >4 (inability to climb more than two flights of stairs) has been used for many years as the discriminator to identify “unfit” patients, this threshold being associated with poor outcomes [24]. Well-­ known by the cardiologists [25] and more recently applied by the anaesthesiologists [26] is the DASI score (a 12 items questionnaire, more objective than the subjective METs assessment). DASI score was recently challenged by Wijeysundera et al. [26] (Measurement of Exercise Tolerance before Surgery, METS) and very recently simplified and recalibrated (4–5 items questionnaire, M-DASI) by Riedel et al. [27] Both DASI and M-DASI are considered accurate and easy-to-use screening tools to identify patients without adequate functional capacity who might benefit from further testing and prehabilitation [26, 27]. McIsaac et al. [10] considered DASI worth to be used as a good screener for the frail surgical patient, since outperformed cardiopulmonary exercise testing and 6-min-walking test in predicting postoperative outcomes [27]. However, McIsaac et  al. [10] and Carli et al. [17] raised concerns on its use, at least as single

14

test, due to the inadequate challenging of the DASI scores in older frail individuals. Further studies are then needed. A time-honoured, simple and easy-to-perform test also in older frail patients, the Timed Up and Go test (TUG), could constitute an appropriate alternative for a reliable (even if broad) estimate of the functional capacity [28]. In short, the subject, standing from a chair, walks for 3 m, returns to the chair and sits. In this test, slow preoperative TUG (>15 s) is associated with an increased risk of 1-year mortality and postoperative complications [17, 28, 29]. Beyond the scope of this chapter is the description of structured exercise programs, essential for a successful prehabilitation and different from the simple “physical activity”. According to Carli et al. [17], physical activity is any body movement that results in quantifiable energy expenditure, while exercise incorporates a planned and structured program with a specific goal of improving fitness. The goal in the case of prehabilitation is a structured program with exercise intensity, frequency, and modality [17].

2.8 Nutrition Suboptimal nutritional state (or overt malnutrition) is highly represented (15–60%) in the older surgical population, cancer diagnoses, and gastrointestinal pathologies playing a relevant role. Vulnerability to every kind of stressors in the entire perioperative period is increased in the undernourished surgical patient [17]. Main consequences are a reduced chance of adequate prehabilitation, an increased risk for postoperative complications, included (among others) delirium, infections, impaired functional recovery, and preclusion of an early and aggressive postoperative rehabilitation. This is why the availability of tools to screen malnutrition (Mini Nutritional Assessment and Canadian Nutrition Screening tool, among the others) [1] is pivotal to start nutritional supplementation using both micro- and macronutrients. Amino acids utilization for anabolic purposes is reduced in elderly patients, even in the presence of resistance exercises, making high-quality protein supplementation (particularly essential amino acids, as leucine) key for a valid anabolic response, crucial for a successful multimodal prehabilitation program and essential for the postoperative exercise therapy [4, 10, 17]. For the interested readers, the 2017 ESPEN guidelines on clinical nutrition in surgery will be extremely helpful [30]. According to Carli et  al. [17], an appropriate functional capacity able to respond to the multifaceted surgical stress should rely upon some essential components of perioperative nutrition. A tentative (but not exhaustive) list should target normoglycemia, provide a protein load adequate to stimulate anabolism, provide energy sufficient to maintain body weight, promote GI tolerance, to enhance immunity.

A. De Gasperi et al.

Immunonutrition, still under discussion among experts, might deserve a place in this multifaceted approach [4].

2.9 Mental Health and Cognitive Dysfunction Biological connections exist between cognitive impairment/ cognitive decline (from mild to severe) and frailty [31]. Even if in the absence of organic causes of anxiety and depression, the older surgical patient might become prone to relevant changes of moods (anxiety, depression, and agitation) in case of a surgical solution proposed for an incoming pathological condition. As underlined by McIsaac et al. [10], early identification of potential postoperative depression, hidden mental health issues, and psychosocial stressors able to negatively impact on discharge pathways or home discharge feasibility, even if considered relevant, is seldom used. The easy-to-use Personal Health Questionnaire (PHQ-2) could be considered by preoperative clinicians as a screening tool for depression, possibly anticipating complex discharge needs or reduced support for going home [10, 32]. In the frail older patient, mild neurocognitive dysfunction is not infrequent and could contribute to postoperative delirium, a condition able to amplify discharge problems, need for postoperative support measures and, in general, adverse outcomes [31–33]. Again, underpinning the need for the preoperative awareness of possible problematic postoperative conditions, the American College of Surgeons and the American Geriatrics Society in 2012 endorsed the use of the Mini-Cog test as a cognitive screener before surgery, now present in the best practice guidelines for the preoperative assessment of the older surgical patients [33]. A “bundled approach” to implement new forms of prehabilitation targeting the prevention of postoperative delirium is aegerly awaited [33–36]. It might should include not only the avoidance of well-known perioperative delirium triggers, but a wider and more comprehensive “environmental” program, including mental work aiming at attention, acuity and interaction, orientation, nutrition, and mobilization. In a recent report by Chen et  al., similar approaches were associated with lower delirium rates in surgical patients [33]. Reducing the postoperative delirium and in general the postoperative alterations of moods and the cognitive dysfunction should have a significant impact on the entire postoperative period. The positive role of cognitive prehabilitation in its broadest sense and the favourable reflexes on the entire perioperative period are more than promising [36] and do require further multidimensional and multidisciplinary efforts involving physicians, health care providers, patients, and families. An interesting example is the Hospital Elder Life Program [37], an innovative model of hospital care aiming at preventing delirium and mental and physical decline in hospitalized older adults. Main targets

2  The Frail Patient in the Operating Room: Practical Steps to Reduce the Operative Risk

are to improve patients’ outcomes, to provide cost-effective care, and to maximize independence at discharge while assisting the transition from hospital to home. To reduce unplanned hospital readmission, implementing multidisciplinary multitasking intervention protocols is one of the main goals of the program [37].

2.10 Solid Organ Transplant Surgery and Frailty: Times Are (a)Changing In individuals suffering for end-stage organ failure and candidates for solid organ transplant (SOT) surgery, frailty is “an independent domain of risk, overlapping with, but distinct from, comorbidities (among others physiologic aging) and disability”: signs of frailty may overlap with characteristics of the index failing organ [38]. The associated dysregulation of multiple physiological systems may cause, among major adverse responses, an altered immune response, neuroendocrine changes, sarcopenia and physical disability, cognitive impairment, all leading to the inability to maintain homeostasis. Frailty, even if considered a useful definition while assessing SOT candidates, is still seldom included in the preoperative transplant assessment (10  mmHg), decreased cardiac function can be suspected as the primary problem, so addressing the clinician to explain why the heart function is poor. Notable exceptions are the use of high positive end-expiratory pressure and increased abdominal pressure [36]. Conversely, decreased blood pressure with low CVP values indicates lower than normal venous return. The heart function is probably normal and providing more volume will probably solve the problem. When the effect of volume is uncertain, a fluid challenge may be the most reasonable choice, provided that it is sufficient to raise the CVP by 2 mmHg or more, so that Starling’s law is tested. In Table 3.1, a summary of the dominant process responsible for arterial hypotension and the main therapeutic interventions are provided in accordance with the

respective deviation of cardiac output and CVP from the normal value. The volume bolus can be repeated until CVP increases by 2 mmHg or no further increase of cardiac output occurs. The approach outlined above requires the measurement of cardiac output or at least a surrogate. At the most basic level, the adequacy of cardiac output can often be inferred by clinical examination, while CVP values are easily obtained as almost all high-risk patients are equipped with a central venous line. A clear sensorium, warm extremities, normal renal function probably means that cardiac output is adequate. If any doubt persists, the measurement of central venous oxygen saturation and arterial blood lactates help to assess the adequacy of tissue perfusion. Abnormal numbers almost always indicate insufficient cardiac output for tissue needs, although normal or supra-normal ScvO2 levels cannot rule out inadequate peripheral O2 uptake (e.g., sepsis). Respiratory variations in CVP can also help to predict fluid responsiveness (Fig.  3.8) [37]. The inspiratory fall of pleural pressure in spontaneously breathing patient increases the transmural pressure of cardiac chambers so moving the cardiac function curve to the left with respect to the venous return curve. If the venous return curve intersects the ascending part of the cardiac function curve, then the CVP falls during inspiration, and the output from the right heart transiently increases because of increased venous return (panel

Table 3.1  Dominant process and therapeutic intervention during arterial hypotension and corresponding CVP deviation Cardiac output ↓ =↑ ↓

CVP ↓ =↓ ↑

Blood pressure ↓ ↓ ↓

Dominant process ↓ venous return ↓ vascular resistance ↓ cardiac function

NORMAL CARDIAC FUNCTION

a

Therapeutic intervention Volume infusion Vasopressors Inotropic drugs

ABNORMAL CARDIAC FUNCTION

b

CVP

CVP

INSP

INSP Fig. 3.8  Inspiratory variations of CVP during normal (panel A) and abnormal cardiac function (panel B). Patients with an inspiratory decrease of CVP have an increase of venous return during the inspiratory phase and they can increase their cardiac output after a fluid volume bolus (panel A). Conversely patients who do not show any

respiratory change of CVP cannot increase the venous return during inspiration as their venous return function curve intersects the flat part of the cardiac function curve (panel B). These patients will probably not beneficiate from a fluid bolus to increase their cardiac output

26

A). However, if the venous curve intersects the plateau of the cardiac function curve, CVP and hence SV will not change with inspiration (panel B). As a corollary, the absence of inspiratory fall in CVP means that the patient will probably not be a fluid-responder [37]. The test is most useful when negative, provided that pleural pressure falls sufficiently to rule out the inadequate decrease with inspiration. The fall of CVP does not invariably indicate volume responsiveness: active expiratory efforts must be ruled out as they cause CVP to rise during expiration so giving the false impression of inspiratory fall of pressure. Today, continuous positive airway pressure or noninvasive ventilation is increasingly employed as preventive or therapeutic measures in high-risk patients. Positive pressure breathing shifts the cardiac function curve to the right: if the venous function curve intersects the ascending part of the cardiac function curve, the venous return and cardiac output will be diminished, but CVP will rise due to transmission of the positive pleural pressure. This means that the patient with the inspiratory fall of CVP during spontaneous breathing will reduce the venous return when a positive pressure is applied. The microcirculation includes arterioles, capillaries, and small veins. The capillary section ensures the adequate O2 supply to cells by diffusion not convection. About 4 × 1010 units form the capillary network, with only 1010 open at each time. This is because of the enormous surface (about 500  m2), so that microcirculatory perfusion is physiologically inhomogeneous. Three distinct mechanisms regulate the blood flow through the capillaries. They respond to myogenic, shear stress, and metabolic stimuli, preferentially operating at distinct vessel segments. The myogenic and metabolic responses are most active in the terminal arteries, while the shear stress acts upon vessels of greater diameter (small arteries and arterioles). The most important of the three auto-regulatory systems is the metabolic one which relies upon the sensing of PO2 in the tissues. When PO2 reduces below the hypoxic threshold, feeding arteries dilate to provide more flow and hence more O2 to the cells. Conversely, the blood flow reduces in well-oxygenated tissues. Thus, O2 flow is carefully regulated through this negative feedback. The second regulatory system is the myogenic reflex (Bayliss’s reflex). It operates through the increase of arteriolar tone in response to increased arterial pressure. According to Poseuille’s law, any rise of pressure causes the flow to increase proportionately to the vessel resistance. Therefore, any increase in arterial pressure causes the reflex constriction of the vascular smooth muscle, this, in turn, increasing the hydraulic resistance. The opposite occurs with decreased arterial pressure. Bayliss’s reflex acts as a negative feedback, because it allows for constant microcirculatory flow despite upstream pressure variations. The third system operates by increasing O2 flow when O2 demands are

S. Arlati

increased (positive feedback). This mechanism is based upon the release of nitric oxide (NO) by the arteriolar endothelium in response to the shear stress of erythrocytes along the inner vessel surface. Although this mechanism operates in basal conditions, the increase of RBC flow causes more NO to be released in consequence of the increased shear stress. The intrinsic nature of this mechanism guarantees the adequate functional reserve of O2 in response to increased O2 demands. The correct interaction between these three regulatory mechanisms ensures the adequate O2 supply throughout virtually any condition of the entire lifetime. Hemorheology and capillary patency are the main determinants of capillary blood flow. Capillary hemodynamics can be quantified by red cells flux (red blood cells/s) [38] as defined:

Red Blood Cell ( RBC ) flux = V × LD

(3.4)

where V is linear RBC velocity (mm/s) and LD is RBC linear density (RBC/mm) or capillary hematocrit. Oxygen flow in capillaries (O2Fluxcap) is then calculated as

O2 Fluxcap = RBC flux × O2 Sat × K

(3.5)

According to (Eq. 3.4)

O2 Fluxcap = (V × LD ) × O2 Sat × K

(3.6)

where O2Sat is red cell oxygen saturation and K is the oxygen-­ carrying capacity of a single red blood cell (0.0362 mL O2/cell at 100% O2Sat) [39]. The above equation is analogous to the global O2 delivery equation as the term (LD × O2Sat × K) represents the O2 vol/mm, which multiplied by velocity (V mm/s) gives the total O2 capillary delivery (mL/s). Consequently, the capillary oxygen extraction ratio (O2ERcap) will be the difference between the inflow O2, and outflow O2 rate:

O2 ERcap = ( O2 in flow − O2 out flow ) / ( O2 in flow )

(3.7)



O2 ERcap = 1 − ( O2 out flow / O2 in flow )

(3.7a)

By rearranging (Eq. 3.4) as V = RBCflux/LD, it becomes evident that RBC velocity is an inverse function of capillary hematocrit. Reducing LD increases the linear velocity of RBC into the capillaries, thus reducing the transit time and increasing the PO2 of the red cells who leave the capillaries. Conversely, increased LD slows down the transit of erythrocytes along the capillary length this, in turn, causing the reduction of PO2 in RBCs. Anemia and polycythemia are both examples of the LD effects of RBC velocity in microcirculation. As blood viscosity is mainly produced by capillary hematocrit (LD), the higher is the number of red blood cells per millimeter of capillary length, and the lower will result the flow. The relationship between capillary hematocrit and O2 flow is curvilinear with a downward concavity

3  The High Risk Surgical Patients: The Pathophysiologic Perspective

(Fig.  3.9) and the maximum value at about 30% of Hct. Surprisingly, extremely low values of hematocrit (≤18%) obstacle the capillary blood flow in the same manner, as very high hematocrit values. The less viscous blood reduces the shear stress on the endothelial wall, so that lesser NO is produced and capillary resistance increases. Therefore, ­ extreme anemia is as well as deleterious as polycythemia for microcirculation. The hemorheological effects of LD are complex as apparent blood viscosity is determined by factors other than capillary hematocrit. Plasma viscosity, RCB aggregation, and deformability give a substantial contribution to blood viscosity in microcirculation [40]. Besides viscosity, microcirculatory resistance to flow also depends on vascular hindrance (H). In a broad sense, vascular hindrance O2 transport (DO2)

Viscosity (η)

10

20

30

40 50 Hematocrit

O2 Flux ÷ 1/(η)

60

70

80

90

DO2 ≈ Htc/(η)

Fig. 3.9  Oxygen transport and blood viscosity are plotted in function of the Hematocrit value. The maximum value of O2 transport is around 40–45% of hematocrit. Maximum O2 transport is a complex function of capillary viscosity and microvessels geometry (hindrance) which in turn determine microvascular rheology. Viscosity increases according to a curvilinear function with its minimum value around 10% of Hematocrit value (see text)

Rescap = H ×η



(3.8)

Hindrance’s contribution to capillary resistance follows either the reduced capillary distending pressure (e.g., hypovolemic shock) or the reduced capillary density by microvascular occlusion or edema accumulation (e.g., distributive shock) as the intercapillary distance increases. Increased microvessels resistance causes the fall of DO2cap with the right shift and flattening of the VO2/DO2 relationship (Fig. 3.10). The shift is even more pronounced if decreased microvascular PO2 occurs with increased capillary resistance [41] because of the greater relevance of diffusive versus convective O2 transport at microcirculatory level (Fig. 3.10). The regulation of the arteriolar diameter is crucial to compensate for changes in capillary resistance. Microcirculatory vasodilation and vasoconstriction have a different source of origin and different spread along the vessel walls [42]. The vasodilatory effect originates in the endothelium of the smallest caliber arterioles, thereafter spreading longitudinally upward, while vasoconstriction originates in the smooth muscle spreading transversally through the vessel wall. The vasodilatory effect is, therefore, more diffuse and with a higher degree of summation as it spreads from the smallest arteries to the feeding-arterioles. Vasoconstriction has more local and scarcely diffuse effects, perhaps because it is potentially hazardous. The actual model of oxygen diffusion has been developed from the observation that the O2 level in blood diminishes along the arterial tree with up to 2/3 lost before entering the capillary bed [43]. It has been observed that arterioles supply oxygen to capillaries by diffusion. Some of the O2 that leaves the arterioles diffuses to erythrocytes flowing through the nearby capillaries resulting in increased RBC SatO2 [44]. There is evidence that considerable spatial het-

a

b Anemic/Stagnant 40

VO2 ml/min/kg

Fig. 3.10  Predicted impact of changes in intercapillary distance (capillary density) on DO2crit because of anemic/ stagnant hypoxia (panel A) and hypoxic hypoxia (panel B). Numbers on the plots correspond to the intercapillary distance (μm). Hypoxic hypoxia shows the greatest impact of reduced capillary density on the VO2/ DO2 relationship

reflects the contribution of vascular geometry to flow. It relates to length (L), radius (R), and number (N) of parallel vessels in a complex way, with L changes being in the same direction that H, the opposite occurring with R and N.  Microvascular resistance is given by the following equation:

Hypoxic 40 VO2 ml/min/kg

0

27

160

160

240 0

5

10 15 DO2 ml/min/kg

240 20

0

5

10 DO2 ml/min/kg

15

20

S. Arlati

28

erogeneity of capillary perfusion [45] and corresponding heterogeneity of O2 delivery exist. The microcirculation supplies O2 to tissues by multiple vessel types, which are functionally connected through both convective (blood flow) and diffusive O2 transfer [46, 47]. The diffusional loss of O2 from the arteriolar tree occurs from the RBCs, which flows near the vessel wall. Therefore, more peripheral RBCs would have lower O2 saturation than those nearer to the lumen center [48, 49]. At vessel bifurcations, the intravascular PO2 gradient affects the convective O2 transport of the downstream branches. For example, if blood flow into a downstream branch is low, only slow plasma and erythrocytes with lower O2 tension will enter this branch (Fig. 3.11). However, if flow increases, a larger cross-sectional area of the upstream flow will enter the branch, thus increasing local DO2cap. According to this view, the metabolic needs are finely tuned by the redistribution of erythrocytes to the microcirculation of the demanding tissue. The erythrocytes, the major supplier of O2, also function as a sensor of O2 requirements. Experimental evidences shown that exposure to reduced pO2 stimulates ATP release from the erythrocytes [50] and that ATP efflux is linearly related to Hb saturation [51]. The importance of hemoglobin desaturation in ATP release has been confirmed in human studies, thus indicating erythrocytes as physiological regulators of hypoxia. Mechanical stimuli as red cells deformation (shear stress) or exposure to reduced oxygen tension cause the controlled release of ATP from the erythrocytes. Importantly, the amount of ATP released is influenced by the magnitude of the stimulus. ATP initiates a conducted vasodilation that extends well beyond the site of initiation so increasing the vascular perfusion as the final result (Fig. 3.11). The ATP-induced vasodilation results from the synthesis of endothelium-derived relaxing factors such as NO and products of arachidonic acid metabolism by puriner-

PO2

PO2

SatO2

ATP synthesis

high O2 demand

Normal O2 demand

vasodilation

Fig. 3.11  Regulation of microvascular flow by the PO2 level within the erythrocytes. At vessel bifurcation the entrance of erythrocytes into a region with high O2 demand results in higher PO2 gradient and more volume of oxygen transferred to tissues. The oxygen saturation of the hemoglobin within erythrocytes is lowered, this in turn stimulating the release of ATP from RBCs. ATP stimulates the endothelium to produce mediators that initiate vasodilation

gic receptors [52]. NO also acts as a feedback mechanism by attenuating the ATP-induced vasodilation when ATP levels are high [53]. This conceptual view suggests that increased DO2cap would result from a more uniform distribution of erythrocytes to already perfused capillaries rather than recruitment of new capillaries [54]. In summary, the release of vasodilator ATP from mobile erythrocytes plays a key role in matching micro-vascular O2 supply with local O2 demands. A finely tuned system regulates both the intraerythrocytic signal pathways and the feedback mechanisms controlling ATP release.

3.1 Anemia According to the World Health Organization, anemia is defined as the reduction of Hb content to less than 13 g/dL in men and 12 g/dL in women [55]. From the pathophysiological viewpoint, anemia becomes relevant when it reduces O2 supply to an extent near to actual metabolic needs. These two statements seem contradictory as any reduction in Hb content causes the reduction of CaO2, so that one could expect anemia as invariably responsible for tissue hypoxia. This is not true unless Hb content becomes lesser than half-normal (≤6  g/dL). The binary nature of DO2 compensates for the decrease of CaO2 with the parallel increase of cardiac output, so keeping DO2 = CaO2 × CO approximately constant. Once cardiac output rises to its maximum, O2ER begins to increase, thus maintaining VO2 constant unless Hb content is severely reduced. In a physiological study, the progressive reduction of Hb in young healthy awake humans increased the cardiac output with unchanged O2ER until the Hb content was decreased to 75  g/L or lesser [56]. Similar results were obtained in anesthetized animals, although the blunted reflex tachycardia caused O2ER to rise well before the hemoglobin threshold of 75 g/L [57]. From the circulatory viewpoint, the decline of hematocrit causes the reduction of blood viscosity with consequent diminution of peripheral vascular resistance and increased cardiac output [58]. At the microcirculatory level, the increased blood flow also allows for capillary recruitment with reduced intercapillary distance and increased DO2cap to the tissue [59]. Finally, the reduction of Hb  70  g/L, while a substantial increase was noted for levels 6 mmHg. Carbonic dioxide is more than 20 times more soluble than O2 [96], so it can reliably diffuse out of the ischemic tissues into the venous blood. This makes PCO2 a more sensitive marker of hypoperfusion than lactates. Where an O2 diffusion barrier exists, as in dysfunctional microcirculation (e.g., sepsis), poor tissue perfusion can be unmasked by the ability of CO2 to diffuse into the venous blood. It has been suggested that the increased Pv-aCO2 gap could reflect microcirculatory alterations undetected by other markers of global tissue ­ hypoxia [97]. However, the Pv-aCO2 gap is a marker of the adequacy of venous blood flow to remove CO2 rather than a marker of tissue hypoxia [98]. Combining ScvO2 as a surrogate for tissue hypoxia and Pv-aCO2 gap as a surrogate for cardiac output, the cardiovascular state of critically ill patients may be assessed during the resuscitation [99]. Both parameters can easily be obtained from a central venous blood sampling. In Table 3.3, the comparison between different indices of hypoperfusion is shown with respect to the most frequent types of shock. A further step toward the monitoring of global tissue hypoxia is represented by the combined evaluation of Pv-aCO2 and the a-vO2 content difference cO2(a-v). The computation of the Pv-aCO2/cO2(a-v) ratio relies upon the marked decrease of aerobic VCO2 with respect to anaerobic CO2 production and reduced VO2 during tissue hypoxia. As a result, the increase of anaerobic CO2 production must raise the VCO2/VO2 ratio. According to the VCO2 and VO2 equations, the respiratory quotient R is independent of the cardiac output:

R = VCO2 / VO2 (3.11)

where [VO2 = a − vO2 × CO ] and [VCO2 = v − aCO2 × CO ] giving the following relationship:

R = v − aCO2 /a − vO2 (3.11a)

Thus, R can be estimated by (Pv-aCO2)/cO2(a-v) [100]. Values of Pv-aCO2/cO2(a-v) greater than 1.4  mmHg/mL

have been observed in two series of septic patients with arterial blood lactates >2 mmol/L [100, 101]. Limitations in monitoring the microcirculation: given the importance of microcirculation in the regulation of O2 delivery to tissue, it is not surprising that its assessment would take on great relevance in optimizing the perfusion of tissues during critical illnesses. Microvascular alterations have been repeatedly demonstrated in either experimental or clinical conditions, including sepsis, hemorrhage, cardiac failure, trauma, and complicated postoperative setting [78– 84]. These alterations are relevant, especially because of their association with outcome [85]. The two main abnormal microvascular findings [76, 77] are: 1. decreased density of perfused vessels 2. increased heterogeneity of flow, that is, the presence of non-perfused capillaries in close proximity with normally or increasingly perfused vessels The investigation of microcirculation is performed by direct and indirect techniques. Direct techniques employ videomicroscopy to allow for the visualization of microvascular perfusion and the characterization of its alterations. Direct videomicroscopy represents the gold standard for the study of the microcirculation. Importantly, these alterations are dissociated from systemic hemodynamic variables and thus cannot be detected using classic macrohemodynamic parameters [102, 103]. The different devices employed are based on the principle that a light reflected by the deeper tissue layer is absorbed by red blood cells allowing for visualization of microvascular perfusion. Unfortunately, these techniques have limitations which prevent their easiness of use at the bedside. First, the video camera can be applied only on thin epithelial surfaces, the most utilized area being the sublingual mucosal surface. Nevertheless, the representativity of the sublingual area has been questioned in the clinical arena [104]. Second, the videomicroscopic techniques are intermittently performed, more often by research teams. The routine use of videomicroscopy is still lacking, even if a nurse-driven approach has been proven feasible [105]. Finally, the investigation of the sublingual area restricts its use to sedated and intubated patients only, although these are the most critically ill patients who would take the greatest advantage from the microcirculatory monitoring. As a result, the video–microscopic techniques are not feasible in many patients. Indirect techniques investigate the microvascular perfusion by (1) assessing the vascular reactivity of the intact

Table 3.3  Indices of hypoperfusion during low and high output states of shock Shock type Low output state (cardiogenic/hypovolemic) High output state (distributive)

Lactate ↑ ↑

O2ER ↑ ↓

Adapted from Vallet et al. [99]

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ScvO2 ↓ ↑

Pv-aCO2 gap ↑ ↑

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3  The High Risk Surgical Patients: The Pathophysiologic Perspective

and damaged endothelium, (2) measuring the extent of endothelial damage, and (3) evaluating microvascular flow by ultrasound contrast media. The first technique employs laser or near-infra-red spectroscopy to estimate regional blood flow after a brief period of vascular occlusion. Damaged endothelium has diminished maximal vasodilatory properties, so that the reperfusion flow is decreased [106, 107]. The major limitation of this technique is that it is affected by local factors as temperature and peripheral ischemia, in addition to the lack of direct measurement of microvascular perfusion. Endothelial damage can be quantified by glycocalyx biomarkers as syndecan-1, heparin sulfate, and hyaluronan. Alterations of glycocalyx may induce microvascular alterations and increased permeability with the development of ­tissue edema [108]. Although easy to measure, these biomarkers do not allow for direct measurement of microvascular perfusion as well as endothelial functions. Moreover, and perhaps more important, the restoration of glycocalyx is challenging at today, so that their utility in monitoring therapeutic interventions is questionable. Contrast-enhanced ultra-sound (CEUS) evaluates the microvascular perfusion by measuring the speed of enrichment of the tissue by ultrasound contrast media [109]. Kidney and liver are the most investigated sites. The limitations of CEUS are its high costs, the need for great ultrasonographic skill, dedicated software, and (low) anaphylactic risks. In addition, the intrinsic nature of CEUS does not allow for the assessment of microvascular perfusion heterogeneity. Finally, CEUS cannot separate regional from microvascular perfusion. In summary:

deficits over time. For example, if a 70 kg healthy male with a basal VO2 of 140 mL/min/m2 suffers an O2 deficit of 40 mL/ min/m2, meaning that VO2 decreases from 140 to 100 mL/ min/m2, the cumulated O2 debt over 2  h will be 4.8  L/m2 (40 mL/min/m2 × 120 min). Figure 3.13 illustrates the difference between oxygen deficit and oxygen debt and how poor their correlation is. At timepoint 1, O2 deficit is 50 mL/min/ m2 and the incurred debt at this point is 750 mL/m2. At timepoint 2, the deficit is at its maximum (60 mL/min/m2) and the debt is increased to 2500 mL/m2. At timepoint 3, the O2 deficit begins to decrease (30 mL/min/m2), and this will continue through timepoint 4 (15 mL/min/m2). However, the debt continues to increase, although the accumulation rate is fading. At timepoint 5, the deficit is null, and no more debt is being accumulated, but now, the overall O2 debt is over 4.6 L/m2. According to this model, it is likely that the debt repayment will be faster as the resuscitation will be prompter. This seems true as patients with prolonged hemorrhagic shock following inadequate resuscitation have an almost 25% in-­ hospital mortality rate primarily from organ failure [112]. As O2 debt accumulates, the likelihood of cellular damage increases because of loss of membrane integrity, cellular swelling and intracellular organelles damage. The cessation of synthetic mechanisms and lysosome activation will finally result in cellular necrosis and digestion [113]. Even at less severe levels of O2 debt, apoptosis ensues with progression to organ dysfunction [114]. Cells with the greatest O2

30’

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O2 DEFICIT ml/min/m2

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1. Perturbation of the microcirculation is frequently observed in severe sepsis and septic shock. 2. Microcirculatory dysfunction plays an important role in the development of multiple organ dysfunctions. 3. Today, the monitoring of microcirculation is impractical because of many limitations of the currently employed techniques [110]. Oxygen debt accumulation/repayment: according to the standard definition of shock, when O2 demand is inadequately matched by O2 supply, DO2 is reduced below DO2crit, and O2 deficit incurs. Oxygen deficit can be calculated as the difference between baseline VO2 and VO2 measured at any given time during the shock period. As a significant time dimension, shock must account for the oxygen debt accumulated over time. By consequence, the O2 deficit accumulated over time is the O2 debt:

Oxygen deficit = VO2 basal − VO2 − t (3.12)

where VO2basal is the basal VO2 and VO2-t, the oxygen consumption at the timepoint t [111]. According to this definition, O2 debt represents the accumulation of multiple oxygen

2500

1350

3850

675

4525

112.5

4637.5

Fig. 3.13  Current and cumulative O2 debts are shown. Note that the current debt decreases after 60 min, while the cumulative debt continues to rise. Therefore, it is the overall debt to be really representative of tissue hypoxia: the greater the debt, the longer will be the time of repayment

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requirements (brain, liver, kidney, heart, and leukocytes) are the most vulnerable to hypoxia-induced injury and death. The relationship between O2 debt and acute death has been quantified experimentally. In a canine study, 120 mL/ min/m2 of O2 debt killed 50% of the studied population, while 140 mL/min/m2 or more resulted invariably fatal [115]. A quantification of the probability of death with increasing O2 debt established an exponential relationship with 95.5 mL/ min/m2, 113.5  mL/min/m2 and 126.5  mL/min/m2 giving, respectively, 25%, 50%, and 75% probability of death [116]. Studies in pigs gave the same results, although at slightly lower values of O2 debt, probably because of their greater adipose mass over the same range of body weight [117]. The relationship between O2 debt accumulation and its repayment has been studied experimentally in 40 dogs bled to achieve 104 ± 7.6 mL/Kg of O2 debt by 71 ± 6.8% withdraw of shed blood volume (SBV) (actual death rate 40%) [118]. Following hemorrhage, the animals were given no initial resuscitation for 2 h and then divided into four groups as follows: fully resuscitated with 5% colloid volume equivalent to 120% of SBV, 8.4% of SBV, 15% of SBV, and 30% of SBV. After a further 2 h delay, the animals were given the remaining portion of the 120% of SBV lost during hemorrhage. This made the final quantity of volume replacement in each animal equal to 120% of SBV. The accumulation rate of the O2 debt continued to rise during the first 2 h after hemorrhage at the same or slightly lower degree, even though no further blood loss occurred. The O2 debt continued to accumulate until the animals received at least 30% of the SBV, but the rate of repayment increased in proportion with the amount of initial resuscitation volume. The lowest rate occurred in those receiving 8% of SBV and increased progressively with the initial resuscitation volume. The mass-­ specific fluid volume in those animals receiving 30% as the initial bolus of SBV was 18 mL/Kg that is 74% of the accumulated O2 debt over the first 2 h. The outcome was scored accordingly with the derangement of physiological organs function and histologic examination developed at 7 day post-­ hemorrhage. Although survivors did not show appreciable differences in vital signs and neurological functions, cellular damage in the liver and kidney was most severe in animals receiving the lowest initial resuscitation volume (8.4% and 15% of SBV) and mild to moderate in those receiving 30% of SBV immediately post-shock. None to mild cellular injury was found in animals receiving the immediate full resuscitation volume. This study implicates that it is the amount of debt repaid within a restricted time window instead of the absolute repayment over a prolonged time that matters about organ damage. Animals receiving 8.4% only as the initial resuscitation volume repaid less than 1/3 of the accumulated debt resulting in subsequent organ failure and death. The minimum volume of fluid resuscitation required for 75% of

oxygen debt repayment was equivalent to at least 30% of SBV (about 20/mL/Kg). Although this experimental study is not a real representation of the clinical situation (colloids given as resuscitation fluids, controlled hemorrhage and no additional trauma imposed, and anesthetized and heparinized animals), its major implication is that at least 2/3 of the incurrent oxygen debt must be repaid as fast as possible (ideally within the first 2 h), to maximize the probability of good clinical recovery after moderate to severe shock. The second implication is that the adequacy of fluid resuscitation must be gauged by the extent to which O2 debt has been repaid within a given time window, rather than in terms of a set fluid volume. In contrast with the discriminative power of O2 debt, simultaneous measurement of cardiac output and DO2 did neither reflect the severity of shock nor the effectiveness of volume resuscitation. This is not surprising as DO2crit only marks the transition at which the O2 debt starts to accumulate. This study demonstrates that without an estimate of the previously incurred debt and the amount of repayment needed on a per-patient basis, any predefined target of DO2 is essentially arbitrary. In previous studies involving high-risk surgical patients, survivors with targeted DO2 values might have never trespassed the critical threshold or, alternatively, the estimated O2 debt was by far lesser, so that resuscitation resulted adequate. By converse, non-survivors may have incurred into a lethal O2 debt, so that no resuscitation would be adequate or debt repayment was so delayed that MODS and death were inevitable. As O2 debt entails the production of metabolic acid as a consequence of anaerobic metabolism, both animal and human studies suggest that either blood or plasma acids levels can be used as a surrogate of tissue hypoxia [116–121]. The relationship between O2 debt and increased base deficit (BD) or lactate levels has been well-established, with increased acidosis being paralleled by increased O2 debt. The opposite occurs during volume resuscitation when O2 debt repayment associates to lactate clearance and BD reduction. The relationship between BD and O2 debt seems to reflect better the effectiveness of resuscitation volume, whereas lactate reflects the overall trend in effectiveness [122]. In accordance with the animal model of O2 debt accumulation and repayment, it seems obvious that single timepoint measurements are of little value unless measured very soon after the initiation of shock (Fig.  3.14). The severity of O2 debt is more accurately reproduced by the area under the curve than by its peak value. Higher peak does not necessarily mean higher cumulative O2 debt. Peak arterial blood lactates are also shown for comparison. Sequential values are much more informative about the severity of shock and the response to resuscitation maneuvers. Persistently, high lactates are thought to be good indicators of permanent impairment of DO2, early inflammatory

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3  The High Risk Surgical Patients: The Pathophysiologic Perspective Lact 8 mmol/l

Lact 5 mmol/l

10

10 21,5 a.u.

41 a.u.

8

8 O2 debt (a.u)

O2 debt (a.u)

Fig. 3.14  Severity of O2 debt is more accurately reproduced by the area under the curve than by its peak value. Higher peak does not necessarily mean higher cumulative O2 debt. Peak arterial blood lactates are also shown

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activation, and subsequent MODS development [123]. Conversely, a positive correlation between the rate of lactate clearance and survival in sepsis, burns, trauma, and cardiac arrest has been documented. Given the importance of the rapid repayment of O2 debt, the sequential assessment of lactate and BD during the early resuscitation seems a good method to assess the effectiveness of post-shock therapies. The assumption that the higher is the level of the acidosis markers in plasma, the greater is the extent of shock is true, but the proportionality of their changes with changes of patient conditions remains unknown. Proportionality is probably not linear due to the exponential rise of mortality when lactates increase above 4  mmol/L [124] and BD becomes lesser than -6 mmol/L [119–121]. A swine model of hemorrhagic shock investigating the extent to which changes in lactate levels corresponded to changes in O2 debt confirmed the individual variability of response. However, sequential lactate determination is the best, although imperfect way to determine the oxygen debt status, unless at present. Another problem is that it is difficult, if not impossible, to determine how much of the accumulated O2 debt can be tolerated before cellular damage becomes irreversible. Although extreme cases are evident “per se”, the question includes the intermediate conditions as no clinical methods exist to effectively track O2 debt accumulation and clearance. Even if VO2 could be measured, as in sedated and ventilated patients, both baseline VO2 and duration of shock before treatment remains largely unknown. Confounding variable as hypothermia, hyperthermia, sedation, anesthesia, and muscular paralysis makes the assessment of “true” baseline VO2 difficult. Therefore, the only way to assess the severity of O2 debt is the wise combination of clinician’s eye, careful monitoring of oxygen and circulatory variables, and sequential assessment of surrogate markers of acidosis. In addition, the prompt recognition of shock limits the accumulation of O2 debt and allows for its quick repayment.

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3.3 Conclusions Experimental evidence suggests that the “golden hour” changes into “two silver hours” [111]. This means that moderate-­to-severe shock requires repayment of approximately 3/4 of the accumulated O2 debt within 2 h. Although studies refer to resuscitation from hemorrhagic shock, the same kinetic of repayment seems applicable to the other types of shock. Nevertheless, the complex nature of cardiogenic and distributive shock (e.g., septic) makes improbable the achievement of O2 debt repayment within the “two silver hours”. Efforts must be committed to: 1. prevent or at least limit as much as possible any further O2 debt accumulation 2. repay the oxygen debt as fast as possible 3. minimize the time of oxygen debt resolution Case History 64 years, male, Caucasian. Scheduled for elective abdominal aortic aneurysm repair. After induction of anesthesia both cardiovascular and hemodynamic parameters are normal (Fig. 3.15; panel A). During the procedure a reduction of cardiac output due to intraoperative blood losses is noted (panel B). Suddenly the systolic pressure drops to 70/45 and heart rate rises to 140 bpm (panel C). Massive transfusion is undertaken and normal systolic pressure is recovered within 60 min (panel B): 1. Given the hemodynamic data, calculate the cumulative O2 debt during the hypotensive episode in accordance with the temporal profile of Fig. 3.16. Assume arterial O2 saturation 97% and consider negligible the amount of dissolved O2 2. Is the O2 debt reversible? 3. Is the Base Excess at timepoint 2: (a) 6 mmol/L 4. At point C (Fig. 3.1), is there an O2 supply dependency or independency? 5. Which of the following microvascular patterns coexists with the microvascular profile of Fig. 3.1 (panel C)? (a) Distributive (b) Congestive/tamponade (c) Hemodilution (d) Tissue Edema 6. What is the most feared complication for this patient? (a) Pancreatitis (b) Severe Sepsis/Septic Shock (c) Multiple organ dysfunction (d) SIRS

a

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Hb 15 CI 2.3 HR 140 AP 110/70 Scv02 53%

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g/dL I/min/m2 bpm mmHg

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indexed VO2 = CI × ( SaO2 − ScvO2 ) ×1.36 × [ Hb ] × 10

Panel A: 3.2  L/min/m2  ×  10  ×  (0.97–0.74)  ×  1.36  ×  15  g/ dL = 150/min/m2 Panel B: 2.3  L/min/m2  ×  10  ×  (0.97–0.53)  ×  1.36  ×  11  g/ dL = 150 mL/min/m2 Panel C: 1.8 L/min/m2 × 10 × (0.97–0.56) × 1.36 × 7.5 g/ dL = 75 mL/min/m2 Therefore, the indexed VO2 remains normal from A to B despite the decrease of indexed DO2 mainly because O2ER has increased (from 0.24 to 0.45). However, the DO2 threshold has been reached. Thereafter O2 extraction decreases to half the normal value reaching 75 mL/min/ m2 (point C). As a corollary note that ScvO2 apparently increases from 53% (panel B) to 56% (panel C), although DO2 has decreased from 334 mL/min/m2 to 227 mL/min/ m2. The apparent increase of DO2 is the consequence of the decreased Hb content. Remember that SatO2 is the given by [HbO2]/[Hbtot]. Thus, the decrease of Hbtot causes the HbO2/Hbtot ratio to increase. According with Fig. 3.16

g/dL I/min/m2 bpm mmHg

b Hb 7.5 CI 1.8 HR 140 AP 75/45 Scv02 56%

40 0

c

Indexed DO2 = [ Hb ] × CI × 1.36 × SaO2 The amount of indexed O2 delivery in panels A, B and C are, respectively: Panel A: (15  g/dL  ×  1.36  ×  0.97)  ×  3.2  L/min/ m2 × 10 = 633 mL/min/m2 Panel B: (11  g/dL  ×  1.36  ×  0.97)  ×  2.3  L/min/ m2 × 10 = 334 mL/min/m2 Panel C: (7.5  g/dL  ×  1.36  ×  0.97)  ×  2.3  L/min/ m2 × 10 = 227 mL/min/m2 Therefore, oxygen delivery decrease approximately of 65% from A to C The amount of oxygen extraction can be approximated by the following:

300

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Fig. 3.15  Hemodynamic parameters are shown with respect to the VO2/DO2 plot. Data reflect the cardiovascular status respectively before (b), during (c) and after hemorrhage (a) Fig. 3.16  Time profile and hemodynamic parameters during the hemorrhagic shock

ELAPSED TIME 0

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60 [Hb] 11 g/dL SaO2 97% ScvO2 53% CI 2.3 I/min/m2

[Hb] 11 g/dL SaO2 97% ScvO2 53% CI 2.3 I/min/m2 1

2 [Hb] 7.5 g/dL SaO2 97% ScvO2 56% CI 1.8 I/min/m2

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3  The High Risk Surgical Patients: The Pathophysiologic Perspective

the O2 debt from 0 to 1 is: (150–75) mL/min/ m2 × 30 min = 2250 mL the O2 debt from 1 to 2 is: (150–75) mL/min/ m2 × 30 min = 2250 mL The cumulative O2 debt is, therefore, 2250  +  2250  mL/ m2/60 min = 4500 mL/m2/60 min = 75 mL/min/m2. 2. The O2 debt is 75 mL/min/m2 that is approximately half of the maximum established by animal studies (120– 140 mL/min/m2). 3. BE is probably between −2  mmol/L and −  6  mmol/L.  Given the amount of O2 debt, the aerobic metabolism has probably been switched to anaerobic metabolism. Therefore, the amount of BE at point C is abnormal but lesser than −6 mmol/L in consequence of the short duration of the hypotensive episode. 4. In panel C a status of O2 supply dependence exists as the DO2 is reduced under the critical DO2 threshold. 5. The most probable microvascular pattern in association with the hypovolemic shock of our patient is hemodilution as the reduced RBC mass causes less erythrocytes to flow into the capillary network. Both congestive and tissue edema are improbable, because the filling pressure of the microvessels is low due to hypovolemia, so that tissue edema and capillary congestion are not plausible. The distributive shock is also improbable. Moreover, the studies show the concordance between microcirculation and macrocirculation during the very early phase of hypovolemic shock. 6. The most feared complication is represented by multiple organ dysfunctions due to tissue hypoxia, most notably the liver and kidney. This patient must be carefully observed for the development of acute kidney and hepatic dysfunction during the next days. Although the hypotension was short in duration it is plausible that this patient suffers from diffuse atherosclerosis as witnessed by the aortic aneurysm. SIRS is the second most frequent complication as the inflammatory activation following the ischemia/reperfusion syndrome causes the loss of control of vascular tone with decreased systemic vascular resistance and ensuing hypotension, fever and tachypnea.

References 1. Boyd O, Jackson N.  How is risk defined in high risk surgical patient management? Crit Care. 2005;9:390–6. 2. Lee TH, Marcantonio ER, Mangione CM, et  al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation. 1999;100:1043–9. 3. Shoemaker WC, Montgomery ES, Kaplan E, Elwyn DW. Physiological patterns in surviving and non-surviving shock patients. Use of sequential cardiorespiratory variables in defining criteria for therapeutic goals and early warning of death. Arch Surg. 1993;106:630–6.

37 4. James S, Jhanji S, Smith A, et al. Comparison of the prognostic accuracy of scoring systems, cardiopulmonary exercise testing and plasma biomarkers: a single-Centre observational pilot study. Br J Anaesth. 2014;112:491–7. 5. Older P, Hall A, Hader R.  Cardiopulmonary exercise testing as screening test for perioperative management of major surgery in the elderly. Chest. 1999;116(2):355–62. 6. Lobo SM, Rezende E, Knibel MF, et  al. Early determinants of death due to multiple organ failure after non-cardiac surgery in high-risk patients. Anesth Analg. 2011;112:877–83. 7. Husain FA, Martin MJ, Mullenix PS, et  al. Serum lactate and base deficit as predictors of mortality and morbidity. Am J Surg. 2003;185:485–91. 8. McNelis J, Marini CP, Jurkiewicz A, et al. Prolonged lactate clearance is associated with increased mortality in the surgical intensive care unit. Am J Surg. 2001;182:481–5. 9. Vallet B, Tavernier B, Lund N. Assessment of tissue oxygenation in the critically ill. Eur J Anaesthesiol. 2000;17:221–9. 10. Cain SM, Curtis SE. Experimental models of pathologic oxygen supply dependency. Crit Care Med. 1991;19:603–12. 11. Vincent JL, Roman A, De Backer D, et al. Oxygen uptake/supply dependence. Am Rev Respir Dis. 1990;142:2–7. 12. Squara P. Matching total body oxygen consumption and delivery: a crucial objective? Intensive Care Med. 2004;30:2170–9. 13. Bihari D, Smithies M, Gimson A, Tinker J. The effects of vasodilation with prostacyclin on oxygen delivery and uptake in critically ill patients. N Engl J Med. 1987;317:397–403. 14. Nelson DP, Beyer C, Samsel RW, et al. Pathological supply dependence of O2 uptake during bacteriemia in dogs. J Appl Physiol. 1987;63:1487–92. 15. Duran W, Renkin E.  Oxygen consumption and blood flow in resting mamalians skeletal muscles. Am J Phys. 1974;226:173–7. 16. McCord J.  Oxygen-derived free radicals in post ischemic tissue injury. N Engl J Med. 1985;312:159–61. 17. Schumacker PT, Chandel N, Agusti AG.  Oxygen conformance of cellular respiration in hepatocytes. Am J Phys. 1993;265:L395–402. 18. Kandel G, Aberman A.  A mixed venous oxygen saturation: its role in the assessment of the critically ill patient. Arch Int Med. 1983;143:1400–2. 19. Tanczos K, Molnar Z.  The oxygen supply-demand balance: a monitoring challenge. Best Pract Res Clin Anaestheriol. 2013;27:210–7. 20. Reinhardt K, Bloos F. The value of venous oximetry. Curr Opin Crit Care. 2005;11:259–63. 21. Chawla LS, Zia H, Gutierrez G, et al. Lack of equivalence between central venous and pulmonary artery oxygen saturation. Chest. 2004;126:1891–6. 22. Rivers E.  Mixed versus central venous oxygen saturation may not be numerical equal, but both are still clinically useful. Chest. 2006;129:507–8. 23. Van Beest PA, Wietasch G, Scheeren T, et al. Clinical Revies: use of venous oxygen saturation as a goal—a yet unfinished puzzle. Crit Care. 2011;15:232. 24. Pope JV, Jones AE, Gaieski DF, et al. Multicenter study of central venous oxygen saturation (ScvO2) as a predictor of mortality in patients with sepsis. Ann Emerg Med. 2010;55:40–6. 25. Ince C, Sinaasappel M. Microcirculatory oxygenation and shunting in sepsis and septic shock. Crit Care Med. 1999;27:1369–77. 26. Leach RM, Treacher DF. The pulmonary physician in critical care * 2: oxygen delivery and consumption in the critically ill. Thorax. 2002;57:170–7. 27. Guyton AC.  Determination of cardiac output by equating venous return curves with cardiac response curves. Physiol Rev. 1955;35:123–9.

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28. Guyton AC, Polizo D, Armostron GG.  Mean circulatory filling pressure measured immediately after cessation of heart pumping. Am J Phys. 1954;179:261–7. 29. Deschamps A, Magder S. Baroreflex control of regional capacitance and blood flow distribution with or without alpha adrenergic blockade. J Appl Physiol. 1992;263:HI1755–63. 30. Thiele RH, Nemergut EC, Lynch C III.  The clinical implications of isolated α1 adrenergic stimulation. Anesth Analg. 2011;113:297–304. 31. American College of Surgeons. Advanced trauma life support for doctors-student course manual. 8th ed. Chicago: American College of Surgeons; 2008. 32. Olgivie RI.  Effect of nitroglycerine on peripheral blood flow distribution and venous return. J Pharmacol Exp Ther. 1978;207:372–80. 33. Pouleur H, Covell JW, Ross J Jr. Effects of nitroprusside on venous return and central blood volume in the absence and presence of acute heart failure. Circulation. 1980;61:328–37. 34. Magder S.  Phenylephrine and tangible bias. Anesth Analg. 2011;113:211–3. 35. Permutt S, Riley S.  Hemodynamics of collapsible vessels with tone: the vascular waterfall. J Appl Physiol. 1963;18:924–32. 36. Magder S, Bafaqueeh F. The clinical role of central venous pressure measurement. J Intensive Care Med. 2007;22:44–51. 37. Magder SA, Georgiadis G, Cheong T.  Respiratory variations in right atrial pressure predict response to fluid challenge. J Crit Care. 1992;7:76–85. 38. Nakajima Y, Baudry N, Duranteau J, et  al. Microcirculation in intestinal villi: a comparison between hemorrhagic and endotoxin shock. Am J Respir Crit Care Med. 2001;164(8 part 1):1526–30. 39. Ellis CG, Bateman RM, Sharpe MD, et al. Effect of a maldistribution of microvascular blood flow on capillary O2 extraction in sepsis. Am J Physiol Heart Circ Physiol. 2002;282:H156–64. 40. Baskurt OK, Meiselman HJ. Blood rheology and hemodynamics. Semin Thromb Hemost. 2003;29(5):435–50. 41. Schoemaker PT, Samuel RW.  Analysis of oxygen delivery and uptake relationship in the Krogh tissue model. J Appl Physiol. 1989;67:1234–44. 42. Segal S.  Regulation of blood flow in the microcirculation. Microcirculation. 2005;12:33–45. 43. Duling BR, Berne RM.  Longitudinal gradients in periarteriolar oxygen tension. A possible mechanism for the participation of oxygen in local regulation of blood flow. Circ Res. 1970;27:669–78. 44. Ellsworth ML, Pittman RN. Arterioles supply oxygen to capillaries by diffusion. Am J Physiol Heart Circ Physiol. 1990;258:H1240–3. 45. Tyml K, Ellis CG, Safranyos RG, et  al. Temporal and spatial distributions of red cell velocity in capillaries of resting skeletal muscle, including estimates of red cell transit times. Microvasc Res. 1981;22:14–31. 46. Ellisworth ML, Ellis CG, Popel AS, et al. Role of microvessels in oxygen supply to tissue. NIPS. 1994;9:199–23. 47. Goldman D, Popel AS. A computational study of the effect of capillary network anastomoses and tortuosity on oxygen transport. J Theor Biol. 2000;206:181–94. 48. Carvalho H, Pittman RN. Longitudinal and radial gradients of PO2 in the hamster cheek pouch microcirculation. Microcirculation. 2008;15:215–24. 49. Ellsworth ML, Pittman RN.  Evaluation of photometric methods for quantifying convective mass transport in microvessels. Am J Physiol Heart Circ Physiol. 1986;251:H869–79. 50. Sprague RS, Bowles EA, Hanson MS, et  al. Prostacyclin analogues stimulate receptor-mediated cAMP synthesis and ATP release from rabbit and human erythrocytes. Microcirculation. 2008;15:461–71. 51. Jagger JE, Bateman RM, Ellsworth ML, et al. Role of erythrocyte in regulating local O2 delivery mediated by hemoglobin oxygenation. Am J Physiol Heart Circ Physiol. 2001;280:H2833–9.

52. Ellsworth ML, Ellis CG, Goldman D, et  al. Erythrocytes: oxygen sensors and modulators of vascular tone. Physiology. 2009;24:107–16. 53. Olearczyk JJ, Ellsworth ML, Stephenson AH.  Nitric oxide inhibits ATP release from erythrocytes. J Pharmacol Exp Ther. 2004;309:1079–84. 54. Ellis CG, Wrigley SM, Groom AC.  Heterogeneity of red blood cell perfusion in capillary networks supplied by a single arteriole in resting skeletal muscle. Circ Res. 1994;75:357–68. 55. Blanc B, Finch CA, Hallberg L, et al. Nutritional anemias. Report of a WHO Scientific Group. WHO Tech Rep Ser. 1968;405:1–40. 56. Weiskopf RB, Viele MK, Feiner J, et  al. Human cardiovascular and metabolic response to acute severe isovolemic anemia. JAMA. 1998;279:217–21. 57. Van der Linden P, De Hert S, Mathieu N, et  al. Tolerance of acute isovolemic hemodilution: effects of anesthetic depth. Anesthesiology. 2003;99:97–104. 58. Murray JF, Escobar E, Rapaport E. Effects of blood viscosity on hemodynamic responses in acute normovolemic anemia. Am J Phys. 1969;216:638–42. 59. Messmer K.  Blood rheology factors and capillary blood flow. In: Gutierrez G, Vincent JL, editors. Tissue oxygen-utilization. Berlin: Springer Verlag; 1991. p. 103–13. 60. Sibbald WJ, Doig GS, Morisaki H. Role of RBC transfusion therapy in sepsis. In: Sibbald WJ, Vincent JL, editors. Clinical trials for the treatment of sepsis. Berlin: Springer Verlag; 1995. p. 191–206. 61. Carson JL, Noveck H, Berlin JA, et al. Mortality and morbidity in patients with very low postoperative Hb levels who decline blood transfusion. Transfusion. 2002;42:812–8. 62. Shou H, Perez de Sa V, Sigurdardottir M, et al. Circulatory effects of hypoxia, acute normovolemic hemodilution, and their combination in anesthetized pigs. Anesthesiology. 1996;84:1443–54. 63. Kei T, Mistry N, Tsui AKY, et  al. Experimental assessment of oxygen homeostasis during acute hemodilution: the integrated role of hemoglobin concentration and blood pressure. Intensive Care Med Exp. 2017;5:12. 64. Blow O, Magliore L, Claridge JA, et  al. The golden hour and the silver day: detection and correction of occult hypoperfusion within 24 hours improves outcome from major trauma. J Trauma. 1999;47:964–9. 65. Karimova A, Pinsky DJ.  The endothelial response to oxygen deprivation: biology and clinical implications. Intensive Care Med. 2001;27:19–31. 66. Ince C. Hemodynamic coherence and the rationale for monitoring the microcirculation. Crit Care. 2015;19(Suppl 3):S8. 67. Cortes DO, Puflea F, Donadello K, et al. Normobaric hyperoxia alters the microcirculation in healthy volunteers. Microvasc Res. 2015;98:23–8. 68. Vellinga NA, Inca C, Boerma EC. Elevated central venous pressure is associated with impairment of microcirculatory blood flow in sepsis: a hypothesis generating post hoc analysis. BMC Anesthesiol. 2013;13:17. 69. Hanson J, Lam SWK, Mohanty S, et al. A fluid resuscitation of adults with severe falciparum malaria: effects on acid-base status, renal function and extravascular lung water. Crit Care Med. 2013;41:972–81. 70. Shoemaker WC, Appel PL, Hb K. Role of oxygen in development of organ failure and death in high risk surgical patients. Chest. 1992;102:208–15. 71. Bakker J, Ince C.  Monitoring the coherence between the macro and the microcirculation in septic shock. Curr Opin Crit Care. 2020;26:267–72. 72. Kanoore Edul VS, Ince C, Dubin A.  What is microcirculatory shock? Curr Opin Crit Care. 2015;21:245–52. 73. Dubin A, Pozo MO, Ferrara G, et al. Systemic and microcirculatory responses to progressive hemorrhage. Intensive Care Med. 2009;35:556–64.

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3  The High Risk Surgical Patients: The Pathophysiologic Perspective 74. Van Genderen ME, Klijn E, Lima A, et al. Microvascular perfusion as a target for fluid resuscitation in experimental circulatory shock. Crit Care Med. 2014;42:E96–E105. 75. Langeland H, Lying O, Aadhal P, et  al. The coherence of macrocirculation, microcirculation and tissue metabolic response during nontraumatic hemorrhagic shock in swine. Physiol Rep. 2017;5:e13216. 76. Lam C, Tymil K, Martin C, et  al. Microvascular perfusion is impaired in a rat model of normotensive sepsis. J Clin Invest. 1994;94:2077–83. 77. Farquar I, Martin CM, Lam C, et al. Decreased capillary density in vivo in bowel mucosa of rats with normotensive sepsis. J Surg Res. 1996;61:190–6. 78. Bartels SA, Bezemer R, Milstein DM, et al. The microcirculatory response to compensated hypovolemia in a lower body negative pressure model. Microvasc Res. 2011;82:374–80. 79. Vellinga NA, Ince C, Boerma EC. Elevated central venous pressure is associated with impairment of microcirculatory blood flow in sepsis: a hypothesis generating post-hoc analysis. BMC Anesthesiol. 2013;13:17. 80. Edul VS, Enrico C, Laviolle B, et al. Quantitative assessment of the microcirculation in healthy volunteers and in patients with septic shock. Crit Care Med. 2012;40:1443–8. 81. De Backer D, Creteur J, Dubois MJ, et al. Microvascular alterations in patients with acute severe heart failure and cardiogenic shock. Am Heart. 2004;147:91–9. 82. Tachon G, Harrois A, Tanaka S, et al. Microcirculatory alterations in traumatic/hemorrhagic shock. Crit Care Med. 2014;42:1433–41. 83. den Uil CA, Lagrand WK, van der Ent M, et  al. Conventional hemodynamic resuscitation may fail to optimize tissue perfusion: an observational study on the effect of dobutamine, enoximone and norepinephrine in patients with acute myocardial infarction complicated by cardiogenic shock. PLoS One. 2014;9:e103978. 84. Sakr Y, Dubois MJ, De Backer D, et al. Persistent microcirculatory alterations are associated with organ failure and death in patients with septic shock. Crit Care Med. 2004;32:1825–31. 85. Vellinga NA, Boerma EC, Koopmans M, et al. International study on microcirculatory shock occurrence in acutely ill patients. Crit Care Med. 2015;43:48–56. 86. Kruse O, Grunnet N, Barfold C. Blood lactate as a predictor for in-­ hospital mortality in patients admitted acutely to hospital. Scand J Trauma Resusc Emerg Med. 2011;19:74. 87. Cox K, Cocchi MN, Salsiccioli JD, et  al. Prevalence and significance of lactic acidosis in diabetic ketoacidosis. J Crit Care. 2012;27(2):132–7. 88. Shapiro NI, Howell MD, Talmod R, et al. Serum lactate as a predictor of mortality in emergency department patients with infection. Ann Intern Med. 2005;45(5):524–8. 89. Callaway DW, Shapiro NI, Donnino MW, et  al. Serum lactate and base deficit as predictors of mortality in normotensive elderly blunt trauma patients. J Trauma. 2009;66(4):1040–4. 90. Cocchi MN, Miller J, Hunziker S, et al. The association of lactate and vasopressor need for mortality prediction in survivors of cardiac arrest. Minerva Anestesiol. 2011;77(11):1063–71. 91. Donnino MW, Miller J, Goyal N, et  al. Effective lactate clearance is associated with improved outcome in post-cardiac arrest patients. Resuscitation. 2007;75(2):229–34. 92. Teboul JL, Scheeren T.  Understanding the Haldane effect. Intensive Care Med. 2017;43:91–3. 93. Saludes P, Proença L, Gruartmoner G, et al. In response to: “understanding elevated Pv-aCO2 gap and Pv-aCO2/Cc-aO2 ratio in venous hyperoxia condition”. J Clin Monit Comput. 2017;31:1325–7. 94. Van Beest PA, Lont MC, Holman ND, et  al. Central venous-­ arterial pCO2 difference as a tool in resuscitation of septic patients. Intensive Care Med. 2013;39:1034–9.

39 95. Mahutte CK, Jaffe MB, Sasson CS, et  al. Cardiac output from carbon dioxide production and arterial and venous oximetry. Crit Care Med. 1991;19:1270–7. 96. Pittman RN. Oxygen transport. The regulation of tissue oxygenation 2. San Rafael, CA: Morgan & Claypool Life Sciences; 2016, p. 23–26. 97. Jakob SM, Groeneveld ABJ, Teboul JL.  Venous-arterial CO2 to arterial-venous O2 difference as a resuscitation target in shock states? Intensive Care Med. 2015;41:936–8. 98. Silbert BI, Litton E, Ho KM.  Central venous-to-arterial carbon dioxide gradient as a marker of occult tissue hypoperfusion after major surgery. Anaesth Intensive Care. 2015;43:628–34. 99. Vallet B, Pinsky MR, Cecconi M.  Resuscitation of patients with septic shock: please “mind the gap”! Intensive Care Med. 2013;39:1653–5. 100. Mekontso-Dessap A, Castelain V, Anguel N, et  al. Combination of venoarterial PCO2 difference with arteriovenous O2 content difference to detect anaerobic metabolism in patients. Intensive Care Med. 2002;28:272–7. 101. Mesquida J, Saludes P, Gruartmoner G, et  al. Central venous-­ to-­ arterial carbon dioxide difference combined with arterial-­ to-­venous oxygen content difference is associated with lactate evolution in hemodynamic resuscitation process in early septic shock. Crit Care. 2015;19:126. 102. De Backer D, et al. The effects of dobutamine on microcirculatory alterations in patients with septic shock are independent of its systemic effects. Crit Care Med. 2006;34:403–8. 103. Edul VS, Ince C, Vazquez AR, et  al. Similar microcirculatory alterations in patients with normodynamic and hyperdynamic septic shock. Ann Am Thorac Soc. 2016;13:240–7. 104. Edul VS, Ince C, Navarro N, et al. Dissociation between sublingual and gut microcirculation in the response to a fluid challenge in postoperative patients with abdominal sepsis. Ann Intensive Care. 2014;4:39. 105. Tanaka S, Harrois A, Nicolai C, et al. Quantitative real-time analysis by nurses of sublingual microcirculation in intensive care unit: the MICRONURSE study. Crit Care. 2015;19:388. 106. Doerschug KC, Delsing S, Schmidt GA, et  al. Impairments in microvascular reactivity are related to organ failure in human sepsis. Am J Physiol Heart Circ Physiol. 2007;293:H1065–71. 107. Shapiro NI, Arnold R, Sherwin R, et al. The association of near-­ infrared-­ spectroscopy-derived tissue oxygenation measurement with sepsis syndrome, organ dysfunction and mortality in emergency department patients with sepsis. Crit Care. 2011;15:R223. 108. Cabrales P, Vasquez BY, Tsai AG, et al. Microvascular and capillary perfusion following glycocalyx degradation. J Appl Physiol. 2007;102:2251–9. 109. Harrois A, Grillot N, Figueiredo S, et al. Acute kidney injury is associated with a decrease in cortical renal perfusion during septic shock. Crit Care. 2012;2:44. 110. De Backer D. Is microcirculatory assessment ready for regular use in clinical practice. Curr Opin Crit Care. 2019;25:280–4. 111. Barbee RW, Reynolds PS, Ward KR.  Assessing shock resuscitation strategies by oxygen debt repayment. Shock. 2010;33(2):113–22. 112. Schoemaker WC, Peitzman AB, Bellamy R, et al. Resuscitation from severe hemorrhage. Crit Care Med. 1996;24:S12–23. 113. Cowley RA, Mergner WJ, Fischer SS, et  al. The subcellular pathology of shock in trauma patients: studies using the immediate autopsy. Am Surg. 1979;45:255–69. 114. Guan J, Jin DD, Jin LI, et  al. Apoptosis in organs of rats in early stage after polytrauma combined with shock. J Trauma. 2002;52:104–11. 115. Crowell JW, Smith EE.  Oxygen deficit and irreversible hemorrhagic shock. Am J Phys. 1964;203:313–6.

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116. Dunham CM, Siegel JH, Weireter H, et al. Oxygen debt and metabolic academia as quantitative predictors of mortality and the severity of the ischemic insult in hemorrhagic shock. Crit Care Med. 1991;19:231–43. 117. Rixen D, Raum M, Holzgraefe B, et al. A pig hemorrhagic shock model: oxygen debt and metabolic academia as indicators of severity. Shock. 2001;16:239–44. 118. Siegel JH, Fabian M, Smith JA, et al. Oxygen debt criteria quantify the effectiveness of early partial resuscitation after hypovolemic hemorrhagic shock. J Trauma. 2003;54:862–80. 119. Siegel JH, Rivkind AI, Dala S, et al. Early physiologic predictors of injury severity and death in blunt multiple trauma. Arch Surg. 1990;125:498–508. 120. Davis JW, Shackford SR, Mackersie RC, et al. Base deficit as a guide to volume resuscitation. J Trauma. 1988;28:1464–7.

121. Rixen D, Raum M, Bouillon B, et  al. Base deficit development and its prognostic significance in posttrauma critical illness: an analysis by the trauma registry of the deutsche Gesellschaft fur Unfallchirurgie. Shock. 2001;15:83–9. 122. Rixen D, Siegel JH. Bench to bedside review. Oxygen debt and its metabolic correlates as quantifiers of the severity of hemorrhagic and post-traumatic shock. Crit Care. 2005;9:441–53. 123. Nast-Kolb D, Waydhas C, Gippner-Steppert C, et al. Indicators of the post-traumatic inflammatory response correlate with organ failure in patients with multiple injuries. J Trauma. 1997;42:446–54. 124. Meregalli A, Oliveira RP, Friedman G.  Occult hypoperfusion is associated with increased mortality in hemodynamically stable, high-risk surgical patients. Crit Care. 2003;8:R60–5.

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4

Monitoring and Interpretation of Vital Signs in the High-Risk Surgical Patients Sergio Arlati

Key Points • Vital signs are a condensate of physiology. Their abnormality is synonymous of homeostatic perturbation. • Heart Rate is the major adaptive response for increased or maintained cardiac output. • Tachycardia always means circulatory distress. • Blood pressure results from the heart-pumped flow in the arterial tree. Arterial pressure is the main determinant of blood flow in the different body districts. • Maintenance of blood pressure depends on the adequacy of cardiac output and peripheral vascular resistances. Both parameters need to be carefully evaluated before undertaking any intervention aimed to restore arterial blood pressure. • Respiratory rate is a global measure of the energetic cost of breathing. • The increased elastic load (restrictive diseases) is marked by tachypnea, while chronic airflow diseases entail bradypnea unless decompensated (rapid shallow breathing). • Acute changes of body temperature deeply influence the cardiorespiratory status because of the complex effects derived by preservation, increase or dissipation of the body’s heat. • Shivering is always a stressful condition, especially when advanced coronary disease and severe mitral or aortic stenosis are present. • Pulse oxymetry is largely superior to the human eye as a detector of hypoxia. • Its easiness of use made pulse oximetry the standard of respiratory monitoring in virtually any medical setting and even in private houses. • Caution must be paid during severe anemia because of overestimated oximetry readings.

S. Arlati (*) Intensive Care Unit “G. Bozza”, ASST Grande Ospedale Metropolitano, Niguarda Hospital, Milan, Italy e-mail: [email protected]

Vital signs can be regarded as bridges between physiology and clinical practice. Traditional vital signs are heart rate, arterial pressure, body temperature and respiratory rate. Conventionally consciousness is also included but it will not be dealt here. For four decades, however, peripheral oxyhemoglobin saturation (SpO2) as measured by the pulse oximeter has become the fifth vital sign. Both historical and scientific reasons make the recording of vital signs essential in good clinical practice. Historical reasons rely essentially on the fact that wristwatch and thermometer are all you need to obtain body temperature, respiratory rate, and heart pulse, while arterial pressure measurement requires a ubiquitous device as the sphygmomanometer. More recently the pulse oximeter has become so easiest and cheapest that its use is limitless in hospital wards, ambulatories, and even private houses. Scientific reasons are more complex and date back to the nineteenth century when Claude Bernard first introduced the concept of disease as the perturbation of body’s homeostasis. He defined homeostasis as the active maintenance of the “internal milieu” gradually translating into the well-­being state. As the cell spends energy to keep constant the physical, chemical, and structural integrity so by extension the whole body is thought to maintain constant the water and electrolyte balance as well as the acid–base, and metabolic equilibrium by adequate cardiorespiratory and hepato-renal function. According to this vision, any perturbation that definitely and persistently alters the homeostasis entails the physiopathologic process that ends into illness. There are several levels of evaluation to graduate the deviation from the homeostatic equilibrium. Generally speaking, the more sophisticated is the parameter employed, the more precise its accuracy will be. However, it will necessarily pertain to only one or few particular aspects of homeostasis. For example, high levels of Pro-Brain Natriuretic Peptide (ProBNP) mean that ventricular fibers are excessively stretched because of the abnormally increased end-diastolic volume. By converse, the simpler is the parameter, the coarser its specificity will be. Vital signs have low specificity but suf-

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 P. Aseni et al. (eds.), The High-risk Surgical Patient, https://doi.org/10.1007/978-3-031-17273-1_4

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Heart Rate >140

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>40 10  L/min) as occurs during sepsis. Septic patients require the same adjustments of stroke volume and heart rate as seen during muscu-

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lar exercise, although the sepsis-induced myocardial dysfunction decreases contractility, this in turn limiting ventricular ejection and volume output [5]. Heart rate, therefore, becomes an even more important compensatory mechanism in septic patients. Nevertheless, any parallel increase of heart rate and cardiac output (Fig. 4.3; right) causes the progressive reduction of diastolic time that is the time useful for left ventricular perfusion by coronary blood flow. Heart rate is a major determinant of myocardial oxygen consumption the other two being cardiac contractility and ventricular wall tension. Except at very high values of arterial pressure, changes in heart rate rule the respective changes in myocardial oxygen demand. Therefore, the increase of heart rate increases the myocardial oxygen demand and contemporarily reduces the diastole that is essential for coronary blood supply. In effect, the heart lies in the difficult position of having to generate the arterial pressure that is necessary to achieve the adequate coronary perfusion pressure and hence the coronary blood flow (to be rigorous the pumped flow is the pressure generator). This concept is very important and needs some explanations. Let us consider a heart beating to 75 bpm (1 beat/0.8 s). Every systolic contraction lasts 0.32 s, so that the duration of the diastole is 0.48 s. Such time partition ensures the filling of ventricular chambers (preload). When the heart rate is increased to 125 bpm, both the systolic and diastolic time reduces to 0.24 s each but the reduction is proportionally different being −25% and −50%, respectively. Therefore, the diastolic time halves, while the systole reduces by ¼ only. Such a different impact of the increased heart rate is shown in Fig. 4.4. For example, when the heart beats to 140 bpm, the diastole is reduced to about 1/3 of duration at 60 bpm, while the systole reduces of −35%



0.7 0.6

Diastole

Time sec

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only. This would theoretically impact on the loading of the ventricle, as the faster the heart beats the lesser the ventricle fills. Moreover, the increased heart rate shortens the diastolic time, so reducing the time allowed for O2 extraction by myocardial cells. Increased heart rate also elevates the arterial diastolic pressure, therefore, increasing the coronary perfusion pressure but it also causes the ventricular wall tension to rise (increased afterload). Change in heart rate is, therefore, the dominant factor for changes of myocardial O2 demands. Normal subjects have a coronary reserve large enough to keep the coronary O2 demand/supply adequate even for heart rates greater than 200  bpm as long as wall tension is not excessively increased. This does not hold true for patients with reduced coronary reserve as the increased inotropic and chronotropic states cause the heart rate and systolic peak wall tension to rise thus precipitating myocardial ischemia. The regulation of heart rate is determined by autonomic inputs, namely, the parasympathetic and adrenergic input. The intrinsic heart rate has been studied in more than 400 healthy individuals aged 16–70 years by blocking both the autonomic systems with atropine and propranolol [6]. The intrinsic heart rate was 106 beats/min in 25-year-old subjects with an age-related decrease of 0.057  beats/min/year. Because of the normal resting rate ≤ 70 beats/min, the parasympathetic tone predominates in the resting state. It seems advantageous that both autonomic systems operate in the normal subject as heart rate can rise immediately in case of stressful conditions by increased adrenergic tone [7, 8]. This obviously occurs in disease states, even if it is probably less advantageous. The concept of age-related decrease of the heart rate holds true also for its maximum value. The maximum heart rate declines linearly with age as follows:

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Fig. 4.4  Duration of corresponding systolic and diastolic times with different heart rate values. Increased heart rate causes the diminution of both systole and diastole duration. Diastole is much more decreased than systole (respectively, −50% and 25% at 120 bpm), so that the time available for myocardial perfusion is reduced

210 − ( Age × 0.5 ) for age > 20 years

Thus, the maximum heart rate value of a 40 year healthy man is 210 − (40 × 0.5) = 190 beats/min, and it will reduce to 170 bpm at the age of 80 years. The age-related reduction of the maximum heart rate implicates that the related increase of cardiac output is decreased by aging. Otherwise stated, the heart rate becomes less efficient to match the increase of peripheral O2 needs. The reduced cardiac reserve requires a close monitoring of the oldest surgical patients to prevent or halt any dangerous increase of metabolic requirement in the perioperative period. Fever, shivering, and stressful conditions as pain, fear, anxiety must be adequately prevented or rapidly controlled especially in the eldest. Similarly, hypoxia and anemia must be corrected as soon as possible because of their potential to cause inadequate O2 delivery by the reduced cardiac reserve. The increase of heart rate during exercise occurs through three distinct mechanisms. When the motor inputs travel from the motor cortex to the neurons in the anterior horns of the spinal cord, part of that signal reaches the sympathetic centers in the hypothalamus and the medulla,

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4  Monitoring and Interpretation of Vital Signs in the High-Risk Surgical Patients

thus increasing the adrenergic output to the heart and vessels. This central drive also increases the heart rate in non-­exercise conditions as pain, fear, and anxiety. The second mechanism is regulation by baroreceptors in response to changes in arterial pressure. The third factor operates either in normal and pathologic conditions by activating peripheral afferents in response to the increase of metabolic requirements in exercising as well as ischemic or inflamed tissues [9–11]. The key point is that tachycardia induced by sympathetic afferents does not invariably mean hypovolemia and should not be treated with volume infusion unless signs of hypovolemia are present. The other notable exception is reflex tachycardia in response to decreased peripheral resistances. Again, no volume infusion but vasopressors are required to normalize peripheral vascular tone. Atrial fibrillation is one of the most frequent tachyarrhythmias which occur in both cardiac and non-cardiac patients during the perioperative period. During the acute onset of atrial fibrillation, the atria depolarize at 400–500 per min, but the ventricular rate is considerably lower, usually 140–180 per min, because of blockage through the A–V node. Atrial Fibrillation is often caused by hypovolemia in adjunct to high sympathetic tone (fear, anxiety, and pain) or misuse of beta-adrenergic drugs (dopamine, dobutamine, and epinephrine) to treat episodes of hypovolemia-induced hypotension. Other frequent causes are the sudden decrease of venous return (e.g., Valsalva manoeuver) or the use of positive pressure ventilation. Less frequently, severe causes of sudden onset atrial fibrillation include pulmonary embolism, cardiac ischemia, and new onset of sepsis. The first question to answer in the presence of atrial fibrillation is the patient’s tolerance. Atrial fibrillation may precipitate pulmonary edema or new myocardial ischemia in patients with mitral stenosis or ischemic cardiomyopathy. The increased heart rate causes the diastole to shorten, so that flow across the mitral valve or fixed coronary stenosis is severely reduced. When the mitral valve is significantly narrowed, the increase of flow can only be obtained by increasing the trans-­ valvular pressure gradient, which, in turn, raises the pulmonary vein pressure. In addition, the shortened diastole time may precipitate ischemic signs and symptoms in patients with limited coronary reserve. If pulmonary edema or myocardial ischemia is serious concerns, the rapid control of ventricular rate is an emergency. When atrial fibrillation onsets in non-cardiac patients, the rate control is mandatory, but less urgent. Anyway, the underlying cause (e.g., hypovolemia, electrolyte disturbances, hypoxia, and acidosis) must be aggressively searched and corrected as atrial fibrillation is a marker of perturbed homeostasis. In summary, the increased heart rate is always produced by activation of the adrenergic system. The activation of the orthosympathic system is the rule during actual or anticipated stressful conditions. Tachycardia is an essential part of

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the stress reaction as it contributes to increasing the cardiac output and hence O2 delivery to tissues. It is imperative to search for the cause of tachycardia and to eliminate it, especially in the eldest because of their greater frailty. Beta1-­ adrenergic blockers must be used cautiously especially when the cause of tachycardia remains unidentified.

4.2 Blood Pressure Blood pressure is certainly the most important of vital signs. It is a common experience that profound hypotension is life-­ threatening and that multiple organ damage always follows prolonged tissue hypoperfusion. Clinical signs and symptoms of severe hypotension include anuria, lethargy, ileus, nausea, vomiting, cardiac arrhythmias, mental confusion, and reduced cognitive functions. Occurrence is faster and intensity stronger if concurrent cardiac, renal, metabolic, and atherosclerotic diseases are present. The basic question before going inside the physiological and clinical meaning of arterial pressure is the following: what determines blood pressure? The common belief is that the heart generates a force, arterial pressure, which drives blood around the circulation. However, it is the blood volume forced through the vascular resistances that generate arterial pressure [12]. Therefore, flow generates pressure and not vice versa. However, arterial pressure is a major determinant of regional blood flow, although it is not an indicator of regional blood flow. Otherwise, stated normal values of arterial pressure are not sufficient to ensure the adequacy of flow. Any evaluation of the adequacy of arterial pressure is, therefore, coupled to the adequacy of flow. From a physical standpoint, arterial pressure can be defined as the force that distends the elastic wall of the vessels. This force acts perpendicularly to the vessel wall, so that it can be defined as P = F/S, where P, F, and S are pressure, force, and surface area, respectively. The hydrostatic definition can be viewed dynamically as the force that propels the fluid into a conduit (Pressure = Flow × Resistance). This definition is analog to Ohm’s law for electrical circuits: ε = I × R, where ε is the electrical potential (analogue to hydraulic pressure), I is the intensity of the electrical current (analog to flow), and R is the resistance of the circuit (analog to hydraulic resistance). In addition, pressure can be defined as the hydraulic force that makes work by pushing a pulsatile fluid volume (e.g., Blood Pressure = Cardiac work/systolic volume). Finally, pressure can be related to blood velocity by the following relationship:

P = v max ( 4πL / r 2 )

where υ is viscosity and r and L are, respectively, the radius and length of the conduit. According to this relationship, blood velocity decreases as the cross-sectional area of

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the vascular segment increases. This is what really happens as the blood flows from the aorta to the perfused capillaries, whose cross section is about 700 times larger. The mean blood velocity decreases from 110  mm/s in the ascending aorta to only 0.65 mm/s in human skin capillaries [13, 14]. The second important question is why the pressure is so high? First, a basic principle of cardiovascular physiology is that the circulatory system is pressure regulated, so that blood pressure is kept within a narrow range of values. Such regulation is good for cardiac performances as the left ventricle handles volume loads better than pressure loads. By keeping the pressure constant, the heart works against a relatively constant workload. Second, the systemic circulation has high distributive tasks as it serves different vascular beds with different oxygen requirements and functions. Moreover, the oxygen requirements may increase of manifolds from the rest to exercising conditions. This is particularly true for the muscle and the gut, whose regional blood flow increases markedly during physical activity and digestive processes. Oxygen requirement drives the regional blood flow in muscle, heart, gut, and liver, while the brain and kidney maintain a relatively constant blood flow because of their autoregulatory properties. The constant flow to the kidney relies upon its function: the high flow per minute is essential to purify blood from the wasted products. Finally, the skin has relatively low metabolic needs, but its regional flow may change of manifolds with respect to resting conditions because of its thermoregulatory functions. Blood flow to the skin increases during muscular exercise or the stay in heat environments, the opposite occurs with exposition to low temperatures. The distributive function of the arteries relies upon the structure and function of the smaller vessel (diameter ≤ 0.1 mm). The thickness of smooth muscular layers increases progressively along the arterial tree, the ratio between the vessel wall and the lumen increasing from 1/6 in the aorta (2 mm/12 mm) to 4/3 in the smaller arterioles (20 μm/15 μm). The increased thickness of the smooth muscle layer allows for the active control of the vessel patency by orthosympathic stimulation. Maximal orthosympathic stimuli may even occlude the vessel lumen as occur to skin arterioles of the hands and foots after exposure to very cold temperatures. In an ideal “Newtonian” fluid, the pressure drop (∆P) along the course of the conduit is determined by the following relationship:

∆P = Φ × Res

where Φ and Res are, respectively, flow and resistance. As determined by Poiseuille in the nineteenth century, the resistance to flow depends from the viscosity of the fluid (η), the length (L), and radius (r) of the vessel according to the relationship:

Res = ( 8· L ) / ( πr 4 ) where the fourth power of the radius is the crucial factor.

When the radius of the conduit doubles, a 16-folds decrease of the hydraulic resistance occurs! The opposite occurs when the radius halves (16-folds increase of hydraulic resistance). Such results can be appreciated by this simple common-life example: everybody has experienced the brisk reduction of car speeds when driving on a trafficked motorway after 1/3 reduction of the roadway. According to Poiseuille’s law, the car speed should reduce to 20% only (e.g., from 100  km/h to 20  km/h). This seems surprising, but it is what really happens in a small artery when the flow is reduced to 1/256 because of the reduction of the vessel radius to ¼ only of its diameter. Active smooth muscle contraction is extremely effective in regulating the blood flow through the small arteries. The other factor responsible for the pressure to drop along the vessels is the viscosity of blood. In an ideal flowing fluid, the sliding over each other of the thin layers of the fluid column, as well the contact of the fluid with the vessel wall, cause a frictional loss of energy called “viscosity”. Viscosity causes the pressure drop along the course of the vessels, which is referred to as the resistance to flow. In a non-Newtonian fluid as the blood, viscosity is a non-linear function of hematocrit and plasma proteins (lesser). Values of hematocrit >50% or plasma proteins >9–10 g/L cause the substantial increase of viscosity. Chronic hypoxia (e.g., chronic respiratory failure), right-to-­left cardiac shunt, myeloma, and macroglobulinemia are well-known causes of increased blood viscosity. To summarize, the systemic circulation is a high pressure reservoir with elevated distributive capacities, thus matching the nutritional and functional requirements of a heterogeneous pool of organs and tissues. The high pressure of systemic circulation warrants the body with an immediate reservoir of energy which allows the prompt diversion of flow from one organ to another. The maintenance of high arterial pressure is due to the elastic properties of the great arteries. In the aorta as well as in arteries ≥2 mm diameter, elastic tissue represents over 50% of the medium layer, so that the artery functions as a pressure reservoir. With systole, the elastic energy generated by the distension of arterial walls is stored and subsequently released during diastole. This keeps the diastolic pressure higher than in a non-compliant vessel, so increasing the mean arterial pressure also defined as mean perfusion pressure. The higher is the ejected volume and the more compliant the artery is the higher will be the stored energy and the derived perfusion pressure. Systolic blood pressure offers an overall evaluation of cardiac performance. Its main determinants are (1) initial arterial volume at the start of the ejection, (2) arterial compliance, (3) ejected (stroke) volume, and (4) rate of outflow from the great arteries:

Psyst = ( Stroke Vol + Vi ) − ( Φeff × 60 / HR )  / Cart

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4  Monitoring and Interpretation of Vital Signs in the High-Risk Surgical Patients

where Vi is the initial (pre-systolic) blood volume contained in the arteries, Φeff is the effluent flow, T is the time period (60 sec/HR), and Cart is arterial compliance. The duration of the cardiac cycle (heart rate) also affects the pressure. Diastolic pressure is more dependent on the run-off from the large arteries which in turn depends on peripheral resistances. Heart rate and the initial volume of the artery also affect the diastolic pressure:

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the sympathetic tone so causing generalized vasoconstriction, but local vasodilation prevails in the exercising muscles and the heart. The vasoconstrictive effect in the other districts redirects the flow to the working regions, thus increasing muscular and cardiac perfusion. In contrast to the muscle, the brain and kidney have constant metabolic needs, but they depend on constant regional flow for their function. The constant flow implies no significant changes in arterial pressure. The increased pressure in cerebral vasculature stimulates the Pdia = ( τ × Vi × HR / 60 ) / Cart myogenic “Bayliss” reflex (arteriolar smooth muscle con where τ is the time constant of blood efflux from the arte- traction) so maintaining the flow constant [18, 19]. The rial system and 1/T = HR/60 sec is time−1 (s−1). As a result, inverse occurs with decreased arterial pressure as the vessels diastolic pressure increases as the diastole becomes shorter. dilate. Both mechanisms help to keep constant intracranial However, the shorter diastole means lesser time for coronary blood volume (and flow), thus avoiding the dangerous rise of perfusion. Moreover, the increased heart rate elevates the intracranial pressure. Local metabolic mechanisms are lost metabolic needs of the cardiac muscle. Therefore, heart rate or malfunctioning in sepsis, ischemia, and chronic endotheis a double-edged sword as it elevates the coronary perfusion lial dysfunction [20–22]. According to Poiseuille’s law, the calculation of vascular pressure but also decreases the time for perfusion in the presresistances is obtained by diving the cardiac output by the ence of increased O2 demands. The distribution of local artery resistances is a major difference between the inflow and the lowest outflow presdeterminant of where the blood goes. Therefore, the third sure usually settled at the level of the right atrium (central question is what is resistance? The arterial vessel modifies venous pressure). This is not the case when there are flow-­ the radius by active dilation or constriction [15]. Small diam- limitation phenomena that occur at the arteriolar level. eter changes produce large resistance variations, and each Arteriolar vasoconstriction generates a critical closing presvascular bed has its own resistance characteristics so causing sure, so that the effective flow does not depend on inflow and inter-organs flow distribution. Maximum vessels dilation is outflow pressures but from the difference between the arteset by distension of collagen and elastin fibers [16]. A fully rial and critical closing pressure giving the so-called waterdilated vessel functions like a rigid pipe, where flow increases fall effect [23, 24]. Standard vascular resistances calculated linearly with the increased pressure. As a corollary, the maxi- from arterial and central venous pressure overestimate the mal flow in one organ is the function of its vascular density, true resistance value, the error getting larger as arterial presthat is, the cross-sectional area of its vasculature per gram of sure drops. This is because the error makes up a larger fractissue. For example, the heart has three times the cross-­ tion of the total pressure difference. As a result, there is an sectional area with respect to the muscles. Its basal flow can, “apparent” decrease in systemic resistances as pressure or therefore, increase three times more than the muscular tissue. flow increases. Therefore, the standard calculated resistances Baseline flow is normally set by neural inputs which keep the will fall whether there is or not a change in true resistance. pressure constant, the baroceptors acting as main sensors for The effect of the sympathetic output on critical closing presthis process. During hypotension, vascular resistances sure and true vascular resistance is illustrated in Fig.  4.5, increase disproportionately in non-visceral organs as mus- where a pressure–flow relationship is shown for three differcles and skin, so redirecting flow to more “vital” organs [17]. ent levels of adrenergic tone. The slope of the curve is the Although teleological, the adaptive meaning of this process vascular conductance that is the inverse of resistance (1/R). acts intuitively to preserve metabolically active organs. This As the sympathetic output changes, critical closing pressure probably results from the higher density of adrenergic recep- and conductance vary in the opposite way. High adrenergic tors in visceral organs, the corollary being that vasoactive tone reduces conductance by vasoconstriction, but increases drugs are more active in the viscera. Local distribution of the critical closing pressure. The presence of critical closing flow can, however, overcome the hierarchical order between pressure means that arterial pressure can be regulated in two vital and less vital organs. This occurs every time the com- ways: (1) by a change in the actual resistance (1/slope of the mon needs of the day-life require additional blood to accom- pressure–flow relationship) or (2) by a change in critical plish the functional duties of the involved district. Local closing pressure (X-intercept). If the pressure rises because metabolic needs, flow-mediated vasodilation, and the myo- of increased vasoconstriction, a given change in flow will genic reflex, interact to autoregulate the regional flow distri- produce a greater change in pressure. If the rise in pressure is bution. A good example of their interaction is the exercising due to increased critical closing pressure, the subsequent muscle: the drop of systemic vascular resistance and the change in flow will produce the same change in pressure as stimulation of efferent endings in muscular tissue [9] increase occurred before the increase of critical closing pressure

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S. Arlati Absent Orthosymp. stimulation Rigid Tube

Flow

Increased Orthosymp. stimulation

Maximal Orthosymp. stimulation A

B

C CRITICAL CLOSING PRESSURE

Flow

∆P2 > ∆P1

Pressure

Flow

Fig. 4.5  Influence of orthosympathic stimulation on arterial resistance and critical closing pressure. The slope of the curve represents conductance (1/Res). At maximal stimulation the arterial closure occurs at the highest pressure value. Vasoconstriction increases the hydraulic resistance as reflected by the decreased slope (decreased conductance)

∆P2=∆P1

Pressure

Fig. 4.6  Arterial pressure can be regulated by change in the actual resistance or by change in critical closing pressure. If pressure rises because of increased vasoconstriction a given change in flow will produce a greater change in pressure (left panel). If the rise in pressure is due to increased critical closing pressure the subsequent change in flow will produce the same change in pressure as occurred before the increase of critical closing pressure (right panel)

(Fig. 4.6). To discriminate between change in true resistances and critical closing pressure one should obtain two separate measurements and then plot them on the pressure–flow relationship (Fig. 4.6). Unfortunately, this is difficult to achieve in the intact person, so that critical closing pressure cannot be estimated in the clinical practice. The presence of the critical closing pressure in the vascular system implies that changes in standard vascular resistances have little meaning in comparison to the directional changes in arterial pressure and the cardiac output. The use of vasopressors represents a good example of the utility of such an approach. Normally, the rationale behind the use of vasopressors is to augment the arterial pressure so increasing flow to the vital organs. If vasopressors increase the blood pressure, but the cardiac output does not increase, their clinical utility is doubtful. Conversely, the decrease of blood pressure by proportional decrease of vascular resistances causes the flow to be

­ aintained even at lower pressures. This is why some peom ple, especially women, can have normally functioning organs at systolic arterial pressure of 90 mmHg. Blood pressure is, therefore, a complex function of many interplaying variables, but its usefulness to estimate the actual flow is poor. Nevertheless, physicians continue to look at arterial pressure as a limited but essential tool for the therapeutic goal of increasing tissue perfusion. Emphasis on pressure is misleading without some assessment of the overall flow [25]. The clinical objective of increased arterial pressure is to ameliorate the perfusion of organs, such as the brain and kidney. If this does not occur, the increase of arterial pressure is clinically useless. Careful clinical observation and monitoring are mandatory to predict the usefulness of increased arterial pressure: the improvement of mental status and diuresis together with decreased arterial blood lactates are extremely valuable signs of improved organ perfusion. The key message is that arterial pressure is by no means equivalent to organ perfusion, but its “adequate” values are essential for homeostasis. The concept of “adequacy” relies upon the fact that arterial pressure must be evaluated in conjunction with a constellation of factors that help to decide the use or titration of vasoactive drugs, and fluid volume. Unfortunately, no target values of blood pressure can be recommended as only the pressure–flow combination helps to set the adequate pressure values. For example, a blood pressure of 90/55 mmHg may be adequate in conscious, warmth and urinating patients with normal heart rate and arterial blood lactates. Vice versa, the same blood pressure is deleterious in a tachycardic, oliguric, pale, and cold skin patient, as this clinical picture suggests inadequate tissue perfusion. The final question is how the clinician can determine if rising blood pressure is helpful or harmful. Remember that treatment is aimed to increase flow in some organs! If this does not occur, the treatment is probably useless. Physiologically, the question can be translated as follows: are vasopressors useful to increase the cardiac output of my patient and to decrease the anaerobic metabolism? The reverse is also true: can the suspension of vasopressors maintains or even increases the cardiac output? If reduction of vasopressors does not change flow, the lowering of arterial pressure is probably harmless. The continuous monitoring of arterial pressure and flow is regularly performed in the presence of hemodynamic instability. Most sophisticated hemodynamic monitoring is reserved for the ICU setting and includes the invasive measurement of cardiac output and left filling pressure. However, it is useful to have some integrated cardiovascular parameters that help the clinicians to detect patients with falsely normal or initially lower than normal arterial pressure values as consequence of the abnormal cardiovascular status. The most common bedside descriptors of circulatory inadequacy include hypotension, need for vasoactive drugs, increased right atrial pressure (CVP), abnormal (too high or too low) venous O2 saturation,

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4  Monitoring and Interpretation of Vital Signs in the High-Risk Surgical Patients



PAR = HR × CVP / MAP

It is expressed in beats per minute and adjusts the heart rate by a factor that mirrors the response of the systemic blood pressure to a rough surrogate of cardiac function as CVP.  In normal individuals (heart rate 60–90  beats/min, CVP 4–8 mmHg, and MAP 70–100 mmHg), the PAR ranges from 2.5 to 10  beats/min. The asymptomatic myocardial injury occurs in more than 30% of patients undergoing non-­ cardiac surgery [30]. It is frequently encountered in the post-­ operative period as a consequence of generalized systemic

ABNORMAL CARDIAC FUNCTION

ABNORMAL CARDIOVASCULAR FUNCTION

NORMAL CARDIOVASCULAR FUNCTION

ABNORMAL VASCULAR TONE

PAR 10

and increased arterial blood lactates [26, 27]. In addition, the Shock Index and the pressure adjusted rate (PAR) are composite measures of basic cardiovascular parameters as heart rate, arterial pressure, and CVP, which help clinicians to estimate the adequacy of the cardiovascular status in addition to traditional vital signs [28, 29]. Shock Index is defined as the ratio between heart rate and corresponding arterial systolic pressure value (HR/Psyst) with values >1 indicative of worsening hemodynamic status and shock [28]. The rationale behind Shock Index is that increased heart rate causes the physiological increase of systolic blood pressure. This assumption holds true only if the cardiovascular function is normal (adequate preload, afterload, and contractility). In practice, any heart rate higher than the corresponding value of systolic pressure suggests that the cardiovascular function is abnormal and that abnormality is approaching shock. The higher is the HR/Psyst ratio, the worse the hemodynamic perturbation is. As an example, consider a tachycardic patient with the heart beating at 125 bpm and with 110 mmHg of systolic blood pressure (Shock Index 1.14). The patient’s examination reveals oliguria and pale and cold extremities, but neither altered mental status nor increased arterial blood lactate is present. Both central venous saturation (surrogate of O2 delivery) and PvCO2–PaCO2 gap (surrogate of cardiac output) are abnormal (see Chap. 3). The measurements of central venous pressure or echocardiography are useful to make the discrimination between hypovolemic and cardiogenic “compensated” shock. Patients with severely reduced cardiac output may have normal or even increased arterial pressure due to increased peripheral resistances. The prudent physician will search for inadequate tissue perfusion (venous SatO2 and CO2 gap) so unmasking the flow/pressure relationship as abnormal. Another patient with 140 bpm and Psyst 85 mmHg (Shock Index 1.65) and more severe clinical conditions (anuria, mental confusion, and agitation) has warm skin and fever. This patient is clearly septic, but again, the Shock Index only informs about the severity, not the cause of cardiovascular dysfunction. The PAR is a composite measure that adjusts the cardiovascular function in relation to physiological variables. PAR is calculated as the product of heart rate by the ratio of central venous pressure to mean arterial pressure measured simultaneously:

1 Shock Index

Fig. 4.7  Integrated use of Shock Index and PAR allows for the bedside analysis of cardiac and vascular function. Isolated (yellow square) or complete (red square) abnormalities can be found depending from the patient’s integration of both scores (see text for explanations)

inflammation [31]. Administration of fluids in a hypotensive patient with cardiac dysfunction may increase CVP, resulting in PAR > 10 beats/min. The increase of PAR after volume loading can help to suspect coexistent myocardial dysfunction, and to differentiate it from pure hypovolemic-related hypotension. In effect, PAR is normal (≤10 beats/min) when decreased blood volume is the only responsible for hypotension. Thus, PAR in a hypovolemic patient with 120  bpm, CVP 4  mmHg, and MAP 60  mmHg will be 8  beats/min. Conversely, PAR in a septic patient with 125  bpm, CVP 8 mmHg, and MAP 55 mmHg will be abnormal (16.7 beats/ min) probably as a consequence of septic induced myocardial dysfunction [5]. The combination of SI and PAR might allow the clinical distinction between normal and abnormal cardiovascular function at the bedside. Figure 4.7 illustrates this opportunity by placing the corresponding SI and PAR values on an x–y plot. Four different conditions are dichotomously defined according to the respective cutoff (normal) values. A normal cardiovascular status is highly probable when both SI and PAR are normal. The opposite occurs when both are abnormal. Intermediate conditions might help to suspect the prevalence of abnormal vascular function (SI abnormal and PAR normal) versus poor cardiac function (SI normal and PAR abnormal).

4.3 Respiratory Rate Respiratory rate is one of the most important but neglected clinical sign [32]. Abnormal values have been repeatedly associated with poor outcome, increased rate of adverse events (e.g., cardiac arrest), and need for ICU admission [33, 34]. Abnormal respiratory rate associates with any condition

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that causes hypotension, acidosis, and hypoxia [35]. This frequently occurs with circulatory shock, cardiac failure, asthma, pneumonia, cerebrovascular stroke, diabetic ketoacidosis, drugs overdose, and kidney failure. Respiratory rate is, therefore, an important alert for severe derangement of several body districts. Nevertheless, respiratory rate is the neglected part of monitoring as its recording often lacks on the sheets of patient’s clinical records [36]. Surprisingly, this occurs even when pulmonary pathology is the main cause for hospital admission. One reason might be the inaccurateness of automated recording systems, but the poor appreciation of its physiological meaning is probably more important [37, 38]. To fully appreciate its importance, the first question to answer is: how respiratory rhythm generates? Breathing is the life function that people almost never think about until they are overexerted, or something goes wrong. Again, respiration is the last function to be lost before the onset of brain death. As a corollary, the control of ventilation is one of the most important brain functions. Its two main duties are (1) the establishment of an automatic respiratory rhythm and (2) the needed adjustments to accommodate for the change of metabolic demands (blood PO2 PCO2 and pH), mechanical conditions (e.g., changing posture), and a vast array of non-­ ventilatory behaviors (e.g., speaking, singing, eating, and sniffing). The respiratory rhythm is generated by respiratory-­ related neurons grouped in the central pattern generator (CPG) of the brain medulla. Neurons of CPG are interneurons, pre-motor neurons, and motor neurons innervating the respiratory muscles, such as the diaphragm and external intercostal muscles. These muscles are primarily involved in eupnoea that is defined as the normal respiratory condition of sleeping, resting, and mild muscular exercising. When the neural respiratory output is increased as during heavy exercise, the accessory inspiratory muscles and expiratory muscles become actives. Pre-motor neurons modulate the pattern of activity of accessory respiratory muscles by increasing both the frequency and strength of contraction (rate and depth of breath). The CPG can be viewed as a clock that cycles automatically from inspiration to expiration. This happens because of the tonic drive inputs from both central and peripheral chemoreceptors. However, the output of CPG can vary in response to changes in chemoreceptors stimulation. Peripheral chemoreceptors are located in the carotid and aortic bodies. They are exquisitely sensitive to decreased arterial PO2, but high PCO2 and low pH values can increase their sensitivity to hypoxia. The glossopharyngeal (CN IX) and vagus nerve (CN X) are deputed to convey chemoreceptor stimuli to the CPG. Central chemoreceptors are located on the “brain side” of the blood–brain barrier just beneath the floor of the fourth ventricle. They are quickly sensitive to even small increases of arterial PCO2. Decreased arterial pH is another important although slower stimulus. Arterial PO2 does not stimulate central chemoreceptors at all. In sum-

mary, peripheral and central chemoreceptors use CO2, PO2, and [H+] as a negative feed-back to stabilize arterial blood chemistry. For example, the rise of PaCO2 stimulates the central chemoreceptors to enhance the neural output of CPG so increasing pulmonary ventilation. The vice versa occurs when PaCO2 is low. The decrease of PaO2 to 55 mmHg or less causes the stimulation of CPG by peripheral chemoreceptors. Other sensory inputs derive from stretch receptors (lung parenchyma), irritant receptors (airways), and proprioceptors (rib cage joints, muscles, and tendons). Finally, the higher non-respiratory centers of the CNS interact with CPG to integrate respiration with many non-respiratory activities as speaking, singing, playing a wind instrument, swallowing and vomiting, and, in a general sense, with all aspects of vegetative and emotional life. CPG consists of two pairs of related respiratory neurons located, respectively, on the dorsal (dorsal respiratory groups; DRG) and ventral (ventral respiratory groups; VRG) surface of the medulla, pons, and other parts of the brain stem. Both DRG and VRG contain high densities of neurons that fire in phase with the respiratory cycle. The DRG processes sensory inputs and contains primarily inspiratory pre-motor neurons, the nucleus tractus solitarius being its major component. The major sensory input travels via the IX and X cranial nerves, while the efferent pre-motor output descends to the anterior horn of the spinal cord, where are located the inspiratory motor neurons of the diaphragm and external intercostal muscles. The VRG is primarily motor and contains both inspiratory and expiratory neurons. Its major components are the nucleus retrofacialis or Bötzinger complex (caudal), the nucleus ambiguus and parambigualis (intermediate), and retroambigualis (rostral). Its output consists of neurons innervating the pharynx, larynx as well as thoracic and abdominal viscera. In summary, VRG plays an efferent role, whereas DRG primarily elaborates the afferent inputs. Within the rostral pole of the intermediate VRG lies a group of inspiratory neurons, the pre-Botzinger complex, which is thought to be involved in the generation of the respiratory rhythm, although not definitely proved in humans. Another theory postulates that more than one single CPG exists in the latent state and that each of them can take over the generation of the respiratory rhythm. Such theory has the advantage of physiological redundancy, because the respiratory output can never fail, as it occurs by the replacing activity of multiple cardiac pacemakers. The most common explanation for the origin of respiratory rhythm is that no single region of VRG and DRG is sufficient by itself to generate the rhythm, but that many regions are contemporarily required. If left alone, CPG would regularly oscillate for indefinite periods, so that the respiratory rate is fixed, but the activity of higher CNS centers finely tunes that rhythm. Historically, the transection of the brainstem at midpons and rostral level causes the alteration of the normal respiratory pattern. This led to postulate the existence of an

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4  Monitoring and Interpretation of Vital Signs in the High-Risk Surgical Patients

apneustic center (causing apneusis) and a pneumotaxic center (promoting coordinate respiration). Today, these centers have only a historical significance as their action is not necessary for the generation of the normal respiratory rhythm. The second question is: which inputs influence the rate of the respiratory rhythm? Afferent inputs to the CPG are provided by four groups of receptors: (1) peripheral arterial chemoreceptors, (2) central chemoreceptors, (3) intrapulmonary receptors, and (4) chest wall and muscular mechanoreceptors. Peripheral chemoreceptors in humans are located in the carotid (largely prevalent) and aortic bodies. The carotid bodies are located at the junction between the internal and external carotid arteries. They are small (3–5  mm size, weight 10–12  g) and are perfused by branches of the external carotid artery. The sensory supply is provided by the glossopharyngeal nerve (IX CN), which contains both sympathetic and parasympathetic fibers. Two cell types, the glomus cells (type I) and the sheath cells (type II), populate the carotid bodies. Their highest blood supply in the body (20  mL/min/g) ensures the entire O2 demand by the dissolved oxygen [39]. In comparison, the heart receives only 0.8–1.6 mL/min/g, while the supply of the kidney averages 0.5 mL/min/g [40]. In addition, PaO2 is the specific signal for the glomus cells, so that decreased O2 tension in arterial blood stimulates the chemoreceptors. By converse, they are insensitive to reduced O2 content as occurs in anemia and carbon monoxide poisoning [39]. Carotid bodies exhibit a non-linear response to decreased PaO2 and pH, the greatest stimulus being hypoxemia. When PaO2 falls to 55  mmHg or less, minute ventilation is enhanced by increasing the depth of breaths (VT) and to a lesser extent by raising the respiratory rate. Bilateral carotid bodies resection reduces the resting minute ventilation (VE) and causes the elevation of resting PaCO2 by 2–4  mmHg [41]. More importantly, the ventilatory response to hypoxemia is abolished both at rest and during exercise [41]. Carotid endarterectomy is a complication of unintended carotid body resection [42]. The ventilatory response to hypoxemia varies depending on the level of PaCO2 [43, 44]. The PaO2/VE relationship is exponential with a raising slope as PaCO2 increases. The opposite occurs with hypocapnia [43] (e.g., “rapid shallow breathing”). Hypoxemiainduced hyperventilation causes PaCO2 to decrease, so that the stimulus to central chemoreceptors is blunted. A conflicting situation develops as the respiratory drive is inhibited by decreased stimulation of central chemoreceptors, while the opposite occurs with the high stimulation from peripheral chemoreceptors. The result is the (apparent) difference in the less powerful hypoxemic than hypercapnic stimulus. When hypoxemia is tested in normal volunteers while keeping PaCO2 constant, both stimuli are equally powerful [45]. Caution must be exerted when the combination of hypoxemia and hypercapnia does not trigger venti-

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lation as the reduction of the ventilatory drive must be suspected (e.g., opiates and sedatives). The central chemoreceptors are located in the proximity of the ventral surface of the medulla, behind the parenchymal surface of the blood–brain barrier that delimits the fourth ventricle. Stimulation of central chemoreceptors increases the rate of respiratory rhythm. They respond primarily to the increase of H+ ions in CSF and medullary interstitial fluid [46]. Hydrogen ions enter and exit the CSF as a result of the high CO2 permeability. Elevation of CO2 in arterial blood increases its diffusion in the CSF, where it quickly dissociates as H+ and HCO3− because of carbonic anhydrase. The rise of [H+] in the CSF and medullary interstitium stimulates the central chemoreceptors to increase pulmonary ventilation. Conversely, the decrease of PCO2 (and [H+]) reduces the ventilatory drive [47]. Central chemoreceptors are less sensitive than peripheral chemoreceptors as they adjust blood chemistry for lesser breath-to-breath variations [47]. The response to increased PCO2 is increased by arterial hypoxemia [43]. The slope of the ventilatory response to CO2 increases exponentially as PO2 lowers. Both hypercapnic and hypoxemic responses become weaker with aging [48]. The ventilatory response consists of two phases: the first is rapid, because of the sharp increase of H+ ions in the protein-free CSF solution. The second is slower, as the proteins in the medullary interstitium buffer the [H+] build-up. The relatively slow diffusion of H+ ions through the blood– brain barrier causes metabolic acidosis to be less vigorous as a stimulus than respiratory acidosis [47]. Chronic elevation of PCO2 also displays a weaker effect because of the renal retention of HCO3−. The increased [HCO3−] diffuse gradually into the CSF so buffering the excess of H+ ions [47]. The compensatory response of chemoreceptors during metabolic acidosis/acidemia can be easily overlooked as its main effect is hyperpnea (increased VT) rather than tachypnea. Hyperpnea may be difficult to detect, at least early, as the patient does not complain of dyspnea unless pre-existing thoraco-­ pulmonary dysfunction coexists. When metabolic acidosis becomes severe, the detection of hyperventilation is easier as both VT and RR increase (polypnea). In chronic metabolic alkalosis, the increased [HCO3−] reduces the ventilatory response, so that PaCO2 rises. However, alveolar hypoventilation causes PO2 to decrease, thus stimulating peripheral chemoreceptors [49]. Pulmonary receptors are located in the airways and lung parenchyma. They are innervated by the vagus nerve with myelinated (airways) and unmyelinated C fibers (lung) [50, 51]. There are two types of airways receptors: the slowly adapting receptors (SARs), also known as stretch receptors, and the rapidly adapting receptors (RARs), named irritant receptors. Receptors in lung parenchyma are the juxtacapillary receptors. SARs respond to mechanical stretching by rapidly increasing the neuronal output; after that, they slow

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down over time. Their function may be to inform the brain about lung volume, so optimizing the respiratory output. SARs lie among the airway smooth muscle and are responsible for the Hering–Breuer inflation reflex [51]. In humans, the Hering–Breuer reflex becomes manifest at inspiratory volumes greater than 3  L, so that it is supposed to exert a protective effect against excessive lung inflation [52]. It also prolongs the expiratory time so reducing the respiratory rate. Besides the Hering–Breuer reflex, SARs are thought to participate in ventilatory control by prolonging the time of inspiration when airways obstruction or decreased chest wall compliance occurs so preserving the tidal volume. This provides neural feedback to the CPG, allowing for the most ergonomic combination of VT and RR in response to increased respiratory work. SARs stimulation also prolongs expiration, a very useful measure during airways obstruction. If expiratory time would lengthen without the compensatory decrease of RR, the rise of end-expiratory lung volume would become inevitable (see below). The air trapped in the alveoli increases the resting length of the inspiratory muscles, placing them on a disadvantageous portion of the length–tension curve. Therefore, inspiratory volume must decrease, while respiratory rate increases, thus preserving alveolar ventilation. SARs help to prevent incomplete expiration, therefore, maintaining the end-expiratory volume [53]. RARs are irritant receptors placed between the airway epithelial cells. They respond to noxious stimuli, such as dust, smoke, and foreign bodies [54]. The maximum concentration of RARs is found in the carina and primary bronchi [49]. RARs are also believed to be cough receptors [49], their most important function being the detection of changes in the caliber of the airways. Their stimulation seems to have a role in the sensation of chest tightness, dyspnea, and “rapid shallow breathing” [55, 56]. In summary, SARs and RARs provide CPG with important feedbacks about lung volumes and the presence of irritants. The pulmonary receptors (juxtacapillary receptors) are located adjacent to the capillaries in the alveolar wall. They are probably involved in the sensation of dyspnea when ­congestion of the lung parenchyma is present [57]. Pulmonary receptors are also responsible for “rapid shallow breathing” [58]. Their tonic influence on CPG accentuates the ventilatory response to hypercapnia and hypoxia [59]. Juxtacapillary receptors also increase the respiratory rate during muscular exercise [59]. Mechano-receptors in chest muscles, tendons, and joints respond to changes in length, tension, and movement. Muscle spindle endings are responsible for the increased contraction of respiratory muscles in response to stretching. Tendon organs sense changes in the force of contraction so preventing excessive muscular tension. Tendon receptors seem involved in the coordinated contraction of respiratory mus-

cles [60]. Joint proprioceptors sense the degree of chest wall displacement so influencing both the timing and level of respiratory activity [60]. Muscle, joint, and tendon receptors play a role in increased ventilation during muscular exercise. They also contribute to the sensation of dyspnea when respiratory efforts seem disproportionate with respect to the actual VT [55]. Cortical centers play a role in balancing the need for the chemical control of arterial blood and the implementation of ventilatory adjustments for non-respiratory purposes (e.g., speaking and sniffing) [61]. They also coordinate the breathing rhythm during behavioral activities which need the temporary stop of ventilation (e.g., chewing and swallowing). Finally, the voluntary control over ventilation is exerted by descending cortical pathways to the motor neurons of the medulla and the spinal cord. This control is precise but not absolute as voluntary breath-holding is overwhelmed by the compelling need for breathing. In the clinical setting, clinicians must decide if bradypnea or tachypnea are physiological (adaptive) or pathological. Dyspnea does not help to discriminate as it may be physiological (e.g., exercise, breath-holding, and altitude), pathological (e.g., respiratory diseases), or maladaptive in origin (claustrophobia and panic attacks). In addition, normal or abnormal breathing pattern does not discriminate as both coexist in physiological conditions (e.g., sleep). The change from periodic to regular respiratory rhythm is often seen during transition from phases 1–2 to phases 3–4 [62]. Even arterial blood gases can be inadequate in differentiating normal from abnormal respiratory conditions. As an example, normal O2 values are frequently encountered in asthmatic patients as they hyperventilate to overcome the augmented resistive load. The resulting hypocapnia derives from reduction of the dead space of ventilation and not from stimulation of peripheral chemoreceptors as supplemental O2 does not reduce the ventilatory drive. As a rule of thumb, the contemporary increase of respiratory rate and tidal volume (polypnoea), as well as hyperpnoea (VT increase) rules out a respiratory pathology. Polypnoea and hyperpnoea represent the adaptive response to various physiological stimuli (e.g., muscular exercise, acidosis, altitude, and shivering) by activation of accessory respiratory muscles in a coordinated manner so maintaining the respiratory pattern harmonic. Abnormal patterns include paradoxical motions of the chest wall and abdomen and/or thoraco-­ abdominal asynchronies [63]. In summary, the occurrence of abnormal respiratory patterns, polypnoea, and hyperpnoea require supplemental investigations to distinguish physiological from pathological conditions. The only pattern almost exclusively associated with respiratory pathology is the “rapid shallow breathing”. During “rapid shallow breathing”, the Tobin Index (RR/VT ratio) increases over the upper limit (350  mL/dL of ethanol concentration in blood) [70]. In summary, respiratory rate and rhythm are fundamentals for the patient’s clinical assessment. Their generation and control are highly synchronized by a complex array of coordinate nervous centers in the brain stem. Peripheral and central chemoreceptors inform the respiratory centers about the chemical composition of arterial blood gases. This allows for continuous adjustment of pulmonary ventilation. Arterial

PO2, PCO2, and pH are thus maintained within strict normal limits. Abnormalities of respiratory rhythm are often but not always associated with respiratory and neurological ­diseases. Tachypnea and bradypnea may be physiological (e.g., during exercise or sleep) or pathological. The most important form of tachypnea is the “rapid shallow breathing”. The diagnosis of “rapid shallow breathing” is easy, as in extreme cases, it resembles “panting” and interrupts the most basic activities as talking and drinking. The most important meaning of the pathological increase of RR (e.g., “rapid shallow breathing”) is the augmented cost of respiration by the increased inspiratory load.

4.4 Body Temperature The control of body temperature is crucial for vital functions, and its changes cause profound modifications in many organ systems, such as the brain and circulatory system; moreover, changes in body temperature alert against the presence of disease processes. Temperature plays an important role in physical, chemical, and biological sciences. It influences many properties of the material world as the physical state of matter, density, viscosity, and the vapor tension of gases. Temperature is responsible for the Brownian motion of the molecules and it is a measure of their mean level of kinetic energy. If a solute dissolves into water, the speed of dissolution is proportional to the temperature, and this is why sugar dissolves more rapidly in hot than cold drinks. Temperature is also the main determinant of chemical reactions, so that any change of body temperature varies the speed of reaction in the same direction. The increase of temperature over 42 C° causes cytotoxicity, protein denaturation, and DNA synthesis inhibition [71]. Conversely, the drop of temperature below 27 °C can equally prove fatal because of

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4  Monitoring and Interpretation of Vital Signs in the High-Risk Surgical Patients

irreversible cardiac, respiratory, and hematologic failure [72]. Normal core-body temperature is around 37  °C with daily (circadian rhythm), monthly (menstrual cycle), and lifetime (aging) fluctuations. To ensure optimal physiological functions, humans preserve the core-body temperature (head and trunk) despite the ever-changing environment. Therefore, heat gain always equals heat loss, thus keeping body temperature constant (homeothermy). Mammals produce heat by themselves and disperse or conserve the heat so keeping constant the core-body temperature. Any heat transfer occurs down a thermal gradient in accordance with thermodynamic laws. Radiation, convection, and contact are the involved physical mechanisms. When all these processes are fully saturated, evaporation dissipates the heat in excess (sweating). The following equation resumes the internal and external factors implicated in heat balance:

Heat Storage = M − ( W + v ) ± ( C + Conv + R )

where M is the heat produced by cellular metabolism (mainly muscular tissue). W is the external work done. E is the heat dispersed by water vaporization from the skin surface and respiratory tract. Vaporization depends on the surface area exposed, temperature, and humidity of the environment, and convective air currents around the body. R is the electromagnetic radiation transferred or absorbed from the environment. It includes infrared emissions from the body and ultra-violet absorption from the light sun. C is the heat transferred by direct contact with the external surface. Usually, the heat-­exchanged by contact is minimal unless exposed surface areas are large or big amounts of cold foods and drinks are ingested (e.g., ice cream). Conv is the convection of heat by movement of air or water in contact with the body. The heat transfer to the fluid makes them lesser dense, so that the heated molecules are replaced by cooler ones. Note that the heat flux is bidirectional by convection, contact, and radiation, while it only travels from the body to the environment by evaporation. When the heat storage is zero, the body is thermally balanced and the core-body temperature is constant. Temperature regulation refers to the regulation of the body’s central core. Core temperature refers to the temperature of “deep” organs and viscera with high metabolic levels (brain, heart, and liver). Conversely, peripheral shell body refers to the body skin surface, notably arms and legs. The peripheral shell body is well-suited as a heat exchanger because of its high surface/mass tissue ratio. For example, the surface/mass tissue ratio of the hands is fivefold that of the whole body [73]. Shell temperature is mostly influenced by skin blood flow. When body-core temperature or environmental temperature raises the blood flow to the skin also rises. As human beings are generally warmer than the ambient temperature, the heat normally flows from shell to environment. Peripheral shell temperature is about 4  °C lesser than the core, but this gradient is reduced when the

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body dissipates the heat in excess. Conversely, the cold stress reduces the blood flow to the skin (vasoconstriction), so preserving the core temperature. The hypothalamus acts as coordinator and integrator for thermoregulation. The anterior pre-optic hypothalamus is the main region for autonomic regulation of the temperature [74]. It receives inputs from peripheral and central receptors of both warm and cold type. Cold receptors are more abundant in periphery, while warm receptors are more central (hypothalamus, brain spinal cord, viscera, and great veins).

4.4.1 Effector Organs Response to Increased Body Temperature The mechanism of cutaneous thermoregulation depends on sympathetic and parasympathetic innervation of the haired skin and sympathetic innervation of glabrous skin (palms, soles, and lips). Increased blood flow in glabrous skin is obtained by passive vessel dilation after inhibition of the sympathetic vasomotor tone [75, 76]. In addition, the numerous artero-venous anastomoses allow for the blood to flow directly from arteries to veins, therefore, by-passing constricting arterioles and capillary loops. As a result, blood flow increases of manifolds with respect to basal condition. Haired skin further increases heat loss by parasympathetic vessels dilation. Active vasodilation is at least in part the result of acetylcholine release from nerve endings, so that blood flow can increase from 300 mL/min to the hyperbolic number of 8000 mL/min [77]. Co-transmitters as vasointestinal peptide, substance P, prostaglandins, and transient receptor potential (TRP)V1 receptors also participate in active vasodilation [77]. Sweating is the principal mode of heat dissipation during muscular exercise or when the ambient temperature rises. It is the sole mode of heat loss when the external temperature is higher than the core temperature. Sweating is mediated by sympathetic cholinergic fibers, which innervate the millions of sweat glands regionally distributed throughout the entire body [78]. The availability of water is the main limiting factor for the production of sweat. Dehydration, therefore, limits the regulation of core-body temperature when exercising in a hot environment. As much as 2–3 L/h of sweat is produced in acclimatized persons [79], and 1 L/h in non-acclimatized individuals [80]. The increased sweat rate alters the composition of sweat as its sodium and chloride content reduces.

4.4.2 Effector Organ Responses to Decreased Body Temperature Cold stress reduces the skin blood flow by active vasoconstriction. Heat is conserved by redirecting blood flow to the

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internal (subcutaneous) venous plexus. This widens the gradient between the peripheral shell and core-body ­temperature. Vasoconstrictor nerves are primarily alphanoradrenergic fibers. The brown adipose tissue (BAT) is effective in non-­ shivering thermogenesis, thus contributing heating production during cold exposure. Previously believed important in infants and newborns, recent researches established its efficacy in adults [81]. BAT increases body temperature by raising the metabolic rate. It reduces the efficiency of oxidative phosphorylation, so that less ATP is produced and the remaining chemical-bond energy is transformed into heat. Peripheral and central receptors activate BAT thermogenesis by thermogenin, an uncoupling protein that prevents ATP production by H+ transfer across mitochondrial membranes. Piloerection also minimizes heat loss by sympathetic stimulation of the erector pilii muscle. This muscle is a small band of smooth muscle that connects the base of the follicle to the connective tissue of the basement membrane. Its contraction cause hairs to become upright so creating a tiny insulating layer of warmed air. The “goose-bump” effect is the contraction of erector pilia around the clasped skin follicles. Piloerection is normally considered accessorial in humans, but it becomes relevant during shivering [82]. Shivering is the strongest response to cold exposure. Its activation occurs when physiological mechanisms (vasoconstriction and piloerection) and behavioral changes (clothing, hot drinks, increased muscular activity, and huddled body position) are no longer effective in maintaining the core-body temperature. The onset of shivering means that maximal vasoconstriction has already been achieved [83]. It is initiated by the hypothalamus and mediated by the motor cortex in response to peripheral cold stimuli. During shivering, the energy produced by involuntary, rapidly oscillating contractions of the skeletal muscle is released as heat. At the maximum rate, shivering produces heat equivalent to five times the basal metabolic rate [84]. Neonates have limited shivering c­ apacity because of their immature skeletal muscles [85]. The shivering threshold is typically 1  °C below the vasoconstriction threshold [86]. When a person begins to shiver, he/she is already fairly hypothermic.

4.4.3 Effects of Body Temperature Changes The changing of body temperature affects mainly the cardiovascular and respiratory functions. Increased Temperature: fever is a very challenging condition, because its effects mimic that of body exposure to cold. The opposite occurs, although lesser demanding, with fever descent (e.g., antipyretic drugs). Several pro-inflammatory mediators (e.g., cytokines) stimulate the production of prostaglandins (PGE2) in the preoptic hypothalamus. PGE2 binds

to specific receptors on warm-sensitive cells so inhibiting their activity. The resultant inhibition to warm stimuli initiates peripheral vasoconstriction, BAT thermogenesis, and shivering to gain heat. Non-steroidal inflammatory drugs reduce fever by inhibiting the production of prostaglandins. The rise of fever increases the arterial diastolic pressure by augmentation of peripheral vascular resistance (vasoconstriction) [87]. The augmented afterload is offset by increases venous return (preload) to the core [88]. As a result, the stroke volume is maintained. The rate-pressure product is obtained by heart-rate × Psyst (bpm × mmHg), representing a good surrogate of myocardial oxygen consumption [89]. It increases during cold exposure [87, 90] because of increased myocardial work by the activated sympathetic nervous system. The coronary blood flow of normal individuals is, therefore, expected to increase. Cold exposure can provoke angina in subjects with coronary artery disease (CAD) [91]. A plausible explanation is that an imbalance of the myocardial O2 demand/supply occurs, this, in turn, precipitating myocardial ischemia. The exhaustion of the vasodilator reserve and the diminished flow-mediated vasodilator response of coronary resistance vessels prevent the increase of coronary blood flow in CAD patients. This occurs despite the increase of mean arterial pressure. Small but significant increases in coronary blood flow have been observed in patients with minor atheromas [92]. Cold stress also is a powerful pro-­ arrhythmic stimulus in CAD patients. The pre-existing mismatch between myocardial O2 demand and supply is aggravated by activation of the sympathetic nervous system, so that cardiac arrhythmias may supervene [93]. Shivering furtherly worsens the cardiovascular load as it mimics strenuous physical activity in the cold environment. The reduced vasodilator capacity of CAD limits the increase of coronary blood flow so reducing the ability of metabolic adaptation. Shivering can, therefore, precipitate angina as the metabolic demand increases up to 200–300% of the basal rate [94]. As a rule, the simple exposure to cold in the presence of flow-­ limiting coronary stenosis is not sufficient to cause acute myocardial infarction. However, hypothermia may induce cardiac ischemia and angina when severe CAD is present [95, 96]. Valvular heart diseases: the two main cardiovascular effects of shivering are arterial hypertension and increased heart rate. Tachycardia and hypertension are potentially harmful in severe valvular stenosis. The fixed stroke volume through the narrowed valvular orifice limits the increase of cardiac output during shivering. In addition, the increased heart rate may cause decreased coronary perfusion and reduction of the systolic ejection time. Aortic stenosis is particularly at risk because of ventricular hypertrophy and reduced arterial diastolic pressure. Supraventricular tachyarrhythmias and loss of effective atrial contraction may also deteriorate the hemodynamic conditions. Mitral stenosis suf-

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4  Monitoring and Interpretation of Vital Signs in the High-Risk Surgical Patients

fers from tachycardia by shortening of the diastolic time. Atrial end-diastolic pressure must rise so increasing trans-­ valvular instantaneous flow in order to maintain the cardiac output. However, Poiseuille’s law dictates that even the smallest increase of trans-mitral flow causes a large increase of left atrial pressure. Therefore, the potential for pulmonary congestion because of increased pulmonary venous pressure exists. Moreover, the acute dilation of atria may precipitate tachyarrhythmia which further raises pulmonary venous pressure. Increased systemic vascular resistances are deleterious for both mitral and aortic regurgitation. The increased afterload can worsen the forward cardiac output by augmenting the regurgitant fraction. As a result, sub-endocardial perfusion may decrease because of increased left ventricular end-­ diastolic pressure and stroke work. Finally, cardiac contractility may reduce with increased risk for pulmonary congestion. Altered respiratory function: increased alveolar ventilation in febrile patients aims at boosting the oxygen supply to systemic circulation. Hyperventilation requires the increase of instantaneous flow through the airways. Active exhalation is, therefore, mandatory because of reduced expiratory time. Both restrictive and obstructive respiratory diseases obstacle the increase of alveolar ventilation so causing dyspnea and, eventually, hypoxemia. Reduced pulmonary volume is the rule in postoperative patients, especially during the first week. Perioperative shortness of breath during febrile episodes is quite common in high-risk surgical patients. The reduced pulmonary volume narrows the caliber of the smallest airways, so that the respiratory rate rises disproportionately as the only option to sustain ventilation. The accelerated flow through the narrowed airways often causes wheezing, so that the erroneous diagnosis of asthma is made. The application of continuous pulmonary airways pressure or non-­ invasive ventilation is the sole valuable options to restore pulmonary volume. COPD reduce the patient’s tolerance to increased pulmonary ventilation. The reduced lung elastic recoil impedes the complete exhalation of inspired volume despite active expiration. Expiratory muscles contraction increases the expiratory flow, but the smallest collapsible airways cannot oppose to the external compressive forces of increased pleural pressure. Anticipated expiratory airway closure with increased end expiratory lung volume will, therefore, result because of incomplete exhalation. This phenomenon is responsible for the generation of PEEPi as PALV increases over PATM at zero flow. PEEPi is a compensatory measure as it increases the expiratory flow, but the workload of inspiratory muscles also rises. In fact, the inspiratory flow can only start once the extra alveolar pressure (PEEPi) is overcome, so that more inspiratory pressure must be generated to achieve the actual VT. PEEPi normally amounts to 2–3 cmH2O, but even the smallest shortening of the expira-

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tory time causes the dynamic rise of PEEPi to 6–10 cmH2O in severe COPD patients. Fever-related increases in respiratory rate are usually not well-tolerated by the COPD patient because of the augmented PEEPi. Decreased temperature: cardiovascular adaptations to the decrease of fever mimic the physiological responses to acute heat stress. The need for dissipation of the heat stored during fever redirects blood, and thus heat, to the skin, where heat is dissipated as sweating (water evaporation). Skin blood flow may increase up to 7–8  L/min [97]. Increased peripheral venous pool and arterial vasodilation cause the decrease of venous return and systemic blood pressure, but the increased systolic function maintains the stroke volume unchanged [98]. The increased cardiac output is thus sustained by reflex tachycardia. In high-risk surgical patients, the main cardiovascular concerns consist of diminished arterial diastolic pressure and increased heart rate. The reduction of diastolic pressure results from the combined effects of peripheral arterial dilation and venous pooling of blood in the extremities. Postoperative hypovolemia, opioids drugs, and application of continuous positive end-expiratory pressure may prevent the increase of cardiac output because of significantly reduced venous return. The lack of increased cardiac output may cause hypotension and decreased perfusion pressure. Theoretically, the reduced coronary flow because of lowered diastolic pressure and decreased diastolic time (reflex tachycardia) may result in adverse effects if significant CAD and/ or valvular stenosis are present. At variance with cold exposure, the acute heat stress does not have a relevant impact on respiratory function as both tidal volume and respiratory rate decrease in consequence of reduced metabolic demands.

4.5 Pulse Oximetry Pulse oximetry is a standard of clinical monitoring in many settings, where hypoxemia occurs [99]. It measures the percent of oxygen bound to hemoglobin so allowing for continuous non-invasive measurement of arterial blood saturation. Before its introduction in clinical practice, physicians must rely on arterial blood sampling to identify hypoxemia. The easiness of use made pulse oxymetry the standard of care not only in emergency departments, intensive care units and operating rooms but also in hospital wards, endoscopic suites, and many laboratories (e.g., cardiac catheterization laboratory or sleep laboratory). The accuracy of measurement allows for titration of the inspired fraction of O2 in spontaneously breathing or mechanically ventilated patients. It can also be used as a screening tool for cardiopulmonary diseases. Finally, its safety profile makes contraindications virtually absent, so that any patient is suitable for pulse oximetry monitoring. The human eye is poorly fitted at detecting hypoxemia: cyanosis occurs when at least

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Fig. 4.9  Oxyhemoglobin saturation curve. The arterial and mixed venous points are shown. The SaO2–SvO2 difference is proportional to a-vO2 difference according to the relationship: 1.36 × Hb × (SaO2–SvO2)

SaHbO 2 = HbO 2 / Hb tot

as expressed as a percent value. Oxyhemoglobin saturation can be viewed as the indirect estimate of the affinity of hemoglobin for O2. Affinity is a cumbersome parameter, difficult to obtain, even experimentally. SaHbO2 correlates directly with the oxygen content of blood according to the following relationship:

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O2A-Voff

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O 2 Content = 1.36 mL / g × Hb [ g / dL ] × HbSO 2

where 1.36 is the amount of oxygen bound to 1 g of normal hemoglobin. The normal Hb content (150 g/L) is saturated at 97% in the arterial blood giving (1.36 mL/g × 150 g × 0.97) = 200 mL of O2 content per liter of blood. A normal subject with 5 L/min of cardiac output transports 1000 mL of oxygen per minute, a volume largely exceeding the basal O2 requirement (about 200  mL/min). The extreme cardiovascular performance (up 35–40 L/min) can increase the oxygen delivered to 7–8 L/min so allowing for the astonishing performance of elite athletes and mountaineers. The O2 bound to hemoglobin is about 98% of total O2 content, as at physiological PO2 a very small amount of poorly soluble oxygen is dissolved in plasma. According to Henry’s law, the amount of O2 dissolved in the plasma is proportional to PO2 by the solubility coefficient (0.0031 mL/ mmHg). Thus, at 100 mmHg of PaO2, 1 L of plasma contains only 0.3 mL O2/100 mL or 0.3% vol, which is about 67 times lesser than the O2 bound to hemoglobin. If deoxygenated hemoglobin is equilibrated with alveolar PO2, the four binding sites for O2 become progressively occupied until all of them contain O2. The curve representing the equilibrium binding of O2 to hemoglobin (oxygen saturation curve or oxygen dissociation curve) is shown in Fig. 4.9. It expresses the fundamental relationship between PO2 and the hemoglobin-­bound O2 content. The typical sigmoid shape

100 4 th O 2 molecule more difficult to bind

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Art

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5 g/100 mL of deoxygenated hemoglobin is present in capillary blood. Central cyanosis, the blue coloration of the tongue, and mucous membranes, is believed more reliable as an indicator of hypoxemia, because mucous membranes are rarely affected by hypoperfusion. Cyanosis translates into hemoglobin saturation of about 75%, which is clinically relevant hypoxemia. Detection of cyanosis requires experience and eyesight of the observer [100]. Skin pigmentation and ambient lighting are other relevant factors. Several studies, the earlier dating up to 1947 showed that the human eye, even in ideal condition, cannot detect hypoxemia until oxygen saturation is about 80% (PaO2  ≈  50  mmHg). A pulse oximeter is, therefore, an extensor, not a substitute for clinical senses. In summary, pulse oximetry enters with full rights into the number of vital signs as the fifth member [100]. Functional oxyhemoglobin saturation is defined as the ratio between HbO2 (oxyhemoglobin) and total hemoglobin content:

60 2 nd and 3 rd molecules bind more easily 40

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Fig. 4.10  Affinity for oxygen of the four hemoglobin molecules giving the S-shaped form of the oxyhemoglobin curve. Affinity is highest for the fourth molecule thus flattening the upper part of the curve

reflects the cooperative nature of O2 binding to Hb (Fig. 4.10). This curve is markedly nonlinear through the physiological PO2 range (40–100 mmHg). Conversely, its middle portion (20–80% saturation) is approximately linear. This shape can be viewed as the result of the changing affinity for O2 with increasing PO2. At low and high PO2 values (≤20 mmHg and ≥60 mmHg, respectively), the affinity of hemoglobin for O2 is high, and more molecules are required to further bind Hb to O2. This occurs for the first and fourth binding sites (Fig.  4.10). The opposite occurs for the second and third binding sites, where small PO2 variations cause large changes of HbO2 (steeper portion of the curve). From another point of view, low O2 affinity allows for immediate oxygen release when PO2 decreases even slightly. This is what effectively

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OxyHemoglobin Dissociation Curve

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Fig. 4.11  Changing affinity of Hb for oxygen accounts for SatO2 values ≥90% until PaO2 remains >60  mmHg. When PaO2 drops under 60 mmHg, the decreased affinity allows for the rapid transfer of O2 to tissues

happens when fully oxygenated blood (high PO2) comes in contact with tissues (low PO2). The dissolved O2 in red blood cells diffuses rapidly to tissues, so unbinding the O2 molecules from Hb. Conversely, the high O2 affinity of the fourth molecule keeps the bounded O2 down to a 40 mmHg gradient, from 100 to 60 mmHg PO2 (Fig. 4.11). The high affinity of hemoglobin protects the body against moderate hypoxemia (PaO2 60 mmHg), as occurs when living in altitude or during respiratory diseases. Temperature, pH, PCO2, and 2–3 dyphosphoglycerate [2–3DPG] influence the binding of O2 to Hb. Briefly, the O2 affinity reduces by increased temperature, PCO2 (Bohr effect), [2–3DPG], and reduced pH (rightward shift of O2 dissociation curve). The opposite occurs with decreased temperature, PCO2, [2–3DPG] and increased pH (leftward shift). This is physiologically relevant as increased temperature and PCO2 in exercising muscles favor the O2 unloading from Hb. The 2–3DPG molecule is a charged ion that binds the terminal amino group of beta chains and competes with CO2 for the binding site [101]. It is important in conditions of chronic hypoxia (e.g., acclimatization to altitude, chronic respiratory diseases). Hypoxic hyperventilation causes PCO2 to decrease (leftward shift of the O2–Hb curve) but the increased 2–3DPG shifts the curve back to the right. PO2 in the tissues is normally lower than 60 mmHg. Therefore, O2 transfer from blood to cells is guaranteed by decreased O2 affinity for Hb. The O2 supply is settled to metabolic demands of every single tissue either in resting and non-resting conditions. Figure 4.12 shows the SatO2 value of any single tissue at rest. The PO2 of the resting muscle is about 40 mmHg so reflecting the extraction of about 50 mL of O2 per liter of blood. Oxygen delivery to the exercising muscle increases to 150 mL as PO2 drops to 20 mmHg only. The myocardium

Fig. 4.12  Venous SatO2 value from several vital and non-vital organs is plotted on the oxyhemoglobin curve together with the arterial point. Each organ a-vO2diff is indicated by the vertical distance between the arterial and the respective venous point. Note the different a-vO2diff between the resting and exercising muscle

extracts up to 75% of the arterial O2 content resulting in lesser than 30% of venous O2 saturation in the coronary sinus blood. By contrast, the renal cortex needs so little oxygen that its venous oxygen saturation is near 90%. Therefore, regional venous O2 saturation reflects the amount of O2 extracted from each tissue district. Mixed venous O2 saturation is the weighted mean of venous saturation from all body districts so reflecting the global O2 extraction. Pulse oxymetry provides information about arterial O2 saturation. This parameter, therefore, estimates the global efficiency of O2 uptake by the lungs. Arterial O2 saturation does not give information about the quality of O2 transport and uptake by the tissues. In addition, the flattened part of the upper oxygen dissociation curve does not allow pulse oxymetry to detect hyperoxia, so that it is impossible to know if PaO2 is 100 or 500 mmHg when saturation is 98–100%. Anemia per se does not cause false SpO2 readings, but it rather causes SpO2 to overestimate O2 saturation in patients with true hypoxemia. This occurs, because the reduced hemoglobin content is well-saturated with oxygen. Occult hypoxemia can occur in the anemic patient as SpO2 readings >90% may correspond to PaO2 values  39° or 110  bpm; in children>2SD above age-specific. • Progressive tachypnea >25 bpm non ventilated or > 12 L/ min ventilated; in children>2SD above age-specific. • Thrombocytopenia will not apply until 72 h from initial resuscitation; 2SD above age-specific. • Hyperglycaemia in the absence of pre-existing diabetes mellitus, plasma glucose >200 mg/dL; Insulin resistance (requirements >25% over 24 h). • Inability to continue enteral feeding 24  h, residual >2× feeding rate or abdominal distension or diarrhoea >2500  mL/d for adults, residual 150  mL/h or diarrhoea >400 mL in children. • In addition, infection is demonstrated by at least one of the following: positive culture for infection, pathological tissue source identified clinical response to antimicrobial agents. Clinical state must be evaluated, minor vital signs, IV access, check serum lactate, and blood cultures before administering antibiotics. The initial resuscitation provides haemodynamic support which includes fluid resuscitation with crystalloid fluid, vasopressors if hypotension present to maintain MAP>65 mmHg. Then, start empiric therapy with broad-spectrum antibiotics and continue reassessment for fluids. Taking precautions to prevent and treat sepsis and MOFs include optimize resuscitation and haemodynamic status, prevent organ hypoperfusion, prevent intestinal barrier deterioration with enteral nutrition, performing escharectomy to take away all necrotic tissue.

5.7 Inhalation Injury Inhalation is suspected when a burn injury occurs in a closed space. Signs include hoarseness, carbonaceous sputum, cyanide; upper airway injury due to oedema subsequent to heat; lower respiratory system due to chemical wheeze and dyspnoea, being indicators for inhalation injury. It is possible to identify three different situations: systemic toxicity due to inhalation of gas produced by combustion, such as carbon monoxide or hydrogen or micro-particle inhalation. The treatment is oxygen, in a semi-upright position. Endotracheal intubation or tracheostomy is sometimes suggested if airway patency is compromised, as oedema could have been in

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progress for many hours. Chest radiograph does not exclude the diagnosis of inhalation. Prophylactic antibiotics and corticosteroids are not indicated for the treatment of smoke inhalation injury.

5.8 First-Line Treatment Observation and removal of hazards and risks for operators are mandatory before treating the patient in pre-hospital. Triage depends on the resources and the team must follow the BLS rules for patient monitoring and treatment. If water is readily available, it should be poured directly into the burn area. Ice packs should never be used. During the transfer to the hospital the patient, after the burn injury site has been irrigated with water, should be lain on dry sheets to avoid further temperature loss. It is difficult in the trauma scenario or in the ambulance to calculate the extension of the burned area. The ABA with other International Societies for burn care [8, 9] have developed a formula for the infusion that patients need during transport to the burn centre (Table 5.4). Humidified oxygen should be given to all patients. Table 5.4  Crystalloid resuscitation during transport using Lactated Ringer Solution 95 90–95

Compartmental pressure (mmHg)  20% or unstable patient Check for inhalation injury: Intubation, bronchoscopy, carboxyemoglobin evaluation Central venous catheter Arterial line for continuing blood pressure monitoring Invasive monitoring for unstable patient via arterial lines, SvO2, PiCCO, … Enteral feeding Urinary catheter Core temperature Chest X-ray Blood draw: Electrolytes, BUN, creatinine, blood counts, platelets, coagulation, lactates, albumin or total serum proteins Check other injuries Clean, check the need for escharotomy or fasciotomy Recalculate TBSA and fluid requirements

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TBSA 4 mEq/L are considered as severe hyperlactatemia [29]. Lactic acidosis is a high [AG] metabolic acidosis. In pure cases, the increase in lactate concentration is equivalent to the increase in [AG] and the decrease in plasma [HCO3−] and [BE]. The increase in plasma [AG], however, may be less or greater than the corresponding decrease in [HCO3−] because of the concomitant presence of hyperchloremic acidosis or metabolic alkalosis, respectively. Consequently, the diagnosis of lactic acidosis should always be confirmed by means of direct blood lactate measurement. Lactic acidosis is classified as type A or B according to whether or not there is overt evidence of tissue hypoxia. Type A is associated with clinical conditions, such as shock, extreme anemia, decompensated heart failure, asphyxia, and carbon monoxide poisoning, in which tissue oxygenation is severely compromised. Type B includes a variety of disorders that do not seem associated with impaired oxygen transport. Many hyperlactacidemias found in critically ill patients, especially after resuscitation, have their origin in increased

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aerobic glycolytic activity secondary to a hypermetabolic state [30]. Consequently, there may be some overlap in the classification. Lactate Metabolism

The plasma lactate concentration depends on the balance between its production and removal [29]. At rest, the most important source of circulating lactate are the red blood cells, the skin, and the brain. During exercise, lactate is ­predominantly produced by the skeletal muscle. Lactate is mainly metabolized in the liver and kidneys. The turnover is 15–25 mEq/kg/day. Lactic acid is produced in the cytoplasm according to the following reaction:

piruvate + NADH + H + ↔ lactate + NAD +

The reaction is catalyzed by lactate dehydrogenase, which requires NADH/NAD+ as a cofactor. The cytosolic concentration of pyruvate reflects the balance between its glycolytic production and its oxidative mitochondrial degradation in the Krebs cycle. This reaction produces 36 ATP molecules per glucose molecule. The lactate/pyruvate ratio normally is 10. Lactate increases when pyruvate production exceeds its utilization by the mitochondria. Therefore, any increase in glycolytic activity can increase blood lactate concentrations. Sixty percent of the generated lactate is metabolized in the liver (Cori cycle) and another 30% in the kidney. Since the threshold for renal excretion is 5–6 mEq/L, it is not eliminated in the urine. Mechanisms of Anaerobic Lactate Production

Type A lactic acidosis classically occurs in the setting of anaerobic metabolism. Inadequate perfusion can be global, regional, or microcirculatory. Examples of systemic and regional hypoperfusion are low cardiac output syndrome and intestinal ischemia, respectively. Hypoxia blocks mitochondrial oxidative phosphorylation, decreasing ATP synthesis and NADH re-oxidation. The resulting reduction in the ATP/ADP ratio induces an accumulation of pyruvate due to: (1) increased production secondary to the stimulation of phosphofructokinase, the rate-limiting step of glycolysis and (2) decreased utilization by inhibiting pyruvate carboxylase, which converts pyruvate to oxaloacetate. The increase in the NADH/NAD+ ratio also increases the pyruvate concentration, since it inhibits pyruvate dehydrogenase, necessary for the passage to acetyl-CoA: + piruvate + CoA + NAD ↔ AcetilCoA + CO2 + NADH

In anaerobiosis, the increase in lactate is a consequence of the accumulation of pyruvate and its accelerated conversion

to lactate (increased lactate/pyruvate ratio), which results from the effect of the elevated NADH/NAD+ ratio on lactate dehydrogenase. This reaction allows the formation of NAD+ that is necessary for the functioning of glycolysis and the maintenance of ATP production, which, now under anaerobic conditions, is clearly less efficient (two ATP molecules for each glucose molecule) [31]. In summary, anaerobic metabolism is characterized by hyperlactatemia, increased lactate/pyruvate ratio, increased glucose utilization, and low energy production. At steady state, the lactate/pyruvate ratio depends on

(

lactate / piruvate = K ∗ NADH / NAD +

)

∗

H+

An increase in the NADH/NAD+ ratio or a drop in pH causes an increase in the lactate/pyruvate ratio. The lactate/pyruvate ratio could identify the anaerobic origin of lactate. Its usefulness, however, is limited because of the lack of correlation between plasma and intracellular concentration. Furthermore, pyruvate determination is cumbersome. Thus, the ratio does not adequately reflect the cellular redox potential and its prognostic value is not higher than that of lactate [32]. Mechanisms of Aerobic Lactate Production

Surgical patients can develop hyperlactatemia by mechanisms other than anaerobic glycolysis. They include: 1. Stimulation of aerobic glycolysis: the release of epinephrine during the systemic inflammatory response activates β2 adrenergic receptors in skeletal muscle. This increases the production of cyclic adenylate monophosphate, which stimulates glycogenolysis, glycolysis, and Na+/K+ ATPase. Na+/K+ ATPase consumes ATP and increases ADP levels. This additionally stimulates phosphofructokinase and, therefore, glycolysis, generating greater amounts of pyruvate and lactate. Experimental and clinical studies show that this mechanism is operative in different types of shock [33]. Moreover, it might the main cause of hyperlactatemia in critically ill patients, particularly after hemodynamic resuscitation [30]. Since lactate is an energy fuel in stressful situations, hyperlactatemia can be an adaptive mechanism. Inhibition of lactate synthesis in experimental septic shock decreases ATP and myocardial function, and accelerates death [34]. 2. Reduced lactate clearance: there are conflicting results showing that lactate clearance in sepsis is either normal or decreased [35, 36]. 3. Pulmonary lactate production: in patients with sepsis and acute respiratory distress syndrome, pulmonary production can explain a significant portion of hyperlactatemia [37]. Recent studies confirm that the lung is a major source of lactate production following cardiopulmonary bypass and that lung lactate release may occur as late as 6 h after surgery [38, 39].

6  Acid–Base Abnormalities in Surgical Patients Admitted to Intensive Care Unit

4. Dysfunction of pyruvate dehydrogenase: in septic patients, this alteration may contribute to hyperlactatemia, because the enzyme is involved in the conversion of pyruvate to acetyl-coA, allowing its entry into the mitochondria. In patients with septic shock, stimulation of pyruvate dehydrogenase decreases lactate levels [40]. 5. Protein degradation: protein catabolism releases amino acids that are metabolized to pyruvate and lactate. Although the mechanisms of hyperlactatemia may overlap, some types of surgeries have been associated with particular patterns. In cardiac surgery, hyperlactatemia shows a bimodal distribution. There is an early increment after the initiation of cardiopulmonary bypass that frequently persists until ICU arrival. This “immediate hyperlactatemia” is primarily related to tissue hypoperfusion. Thereafter, a “late hyperlactatemia” develops between 4 and 12 h of the postoperative ICU stay [41]. These patients typically have normal cardiac output, adequate perfusion, and frequently have an associated hyperglycemia. The lactate/pyruvate ratio remains normal. These patients have a benign course and hyperlactatemia spontaneously resolve within 24 h. It is likely multifactorial, resulting from inflammatory changes during tissue injury and cardiopulmonary bypass, and increased exogenous and endogenous catecholamines and steroids. Patients with an isolated type B hyperlactatemia have reassuring outcomes, and neither hyperlactatemia nor the associated hyperglycemia requires treatment [42]. Laparoscopic resection of pheochromocytoma is frequently associated with hyperlactatemia (40.7%), which is severe in 15% of the cases. These findings have been closely related to larger tumor size and higher levels of urine epinephrine, suggesting an aerobic lactate production [43]. In summary, hyperlactatemia should not be considered as an unequivocal indicator of tissue hypoxia but as a biomarker of the stress response. Therefore, lactate could be a misleading goal of hemodynamic resuscitation [44]. Treatment of Lactic Acidosis

As in the other acid–base disorders, it mainly consists in the correction of the underlying cause. For example, the most relevant measures may be cardiovascular resuscitation in shock or withdrawal of metformin or antiretroviral drugs. Alkali administration is controversial in any type of metabolic acidosis. Experimentally, in hypoxemic lactic acidosis, NaHCO3 administration lowers blood pressure and cardiac output [45]. In patients with septic shock and severe lactic acidosis, a small controlled trial showed that the correction of acidemia with NaHCO3 has no beneficial effects on hemodynamics, but produces hypocalcaemia and increases arterial PaCO2. In heart failure, alterations in O2 metabolism and worsening of hyperlactatemia have been observed [46]. NaHCO3 infusion has been associated with multiple adverse effects including hypervolemia, hyperosmolarity, cardiovas-

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cular deterioration, ionic hypocalcemia, hypokalemia, increased CO2 production secondary to H+ buffering with exacerbation of intracellular acidosis, hyperventilation due to paradoxical acidosis of the central nervous system, higher generation of lactate by stimulation of phosphofructokinase, and increased affinity of O2 for Hb. The best evidence regarding alkali therapy is a controlled multicenter study, which included 389 patients with pH ≤7.20, [HCO3−] ≤20 mmol/L) and SOFA score ≥4 or arterial lactate ≥2 mmol/L. Patients were allocated to control group or to receive NaHCO3, in order to maintain an arterial pH >7.30. There was no difference in the primary composite outcome—death from any cause by day 28 and the presence of at least one organ failure at day 7. Nevertheless, NaHCO3 decreased the primary composite outcome and 28-day mortality in the a-priori defined subgroup of patients with acute kidney injury [47]. Alternative alkalis are carbicarb [48], a mixture of NaCO3 and NaHCO3, and THAM (trihydroxymethylaminomethane) [49]. Although in experimental studies, they seem superior to NaHCO3, there is no clinical evidence supporting its use. Dichloroacetate, a potent stimulant of pyruvate dehydrogenase, decreases lactate concentrations, but does not alter the clinical course [40]. Unmeasured Anion Acidosis UA acidosis is defined as the presence of metabolic acidosis due to increased circulating [UA]. [UA] can be quantified by calculating the [AG] or the [SIG]. In two large observational studies, we demonstrated that both variables are interchangeable [19, 28] (Figs. 6.2 and 6.3). Nevertheless, the determination of [AG] is simpler. Since lactate is the only usually measured anion that makes up the [AG], the [UA] can be calculated as follows:

[ UA ] = [ AG ]corrected − [ lactate ]

The origin and characteristics of the UA remain uncertain. However, different anions such as ketoacids, formate, oxalate, Krebs cycle intermediates, salicylate, and drugs can contribute to its generation. Another major cause for increased [UA] is renal failure, especially when estimated glomerular filtration rate values fall below 45–59  mL/ min/1.73 m2 [50]. This condition results in the accumulation of several molecules, such as the negatively charged hippurate and other endogenous organic anions, sulfate, and phosphate. The incidence and significance of [UA] acidosis have not been sufficiently studied in surgical settings. However, in a mixed population of critically ill patients, we showed that it was the most common type of metabolic acidosis, explaining more than the half of the cases. In addition, [UA] behaved as an independent predictor of outcome [28]. In surgical settings, a study found that an elevated [SIG] occurs commonly

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following bypass surgery and appears to be superior to lactate as a mortality predictor [51]. Thus, [UA] acidosis seems to play a relevant role, which was previously unnoticed. Ketoacidosis Diabetic ketoacidosis is a clinical condition generated by an absolute or relative insulin deficiency. It is characterized by hyperglycemia, hyperosmolarity, metabolic acidosis due to accumulation of ketoacids, volume depletion, and different degrees of electrolyte deficiency. Diagnosis of diabetic ketoacidosis is traditionally based on laboratory findings showing hyperglycemia (glucose >250  mmol/L), metabolic acidosis (arterial pH 7.60 [90, 91].

6.2.2.1 Pathophysiology Many processes can primarily increase [BB], but the resulting metabolic alkalosis is rapidly avoided through renal elimination of HCO3− [1]. Therefore, the addition of alkali is only clinically evident as an acid–base disorder when renal HCO3− excretion is altered. Indeed, the persistence of metabolic alkalosis depends not only on the process of generation, but also on the mechanism of maintenance. Generation of Metabolic Alkalosis The plasma [HCO3−] is normally kept in a narrow range of 24 ± 2 mEq/L as a result of the balance between the urinary excretion of all the non-volatile acids produced by metabolism and the complete reabsorption of the filtered HCO3−. Plasma [HCO3−] can increase by three mechanisms: 1. Net loss of [H+]. [BB], [HCO3−] and [BE] increase if the loss of acid from the body exceeds its metabolic generation (negative H+ balance). The eliminated H+ are derived from H2CO3 stores. Consequently, acid secretion is accompanied by equimolar increases in blood [HCO3−]. The most frequent cause of acid loss is from the gastrointestinal tract, especially by vomiting or gastric drainage. Unusually, it occurs with feces, in congenital chloride diarrhea or certain forms of villous adenoma. Renal acid excretion is most commonly caused by loop diuretics, such as furosemide or thiazides. States of adrenocortical hyperfunction also increase renal acid secretion. Although the intracellular displacement of protons in exchange with another cation such as K+ has been advocated as a cause, this mechanism is irrelevant [92]. 2. Alkaline load. [HCO3−] may increase secondary to the administration of NaHCO3 solutions, or precursors such as acetate, citrate, or lactate that are subsequently metabolized to HCO3− in the liver. In oliguric patients, it can be caused by nonabsorbable antacids or cation exchange resins. 3. Disproportionate loss of chloride. [HCO3−] can increase, in the absence of negative proton balance or alkali addition, when there is a loss of extracellular volume with a

6  Acid–Base Abnormalities in Surgical Patients Admitted to Intensive Care Unit

higher proportion of Cl− to HCO3−. The loss of liquid rich in Cl− (gastric, renal) increases the [BB]. This last phenomenon is called volume contraction alkalosis, since the total amount of HCO3− is normal, while the volume of the extracellular fluid decreases, raising the plasma [HCO3−]. The contribution of this mechanism is minor [15]. From Stewart’s perspective, these processes increase the [SID], which decreases water dissociation, causes alkalemia, and increases [HCO3−]. Thus, pH and [HCO3−] are dependent variables that change secondarily to [SID] modifications [15]. Maintenance of Metabolic Alkalosis Metabolic alkalosis is maintained by the renal inability to eliminate the excess of HCO3−. The involved mechanisms are: (1) decrease in filtered HCO3− because of a decline in glomerular filtration rate; (2) increase in HCO3 reabsorption due to volume and Cl− depletion; and (3) increase in the secretion of H+ and NH4+ associated with hypokalemia, increased aldosterone activity or genetic alterations in ion transport. Some clinical situations can simultaneously activate more than one of these mechanisms.

6.2.2.2 Causes of Metabolic Alkalosis The causes of metabolic alkalosis are shown in Table 6.3. In patients undergoing major surgery, many factors contribute to the development of metabolic alkalosis in the perioperative period. Dehydration or hypovolemia produced by fasting and bowel preparation, are frequent findings. This clinical situation has been described as “contraction alkalosis” and it is associated with bicarbonate reabsorption and chloride depletion [93]. Hypochloremic metabolic alkalosis has been preoperatively reported in around 25% of patients [94]. Other major causes in surgical patients are the Cl− loss through nasogastric tubes (>1 L/day) or enterocutaneous fistulas, hypovolemia, diuretics use, or renal compensation for hypercapnia. Hypochloremia and hypokalemia may occur in >50% of these patients because of these mechanisms. Hypokalemia is also a known etiology of metabolic alkalosis. Proposed mechanisms are increased H+ secretion in proximal and distal nephron, increased HCO3−reabsorption in proximal tubule and ammoniagenesis stimulation. Since hypokalemia can exacerbate metabolic alkalosis, the adequate management should include the K+ administration [95, 96]. Metabolic alkalosis is a well-known complication of massive blood transfusion. The explanation is the hepatic conversion of citrate to HCO3− [97]. Rates of 40–100% [98, 99] have been reported in patients who received massive blood transfusion in orthotopic liver transplantation, 40–64% in adult surgical patients [100–102], and 49–52% in pediatric patients after open-heart surgery [103].

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Table 6.3  Causes of metabolic alkalosis Chloride losses  Digestive    Gastric fluid losses    Loss from feces    Congenital chloride diarrhea     Villous adenoma  Renal    Loop and thiazide diuretics    Bartter and Gitelman syndromes    Posthypercapnic state  Skin    Cystic fibrosis States that present or simulate mineralocorticoid hyperactivity  Primary hyperaldosteronism  Cushing’s syndrome  Apparent excess of mineralocorticoids    Primary excess of deoxycorticosterone: 11β- and 17α-hydroxylase deficiency    Drugs: Liqueurs (glycyrrhizic acid), carbenoxolone  Bartter syndrome  Secondary hyperaldosteronism    Accelerated and malignant hypertension    Edematous states Administration of alkali  Solutions containing bicarbonate, citrate, acetate and sodium lactate  Dairy-alkaline syndrome  Combination of non-absorbable antacids and cation exchange resins Severe potassium depletion Miscellaneous  High doses of β-lactam antibiotics  Hypoalbuminemia

The use of balanced crystalloid instead of chloride-rich solutions leads to higher incidence of severe metabolic alkalosis. In addition, large amounts of balanced crystalloids may cause dilutional metabolic alkalosis by diluting Atot [78]. Since hypoalbuminemia is almost a ubiquitous finding in critically ill patients, it might be another cause of metabolic alkalosis. This is explained by the loss of the normal buffering plasma proteins, which act as weak acids under physiologic conditions. Nevertheless, the issue is controversial. The “primary hypoproteinemic alkalosis” was described in eight hypoalbuminemic ICU patients with increased [HCO3−] and [BE], and without alterations in [AG], [SID], and osmolarity [104]. In a series of 700 critically ill patients with hypoalbuminemia, however, we could only identify one patient fulfilling these criteria [19]. Actually, the loss of weak acid secondary to hypoproteinemia is compensated by a renal-­ mediated increase in [Cl−], so [SID] decreases without changes in pH and [HCO3−] [105]. Critically ill patients fre-

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quently have hypoalbuminemia, but they are not usually alkalemic (normal pH, [HCO3−], and [BE]), and their [SID] is also reduced. Consequently, it would seem more appropriate to consider this as a physiologic compensation for a decreased [Atot], rather than a complex acid–base disorder, such as a mixed metabolic acidosis/hypoalbuminemic alkalosis [18, 105]. Response of Metabolic Alkalosis to Chloride Administration The different responses to the administration of Cl− solutions not only point out the underlying mechanisms but also have important diagnostic and therapeutic connotations (Table 6.4). The most frequent causes of metabolic alkalosis are associated with Cl− depletion. These disorders are corrected by administration of Cl−solutions. Characteristically, the [Cl−]urinary is 20 mEq/L. A particular situation is that of edematous states with effective arterial hypovolemia, such as cirrhosis, nephrotic syndrome, and cardiac failure. Although these patients usually have [Cl−]urinary 1000 mEq. A central venous catheter and careful monitoring are required. In primary mineralocorticoids excess, their source must be removed (surgery, chemotherapy) or their effects blocked. In primary hyperaldosteronism, spironolactone is effective and K+ supplements can improve alkalosis and high blood pressure. In Bartter and Gitelman syndromes, hypokalemia and hypomagnesemia must be corrected. In Bartter syndrome, inhibitors of angiotensin-converting enzyme and prostaglandin synthesis are helpful. In Gitelman syndrome, any K+ sparing diuretic can be useful, while in Liddle’s syndrome, amiloride is the choice [107]. A detailed analysis of the ­treatment of the different states is out of the scope of this chapter.

6.2.3 Complex Metabolic Disorders Complex metabolic acid–base disorders (acidosis plus alkalosis) are frequently found in surgical patients. As a result, severe abnormalities might not be evident, because metabolic acidosis may be masked by the simultaneous presence of metabolic alkalosis. Indeed, pH, PCO2, [HCO3−], and [BE] could be normal. The diagnosis should be performed through the analysis of the ∆[AG]/∆[EB] and the ∆[AG]/∆[HCO3−] ratios: mixed metabolic disorders are characterized by increases in [AG] greater than the decreases in [EB] and [HCO3−] [8]. Using the Stewart’s approach, the diagnosis is based on [SID] and [Atot] changes [15]. In a series of 152 critical patients, the Stewart’s approach could detect metabolic acidosis in some patients with normal [HCO3−] and [BE] levels. In those patients, the metabolic acidosis with a low [SID] was counterbalanced by an alkalinizing processes, mostly by hypoalbuminemia [16]. In another series of critically ill patients with severe hyperlactatemia, we found that: 20% of them had normal pH, [HCO3−], and [BE] levels because of a concomitant presence of hypochloremic metabolic alkalosis. Both the conventional and the Stewart’s approach allowed the correct identification of mixed metabolic acidosis and alkalosis [108]. Therefore, a correct diagnosis of acid–base disorders requires the assessment of the changes in [Cl−], [HCO3−], [BE], and [AG].

6.3 Respiratory Acid–Base Disorders Alveolar ventilation is normally adjusted to maintain the arterial PCO2 between 35 and 45 mmHg. When alveolar ventilation is increased or decreased out of proportion to CO2 production, a respiratory acid–base disorder arises.

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6.3.1 Physiopathology Respiratory acidosis is an alteration characterized by elevated arterial PCO2 and decreased pH.  On the contrary, respiratory alkalosis is defined by reduced PCO2 and increased pH. Both types of disorders are frequently observed in the postoperative period. Any change in the PCO2 determines a [HCO3−] modification in the same direction, to lessen the effect on the pH.  The magnitude of the change in HCO3− depends on whether the respiratory alteration is acute or chronic [2]. In chronic processes, it is higher because of the time of renal mechanisms. Acute variations in blood PCO2 determine modifications in [H+] and [HCO3−] according to the carbonic acid equilibrium equation. Therefore, there are no significant changes in either plasma [BE] or [SID] [109]. If the PCO2 alteration remains over time, renal compensatory mechanisms are activated and both, plasma [BE] and [SID], are modified to decrease the impact on [H+]. The metabolic response to respiratory disorders begins in minutes and takes effect over a period of hours to days [110, 111]. Like metabolic disorders, the compensatory response should set [HCO3−] within the expected values (Table 6.5). In respiratory acidosis, the kidney acidifies the urine by increasing the reabsorption of filtered HCO3− and the NH4Cl excretion, in order to increase plasma [BE] and [SID]. The renal compensation process produces hypochloremia [112, 113]. The traditional approach considers that the compensation is primarily due to an increase in renal bicarbonate generation, while the Stewart’s approach states that the compensation is mediated by Cl− excretion to maintain extracellular electroneutrality [15–18]. In respiratory alkalosis, the kidney responds by alkalizing the urine through the inhibition of HCO3 reabsorption and ammoniagenesis. The filtered HCO3− is excreted along with urinary cations, mainly sodium. The compensation induces hyperchloremia. According to the traditional approach, the compensation is primarily dependent on the renal loss of HCO3−, whereas the Stewart’s approach interprets that the mechanism is the renal retention of chloride to maintain electroneutrality [15–18].

Table 6.5  Metabolic compensatory responses in respiratory disorders Disorders Acute respiratory acidosis Chronic respiratory acidosis Acute respiratory alkalosis Chronic respiratory alkalosis

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[HCO3−] (mEq/L) 24 + (0.1 * ∆PCO2) 24 + (0.35 * ∆PCO2) 24 − (0.2 * ∆PCO2) 24 − (0.5 * ∆PCO2)

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6.3.2 Clinical Manifestations The main clinical effects of hypercapnia are mediated by vasodilation of different vascular beds. Brain manifestations such as intracranial hypertension, papilledema, anxiety, confusion, headache, delirium, aggressiveness, stupor and coma have been described. In addition, negative inotropic effects, systemic vasodilation and release of catecholamines can be present. Increases in the adrenergic tone and in the levels of renin, corticosteroids, aldosterone and ADH can lead to renal water and sodium retention. Acute hypercapnia and acidosis shift the hemoglobin dissociation curve to the right. Unlike hypercapnia, hypocapnia induces vasoconstriction. In acute respiratory alkalosis, blood flow could decrease in heart, brain, skin, and kidney, but increase in skeletal muscle. Hypocapnia increases the affinity of hemoglobin for oxygen, which determines an improvement in the capacity to incorporate oxygen at the pulmonary level but a difficulty in transferring it to the tissues. Oxygen consumption increases, probably due to the higher adrenergic tone. Precordial pain and electrocardiographic changes in the ST segment consistent with ischemia; and neurologic effects such as dizziness, perioral paresthesia, cramps, and exceptionally generalized seizures have been described. They are related to ionic hypocalcemia. Bronchoconstriction, increased microvascular permeability of the tracheal mucosa, and decreased lung compliance can also occur.

6.3.3 Treatment Therapeutic management should be directed at the underlying cause (Table 6.6). In postoperative respiratory acidosis, the most important threat is not acidosis but hypoxemia. Accordingly, supplemental oxygen is always required. While the underlying causes are being investigated, an attempt should be made to reverse the effect of sedatives, narcotics and, if necessary, endotracheal intubation should not be delayed. Noninvasive ventilation is another treatment option that is useful in selected patients, particularly those with normal state of consciousness. Thus, the clinical condition of the patient rather than absolute arterial PCO2 value should be considered for the decision of tracheal intubation [114].

F. D. Masevicius and A. Dubin Table 6.6  Causes of respiratory acid base disorders Respiratory acidosis Large airway obstruction  Physical/mechanical obstruction (aspiration, mass lesion, plug or kink in endotracheal tube, tracheal collapse) Intrinsic pulmonary and small airway disease  Severe pulmonary edema  Pneumonia

 Asthma  Chronic obstructive pulmonary disease Respiratory center depression  Drug induced (opioids, barbiturates, inhalant anesthetics)  Neurologic disease (e.g., brainstem or cervical spinal cord lesion) Restrictive extrapulmonary disorders  Diaphragmatic hernia  Pleural space disease (e.g., pneumothorax, pleural effusion) Neuromuscular disease  Drug induced (anesthetic drugs, muscle relaxants, aminoglycosides)  Electrolyte abnormalities (eg, hypokalemia)  Myasthenia gravis  Tetanus, botulism  Tick paralysis Increased CO2 production with impaired alveolar ventilation  Heat stroke  Malignant hyperthermia  Ineffective mechanical ventilation  Marked obesity (Pickwickian syndrome)

Respiratory alkalosis Hypoxemia or tissue hypoxia  Pulmonary disorders (pneumonia, edema, pneumothorax, pulmonary embolism, bronchial asthma, interstitial pneumonitis, fibrosis)  Cardiovascular disorders (congestive heart failure, hypotension, shock) Respiratory center stimulation  Drugs and hormones (salicylates, methylxanthines, β-adrenergic agonists, progesterone) Hypocapnia secondary to CNS lesions  Central hyperventilation  Cheyne–stokes  Biot’s respiration

Accidental induction of hypocapnia  Cardiopulmonary bypass  High-frequency modes of ventilation  Extracorporeal membrane oxygenation Miscellaneous  Fever, sepsis, pain, pregnancy, hepatic failure

6  Acid–Base Abnormalities in Surgical Patients Admitted to Intensive Care Unit

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Hatherill M, Waggie Z, Purves L, Reynolds L, Argent A. Correction 2005;365:871–5. of the anion gap for albumin in order to detect occult tissue anions 34. Levy B, Mansart A, Montemont C, Gibot S, Mallie JP, Reanault V, in shock. Arch Dis Child. 2002;87:526–9. et  al. Myocardial lactate deprivation is associated with decreased 12. Carvounis CP, Feinfeld DA.  A simple estimate of the effect cardiovascular performance, decreased myocardial energetof the serum albumin level on the anion gap. Am J Nephrol. ics, and early death in endotoxic shock. Intensive Care Med. 2000;20:369–72. 2007;33:495–502. 13. Taylor D, Durward A, Tibby SM, Thorburn K, Holton F, Johnstone 35. Levraut J, Ciebiera JP, Chave S, Robary O, Jambou P, Carles IC, et al. The influence of hyperchloraemia on acid base interpretaM, et  al. Mild hyperlactatemia in stable septic patients is due to tion in diabetic ketoacidosis. Intensive Care Med. 2006;32:295–301. impaired lactate clearance rather than overproduction. Am J Respir 14. Corey HE. The anion gap (AG): studies in the nephrotic syndrome Crit Care Med. 1998;157:1021–6. and diabetic ketoacidosis (DKA). J Lab Clin Med. 2006;147:121–5. 36. Michaeli B, Martinez A, Revelly JP, Cayeux MC, Chiolero RL, 15. Stewart PA. Modern quantitative acid-base chemistry. Can J Physiol Tappy L, et  al. Effects of endotoxin on lactate metabolism in Pharmacol. 1983;61:1441–61. humans. Crit Care. 2012;16:R139. 16. Fencl V, Jabor A, Kazda A, Figge J. Diagnosis of metabolic acid-­ 37. Brown SD, Clark C, Gutierrez G.  Pulmonary lactate release in base disturbances in critically ill patients. Am J Respir Crit Care patients with sepsis and the adult respiratory distress síndrome. J Med. 2000;162:2246–51. Crit Care. 1996;11:2–8. 17. Boniatti MM, Cardoso PR, Castilho RK, Vieira SR. Acid-base dis38. Bendjelid K, Treggiari MM, Romand JA. Transpulmonary lactate orders evaluation in critically ill patients: we can improve our diaggradient after hypothermic cardiopulmonary bypass. Intensive Care nostic ability. Intensive Care Med. 2009;35:1377–82. Med. 2004;30:817–21. 18. Kellum JA. Determinants of blood pH in health and disease. Crit 39. Gasparovic H, Plestina S, Sutlic Z, Husedzinovic I, Coric V, Care. 2000;4:6–14. Ivancan V, et al. Pulmonary lactate release following cardiopulmo19. Dubin A, Menises MM, Masevicius FD, Moseinco MC, nary bypass. Eur J Cardiothorac Surg. 2007;32:882–7. Kutscherauer DO, Ventrice E, et al. Comparison of three different 40. Stacpoole PW, Wright EC, Baumgartner TG, Bersin RM, Buchalter methods of evaluation of metabolic acid-base disorders. Crit Care S, Curry SH, et al. A controlled clinical trial of dichloroacetate for Med. 2007;35:1264–70. treatment of lactic acidosis in adults. The Dichloroacetate-Lactic 20. Masevicius FD, Dubin A. Has Stewart approach improved our abilAcidosis Study Group. N Engl J Med. 1992;327:1564–9. ity to diagnose acid-base disorders in critically ill patients? World J 41. O’Connor E, Fraser JF.  The interpretation of perioperative lacCrit Care Med. 2015;4:62–70. tate abnormalities in patients undergoing cardiac surgery. Anaesth 21. Lawton TO, Quinn A, Fletcher SJ. Perioperative metabolic acidosis: Intensive Care. 2012;40:598–603. the Bradford Anaesthetic Department Acidosis Study. J Intensive 42. Minton J, Sidebotham DA. Hyperlactatemia and cardiac surgery. J Care Soc. 2019;20(1):11–7. Extra Corpor Technol. 2017;49:7–15. 22. Silva JM Jr, Ribas Rosa de Oliveira AM, Mendes Nogueira FA, 43. Wu S, Chen W, Le Shen LX, Zhu A, Huang Y. Risk factors of post-­ Vianna PMM, Prata Amendola C, Carvalho Carmona MJ, et  al. operative severe hyperlactatemia and lactic acidosis following lapaMetabolic acidosis assessment in high-risk surgeries: prognostic roscopic resection for pheochromocytoma. Sci Rep. 2017;7:403. importance. Anesth Analg. 2016;123:1163–71. 44. Hernández G, Ospina-Tascón GA, Damiani LP, Estenssoro E, 23. Emmett M, Narins RG.  Clinical use of anion gap. Medicine. Dubin A, Hurtado J, et al. Effect of a resuscitation strategy target1977;56:38–54. ing peripheral perfusion status vs serum lactate levels on 28-day 24. Harrington JT, Cohen JJ. Metabolic acidosis. In: Cohen JJ, Kasssirer mortality among patients with septic shock: the ANDROMEDA-­ JP, editors. Acid-base. Boston: Little, Brown and Company; 1984. SHOCK randomized clinical trial. JAMA. 2019;321:654–64. p. 121–225.

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92 45. Cooper DJ, Walley KR, Wiggs BR, Russell JA. Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. A prospective, controlled clinical study. Ann Intern Med. 1990;112:492–8. 46. Bersin RM, Chatterjee K, Arieff AI. Metabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart disease. Am J Med. 1989;87:7–14. 47. Jaber S, Paugam C, Futier E, Lefrant JY, Lasocki S, Lescot T, et  al. Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial. Lancet. 2018;392:31–40. 48. Bersin RM, Arieff AI.  Improved hemodynamic function during hypoxia with Carbicarb, a new agent for the management of acidosis. Circulation. 1988;77:227–33. 49. Nahas GG, Sutin KM, Fermon C, Streat S, Niklund L, Wahlander S, et al. Guidelines for the treatment of acidaemia with THAM. Drugs. 1998;55:191–224. 50. Abramowitz MK, Hostetter TH, Melamed ML.  The serum anion gap is altered in early kidney disease and associates with mortality. Kidney Int. 2012;82:701–9. 51. Durward A, Tibby SM, Skellett S, Austin C, Anderson D, Murdoch IA.  The strong ion gap predicts mortality in children following cardiopulmonary bypass surgery. Pediatr Crit Care Med. 2005;6:281–5. 52. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32:1335–43. 53. Adrogué HJ, Wilson H, Boyd AE, Suki WN, Eknoyan G. Plasma acid-base patterns in diabetic ketoacidosis. N Engl J Med. 1982;307:1603–10. 54. Adrogué HJ, Barrero J, Eknoyan G.  Salutary effects of modest fluid replacement in the treatment of adults with diabetic ketoacidosis. Use in patients without extreme volume deficit. JAMA. 1989;262:2108–13. 55. Mahler SA, Conrad SA, Wang H, et  al. Resuscitation with balanced electrolyte solution prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis. Am J Emerg Med. 2011;29:670–4. 56. Chua HR, Venkatesh B, Stachowski E, Schneider AG, Perkins K, Ladanyi S. Plasma-lyte 148 vs 0.9% saline for fluid resuscitation in diabetic ketoacidosis. J Crit Care. 2012;27:138–45. 57. Okuda Y, Adrogue HJ, Field JB, Nohara H, Yamashita K.  Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis. J Clin Endocrinol Metab. 1996;81:314–20. 58. Hale PJ, Crase J, Nattrass M. Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis. Br Med J (Clin Res Ed). 1984;289:1035–8. 59. American Diabetes Association. Standards of medical care in diabetes—2016. Diabetes Care. 2016;39(Suppl 1):S1–S110. 60. Burke KR, Schumacher CA, Harpe SE.  SGLT2 inhibitors: a systematic review of diabetic ketoacidosis and related risk factors in the primary literature. Pharmacotherapy. J Human Pharmacol Drug Ther. 2017;37:187–94. 61. Bonanni FB, Fei P, Fitzpatrick LL.  Normoglycemic ketoacidosis in a postoperative gastric bypass patient taking canagliflozin. Surg Obes Relat Dis. 2016;2:e11–E12. 62. Kraut JA, Madias NE. Differential diagnosis of nongap metabolic acidosis: value of a systematic approach. Clin J Am Soc Nephrol. 2012;7:671–9. 63. Goldstein MB, Bear R, Richardson RM, Marsden PA, Halperin ML. The urine anion gap: a clinically useful index of ammonium excretion urine anion gap: a clinically useful index of ammonium excretion. Am J Med Sci. 1986;292:198–202. 64. Masevicius FD, Tuhay G, Pein MC, Ventrice E, Dubin A. Alterations in urinary strong ion difference in critically ill patients with meta-

F. D. Masevicius and A. Dubin bolic acidosis: a prospective observational study. Crit Care Resusc. 2010;12:248–54. 65. Scheingraber S, Rehm M, Sehmisch C, Finsterer U. Rapid saline infusion produces hyperchloraemic acidosis in patients undergoing gynecologic surgery. Anesthesiology. 1999;90:1265–70. 66. Masevicius FD, Vazquez AR, Enrico C, Dubin A.  Urinary strong ion difference is a major determinant of plasma chloride concentration changes in postoperative patients. Rev Bras Ter Intensiva. 2013;25:197–204. 67. Brunner R, Drolz A, Scherzer TM, Staufer K, Fuhrmann V, Zauner C, et al. Renal tubular acidosis is highly prevalent in critically ill patients. Crit Care. 2015;19:148. 68. Kellum JA, Bellomo R, Kramer DJ, Pinsky MR. Etiology of metabolic acidosis during saline resuscitation in endotoxemia. Shock. 1998;9:364–8. 69. McDougal WS.  Metabolic complications of urinary intestinal diversion. J Urol. 1992;147:1199–208. 70. Alemozaffar M, Nam CS, Said MA, Patil D, Carney KJ, David S, et al. Avoiding the need for bowel anastomosis during pelvic exenteration—urinary sigmoid or descending colon conduit—short and long term complications. Urology. 2019;129:228–33. 71. Kellum JA, Song M, Li J. Lactic and hydrochloric acids induce different patterns of inflammatory response in LPS-stimulated RAW 264.7 cells. Am J Phys. 2004;286:R686–92. 72. Kellum JA, Song M, Almasri E. Hyperchloremic acidosis increases circulating inflammatory molecules in experimental sepsis. Chest. 2006;130:962–7. 73. Pedoto A, Caruso JE, Nandi J.  Acidosis stimulates nitric oxide production and lung damage in rats. Am J Respir Crit Care Med. 1999;159:397–402. 74. Pedoto A, Nandi J, Oler A, Camporesi EM, Hakim TS, Levine RA.  Role of nitric oxide in acidosis-induced intestinal injury in anesthetized rats. J Lab Clin Med. 2001;138:270–6. 75. Kellum JA.  Fluid resuscitation and hyperchloremic acidosis in experimental sepsis: improved short-term survival and acidbase balance with hextend compared with saline. Crit Care Med. 2002;350:300–5. 76. Suetrong B, Pisitsak C, Boyd JH, Russell JA, Walley K.  Hyperchloremia and moderate increase in serum chloride are associated with acute kidney injury in severe sepsis and septic shock patients. Crit Care. 2016;20:315. 77. Shaw AD, Bagshaw SM, Goldstein SL, Scherer L, Duan M, Schermer CR.  Major complications, mortality, and resource utilization after open abdominal surgery: 0.9% saline compared to plasma-lyte. Ann Surg. 2012;255:821–9. 78. Yunos NM, Kim IB, Bellomo R, Bailey M, Ho L, Story D.  The biochemical effects of restricting chloride-rich fluids in intensive care. Crit Care Med. 2011;39:2419–24. 79. Yunos NM, Bellomo R, Hegarty C, Story D, Ho L, Bailey M.  Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA. 2012;308:1566–72. 80. Boniatti MM, Cardoso PR, Castilho RK, Vieira SRR. Is hyperchloremia associated with mortality in critically ill patients? A prospective cohort study. J Crit Care. 2011;26:175–9. 81. Morgan TJ, Venkatesh B, Hall J. Crystalloid strong ion difference determines metabolic acid base change during in vitro hemodilution. Crit Care Med. 2002;30:157–60. 82. Weinberg L, Harris L, Bellomo R, Ierino FL, Story D, Eastwood G, et al. Effects of intraoperative and early postoperative normal saline or plasma-Lyte 148 on hyperkalaemia in deceased donor renal transplantation: a double-blind randomized trial. Br J Anaesth. 2017;119:606–15. 83. Adrogué HJ, Madias NE.  Changes in plasma potassium concentration during acute acid-base disturbances. Am J Med. 1981;71:456–67.

6  Acid–Base Abnormalities in Surgical Patients Admitted to Intensive Care Unit 84. Waters JH, Gottlieb A, Schoenwald P, Popovich MJ, Sprung J, Nelson DR.  Normal saline versus lactated Ringer’s solution for intraoperative fluid management in patients undergoing abdominal aortic aneurysm repair: an outcome study. Anesth Analg. 2001;93:817–22. 85. Pfortmueller CA, Funk GC, Reiterer C, Schrott A, Zotti O, Kabon B, et al. Normal saline versus a balanced crystalloid for goal-directed perioperative fluid therapy in major abdominal surgery: a doubleblind randomised controlled study. Br J Anaesth. 2018;120:274–83. 86. Semler MW, Self WH, Wanderer JP, Ehrenfeld JM, Wang L, Byrne DW, et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378:829–39. 87. Self WH, Semler MW, Wanderer JP, Wang L, Byrne DW, Collins SP, et  al. Balanced crystalloids versus saline in noncritically ill adults. N Engl J Med. 2018;378:819–28. 88. Zampieri FG, Machado FR, Biondi RS, Freitas FGR, Veiga VC, Figueiredo RC, et  al. Effect of intravenous fluid treatment with a balanced solution vs 0.9% saline solution on mortality in critically ill patients: the basics randomized clinical trial. JAMA. 2021;326:1–12. 89. Evans L, Rhodes A, Alhazzani W, Antonelli M, Coopersmith CM, French C, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021. Intensive Care Med. 2021;47(11):1181–247. 90. Wilson RF, Gibson D, Percinel AK, Ali MA, Baker G, LeBlanc LP, et al. Severe alkalosis in critically ill surgical patients. Arch Surg. 1972;105:197–203. 91. Anderson LE, Henrich WL.  Alkalemia-associated morbidity and mortality in medical and surgical patients. South Med J. 1987;80:729–33. 92. Adler S.  Potassium transport: physiology and pathophysiology. Curr Top Membr Transp. 1987;28:421–40. 93. Marino PL. Acid-base interpretations. In: Marino PL, editor. The ICU book. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2007. p. 540, 568. 94. Freeman BD. Fluid and electrolyte abnormalities. In: Mulholland MW, Doherty GM, editors. Complications in surgery. Philadelphia: Lippincott Williams & Wilkins; 2006. p. 148. 95. Hossain SA, Chaudhry FA, Zahedi K, et al. Cellular and molecular basis of increased ammoniagenesis in potassium deprivation. Am J Renal Physiol. 2011;301:F969–78. 96. Hamm LL, Hering-smith KS, Nakhoul NL. Acid-base and potassium homeostasis. Semin Nephrol. 2013;33:257–64. 97. Yendt ER. Citrate intoxication. Can Med Assoc J. 1957;76:141–4.

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98. Contreras G, Garces G, Reich J, Banerjee D, Young L, Cely C, et  al. Predictors of alkalosis after liver transplantation. Am J Kidney Dis. 2002;40:517–24. 99. Raj D, Abreo K, Zibari G.  Metabolic alkalosis after orthotopic liver transplantation. Am J Transplant. 2003;3:1566–9. 100. Driscoll DF, Bistrian BR, Jenkins RL, Randall S, Dzik WH, Gerson B, et al. Development of metabolic alkalosis after massive transfusion during orthotopic liver transplantation. Crit Care Med. 1987;15:905–8. 101. Okusawa S, Aikawa N, Abe O. Postoperative metabolic alkalosis following general surgery: its incidence and possible etiology. Jpn J Surg. 1989;19:312–8. 102. Hodgkin JE, Soeprono FF, Chan DM.  Incidence of metabolic alkalemia in hospitalized patients. Crit Care Med. 1980;8:725–8. 103. van Thiel RJ, Koopman SR, Takkenberg JJ, Tem Harkel ADJ, Bogers AJJC. Metabolic alkalosis after pediatric cardiac surgery. Eur J Cardiothorac Surg. 2005;28:229–33. 104. McAuliffe JJ, Lind LJ, Leith DE, Fencl V.  Hypoproteinaemic alkalosis. Am J Med. 1986;81:86–90. 105. Wilkes P. Hypoproteinemia, strong-ion difference, and acid-base status in critically ill patients. J Appl Physiol. 1998;84:1740–8. 106. Weiner M, Epstein FH. Signs and symptoms of electrolyte disorders. Yale J Biol Med. 1970;43:76–109. 107. Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000;11:369–75. 108. Tuhay G, Pein MC, Masevicius FD, Olmos Kutscherauer D, Dubin A.  Severe hyperlactatemia with normal base excess: a quantitative analysis using conventional and Stewart approaches. Crit Care. 2008;12:R66. 109. Barker ES, Singer RB, Elkinton JR, Clark JK. The renal response in man to acute experimental respiratory alkalosis and acidosis. J Clin Invest. 1957;36:515–29. 110. Schwartz WB, Falbriard A, Lemieux G. The kinetics of bicarbonate reabsorption during acute respiratory acidosis. J Clin Invest. 1959;38:939–44. 111. Ramadoss J, Stewart RH, Cudd TA.  Acute renal response to rapid onset respiratory acidosis. Can J Physiol Pharmacol. 2011;89:227–31. 112. Sullivan WJ, Dorman PJ. The renal response to chronic respiratory acidosis. J Clin Invest. 1955;34:268–76. 113. Levitin H, Branscome W, Epstein FH.  The pathogenesis of hypochloremia in respiratory acidosis. J Clin Invest. 1958;37:1667–75. 114. Adrogue HJ, Madias NE.  Management of life-threatening acid-­ base disorders: part II. N Engl J Med. 1998;338:107–11.

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7

Pre-operative Cardiovascular Risk Assessment in Non-cardiac General Surgery Andrea Farina, Mauro Zago, and Stefano Savonitto

Key Points • International clinical practice guidelines are of great help for risk stratification of cardiovascular complications in general surgery. • Patients with acute coronary syndromes and severe valvular disease should get specific cardiac treatment before deferrable surgery. • Besides these cases, only patients with functional limitation 2 mg/dL). It provides an estimate of the risk of major CV complications (heart attack, cardiac arrest, pulmonary oedema, and complete AV block), with a score of 2 identifying moderate risk (7%) and 3 identifying high risk (11%). • The second model, derived from the American College of Surgeons database, is based on five variables: type of surgery, functional status, creatinine >1.5  mg/dL, ASA (American Society of Anaesthesiologists) class, and age. It may be obtained using an online calculator and provides a better-performing estimate of 30-day heart attack/ cardiac arrest risk than Lee’s index, especially in vascular patients [13].

7.4.1 Heart Failure (HF) Among the anamnestic data, one of the most negative prognostic factors is a history of HF, especially if associated with an ejection fraction  50 mmHg: in these cases, percutaneous commis- pulmonary exercise testing or estimated from a standardized surotomy (PMC) should be considered (class IIa—LOE clinical questionnaire, such as the Duke Activity Status C), whereas a surgical approach should be reserved for Index; more commonly, a subjective estimate by the doctor symptomatic patients with unfavourable characteristics based on simple anamnestic data is used, which is a less prefor PMC. Control of heart rate and, possibly, maintenance cise method but retains prognostic value [39–41]. The two of sinus rhythm are always essential, clinically relevant cutoffs are 4 METs (good capacity) and –– severe aortic or mitral regurgitation with symptoms or 10 METS (excellent), corresponding, respectively, to a significant reduction of ejection fraction, patient able to climb one floor of stairs (two flights) or engage in strenuous sporting activity.

7.4.4 Arrhythmias Management follows general guidelines outside the surgical setting, whereas most important is an echocardiographic assessment of any underling structural heart disease. Indications to therapy are as follows: –– AF or flutter: rhythm or rate control and anticoagulation as indicated. –– non-sustained ventricular tachycardia (VT): correction of triggers, –– sustained VT: beta-blockers, antiarrhythmic drugs, electrical cardioversion, correction of ischemia, –– third or second Mobitz 2 AV block or symptomatic asystolic pauses: temporary/permanent pacing, –– bifascicular block: availability of external pacing and of isoprenaline,

• If the patient is capable of ≥4 METS without symptoms his prognosis is good and no further tests are also indicated before high-risk NCS. • If FC is 2 (class I-LOE C) and may be considered also in intermediate-risk surgery with Lee index ≥1 (class IIB-LOE C). According to AHA/ ACC guidelines, there is a class IIa indication to pharmacologic stress test in patients with elevated perioperative risk and FC 2 and FC 65 years of age or >45 years with significant CV disease or risk factors; they also give a strong recommendation to cTn dosing in patients with pre-operative positive natriuretic peptides or otherwise deemed to be high risk.

7.8 Management of Perioperative Antithrombotic Therapy 7.8.1 Antiplatelet Therapy

7.7.4 Biomarkers

Low-dose aspirin (75–100  mg daily) causes a minimal increase in perioperative bleeding and has a powerful effect in preventing perioperative complications in patients with vascular disease [54, 55]. On the other hand, inhibitors of the platelet P2Y12 receptor, such as ticlopidine, clopidogrel, and the more powerful prasugrel and ticagrelor, cause a significant increase in surgical bleeding, including the need for haemostatic reoperation [34]. DAPT using aspirin and a P2Y12 receptor blocker is the standard antithrombotic therapy after an ACS, particularly after stent implantation. Several registry data have shown that about 5% of patients with the previous PCI and coronary stenting undergo NCS during the recommended period of DAPT needed to prevent stent thrombosis [34]. DAPT has been traditionally continued for 1 year after an ACS and for 6 months in the context of CCS. However, based on improvements in stent technology and operator skills, current guidelines have taken a more tailored approach to the recommendations on DAPT duration [56]:

Pre-operative measurement of natriuretic peptides (BNP or NT-proBNP) can assist in risk stratification of heart failure patients and in therapeutic optimization [50]; in certain situations, it can be more cost-effective than echocardiography [51]. It is also useful in PAH, where a BNP 38.3  °C or a temperature of >38.0  °C sustained over 2 h and an absolute neutrophil count (ANC) of 14  mg/dL or 3.5  mmol/L) is treated with IV isotonic saline solution, SC calcitonin administration, and IV bisphosphonates therapy. • Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is caused by an unregulated production of the antidiuretic hormone (ADH), which leads to water retention and hyponatremia. Cancer-related SIADH is most often found in small cell carcinoma of the lung, as a consequence of ectopic secretion of ADH. Symptomatic hyponatremia is treated with IV hypertonic 3% saline. Patients with mild symptoms can be managed with a less aggressive therapy: fluid restriction, oral salt tablets, or urea.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 P. Aseni et al. (eds.), The High-risk Surgical Patient, https://doi.org/10.1007/978-3-031-17273-1_10

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• Neuro-oncologic emergencies are clinical conditions that can occur in cancer patients as a direct effect of the tumor on the nervous system or as a complication of cancer treatments. In this chapter, we focus on a frequent cancer-related neuro-oncologic emergency, that is Neoplastic Epidural Spinal Cord Compression (ESCC), and chemotherapy-induced Myasthenic Crisis (MC). ESCC is caused by displacement or compression of the spinal cord by a metastatic tumor in the vertebral bones. Definitive treatment with neurosurgery and/or radiotherapy should be promptly carried out, especially if motor findings are present. Chemotherapyinduced Myasthenic Crisis (MC) is a life-threatening condition that can rarely occur as a worsening of myasthenia gravis after starting chemotherapy for thymomas.

10.1 Introduction Overall survival of oncologic patients has improved in the last decades, thanks to clinical research and the development of increasingly innovative treatments; nonetheless, cancer remains a disease with elevated morbidity and mortality rates. Cancer patients may often experience emergency clinical conditions during the disease course, with several oncological emergencies occurring both as the first presentation of the disease or during the treatment course. In this chapter, we focus on major and well-known oncologic emergencies with the purpose of providing a practical guide for their diagnosis and management.

10.2 Febrile Neutropenia (FN) FN is one of the most common oncologic emergencies and it remains a serious complication of cancer chemotherapy (ChT). FN is defined as an oral temperature of >38.3 °C or a temperature of >38.0 °C sustained over 2 h and an absolute neutrophil count (ANC) of  60 years

Weight 5 3 5 4 4 3 3 2

Reproduced with permission from: Yu JB, Wilson LD, Detterbeck FC et  al. Superior Vena Cava Syndrome—A Proposed Classification System and Algorithm for Management. J Thorac Oncol.2008 Aug 1;3 (8):811–4. All rights reserved

Table 10.1  Febrile neutropenia and neutrophil count decreased grading according to CTCAE v. 5.0 Febrile neutropenia

Neutrophil count decreased

Grade 1 –

Grade 2 –

40 kg m−2 in almost one-half of patients with OSA. 30.1.2.6 Frailty Frailty is most commonly found in older patients, and this population is increasing disproportionately worldwide. In 2015, an estimated 8.5% of the world’s population was 65  years or older (defined as older adults or elderly). It is estimated that this will increase to be more than 12% by the year 2030 and 17% by 2050. Surgery in this age group will become more common.

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Older surgical patients have higher rates of adverse health outcomes, including major complications, prolonged hospital stay, readmission, and unplanned discharge to care facilities. Frailty is generally conceptualised as a state of increased vulnerability resulting from age-associated declines in physiological reserves and function across multiple organ systems. Increasing age has a clear correlation with frailty; however, ageing alone is not necessarily synonymous with frailty. Ageing is often conceptualised as an accumulation of deficits due to incidental damage throughout life, resulting in an increased risk of death.

30.1.2.7 Aetiology Dysregulation of the immune and endocrine systems, basal metabolism, and factors, such as genetics, mitochondrial dysfunction, poor nutrition, and reduced physical activity have been linked to frailty development. Inflammaging has been defined as the presence of a low-­ grade chronic pro-inflammatory state. Increased levels of pro-inflammatory cytokines characterize this (interleukin-6, tissue necrosis factor-alpha and C-reactive protein and leucocytes. Immune dysregulation leads to a catabolic state, with resultant anorexia, sarcopenia, loss of adipose tissue, anaemia, and subclinical cardiovascular disease. Ageing leads to mitochondrial dysfunction: they are ubiquitous intracellular organelles responsible for energy production through oxidative phosphorylation. They contain their DNA encoding several key proteins of the respiratory chain. Mutations in mitochondrial DNA lead to excessive production of reactive oxygen species, damaging macromolecules, and impairing cellular and tissue function. Reduced levels of oestrogen, testosterone, and dehydroepiandrosterone sulphate (DHEA-S) are associated with ageing. In frail individuals, the circulating levels of these hormones are significantly lower. DHEA-S plays an essential role in maintaining muscle mass and indirectly prevents activation of the inflammatory pathways that lead to reduced muscle mass.

30.2 Risk Factors for Extubation Failure Patient-related risk factors –– Age >65 years –– Heart disease or lung disease –– BMI >30 Risk factors related to acute pathology –– Neurological deficits –– Difficulty in protecting the airways –– Inability to manage airway secretions

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–– –– –– ––

Difficult or prolonged respiratory weaning Cardiogenic respiratory failure Secondary intubation to pneumonia Positive water balance The ASA Physical Status Classification System has been used for over 60 years. The purpose of the system is

to assess and communicate a patient’s pre-anesthesia medical co-­morbidities. The classification system alone does not predict the perioperative risks but is used with other factors (type of surgery, frailty, and level of deconditioning); it can be helpful in predicting perioperative risks (see Table 30.1).

Table 30.1  ASA Physical Status Classification System, American Society of Anesthesiologist ASA classifiction Definition ASA I A normal healthy patient ASA II A patient with mild systemic disease

ASA III

A patient with severe systemic disease

ASA IV

A patient with severe systemic disease

ASA V

A moribund patient who is not expected to survive without the operation

ASA VI

A declared braindead patient whose organs Are being removed for donor purposes

Adult Examples, Including, but not Limited to: Healthy, nonsmoking, no or minimal alcohol use. Mild diseases only without substantive functional limitations. Current smoker, social alcohol drinker, pregnancy, obesity (30 3 months) of MI, CVA, TIA, or CAD/stents. Recent (250 mL should be carefully monitored in the postoperative course [23]. Embolization is the first-line treatment in almost all centers, whether bleeding occurs early or late [24]. The catheter-­ directed angiography can also identify the origin of the bleeding and can successfully provide a minimally invasive treatment, preserving the residual renal function without the need for re-operation [25] (Fig. 33.1).

33  Endovascular Management of Post-Operative Bleeding

33.7 After Liver Transplantation There have been several studies that examine the incidence of gastrointestinal bleeding after a liver transplant. One of them described an 8.9% cumulative risk of gastrointestinal bleeding in the post-liver transplant setting [26]. Because of the higher prevalence of gastrointestinal bleeding in patients receiving small-for-size liver grafts, gas-

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trointestinal bleeding must be anticipated and promptly diagnosed and treated [27]. The first-line treatment option should be the endovascular approach (Fig.  33.2), but surgical treatment remains the treatment of choice for major venous bleeding, especially when the source is the vena cava or portal vein anastomosis [28].

a

b

c

d

Fig. 33.1  Bleeding after partial nephrectomy. (a) CT arterial phase axial view, (b) CT arterial phase coronal view, (c) DSA before embolization with coils, (d) Final DSA

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a

b

c

d

Fig. 33.2  Bleeding after liver transplant. (a) CT arterial phase. (b) Distal DSA. (c) Proximal DSA. (d) Final DSA after embolization with coils

33.8 After Digestive Tract Surgery In general, postoperative bleeding after colorectal procedures is a rare complication. The risk depends on the performed surgical procedure, the co-morbidities of the patient, and in individual cases on an impaired clotting system [29] (Fig. 33.3). The choice of materials, embolic agent, and operator expertise are critical to ultimate success. Smaller blood vessels typically require femoral access with a 5F sheath, distal catheterization with microcatheters, followed by deployment

of microcoils, gel-foam slurry, beads, and glue, based on operator familiarity. In hemodynamically unstable patients, the entity of bleeding is usually bigger, and the IR must be more aggressive to save the life of the patient by rapidly controlling exsanguinating hemorrhage. As the procedure should be done in the shortest time possible, the expertise of IR and the ability with material plays a crucial role. There are no large series in the literature because this is not common complication. Thus, there are no practical guidelines, and we can provide recommendations to avoid complications or unsuccessful surgical procedures [11].

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d

e

Fig. 33.3  Duodenal bleeding after endoscopy stent. (a) CT arterial phase, (b) DSA with 5Fr catheter, (c) DSA befor embolization with glue, (d) Embolization with glue, (e) Final DSA

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References 1. Spahn DR, et al. The European guideline on management of major bleeding and coagulopathy following trauma: fifth edition. Crit Care. 2019;23(1):98. https://doi.org/10.1186/s13054-­019-­2347-­3. 2. Cosmi B, et  al. Assessment of the risk of bleeding in patients undergoing surgery or invasive procedures: guidelines of the Italian Society for Haemostasis and Thrombosis (SISET). Thromb Res. 2009;124(5):e6. https://doi.org/10.1016/j. thromres.2009.08.005. 3. Lee HG, Heo JS, Choi SH, Choi DW. Management of bleeding from pseudoaneurysms following pancreaticoduodenectomy. World J Gastroenterol. 2010;16(10):1239–44. https://doi.org/10.3748/wjg. v16.i10.1239. 4. Adam G, et  al. Endovascular treatment of delayed hemorrhage developing after the pancreaticoduodenectomy procedure. Wien Klin Wochenschr. 2014;126(13–14):416–21. https://doi. org/10.1007/s00508-­014-­0557-­x. 5. Yekebas EF, et  al. Postpancreatectomy hemorrhage: diagnosis and treatment—an analysis in 1669 consecutive pancreatic resections. Ann Surg. 2007;246(2):269–80. https://doi.org/10.1097/01. sla.0000262953.77735.db. 6. Sanjay P, Kellner M, Tait IS.  The role of interventional radiology in the management of surgical complications after pancreatoduodenectomy. HPB. 2012;14(12):812–7. https://doi. org/10.1111/j.1477-­2574.2012.00545.x. 7. Jamieson GG, Corbel L, Campion JP, Launois B. Major liver resection without a blood transfusion: is it a realistic objective? Surgery. 1992;112(1):32–6. Accessed: May 22, 2021. [Online]. Available: https://europepmc.org/article/med/1320298. 8. Melendez JA, et al. Perioperative outcomes of major hepatic resections under low central venous pressure anesthesia: blood loss, blood transfusion, and the risk of postoperative renal dysfunction. J Am Coll Surg. 1998;187(6):620–5. https://doi.org/10.1016/ S1072-­7515(98)00240-­3. 9. Romano S, et al. MDCT imaging of post interventional liver: a pictorial essay. Eur J Radiol. 2005;53(3 SPEC ISS):425–32. https:// doi.org/10.1016/j.ejrad.2004.12.019. 10. García-Blázquez V, Vicente-Bártulos A, Olavarria-Delgado A, Plana MN, Van Der Winden D, Zamora J. Accuracy of CT angiography in the diagnosis of acute gastrointestinal bleeding: systematic review and meta-analysis. Eur Radiol. 2013;23(5):1181–90. https:// doi.org/10.1007/s00330-­012-­2721-­x. 11. Tasu JP, et  al. Postoperative abdominal bleeding. Diagn Interv Imaging. 2015;96(7–8):823–31. https://doi.org/10.1016/j. diii.2015.03.013. 12. Vu M, Anderson SW, Shah N, Soto JA, Rhea JT.  CT of blunt abdominal and pelvic vascular injury. Emergency Radiology. 2010;17(1):21–9. https://doi.org/10.1007/s10140-­009-­0813-­y. 13. Ye X, Lafuma A, Torreton E, Arnaud A.  Incidence and costs of bleeding-related complications in French hospitals following surgery for various diagnoses. BMC Health Serv Res. 2013;13(1):1–8. https://doi.org/10.1186/1472-­6963-­13-­186. 14. Rahbari NN, et al. Post-hepatectomy haemorrhage: a definition and grading by the international study Group of Liver Surgery (ISGLS).

F. Barbosa et al. Liver Transplant Unit, R Prince Alfred Hosp. 2011;18:19. https:// doi.org/10.1111/j.1477-­2574.2011.00319.x. 15. Lim C, Dokmak S, Farges O, Aussilhou B, Sauvanet A, Belghiti J. Reoperation for post-hepatectomy hemorrhage: increased risk of mortality. Langenbeck's Arch Surg. 2014;399(6):735–40. https:// doi.org/10.1007/s00423-­014-­1189-­3. 16. Russell MC.  Complications following hepatectomy. Surg Oncol Clin North Am. 2015;24(1):73–96. https://doi.org/10.1016/j. soc.2014.09.008. 17. Yang T, et al. Risk factors of hospital mortality after re-laparotomy for post-hepatectomy hemorrhage. World J Surg. 2013;37(10):2394– 401. https://doi.org/10.1007/s00268-­013-­2147-­x. 18. Lermite E, et al. Complications after pancreatic resection: Diagnosis, prevention and management. Clin Res Hepatol Gastroenterol. 2013;37(3):230–9. https://doi.org/10.1016/j.clinre.2013.01.003. 19. Wente MN, et  al. Postpancreatectomy hemorrhage (PPH)-an International Study Group of Pancreatic Surgery (ISGPS) definition. Surgery. 2007;142(1):20. https://doi.org/10.1016/j. surg.2007.02.001. 20. Kim Y, Lee J, Yi KS, Lee SH, Cho BS, Park KS.  Transcatheter arterial embolization for late postpancreatectomy hemorrhage of unusual origin (dorsal pancreatic artery): a report of three cases. Iran J Radiol. 2019;16(2) https://doi.org/10.5812/iranjradiol.82464. 21. Schäfer M, Heinrich S, Pfammatter T, Clavien PA.  Management of delayed major visceral arterial bleeding after pancreatic surgery. HPB. 2011;13(2):132–8. https://doi. org/10.1111/j.1477-­2574.2010.00260.x. 22. Jung S, Min GE, Chung BI, Jeon SH.  Risk factors for postoperative hemorrhage after partial nephrectomy. Korean J Urol. 2014;55(1):17–22. https://doi.org/10.4111/kju.2014.55.1.17. 23. Fardoun T, et al. Predictive factors of hemorrhagic complications after partial nephrectomy. Eur J Surg Oncol. 2014;40(1):85–9. https://doi.org/10.1016/j.ejso.2013.11.006. 24. Zorn KC, Starks CL, Gofrit ON, Orvieto MA, Shalhav AL.  Embolization of renal-artery pseudoaneurysm after laparoscopic partial nephrectomy for angiomyolipoma: case report and literature review. J Endourol. 2007;21(7):763–8. https://doi. org/10.1089/end.2006.0332. 25. Jeon CH, Seong NJ,Yoon CJ, Byun S-S, Lee SE. Clinical results of renal artery embolization to control postoperative hemorrhage after partial nephrectomy. Acta Radiol Open. 2016;5(8):205846011665583. https://doi.org/10.1177/2058460116655833. 26. Fidan C, et al. Postoperative gastrointestinal bleeding after an orthotopic liver transplant: a single-center experience. Exp Clin Transplant. 2014;12(SUPPL. 1):159–61. https://doi.org/10.6002/ect.25Liver.P38. 27. Hirata M, et al. Gastrointestinal bleeding after living-related liver transplantation. Dig Dis Sci. 2002;47(11):2386–8. https://doi.org/1 0.1023/A:1020570901035. 28. Jung JW, et  al. Incidence and management of postoperative abdominal bleeding after liver transplantation. Transplant Proc. 2012;44(3):765–8. https://doi.org/10.1016/j. transproceed.2012.01.011. 29. Kirchhoff P, Clavien PA, Hahnloser D. Complications in colorectal surgery: risk factors and preventive strategies. Patient Saf Surg. 2010;4(1):1–13. https://doi.org/10.1186/1754-­9493-­4-­5.

Evaluation and Management of Malnutrition in the High-Risk Surgical Patient

34

Biljana Andonovska and Alan Andonovski

Key Points • Prevalence of malnutrition in all surgically treated patients is high and has a negative impact on clinical outcomes. • To achieve better clinical results in surgical patients, a good perioperative nutrition strategy is necessary. • Assessment of nutritional status is equally important as the primary diagnosis in hospitalized patients. • Many different measures, techniques and scores have been proposed, but no indicator has been accepted as the golden standard for the determination of the nutritional status. • Indirect calorimetry is a recommended method for the precise determination of energy expenditure and requirements. • Oral nutrition is the best nutritional support. • In patients who cannot be fed perioperatively for more than 5  days or in cases when over 50% of the recommended intake with oral nutrition cannot be maintained for more than 7 days, enteral nutrition is advised without delay. • If energy and nutritional requirements (5% over 3 months and reduced BMI or a low fat-free mass index (FFMI) [7] However, the use of BMI as a measure for the assessment of the nutritional status has shown poor sensitivity in overweight patients. Firstly, patients with a higher fat mass index can experience a significant change in the nutritional status prior to assessing whether they have abnormal status or have been nutritionally exhausted. Furthermore, this category of patients is associated with cardiovascular (heart) diseases, diabetes, hypertension and increased morbidity. Hence, there is a dilemma whether the increased incidence of perioperative morbidity in patients with increased BMI correlates with associated diseases or whether these patients are really undernourished? Conditions like kidney failure, liver diseases or malig-

nancy can lead to generalized edema or ascites, which can also influence the results and their interpretation. In spite of this, BMI is a useful tool, especially relevant for surgical patients with lower index levels, who, in fact, can benefit from nutritional support [8]. The limitations discovered by measuring only the body weight have led to the evolution of anthropometry. To monitor the subcutaneous fat deposits, skinfold thickness is measured and highly correlates with body fat percentage. The thickness of subcutaneous fat deposits varies in different body parts, and consequently for accurate assessment of fat deposits, a combination of measures is necessary. One of the recommended measurements of subcutaneous adipose tissue is measuring the triceps skinfold thickness (TSF). Another indicator of nutritional assessment is the determination of muscle mass. Skeletal muscle mass is 40% of the body weight and 60% of the total body mass. One of the better parameters for determining skeletal muscle mass is the determination of midarm muscle circumference (MAMC). Neglected parameters for assessing the nutritional status are monitoring the functional capacity and muscle power. The decrease in muscle power (e.g., weak power of the hands and lack of strength in the respiratory muscle) is a better predictor of postoperative complications than the loss of weight or arm muscle circumference. Although these parameters look useful, they have a limited practical application due to the indispensable cooperation with the patient and the influence of the drugs such as narcotic analgesics or sedatives on the examined measurements [9]. A new technique that enables the assessment of the muscle compartment, and correlates with the other anthropometric, biochemical and inflammatory parameters is the measurement of m. adductor pollicis thickness (TAPM). This method identifies the changes in the whole body and can be useful in the detection of early changes associated with malnutrition along with the assessment of nutritional recovery [10]. In addition to anthropometric methods, there are also other techniques for the quantification of the muscle mass. Ultrasonography is also a new technique, which is non-­ invasive and cheap and is realized at the patient’s bedside. It helps in identifying muscle structure and morphology. Campbell et  al. have shown that ultrasonography detects muscle wasting in edematous patients with multiorgan failure. The results obtained with ultrasonography correlate with the results obtained with CT diagnostic techniques. In monitoring muscle wasting, m. quadriceps femoris is observed. This muscle has clear anatomy that can be easily visualized even in cases of reduced muscle architecture [11, 12]. Age, degree of hydration, and physical activity might influence the measured anthropometric parameters, but these measures are essential for assessing the nutritional status of a patient.

34  Evaluation and Management of Malnutrition in the High-Risk Surgical Patient

34.2.3 Biochemical Analyses The development and identification of different types of underfeeding have shown that medical history and physical examination are not sufficient for assessing the nutritional status. Biochemical analyses, especially of serum proteins, are of great importance. Albumin is a hepatic protein with a half-life of 14–20 days. Serum concentration reflects the synthesis, degradation, loss and exchange between intra- and extravascular space. There are processes that change the level of albumin, and hence it is not a specific serum marker of undernourishment. This is particularly valid for acute conditions where a large number of infectious and inflammatory processes have an impact on serum albumin concentration. In spite of this, medical doctors rely on the albumin level as a parameter for the assessment of the patient’s nutritional status. A low serum albumin concentration is linked with a high incidence of clinical complications, morbidity and mortality. Albumin level under 35 g/L as a unique parameter of undernourishment has a low specificity for identification of the nutritional status, but as a predictor, it shows a significant increase in morbidity and prolonged hospital stay. On the other hand, albumin level under 25 g/dL points out increased mortality and severe malnutrition [13]. Other markers such as prealbumin and transferrin are popularized because of their high sensitivity to nutritional status changes and their ability to reflect the protein loss specifically. Still, their unreliable reactions to stress or disease and the huge costs for testing make them less safe and inappropriate for universal application as clinical markers of the nutritional status. Insulin-like growth factor, serum cholesterol, urinary urea nitrogen, creatinine-height index, and delayed cutaneous hypersensitivity have attributes that correlate well with the condition of nutrition and are applied as clinical markers of the nutritional status.

34.2.4 Nutritional Risk Screening and Assessment Tests There are also screening and nutritional status tests to assess nutritional status. Some of these tests are designed to quickly identify patients at risk for developing malnutrition, while other tests provide detailed nutritional assessment and identify patients at higher risk of complications and increased mortality. In a large prospective study comprising 100 patients, who had undergone of the major gastrointestinal tract surgery, Sungurtekin et al. detected that 44% of patients were undernourished according to subjective global assessment (SGA), and 61% were undernourished according to Nutritional Risk Screening (NRS) [14].

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SGA is a marker that integrates data obtained from the medical history, clinical examination, and X-ray imaging. In line with the results obtained by the application of this method, patients were classified as follows: 1. Well-nourished (Grade A). 2. Moderately malnourished or at risk of malnutrition (Grade B). 3. Severely malnourished (Grade C). SGA and albumin levels are important for the differentiation of patients with a high nutritional risk from patients with a low nutritional risk [15]. NRS - 2002 is the method that assesses the weight loss, BMI, food intake, and severity of the disease. Based on this screening, patients can be classified with the following: –– No risk of malnutrition with value 0 –– Mild risk of malnutrition with a value of 1–2 –– Moderate risk of malnutrition with a value of 3–5 –– Severe risk of malnutrition with a value >5 [16] –– Some studies show that patients, who suffer from severe illness and have serious nutritional risk as SGA- level B and NRS 2002 more than 3 points, would benefit from perioperative nutritional support in the postoperative recovery and their clinical results [17].

34.3 Problems During the Perioperative Period Preoperatively patients encounter gastrointestinal abnormalities (mechanical obstruction, malabsorption, adverse effects associated with drugs and treatment such as nausea and vomiting), metabolic disturbances, diagnostic procedures involving preoperative fasting, and all these lead to disorders in nutritional support and undernutrition [17, 18]. Surgery itself is a challenge for the surgeon, and hence, he/she has to balance the extent of the surgical technique with the ability of the patient’s body to cope with the metabolic load. This mainly refers to the cardiopulmonary capacity, the presence of inflammation, infection, or sepsis. If the extent and risk of surgery are not adjusted to the capacity of the patient to generate an adequate host response, then there is a high risk of complications including dehiscence of anastomosis and wounds, infectious complications, and death. Following abdominal surgery, postoperative ileus is a common issue; on the other hand, intraoperative manipulation in the abdominal cavity subsequently leads to panenteric inflammation and dysmotility [19]. Traditionally, many patients undergoing major gastrointestinal resections receive a large amount of crystalloids intravenously during and after surgery. Excessive administration of fluids would result in body weight gain and even edema. This may cause postoperative ileus and delayed gastric emptying [20].

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After surgery, patients also encounter several other barriers to adequate food intake, including surgical response to stress as well as organizational barriers in the hospitals. In general, all these adverse events have an impact on postoperative nutrition. The surgeon should predict the patient’s ability for adequate postoperative oral feeding. If serious problems are on the way that may jeopardize enteral nutrition, it is reasonable to provide access to long-term nutrition (jejunostoma, nasojejunal tube, or needle catheter jejunostomy [NCJ]) at the end of every major gastrointestinal surgery [21–25].

34.4 Energy Requirements Determination of the energy requirements is one of the most provocative challenges in surgical patients and is vital for determining the energy target that would shape the nutrient delivery. Overnutrition and undernutrition are associated phenomena in hospital patients. It is considered that uncomplicated surgery has energy requirements of 1.0–1.15  ×  BMR (basal metabolic rate) while complicated surgery requires 1.25–1.4 × BMR in order to meet the patient’s needs [26]. It is still under debate how much energy surgical patients should receive. In general, 25 kcal/kg/day is considered as an appropriate energetic target for surgical patients, but patients with sepsis, trauma or complicated surgery may require almost twice as much energy [27] (Table 34.1). Indirect calorimetry is a recommended method for precisely determining of the energy expenditure and requirements by the American Society of Parenteral and Enteral Nutrition (ASPEN) and the ESPEN. This method calculates rest energy expenditure (REE), the amount of energy in calories required for basic metabolic processes of the body during a non-active period of 24 h. It is measured indirectly with indirect calorimetry equipment (metabolic cart) by analysis of respiratory gases (usually expired) to derive the volume of air passing through the lungs, the amount of oxygen extracted from it, and the amount of carbon dioxide, as a by-product of metabolism, expelled to atmosphere all computed to represent values corresponding to 1-min time intervals.

Table 34.1  Examples for nutrition requirements Descriptor Open abdomen Low-output gastrointestinal fistula High-output gastrointestinal fistula Short bowel syndrome

Energy 25–35 kCal/kg 25 kCal/kg 30 kCal/kg 32 kCal/kg

Protein 1.5–2.5 g/kg 1–1.5 g/kg 1.5–2 g/kg 1–1.5 g/kg

The respiratory quotient (RQ) can also be calculated with these measurements except REE.  The abbreviated Weir equation is used to calculate the 24-hour energy expenditure. Abbreviated Weir Equation:

REE = 3.9 (VO2 ) + 1.1(VCO2 )  1.44



VO 2 = oxygen uptake ( mL/min )



VCO 2 = carbon dioxide output ( mL/min )



Respiratory quotient ( RQ ) = VCO 2 / VO 2 [ 28]

The amount of lean body mass is the primary determinant of REE, but multiple other factors can influence REE, such as age, sex, presence of fever or inflammation, thyroid function, etc. Sedation, analgesics, and neuromuscular blocking agents reduce REE, while pressors raise REE. The respiratory quotient (physiologic range 0.67–1.2) reflects substrate oxidation and has different values such as 1.0 for glucose, 0.81 for proteins, and 0.69 for lipids. It is theoretically useful in assessing a nutrition regimen, as overfeeding or excessive carbohydrate administration increases VCO2 and leads to an RQ  >  1.0, while underfeeding with associated lipolysis decreases the RQ. According to some specialists, despite the theoretical usefulness of the RQ in nutrition titration, it has a low sensitivity and specificity as an indicator of over- and underfeeding [29]. However, in general, the method of inidirect calorimetry uses expensive equipment; it also requires technical expertise, which makes this method unavailable for many institutions. For easier calculation of energy expenditure and requirements, some researchers have attempted to find some equation to calculate the REE measuring only VCO2 with ventilator devices. The modified Weir equation (REE, kcal/ day = 5.5 × VCO2L/min) × 1440 using a fixed RQ of 0.89) was later improved by Sandra Stapel et al., who proposed an even more sophisticated approach to achieving better accuracy using VCO2 alone in ventilated surgical patients, extracting RQ from the nutrition regimen for each evaluation and not using a fixed value [30]. There are more than 200 prediction equations for the determination of energy requirements. They are based on age, gender, height, weight, and disease severity. One of the most frequently used formulas for predicted energy expenditure is the Harris-Benedict equation, and they take into account gender, age, height and weight. Harris-Benedict Equations (calories/day):



Male : ( 66.5 + 13.8 × weight ) + ( 5.0 × height ) − ( 6.8 × age )

34  Evaluation and Management of Malnutrition in the High-Risk Surgical Patient



Female : ( 665.1 + 9.6 × weight ) + (1.8 × height ) − ( 4.7 × age ) weight in kilograms, height in centimetres, age in years [31].

There is no consensus on which prediction equations are the most suitable for surgical patients. Many problems exist regarding these equations, and the precision varies significantly depending on the heterogeneity of the pathology, stress factor, different body constitution and treatment. Studies have shown that the result of the energy r­ equirements calculated using the prediction equations deviates from the actual requirements for 500  kcal or more, which leads to overfeeding or underfeeding. However, in the absence of indirect calorimetry as a method, prediction equations are widely used and recommended by the international associations [32].

34.5 Nutritional Therapy From a technological point of view, diet is defined as the provision of the right amount of nutrients, carbohydrates, fat, proteins, vitamins, electrolytes and water. Nutrition can be oral, enteral, and parenteral.

34.5.1 Oral Nutrition According to the generally accepted nutritional postulates, oral nutrition is the best method of nutritional support. Oral nutrition is feeding by mouth and should always be advised when the patient is capable of food intake. Intake of solid food is allowed until 6  h preoperatively, and fluids are allowed to be taken up to 2 h preoperatively in elective surgery. Exemptions from the rules are patients at risks, such as patients who are to be subjected to emergent surgical intervention, patients with delayed gastric emptying, or patients with gastroesophageal reflux [33]. It is a general attitude that oral intake of nutrients has to continue without interruption post-surgery considering the individual tolerance and type of surgical intervention.

34.5.2 Nutritional Therapy In a narrow clinical sense, nutritional therapy refers to enteral or parenteral nutrition. Perioperative nutritional therapy is indicated in patients who are to be subjected to major surgery, in patients with malnutrition and in patients with severe nutritional risk. For surgical patients, “severe” nutritional risk has been defined

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according to the ESPEN working group (2006) as the presence of at least one of the following criteria: Weight loss >10–15% within 6 months BMI 5 Serum albumin 500 mL/day) Intestinal obstructions or ileus Intestinal ischaemia Intractable vomiting Profuse diarrhea Severe enterocolitis Aggressive support not warranted

the application of enteral nutrition is contraindicated. The need to satisfy energy and nutritional requirements has led to the onset of another type of nutrition – parenteral nutrition (PN), which was applied for the first time in 1968 and was widely accepted in the following years [41]. Parenteral nutrition is the delivery of all necessary energy and nutritional nutrients in the form of a solution via circulation (via peripheral or central vein approach).

Table 34.3  Complications of Enteral Feeding Complications of enteral feeding Gastrointestinal complications  –  Distension  –  Nausea and vomiting  –  Diarrhoea /constipation Mechanical complications  –  Malposition/blockage of feeding tube  –  Sinusitis  –  Ulcerations/erosions Metabolic complications Infectious complications  –  Aspiration pneumonia  –  Bacterial contamination

Depending on the spectrum and quantity of nutrients delivered in the organism, parenteral nutrition can be partial (supplementary) or total. Total parenteral nutrition is the method of nutritional support when nutrition is provided exclusively via the parenteral route. On the other hand, supplementary parenteral nutrition is a method of nutritional support that aims to supplement the deficit of energy from enteral nutrition until 100% of daily energy needs are achieved. This approach is based on the assumption that energy delivery near 100% of the anticipated daily needs can improve patients’ clinical results. According to the ESPEN recommendations, administration of parenteral nutrition in surgical patients has proven to be of benefit when energy and nutritional requirements (7 days [43]. Nutritional support with the parenteral method preoperatively in a period of 7–14 days results in a reduction of mortality and incidence of postoperative complications from one side, and to the recovery of physiological functions and increase in body proteins, from the other side [44]. Regarding the postoperative period, the administration of parenteral nutrition is beneficial in undernourished patients where enteral nutrition is impossible or insufficient and in patients where postoperative complications cause functional gastrointestinal disorders and, hence, energy requirements of the organism cannot be met by oral or enteral nutrition within 7 days. Parenteral nutritional solutions contain more than 40 different components including water, macronutrients (carbohydrates, lipids, and amino acids), electrolytes, micronutrients (trace elements, vitamins) and other additives (e.g., gluta-

34  Evaluation and Management of Malnutrition in the High-Risk Surgical Patient Table 34.4  Side effects after parenteral nutrition Mechanical complications

Metabolic complications

Septic complications Allergic complications Psychological complications

Low position of the central venous catheter:  –  Pneumothorax  –  Hemothorax  –  Chylothorax  –  Fluid in thorax  –  Cardiac injury  –  Cardiac arrhythmia, Central venous catheter obstruction (partial or total)  –  Air embolism  –  Thrombosis  –  Embolism Hyperglycemia Hypoglycemia Hyperosmolarity Hyperlipidemia Hyperammonemia Electrolyte imbalance Deficiency in trace elements and vitamins Atrophy of intestinal villi Infections of the catheter Lipids and proteins

mine, insulin, and heparin). They can be administered as separate components or in the form of an “all-in-one bag system” applied in hospitals or as industrially ready products. Application of separate components requires numerous manipulations with intravenous line and is associated with an increased risk of administrative errors, including septic and metabolic complications. Therefore, a three-chamber bag or pharmacy prepared should be preferred instead of a multi-bottle system [30]. Parenteral nutrition can be administered by central or peripheral vein route. The peripheral vein route is suitable for the delivery of nutrient mixtures with smaller osmolality (3 g/dI after the end of surgery compared to postoperative baseline level and/or any postoperative transfusion of PRBCs for a falling hemoglobin and/or the need for invasive re-intervention (e.g. embolization or re-laparotomy) to stop bleeding. To diagnose PHH (and to exclude other sources of haemorrhage) evidence of intraabdominal bleeding should be obtained such as frank blood loss via the abdominal drains if present (e.g. haemoglobin level in drain fluid >3 g/dl) or detection of anintra-abdominal haematoma or active haemorrhage by abdominal imaging (ultrasound, CT, angiography). Patients who are transfused immediately postoperatively for intra-operative blood loss by a maximum of two units of PRBCs (.e. who do not haveevidence of active haemorrhage) are not diagnosed with PH.

A → PHH requiring transfusion of up to 2 units of PRBCs GRADING

B → PHH requiring transfusion of >2 units of PRBCs but manageable without invasive intervention C → PHH requiring radiological interventional treatment (e.g embolization) or re-laparotomy

Clinical presentation depends on portal vein thrombosis (PVT) grade. The classification used is generally the Yerdel Classification, also used for spontaneous thrombosis (Fig. 44.2) [7]. PH-PVT of low grade usually occurs accidentally on a routine CT scan after surgery, whereas severe PH-PVT usually presents with refractory ascites and eventually hepatic failure. A few articles have described risk factors for PH-PVT, which seem to be associated with right hepatectomy, caudate lobectomy, splenectomy, larger resection volume, longer operation time, longer duration of Pringle’s maneuver, PV segmental resection, PV angle in the residual liver, age over 70 years, and postoperative bile leakage [8]. Manipulation of the vascular tree or thermal damage of a vessel with energy devices can result in a turbulent flow and consequent PVT. There is no clear evidence that laparoscopic or laparotomic surgery results in a higher incidence of PVT. The early detection of PH-PVT is crucial for a successful treatment. Depending on the grade of thrombosis and the patient’s clinical status, the treatment may consist of oral anticoagulant therapy and monitoring, if possible depending on the time before surgery, interventional radiology with the positioning of a stent, venous angioplasty, and thrombolysis or surgical thrombectomy after the failure of other therapy. If a good result is not achieved, a cavernous transformation and/ or stenosis of the portal vein can lead to liver failure. However, partial or complete portal vein recanalization under anticoagulation therapy is possible in about one-third of patients. There are not several reports dealing with arterial thrombosis after liver resection; this can happen as a specific complication during vascular reconstruction and can be due to

technical errors or an increase of turbulence of the flow due to collection or infection status. Treatment can be radiological or surgical, aimed to restore vascular flow as soon as possible to avoid ischemia of the remnant liver.

44.1.2 Bile Leakage The incidence ranges between 4 and 17%. The most common causes of bile leakage are a truncation of the distal bile duct in the residual liver, especially in the resected liver surface, leakage at the bile duct-intestinal anastomosis, incomplete suture around the T-tube, and injury to the bile duct. Risk factors, identified by different authors, are multiple resections, traumatized liver surface, and intraoperative bleeding [9–11]. There are different definitions of bile leak. Some authors consider a bile leak when a bilirubin concentration in the drain fluid is greater than an absolute value (10  mg/dL) in two or more consecutive measurements. For ISGLS, the definition and grading of bile leakage are shown in Table 44.2 [12]. The impact of a bile leak on morbidity and mortality is closely related to the grade of the fistula (Table 44.3). Various techniques have been described to control a bile leakage detected during surgery, ranging from covering the cut liver surface of the remnant liver with gauze to intraoperative cholangiography and indocyanine green fluorescein. Different biological glue can be applied to the cut surface of the remnant liver. Biliary drainage (percutaneous transhepatic or percutaneous transabdominal drainage with or without endoscopic stenting) is effective in treating most cases of biliary leakage

478

A. Mariani et al.

a

b

Grade I

20%

52%

c

Grade II

Grade III

d

Grade IV 20%

18%

Fig. 44.2  Yerdel classification of portal vein thrombosis. The classification divides the portal vein thrombosis into 4 grades. Grade I: The thrombosis of portal vein affects 3) and associated high-grade non-renal injuries [10]. The next step following the failure of conservative management is angiographic embolisation and/ or surgery.

2020

2020

2019

Desai [40]

Xu [41]

Khoschnau [42] Salem [43]

2018

2018

Mann [46]

Single centre, Canada

National database, Japan Multicentre, Australia Single centre, China Single centre, Qatar Single centre, South Africa Single centre, Denmark National database, Usa Multicentre, Usa

Location

2004–2018, retrospective 2002–2012, retrospective 2011–2018, prospective 2014–2017, retrospective 2012–2016, retrospective 2010–2015, retrospective 2010–2016, retrospective 2014–2017, prospective 2004–2014, retrospective

Study period and type

b

a

26.9% underwent laparotomy but no renal exploration 34.6% underwent laparotomy but no renal explorations c Embolisation data only available from 2013 to 2016

2019

2019

Maibom [44] El hechi [45] Keihani [6]

2019

2020

Author Nakao [39]

Year

368

431

1842

107

223

152

160

668

3550

89%

71%

0%

93%

56%

100%

100%

100%

100%

Injury type Blunt

11%

29%

100%

7%

44%

0%

0%

0%

0%

III: 25.6%, IV: 43.1%, V: 31.3% I–II: 52%, III: 29.6%, IV–V: 18.4% I: 20.2%, II: 23.3%, III: 25.5%, IV: 17% V: 13.9% I: 20% II: 4%, III: 33%, IV: 33%, V: 10% I: 3.1%, II: 6.3%, III: 19.5%, IV: 61.8%, V: 9.2% III (55%), IV (33%), V (12%) I: 16.6%, II: 22.8%, III: 36.4%, IV: 20.9%, V: 3.3%

I: 39.7%, II: 10.1%, III: 29.3%, IV: 16.8%, V: 4.2% –

Penetrating Aast grade distribution

Table 66.2  Summary of recent papers reporting data on the management and outcomes associated with renal trauma

90.5%

70%

51.1%b

92%

79.8% a

92.9%

10%

92.8%

6.6%

11%

0.5%c

7%

2.7%

–

46.3%

2.3%

Management Conservative Minimally invasive – 33.5%

2.9%

19%

48.9%

1%

15.8%

7.1%

37.5%

4.9%

–

Open

2.4%

13%

40.1%

1%

12.2%

3.3%

–

4.9%

5.4%

8%

11.2%

3.7%

8.1%

11.2%

1.9%

0%

Nephrectomy Mortality 3.8% 9.5%

720 P. Gravestock et al.

66  Updates in the Management of Complex Renal Trauma

66.14 Angiography and Embolisation Minimally invasive interventional radiology techniques are reserved for patients who fail conservative management. Renal artery embolisation is a procedure whereby the renal artery, or some of its branches (selective angioembolisation), are occluded endovascularly. Since its advent in the 1970s it has played a developing role in the management of renal trauma. Typically performed via a transfemoral approach, it is generally a safe procedure with lower rates of complication than surgery and minimal impact on renal function [47]. Principally, embolisation of as distal an arterial branch as possible to minimise parenchymal loss is achieved using coils or liquid embolic agents [48]. Indications for angiography and selective angioembolisation include, but are not limited to, active extravasation of contrast, av fistula, pseudoaneurysm, non-resolving visible haematuria and progressively lowering haemoglobin concentrations in patients undergoing expectant management [49]. Success rates for treating haemorrhage in renal trauma are generally high, ranging from 85 to 100%, though there is wide variation in grade 5 trauma with success rates reported in the literature of 0–100% [20, 47, 49–51]. Repeated intervention is often required and success rates for this are equally variable [52]. Following failed embolisation, surgery usually results in nephrectomy [50, 52].

66.15 Iatrogenic Renal Vascular Injury Iatrogenic injuries typically result from nephron-sparing surgery, predominately partial nephrectomy and percutaneous

721

intervention to the kidney from procedures such as nephrolithotomy, nephrostomy and renal biopsy [48, 53]. With an increase in the number of these procedures, particularly a shift toward nephron-sparing surgery, an increasing incidence of iatrogenic renal vascular injury has been observed [54]. These injuries include active bleeding, arterio-urinary fistula, arteriovenous (AV) fistula or pseudoaneurysm (PSA) formation. The majority of iatrogenic renal artery injuries can be managed conservatively or percutaneously. Arterio-urinary fistula generally close without intervention and bleeding post procedures can be embolised with high levels of success, up to 98% in some case series [48, 53, 55]. AV fistulas are relatively common with an incidence post renal biopsy of almost 15%. Though many of these heal spontaneously, those that persist typically have a high flow or are large in size and risk of rupture may necessitate intervention [48]. Pseudoaneurysm or false aneurysms are a contained injury to the vessel wall, typically between the media and adventitia or in some cases the surrounding tissue [56, 57]. These are rare, estimated to occur in 1–2% of partial nephrectomies, and more commonly in procedures undertaken using a minimally invasive technique [54, 57]. Patients are almost always symptomatic, the predominant feature being haematuria which presents on average 2 weeks postoperatively, with flank pain and anaemia also commonly present [54, 57]. Treatment of AV fistula and pseudoanuresym is with angioembolisation, success rates of which are reported as up to 96%, an example is shown in Fig. 66.4 [54].

Fig. 66.4  Angiographic images of a left kidney pre and post-endovascular embolisation. Contrast extravasation is present on the left image, however on the right image coil embolisation has occurred with no further extravasation seen

722

P. Gravestock et al.

Acute Assessment

Investigation

Assessment

Grade I-III Haemodynamically stable

Contrast Enhanced CT + delayed phase

Suspected or confirmed renal trauma Normal IVP Emergency Laparatomy and IVP

Conservative Management

Grade IV Grade V

Haemodynamically unstable

Management

Ureteric Stent Insertion

Angioembolisation

Abnormal IVP Pulsatile expansile perirenal haematoma

Surgical Exploration

Fig. 66.5  Initial Management algorithm for renal trauma (adapted from the WSES-AAST Guidelines [32] and previous review by Veeratterapillay et al. [58])

66.16 Indications for Surgery Open surgical management is indicated in haemodynamically unstable patients unresponsive or transiently responsive to fluid resuscitation or in the case of failed conservative and minimally invasive management (Fig. 66.5). Further indication for renal exploration would be a pulsatile perirenal haematoma noted at a laparotomy performed for other injuries, as this would be suspicious for a pedicle avulsion injury [32]. Extravasation of urine occurs in 29% of patients with high-grade (III-V) renal injury and resolves without intervention in >90% of cases [59, 60]. Extravasation of urine or urinoma with co-existent pancreatic or colonic injury however should be considered for drainage or repair, as this is at high risk of sepsis [58]. Table 66.2 summarises recent studies of patients presenting with renal trauma; between 1 and 51% of patients underwent open surgery, with up to 35% of patients undergoing laparotomy for concomitant injuries with no concurrent renal exploration. Nephrectomy rates varied between 1 and 40% and mortality between 0 and 11%. The studies with the highest rates of open management, nephrectomy and mortality had higher proportions of penetrating trauma and higher grades of trauma.

66.17 Intraoperative Intravenous Pyelography (IVP) Whilst not a form of imaging now used routinely, patients who are haemodynamically unstable and transferred for emergency laparotomy without prior imaging should be considered for a one-shot intraoperative intravenous pyelogram (IVP). IVP is performed using an infusion of 2 mL/kg of radiographic contrast followed by a plain abdominal film for 10 min [61]. This can be helpful in determining the presence of an ipsilateral renal injury and confirm the presence of a contralateral kidney. This is important, as in the absence of a contralateral kidney, nephron-sparing surgery becomes imperative.

66.18 Surgical Technique Surgical management aims to control bleeding and, if possible, preserve the kidney. A transabdominal approach, a midline incision is most commonly undertaken, particularly in the unstable trauma patient, wherein co-existent ­intraabdominal injuries are common. Following midline incision, the transverse colon and small bowel are retracted superiorly to allow access to the retroperitoneum. Once exposed an incision is made into the peritoneum over the aorta above

66  Updates in the Management of Complex Renal Trauma

the inferior mesenteric artery and extended to expose the anterior aorta and left renal vein. Large perirenal haematoma’s can distort this anatomy and make this difficult to identify, in which case the inferior mesenteric vein should be located and an incision made medial to it; this can be extended up to the ligament of Trietz following which the left renal vein and anterior aorta can be identified as before [62]. The next step involves exposing the remaining renal vasculature. At this stage the renal artery and vein of the affected kidney should be looped to facilitate rapid occlusion should significant bleeding occur that cannot be controlled by manual pressure. Once vascular control is achieved the renal fascia can be incised and the kidney exposed. Whilst a pulsatile, expanding renal haematoma should always be explored, a stable and non-expanding haematoma which has not been imaged should only be explored if it is the sole cause of haemodynamic instability or in the case of a penetrating injury [32]. The decision of reconstruction vs nephron-sparing surgery vs nephrectomy is a fluid one and should be guided based on the grade of injury, ongoing haemorrhage, ability to achieve vascular control and presence/absence of a normal contralateral kidney. Reconstruction principally involves the adequate debridement of non-viable tissue and careful vascular control with single suture ligation of bleeding parenchymal vessels. If a collecting system injury is present than a watertight closure with a continuous suture is performed. Capsular tissue should be preserved if possible to facilitate closure, however in cases when an insufficient capsule is present then a pedicle omental

723

flap can be used. Capsular closure is performed by the approximation of laceration margins using interrupted sutures over a haemostatic bolster such as gel foam or surgical to reduce urinary extravasation. If it is not possible to reconstruct a renal pole injury then a formal partial nephrectomy may be required. Drains should be placed where possible and appropriate [62]. In the case of vascular injuries involving the renal pedicle, repair has a low success rate, with renal function preserved in only about 25% of cases. In the context of these poor results, it should therefore only be performed in patients with solitary kidneys or bilateral renal injuries, otherwise, a nephrectomy should be undertaken [63]. Likewise, a nephrectomy is indicated if a kidney is unable to be repaired due to extensive injury, or if the patient is haemodynamically unstable as a life-saving intervention.

66.19 Complications The risk of complication is determined by the cause, grade and management. Repeated cross-sectional imaging is recommended in all high-grade injuries or in any injury if patients exhibit signs of bleeding or infection.

66.20 Urinary Extravasation An analysis of collecting system injury and urinary extravasation revealed an incidence of over 50% in patients with Grade IV/V injuries, an example of this is shown in Fig. 66.6

Fig. 66.6  Sagittal CT images of a large urinoma following a road traffic collision

724

[59]. A high proportion of urinary extravasation will resolve spontaneously, however if it persists then complications can arise and as a result, ureteric stenting is often used to try and prevent further issues such as urinoma formation or perinephric infection. Approximately 30% of patients with urinary extravasation receive ureteric stents either in a delayed or immediate fashion [59]. Guidance suggests that urinary drainage should be performed in enlarging urinoma or those with signs of infection, increasing pain, fistula or associated ileus. This can be achieved by ureteric stenting or percutaneous drainage [27, 31, 32].

66.21 Delayed Bleeding Bleeding at 2–3 weeks can occur and is usually a result of arteriovenous malformation or pseudoaneurysms. Pseudoaneurysms are a contained injury to a vascular wall, typically occurring between the media and adventitia layers and can result from blunt or penetrating trauma [56, 64]. Both pseudoaneurysms and AV malformations are safely and effectively treated by angioembolisation techniques [56, 64].

66.22 Decreased Function Post-injury renal function reduction is common and has been shown to directly correlate with the AAST grade and is independent of mechanism, with a reduction of function of around 30 and 70% in grade 4 and 5 injuries respectively [65]. The renal function appears to be better preserved in a patient undergoing conservative management or angioembolisation [41].

66.23 Hypertension Post-trauma hypertension is a rare complication, more common in young men and attributed in most cases to excess renin secretion. Estimates of incidence vary from 0.5 to 5%, as it is difficult to attribute the cause of hypertension to the previous trauma, particularly in longer follows up periods [66, 67].

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726 58. Veeratterapillay R, Fuge O, Haslam P, Harding C, Thorpe A. Renal trauma. J Clin Urol. 2017;10(4):379–90. 59. Keihani S, Anderson RE, Fiander M, McFarland MM, Stoddard GJ, Hotaling JM, Myers JB. Incidence of urinary extravasation and rate of ureteral stenting after high-grade renal trauma in adults: a meta-­ analysis. Transl Androl Urol. 2018;7(Suppl 2):S169–78. 60. Alsikafi NF, McAninch JW, Elliott SP, Garcia M.  Nonoperative management outcomes of isolated urinary extravasation following renal lacerations due to external trauma. J Urol. 2006;176(6 Pt 1):2494–7. 61. Morey AF, McAninch JW, Tiller BK, Duckett CP, Carroll PR. Single shot intraoperative excretory urography for the immediate evaluation of renal trauma. J Urol. 1999;161(4):1088–92. 62. Metro MJ, McAninch JW.  Surgical exploration of the injured kidney: current indications and techniques. Int Braz J Urol. 2003;29(2):98–105.

P. Gravestock et al. 63. Bittenbinder EN, Reed AB.  Advances in renal intervention for trauma. Semin Vasc Surg. 2013;26(4):165–9. 64. Garg P, Paruthi C, Bhardwaj K, Krishnan V, Bajaj SK, Misra RN. Interventional radiology in the management of renal vascular injury: a prospective study. Indian J Urol. 2020;36(4):303–8. 65. Tasian GE, Aaronson DS, McAninch JW.  Evaluation of renal function after major renal injury: correlation with the American Association for the Surgery of Trauma Injury Scale. J Urol. 2010;183(1):196–200. 66. Monstrey SJ, Beerthuizen GI, van der Werken C, Debruyne FM, Goris RJ.  Renal trauma and hypertension. J Trauma. 1989;29(1):65–70. 67. Chedid A, Le Coz S, Rossignol P, Bobrie G, Herpin D, Plouin PF. Blunt renal trauma-induced hypertension: prevalence, presentation, and outcome. Am J Hypertens. 2006;19(5):500–4.

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67

Aris Koryllos, Klaus-Marius Bastian, and Corinna Ludwig

Key Points • Thoracic trauma is the third most common cause of death in trauma patients. • Incidence rates of pulmonary contusion can vary between 17 and 75%, thus clinical investigation for pulmonary contusions after severe blunt chest trauma could be of great importance. • Main symptom of pulmonary lacerations is air leakage and pneumothorax. • Airway-related injuries include traumas of the trachea or the central bronchi. They are extremely rare (incidence 0.8–5%). Pre-hospital mortality rate can reach up to 81%. • Rib fractures are one of the most frequent chest wall injuries, occurring in 10–40% after blunt chest trauma and approximately 10% of all trauma cases. • Rib fracture osteosynthesis should be considered in all patients with flail chest and in patients with multiple fractures or in severe (bicortical) displaced fractures.

67.1 Introduction Thoracic trauma is the third most common cause of death in trauma patients [1]. Thoracic trauma can lead to life-­ threatening injuries such as tension pneumothorax, massive parenchymal bleeding, or fail-chest with respiratory insufficiency. In most cases, conservative treatment with chest tube insertion is sufficient to stabilize the patient. Chest trauma in addition to brain injury is associated with a decreased chance of good neurologic recovery [2]. Identification of those patients with more complex lesions is mandatory. In 2019, 36699 patients were documented in the German TraumaRegister DGU® (TR-DGU—Annual Report 2020). Of these 29,345, with a maximal AIS (Abbreviated Injury Scale) 2 or ≥3 scores (MAIS), were selected to analyze the A. Koryllos · K.-M. Bastian · C. Ludwig (*) Department of Thoracic Surgery, Florence Nightingale Hospital, Düsseldorf, Germany

severity of trauma and outcome in Germany. The ISS (Injury Severity Score) [3] was ≥16 in 53% of the patients. Severe thoracic trauma with an AIS >3 prevailed in 37%, underlining the frequency of severe chest trauma. The average age was 53 years, with a 70% male predominance. Pre-clinical chest-tube insertion was found in 3.9% and in-hospital in 10%. Surgery of any kind was necessary for 66.4%, whereas 86% required ICU care. In-hospital mortality was 11.9%. The data retrieved from TR-DGU underline that complex chest trauma is not rare in Germany. Thoracic surgeons are only part of the core trauma team in German national trauma teams, unlike regional and local trauma teams where a thoracic surgeon may not even be available. We believe that the profound knowledge of thoracic surgeons is very important in trauma patient care and therefore plead for early involvement and interdisciplinary treatment of these high-risk surgical patients. Would we treat traumatic brain injury without consulting a specialist? In this chapter, we will concentrate on identifying and treating parenchymal, airway and chest wall injuries in trauma patients.

67.2 Pulmonary Parenchyma and Airway-­ Related Injuries 67.2.1 Pulmonary Injuries 67.2.1.1 Pulmonary Contusions Pulmonary contusions without lung lacerations occur usually after blunt chest trauma and are defined as the destruction of lung parenchyma with signs of alveolar hemorrhage [4, 5]. The pathophysiology of the injury can be described as an acute transmission of kinetic energy to the lung parenchyma. Cadaver studies have found that the speed of the impulse and the resulting compression are the most important factors for visceral organ damage [6]. Incidence rates can vary between 17 and 75%, thus clinical investigation for pulmonary contusions after severe blunt chest trauma could

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 P. Aseni et al. (eds.), The High-risk Surgical Patient, https://doi.org/10.1007/978-3-031-17273-1_67

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be of great importance [7]. Parenchymal injuries can occur in the first 24 h after the initial trauma and can resolve radiologically and clinically after 3–14 days [3]. Clinical manifestation can consist of respiratory distress with or without hypercapnia or hypoxemia. This can be the result of reduced pulmonary perfusion, impaired respiratory movement of the chest wall and diaphragm (due to chest trauma) or increased intrapulmonary shunting [8]. Clinical examination shows symptoms of chest pain and dyspnea. Normally, a chest X-ray in combination with an arterial blood gas probe is used for emergency diagnosis [9]. A CT scan of the chest can help evaluate the size of the contusion and the number of affected lobes. Some authors suggest that this correlates with the clinical outcome [7]. Additionally, a CT scan can help differentiate between lung contusion and pulmonary hematoma. Radiological findings include consolidation areas combined with ground glass opacities. Treatment of pulmonary contusions is mainly supportive and includes oxygen therapy, fluid management and sufficient analgesia. Although many centers additionally administer antibiotics, there are no sufficient data in the literature to justify such treatment, especially when no lung lacerations, pleural effusions or further risk factors for secondary empyema are present. Incidence of acute respiratory distress syndrome [10] in patients with pulmonary contusions can rise up to 50–60%, but in most cases, severe lacerations of the parenchyma and multiple rib fractures are also present [8]. In a big cohort study with n: 5042 chest trauma patients, Danilovic et  al. described only an 8% ratio of mechanical ventilation for isolated pulmonary contusions without additional chest injuries [5]. In case of respiratory insufficiency, non-invasive respiratory support should be favored over invasive ventilation if possible [11]. There is no evidence for pharmacological treatment of pulmonary contusions. The use of steroids still remains controversial [3].

67.2.1.2 Pulmonary Lacerations In contrast to contusions, pulmonary lacerations are defined by damage to the parenchymal tissue of the lung, usually caused by penetrating or non-penetrating injuries and rib fractures [7] (Fig. 67.1). Their incidence varies between 4.4 and 12% [12]. They can be divided into four different types [13]: Type 1: lacerations caused by compression-induced lung rupture (most common type). Type 2: lacerations caused by compression and occurring in the lower lobes and paraspinal region. Type 3: lacerations are usually seen as a result of pleural puncture of rib fractures and are associated with pneumothorax. Type 4: lacerations caused by rupture of pleural adhesions with no characteristic radiological findings.

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Fig. 67.1  Left basal laceration after rib fracture with rib fragment dislocation

The main symptom of pulmonary lacerations is air leakage and consequently pneumothorax [14]. Hemothorax can also develop if the pleural cavity is opened. Deep pulmonary lacerations are present in 50% of patients with intrathoracic hemorrhage in blunt chest trauma [15]. Pneumatocele has also been described as a possible consequence of lung lacerations. In cases of deep parenchymal lesions with active bleeding in traumatized pulmonary cavities blood and air, leakage can lead to hemato-pneumocele. This can lead to secondary infection after the bleeding has stopped [16]. Therapy of pulmonary lacerations varies according to severity. In most cases a chest tube is sufficient. Surgical intervention should be always considered if persistent bleeding and hemodynamic instability are present. Pulmonary resection (i.e., lobectomy) may even be indicated in cases of severe lacerations. Mortality is reportedly higher in cases of bilateral and/or major lacerations [12]. The healing process of pulmonary lacerations is longer than that of contusions and can last several months [12]. Some authors also suggest a surgical intervention in cases of severe air leakage without the presence of hemodynamic instability or active bleeding. There is no evidence in the literature for favouring surgery over supportive care for such cases. Our personal experience showed that patients with severe pulmonary lacerations usually have multiple traumatic lesions in different organs as a result of highimpact accidents and conservative management is usually initially adequate for these critical patients.

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Fig. 67.2  Fracture of the cricoid cartilage after blunt chest and neck trauma, subcutaneous emphysema

67.2.2 Airway-Related Injuries Airway-related injuries include traumas of the trachea or the central bronchi. They are extremely rare (incidence 0.8–5%) but when present are often accompanied by high mortality rates [17]. Non-iatrogenic tracheobronchial injuries usually occur after road accidents, crush injuries, stab injuries, gunshots, hyperextension of the neck, hanging or strangulation (Fig. 67.2). Pre-hospital mortality rate can reach up to 81% [18]. In cases of non-penetrating-injuries, the trauma mechanism consists of sudden force from anterior to posterior above the carinal level or rapid deceleration with the tear of the cricoid or severe compression of the thorax while the glottis is closed [19]. In non-iatrogenic tracheobronchial injuries, concomitant traumatic lesions very frequently involve osseous structures of the thorax (ribs, sternum, spine), lungs; diaphragm, spleen, liver; great vessels, heart; brain. However, airway injuries could also be the result of medical interventions in critical trauma patients, since 92% of all tracheobronchial injuries occur after oral intubation or emergency tracheotomy [20]. Diagnosis of airway-related injuries after blunt chest trauma is not trivial. In cases of penetrating injuries, the suspicion of tracheal or bronchial tear correlates to the location of the penetration but diagnosis can be difficult and delayed in cases of blunt force trauma [21]. Because of the severe

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concomitant injuries, tracheobronchial trauma can be challenging to differentiate. Symptoms include subcutaneous or mediastinal emphysema, dyspnea, hemoptysis, stridor, persistent atelectasis or pneumothorax, massive air leakage or alterations in phonation [22]. Imaging modalities such as chest X-ray or ultrasound can be insufficient due to mediastinal and subcutaneous emphysema, thus making CT-scan and mainly bronchoscopy inevitable for accurate diagnosis, localization of the tear and evaluation of its extent. Most non-iatrogenic tracheobronchial injuries after blunt chest trauma are located within 1cm from the main carina [21]. Cardillo et al. proposed an endoscopic classification of the tracheal tears based on the lacerated layers of the trachea, but validation data are still rare and the clinical importance has yet to be justified [23]. Management and approach of airway-related injuries should correlate with the current adult advanced life support guidelines, meaning: As long as a stable airway can be established and ventilation is adequate, the treatment of tracheobronchial injury can be postponed until other life-threatening injuries are repaired and the patient is stabilized [10]. But immediate intervention should be considered if the bronchial or tracheal tear does not allow sufficient ventilation or oxygenation [24]. A general recommendation for ideal management of airway-related injuries is difficult to generate, hence every case is individual and unique considering the patient’s general status, concomitant injuries and anatomy. Nevertheless, it is important to mention that a substantial number of tracheobronchial injuries can be treated conservatively when the respiratory status allows [23]. In recent years, there has been an increase in publications supporting conservative treatment, but only patients with stable respiratory status were treated [25]. Endoscopic suturing by means of rigid bronchoscopy has also been reported, but it is technically feasible only if patients can tolerate jet ventilation, which makes it an attractive option for fairly respiratory-­ stable patients [26]. The main goal of emergency treatment is to maintain airway continuity and repair or temporarily “bridge” the damaged area. Adversely to the respiratory stress of the patient’s positive pressure ventilation can lead to exacerbation of the critical situation [27]. If the tear is unusually located in the upper level of the trachea, an emergency tracheotomy caudal to the lesion could facilitate safe respiratory conditions after the placement of the tracheal cannula underneath the tear. Unfortunately, most of the tears are within a radius of 1cm from the main carina making the above treatment rather futile. Guided by bronchoscopy, placement of endotracheal tubes in the left or right main bronchus could allow temporary stability for further surgical management, but in cases of main bronchi involvement, it could result lead to negative results and enhancement of the tear. In severely-injured polytrauma patients with no respiratory stability even after con-

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trolled placement of an endotracheal tube, case reports of extracorporeal oxygenation have been documented in recent years as a bridge to recovery or to allow surgical management [28, 29]. If surgical management is indicated, most surgeons prefer an antero- or posterolateral right thoracotomy or a median sternotomy for access. Surgical treatment includes primary sutures or resection with anastomosis or bronchoplasty [30]. Esophageal injury associated with tracheobronchial injuries should also be excluded because, if missed, complications such as mediastinitis and tracheoesophageal fistula may develop [4]. In conclusion, airway-related injuries in complex chest trauma patients are associated with high mortality rates and the prognosis is poor mostly because of the concomitant injuries. The main problem of their management is respiratory instability in combination with multiple organ damage/ failure. Goal for the treating multidisciplinary team is to maintain airway continuity/stability and repair or temporarily “bridge” the damaged area.

67.3

Fig. 67.3 Localization of rib fractures by the method of Ritchie et al. A anterior, AL antero-lateral, L lateral, P postero-lateral, P posterior

Chest Wall Injuries

Rib fractures are one of the most frequent chest wall injuries, occurring in 10–40% after blunt chest trauma and approximately 10% of all trauma cases [31]. In younger patients, rib fractures are caused by highenergy trauma, such as car accidents, whereas they result from low-energy trauma i.e. tripping in the elderly [32]. Rib fractures are associated with a significantly higher morbidity and mortality, with regards to older age, a total number of ribs fractured and the presence of a flail chest. A flail chest is defined as a fracture of three or more consecutive ribs in two or more places [33, 34]. The treatment of rib fractures is focused on pain reduction, quick mobilization and prevention of pneumonia. Longterm complications such as restrictive pulmonary disease, pseudoarthrosis and chronic chest pain syndrome are to be avoided by surgical therapy [31–33].

67.3.1 Classification At this time, there is no accepted classification for rib fractures. The Müller AO (Arbeitsgemeinschaft für Osteosynthesefragen) classification system is a method of categorizing injuries according to their localization and severity, but rib fractures are not included in the Müller AO classification system. Bemelman et al. have developed a new classification system based on the Müller AO-classification [35]. An interesting method to illustrate the localization of rib fractures has been described by Ritchie et  al. Using this method, the location of the fracture can be estimated based only on the impact at trauma (Figs. 67.3, 67.4, 67.5, and 67.6) [32]

Fig. 67.4 If the power comes only from the sternum (i.e. CPR) most of the fractures are in A-AL (yellow)

67.3.2 Diagnostics In the ATLS primary survey and in the emergency room, it is important to exclude life-threatening injuries such as pneumothorax, hemothorax and lacerations of the lung. For this, ultrasound is a good clinical tool (eFAST) but it is of no help in detecting rib fractures. The conventional chest X-ray may show some rib fractures. The CT scan is the “gold standard”

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Updates in the Management of Complex Chest Trauma

731 Table 67.1 Indications and contraindications based on Pieracci et al. [31] Indication All patients with flail chest Patients with multiple, severe (bicortical) displaced fractures Patients who fail early, optimal non-operative management Patients with chronic pain and/ or instability due to pseudoarthrosis

Contraindication Repair of ribs 1, 2, 11, and 12 do not confer additional benefit Fractures within 2.5 cm of the transverse process Bone loss and fracture gaps >10 mm should not be bridged using only a plate Life-limiting injuries or illnesses

67.3.3 Indication and Contraindication for Osteosynthesis of the Ribs

Fig. 67.5 If the power comes from the whole ventral body (i.e. car accident with the punch of the steering wheel) the rib fractures are often located in L [7]

Rib fracture osteosynthesis should be considered in all patients with flail chest and in patients with multiple fractures or in severe (bicortical) displaced fractures. In multiplefracture series [11], both fracture lines should be stabilized wherever possible [31]. Stabilization of a fracture of the ribs 1, 2, 11, and 12 has no additional benefit in terms of either chest wall stability or pain control. If the fracture is within 2.5 cm of the transverse process, the osteosynthesis will be very critical because the distance to the transverse process of the spine is too short to drill for a minimum of three screws to fix the plate. Proximity within 2.5 cm of the costal cartilage is also a problem and the fracture should be repaired by fixation of the cartilage to the sternum [32, 37] (Table 67.1). Conservative management is an alternative whenever surgery is not possible. Analgetics such as PDA and intensive respiratory physiotherapy may also lead to good results, especially if the morbidity and preoperative mortality do not allow an operation [18]. In cases in which optimal conservative management has failed, osteosynthesis can be performed later to treat chronic pain and instability due to pseudoarthrosis [18].

67.3.4 Surgical Approaches Fig. 67.6 If the power comes from the side (i.e. tripping, falls) the fractures are often located in PL to P (blue)

to detect every injury to the chest [30]. A 3D reconstruction of the CT scan can be helpful to plan the operation and visualize the fracture lines [31, 36].

There are several ways to stabilize the rib fracture (osteosynthesis plates, internal fixation system / intramedullary splint and rib brackets). We prefer a hybrid technique including video-assisted thoracoscopic (VATS) [30] inspection of the thorax, localization of the rib fracture and impaction of the chest wall. With VATS one can precisely determine the incision placement and define

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Fig. 67.7  Chest X-ray after chest tube insertion, with complete atelectasis of the left lung

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Fig. 67.8  CT trauma scan; flail chest and complete atelectasis of left the upper lobe

the perfect access for osteosynthesis. This method will help to minimize morbidity and damage to chest wall muscles from muscle division and obtain a good cosmetic result. Once the muscle has been carefully split, we use a small soft tissue retractor. With this soft retractor, it is possible to reach at least three ribs cranial and caudal to the fracture [38]. For stabilization, we prefer a plate system with self-drilling, stable angle, and bicortical screws. Once the fracture has been repositioned, additional video thoracoscopy [30] may help to evaluate the position of the screws, and the shape of the chest wall and exclude any further injury within the pleural space. Not every rib fracture must be stabilized to reshape the chest wall. As seen in Fig. 67.13, two plates were sufficient to bring the chest wall to an acceptable anatomical position. Chest tube placement is helpful to detect postoperative bleeding after osteosynthesis [36, 38]. Case 1 82-year-old woman with a flail chest and hemo-­pneumothorax after falling from eight meters high. After emergency treatment of the hemothorax with a chest tube, she was stabilized in ICU.  Despite intensive physiotherapy and pain control during her intensive care stay, she developed complete atelectasis of the left lung (Figs.  67.7 and 67.8 X-ray and CT Thorax before bronchoscopy). This led to the indication of rib osteosynthesis.

Fig. 67.9  Chest X-ray after bronchoscopy

Preoperative bronchoscopic inspection revealed MRSA pneumonia with signs of infection in her blood values. Under these circumstances, the operation was postponed. Conservative therapy was intensified (Fig.  67.9: After routine bronchoscopy). Outpatient visit 4  weeks later (Fig. 67.10: X-ray after conservative treatment).

67  Updates in the Management of Complex Chest Trauma

Fig. 67.10  Final chest X-ray after conservative treatment

Case 2 A 61-year-old woman fell on her left side against the bathtub. Initial treatment was conservative with respiratory physiotherapy, oral analgetics, and epidural analgesia. Four days later, she suddenly had more pain and required oxygen. Figures 67.11 and 67.12 shows that the fractured ribs number 4–7 were now dislocated and there was a new pleural

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Fig. 67.12  X-Ray 4 days later with left side pleural effusion and secondary dislocation of the rib fractures on the left side

effusion. With surgical treatment of rib fracture by osteosynthesis as described above, the patient was able to leave the hospital without pain and required only mild oral analgesia (Fig. 67.13).

Fig. 67.11  Trauma CT-scan with rib fracture 5 and 7, initially without dislocation

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11. Marasco S, Lee G, Summerhayes R, et al. Quality of life after major trauma with multiple rib fractures. Injury. 2015;46:61–5. https:// doi.org/10.1016/j.injury.2014.06.014. 12. Huber S, Biberthaler P, Delhey P, et  al. Predictors of poor outcomes after significant chest trauma in multiply injured patients: a retrospective analysis from the German Trauma Registry (Trauma Register DGU(R)). Scand J Trauma Resusc Emerg Med. 2014;22:52. https://doi.org/10.1186/s13049-­014-­0052-­4. 13. Hollister M, Stern EJ, Steinberg KP.  Type 2 pulmonary laceration: a marker of blunt high-energy injury to the lung. AJR Am J Roentgenol. 1995;165:1126. https://doi.org/10.2214/ ajr.165.5.7572488. 14. ATLS Subcommittee; American College of Surgeons’ Committee on Trauma; International ATLS Working Group. Advanced trauma life support (ATLS(R)): the ninth edition. J Trauma Acute Care Surg. 2013;74:1363–6. https://doi.org/10.1097/TA.0b013e31828b82f5. 15. Nishiumi N, Inokuchi S, Oiwa K, et  al. Diagnosis and treatment of deep pulmonary laceration with intrathoracic hemorrhage from blunt trauma. Ann Thorac Surg. 2010;89:232–8. https://doi. org/10.1016/j.athoracsur.2009.09.041. 16. Karmy-Jones R, Jurkovich GJ. Blunt chest trauma. Curr Probl Surg. 2004;41:211–380. https://doi.org/10.1016/j.cpsurg.2003.12.004. 17. Schneider T, Volz K, Dienemann H, et  al. Incidence and treatment modalities of tracheobronchial injuries in Germany. Interact Fig. 67.13  X-ray after osteosynthesis of the ribs 5 and 7 Cardiovasc Thorac Surg. 2009;8:571–6. https://doi.org/10.1510/ icvts.2008.196790. 18. Cheaito A, Tillou A, Lewis C, et  al. Traumatic bronchial injury. Int J Surg Case Rep. 2016;27:172–5. https://doi.org/10.1016/j. References ijscr.2016.08.014. 19. Shemmeri E, Vallieres E.  Blunt tracheobronchial trauma. 1. Krug EG, Sharma GK, Lozano R.  The global burden of injuries. Thorac Surg Clin. 2018;28:429–34. https://doi.org/10.1016/j. Am J Public Health. 2000;90:523–6. https://doi.org/10.2105/ thorsurg.2018.04.008. ajph.90.4.523. 20. Evagelopoulos N, Tossios P, Wanke W, et  al. Tracheobronchial 2. Schieren M, Wappler F, Wafaisade A, et al. Impact of blunt chest rupture after emergency intubation. Thorac Cardiovasc Surg. trauma on outcome after traumatic brain injury—a matched-­ 1999;47:395–7. https://doi.org/10.1055/s-­2007-­1013183. pair analysis of the TraumaRegister DGU(R). Scand J Trauma 21. Kiser AC, O’Brien SM, Detterbeck FC.  Blunt tracheobronchial Resusc Emerg Med. 2020;28:21. https://doi.org/10.1186/ injuries: treatment and outcomes. Ann Thorac Surg. 2001;71:2059– s13049-­020-­0708-­1. 65. https://doi.org/10.1016/s0003-­4975(00)02453-­x. 3. Cohn SM, Dubose JJ.  Pulmonary contusion: an update on recent 22. Mohammadzadeh AR, Kayalha H. Delayed diagnosis of bronchial advances in clinical management. World J Surg. 2010;34:1959–70. transection following blunt chest trauma. Asian Cardiovasc Thorac https://doi.org/10.1007/s00268-­010-­0599-­9. Ann. 2017;25:540–3. https://doi.org/10.1177/0218492317728665. 4. Farzanegan R, Alijanipour P, Akbarshahi H, et  al. Major airways 23. Cardillo G, Carbone L, Carleo F, et  al. Tracheal lacerations after trauma, management and long term results. Ann Thorac Cardiovasc endotracheal intubation: a proposed morphological classificaSurg. 2011;17:544–51. https://doi.org/10.5761/atcs.oa.11.01679. tion to guide non-surgical treatment. Eur J Cardiothorac Surg. 5. Pozgain Z, Kristek D, Lovric I, et al. Pulmonary contusions after 2010;37:581–7. https://doi.org/10.1016/j.ejcts.2009.07.034. blunt chest trauma: clinical significance and evaluation of patient 24. van Roozendaal LM, van Gool MH, Sprooten RTM, et al. Surgical management. Eur J Trauma Emerg Surg. 2018;44:773–7. https:// treatment of bronchial rupture in blunt chest trauma: a review of litdoi.org/10.1007/s00068-­017-­0876-­5. erature. J Thorac Dis. 2018;10:5576–83. https://doi.org/10.21037/ 6. Viano DC, Lau IV.  A viscous tolerance criterion for soft tisjtd.2018.08.22. sue injury assessment. J Biomech. 1988;21:387–99. https://doi. 25. Tazi-Mezalek R, Musani AI, Laroumagne S, et  al. Airway stentorg/10.1016/0021-­9290(88)90145-­5. ing in the management of iatrogenic tracheal injuries: 10-year 7. Elmali M, Baydin A, Nural MS, et al. Lung parenchymal injury and experience. Respirology. 2016;21:1452–8. https://doi.org/10.1111/ its frequency in blunt thoracic trauma: the diagnostic value of chest resp.12853. radiography and thoracic CT. Diagn Interv Radiol. 2007;13:179–82. 26. Welter S, Krbek T, Halder R, et  al. A new technique for com8. Ganie FA, Lone H, Lone GN, et  al. Lung contusion: a clinico-­ plete intraluminal repair of iatrogenic posterior tracheal lacerapathological entity with unpredictable clinical course. Bull Emerg tions. Interact Cardiovasc Thorac Surg. 2011;12:6–9. https://doi. Trauma. 2013;1:7–16. org/10.1510/icvts.2010.248641. 9. Klein Y, Cohn SM, Proctor KG. Lung contusion: pathophysiology 27. Self ML, Mangram A, Berne JD, et al. Nonoperative management of and management. Curr Opin Anaesthesiol. 2002;15:65–8. https:// severe tracheobronchial injuries with positive end-expiratory presdoi.org/10.1097/00001503-­200202000-­00010. sure and low tidal volume ventilation. J Trauma. 2005;59:1072–5. 10. Soar J, Nolan JP, Bottiger BW, et  al. European Resuscitation https://doi.org/10.1097/01.ta.0000188643.67949.82. Council Guidelines for Resuscitation 2015: section 3. Adult 28. Chung J, Berguson M, Mendelson A, et al. Cross-field ventilation advanced life support. Resuscitation. 2015;95:100–47. https://doi. for treatment of harlequin syndrome in traumatic tracheobronchial org/10.1016/j.resuscitation.2015.07.016. injury repair using intraoperative venoarterial extracorporeal mem-

67  Updates in the Management of Complex Chest Trauma brane oxygenation. J Cardiothorac Vasc Anesth. 2019;33:3090–4. https://doi.org/10.1053/j.jvca.2019.03.033. 29. Moon SH, Kim KN, Jung JJ, et  al. Heparin-free veno-venous ECMO applied to a patient with severe lung contusion and hypovolemic shock due to trauma. Ulus Travma Acil Cerrahi Derg. 2018;24:497–500. https://doi.org/10.5505/tjtes.2018.33802. 30. Ludwig C, Koryllos A. Management of chest trauma. J Thorac Dis. 2017;9:S172–7. https://doi.org/10.21037/jtd.2017.03.52. 31. Pieracci FM, Majercik S, Ali-Osman F, et  al. Consensus statement: surgical stabilization of rib fractures rib fracture colloquium clinical practice guidelines. Injury. 2017;48:307–21. https://doi. org/10.1016/j.injury.2016.11.026. 32. Liebsch C, Seiffert T, Vlcek M, et  al. Patterns of serial rib fractures after blunt chest trauma: an analysis of 380 cases. PLoS One. 2019;14:e0224105. https://doi.org/10.1371/journal.pone.0224105. 33. Cannon RM, Smith JW, Franklin GA, et al. Flail chest injury: are we making any progress? Am Surg. 2012;78:398–402. 34. Dehghan N, de Mestral C, McKee MD, et al. Flail chest injuries: a review of outcomes and treatment practices from the National

735 Trauma Data Bank. J Trauma Acute Care Surg. 2014;76:462–8. https://doi.org/10.1097/TA.0000000000000086. 35. Bemelman M, Baal MV, Raaijmakers C, et  al. An interobserver agreement study with a new classification for rib fractures. Chirurgia (Bucur). 2019;114:352–8. https://doi.org/10.21614/ chirurgia.114.3.352. 36. Cooper A, Edwards M, Brandling J, et al. Taxonomy of the form and function of primary care services in or alongside emergency departments: concepts paper. Emerg Med J. 2019;36:625–30. https://doi.org/10.1136/emermed-­2018-­208305. 37. Hennon M, Yendamuri S.  Video assisted thoracoscopic surgery vs. thoracotomy for lobectomy: why are we still talking about this? J Thorac Dis. 2019;11:S1284–5. https://doi.org/10.21037/ jtd.2019.04.106. 38. Schulz-Drost S, Grupp S, Pachowsky M, et al. Stabilization of flail chest injuries: minimized approach techniques to treat the core of instability. Eur J Trauma Emerg Surg. 2017;43:169–78. https://doi. org/10.1007/s00068-­016-­0664-­7.

Updates in the Management of Complex Cardiac Injuries

68

Riyad Karmy-Jones, Megan R. Lundeberg, and William B. Long III

Key Points 1. Managing cardiac trauma requires a high degree of suspicion and a low threshold for operation. 2. When performing antero-lateral thoracotomy it is important to follow the inframammary crease upwards (cephalad) to cross near the mid sternum, which permits a proper ‘clamshell” incision. 3. Sternotomy is an excellent approach for penetrating trauma between the anterior mid-clavicular lines (“cardiac box”). 4. Cardiopulmonary bypass is rarely needed in the emergent setting. Its role is to either assist in resuscitation and/or repair complex injuries but can only be employed once the source of hemorrhage is controlled. 5. Echocardiography cannot absolutely rule out cardiac injury in the setting of hemothorax. 6. The most common procedure is the repair of a myocardial laceration with a pledgeted mattress suture; pericardium can serve as a pledget. 7. The incidence of postoperative complications including missed or delayed injuries and pericarditis is high enough that follow-up should be performed on all patients. Echocardiography is an excellent tool for this. 8. The operative management of cardiac trauma will vary from region to region, and the team should use the approach they are most comfortable with given their resources.

R. Karmy-Jones (*) Divisions of Thoracic and Vascular Surgery, PeaceHealth Southwest Washington Medical Center, Vancouver, WA, USA Trauma/Critical Care, Legacy Emanuel Medical Center, Portland, OR, USA e-mail: [email protected] M. R. Lundeberg · W. B. Long III Trauma/Critical Care, Legacy Emanuel Medical Center, Portland, OR, USA

68.1 Introduction Cardiac trauma represents one of the highest intensity situations, leading to stress and anxiety. The adage “the enemy in the operating room is tension” seems designed for this scenario. It would not be unreasonable to describe all cardiac injuries as complex, based on the high mortality rate if not acted upon immediately. And yet, the actual procedure most commonly performed is simple mattress suture(s). The stress is created by the need to diagnose and intervene immediately in most cases, often while conducting resuscitative measures, sometimes while unsure of the diagnosis, and occasionally have low confidence in one’s own experience and skill. We recognize that a significant number of patients will have extra-cardiac injury that requires diagnosis and management concurrently, however, this chapter seeks to put into perspective the management of operable injuries to the heart, the majority of which will be performed within minutes of patient arrival. In this chapter, we are focusing on injuries that require operative intervention. Apart from “simple” cardiac penetrating injuries, the majority of reported experiences with complex cardiac injuries include case reports and small series which reflect years or decades of experience. These reports provide valuable insight but given the scope of this chapter, we are not able to give credit to all our colleagues who have advanced the care of these patients. This chapter, therefore, reflects our individual biases, focused primarily on the experiences of our civilian North American trauma center experiences.

68.2 A Brief History Descriptions of cardiac injuries, particularly from penetrating trauma, have been described as early as the Iliad [1]. The reports stress the role of exsanguination, pericardial tamponade, post-cardiac injury pericarditis and the rare case of spontaneous healing [2]. Through most of the nineteenth

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century, surgeons had a fatalistic approach to managing these “uniformly fatal” injuries, with Billroth commenting in 1881 that “any surgeon who would attempt to suture a wound of the heart should lose the respect of his colleagues” [2]. However, there was interest in attempting repairs. Block, in 1882, using a rabbit model, demonstrated that it was possible to repair ventricular lacerations [3]. In 1895 Cappelen repaired a left ventricular stab wound via left thoracotomy. The patient survived three days before succumbing to sepsis (although the description also suggests post-pericardiotomy pericarditis) [4]. In 1896, Rehn successfully repaired a right ventricular laceration, just as a new age of anesthetic techniques became available [5]. In the United States, Hill collated 17 cases from the world literature, described a 41% survival rate, and in 1902 was the first to report on successful suture repair of a left ventricular wound [6, 7]. Spangaro in 1906 described left antero-lateral thoracotomy and Duval in 1907 described what would become known as a median sternotomy [8, 9]. In 1926 Beck reviewed the literature to date and described the physiology of tamponade, both acute and chronic, giving rise to the clinical triad that bears his name [10]. Experience with cardiac injury increased during the Second world war [2]. Beck, in 1942, stressed the role of mattress sutures placed deep into coronary arteries when lacerations were in close proximity [11]. Blalock and Ravitch described the use of pericardiocentesis both as a temporizing measure and possibly as a definitive treatment [12]. Harken, in 1946, described the management of retained foreign bodies in a paper that still has relevance today [13]. Beall and colleagues wrote a series of papers beginning in 1961 recommending emergency department thoracotomy, describing cardiopulmonary bypass (CPB) to permit repair of complex intracardiac injuries, and advocating immediate repair of cardiac injuries without delaying for pericardiocentesis [14–16]. The history of blunt cardiac trauma is sparser. Borsch described blunt injury with valvular disruption in 1676, which was followed by the report of Berard in 1826 [17, 18]. It took a span of nearly 150 years before Desforges and colleagues reported repair of atrial-superior vena cava rupture [19]. With the increase in motor vehicle traffic especially, the incidence of clinically diagnosed blunt cardiac injury has increased. We are now in an era where the principles described by our forebearers still apply. Early recognition and repair of cardiac injuries are critical for survival; the techniques (particularly of suturing ventricular lacerations) are still relevant; concomitant product-based resuscitation is vital; cardiopulmonary bypass can is select cases be all that makes recovery possible. The most important message passed on by our forebears is to have a high degree of suspicion and a very low degree of hesitancy.

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68.3 Incidence The incidence of penetrating cardiac injury varies widely, depending on the clinical environment, nature of the review, and presentation. Rhee et al described an overall incidence of 1 per 201 admissions after penetrating injury [20]. Siemens et al noted that 65% of patients with a penetrating parasternal injury sustained cardiac injury [21]. Among patients undergoing thoracotomy for hemorrhage, cardiac injuries were described in 16–52% following stab wounds and 10–37% following gunshot wounds [22–24]. Penetrating cardiac injuries can result from blunt trauma if fragmented ribs, or rarely sternum, lacerate the myocardium [25]. How many patients suffer a penetrating cardiac injury and survive to reach a hospital is also murky, but a reasonable guess is that it is in the 10% range. Because the ventricles are anterior, the incidence of chamber injury has been estimated and generally accepted to be right ventricle 40–45%, left ventricle 35–40%, and either right atrium 5–24% and left atrium < 5% [25, 26]. Because of its posterior position, penetrating injury to the left atrium implies either through and through injury to the heart via postero-lateral injury with associated spine, aortic and other mediastinal injury that limits the chance of survival. Coronary artery injury is estimated to occur in less than 5% of those who survive to reach the hospital, the most common being the left anterior descending coronary artery [25]. The incidence of complex cardiac injury, defined as coronary, septal and/or valvular injury, in patients arriving at the hospital and undergoing management is less than 10% [26]. The presence of associated injuries similarly varies, based on mechanism and multiplicity of injuries. The nature of the wounding device and the path it takes also affect how much of the heart is affected. A small knife can create a pinpoint injury, while a larger knife can cause through and through injuries, wide lacerations anteriorly etc. The situation is the same with gunshot wounds, depending on caliber and velocity, and of course in the military setting, high-velocity weapons or blast injuries with shrapnel can macerate the heart. Survival is greater following stab wounds and with single chamber injuries. In one study mortality following stab wounds to the heart was 39%, and following gunshot wounds 69% [22]. The incidence of blunt cardiac injuries is even harder to define, not in a small part due to the spectrum of injuries it presents. Typically, blunt cardiac injury rarely occurs in isolation and represents of the spectrum of injuries, ranging from “contusion” to frank rupture. The outcome is often linked to associated injuries, such as intracranial hemorrhage. Blunt cardiac rupture has been described as having a 90% immediate mortality and responsible for as many as 30% of

68  Updates in the Management of Complex Cardiac Injuries

deaths [27]. Of those victims who arrive with a detectable vital sign, survival has been recorded in 20–50%, although there appears to be a survival advantage if the patient is taken directly to the operating room [28]. The various mechanisms described include laceration from bony fractures, acute right atrial distension from compression of the abdomen, deceleration stress at the atrial-caval junctions, direct compression and/or delayed necrosis due to “contusion” or coronary artery injury [27]. The right side of the heart is affected more commonly than the left and has a higher survival rate (Table 68.1) [29]. Other surgical blunt injuries, including coronary, valve and septal defects, have a similar proposed mechanism and may present in a delayed fashion. Coronary injuries typically occur from direct trauma. Valve and septal injuries can occur as a consequence of ischemic necrosis. Valve rupture has been described in 5% of autopsy series, but clinically is relatively rare, with a slight preponderance involving the aortic valve more than the mitral valve [30]. The left-sided valves appear to be at more risk due to exposure to higher pressures. The mitral valve is at risk during early systole when the ventricle is full and the aortic valve still open leading to pressure load on the valve as well as in late diastole in conjunction with a compression of aortic outflow. The aortic valve is at risk from direct compression as well as during early diastole when the ascending aorta is still “full” and the ventricle empty leaving no sub valvular support to mitigate against sudden pressure increase against the valve. The relatively rare incidence of patients with operable cardiac injury surviving to reach the hospital means that our approach must be based on resuscitation principles, a high index of suspicion, and much of the surgical techniques derive from our experience with less acute or elective operations.

68.4 Initial Management and Assessment It is most practical to consider the diagnosis and management of cardiac injury in the context of chest injury rather than in isolation. Patients can be categorized into three groups: in arrest, unstable, or stable. In arrest implies the patient has no signs of life and/or is undergoing cardiopulTable 68.1  Blunt cardiac rupture: location and mortality

Incidence % (range) Survival % (range)

Right atrium 43% (35– 50%) 41% (38– 44%)

Right Left atrium ventricle 22% 26% (16–33%) (16–38%)

Left ventricle 10% (8–13%)

2% (0–50%)

33% (0–100%)

58% (0–33%)

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monary resuscitation (CPR) [31]. Unstable can be defined as evidence of shock or impending collapse including systolic blood pressure 120 beats per minute, not explained by pain, anxiety and/or hypoxemia. Philosophically a patient in arrest may be a candidate for immediate thoracotomy, and an unstable patient should be moved to the operating room as soon as possible with minimal delay for extraneous testing and a stable patient is one in whom there is time to consider different diagnostic and therapeutic options [32]. Obviously, patients can move from one category to another (usually worsening) and to some extent the patient status is a clinical judgement. The approach will differ depending on the mechanism, presentation and institution. An overriding theme in civilian centers is to follow the principles of trauma resuscitation, addressing Airway, Breathing, Circulation and Disability. In the military and mass casualty scenario, there is more emphasis on arresting catastrophic hemorrhage that is externally controllable first [33]. Clinical findings (if not in arrest) classically include jugular venous distention, muffled heart sounds and/or pulsus paradoxus. Unfortunately, Beck’s (acute) triad is present in perhaps only 10% of patients with documented cardiac injury [34]. As a practical matter, in the very acute phase, the clinical exam rarely gives direct evidence of cardiac injury. Penetrating injuries that are anterior between the nipple or mid-clavicular lines (the “cardiac box”) usually immediately alert the team to the possibility of cardiac injury as does a clearly fractured sternum following blunt trauma. In the setting of multiple stab wounds, gunshot wounds and blunt trauma usually the diagnosis is made after imaging, surgical exploration and/or repeat examination once the patient has stabilized. The primary tool to make the diagnosis is clinical suspicion. Initial management includes consideration of where any operation, including ERT, is to be performed. There is data that suggests the higher level of functionality of the room the surgery is being performed (i.e. operating room > ‘shock room” > emergency department) has an independent survival advantage for both gunshot wounds and blunt cardiac rupture. It has been hypothesized that optimal lighting, equipment and operating team leads to better exposure and more options with improved outcomes [22, 23, 28]. The ability of any giving institution to rapidly move a patient to a higher level of operating suite, including having direct-to-OR pathways, will permit increased flexibility in operative approach, even in patients in extremis. In patients who present without signs of life, the immediate question is whether a resuscitative thoracotomy (ERT) should be performed. Assuring airway control, ruling out easily treatable causes of shock (such as pneumothorax) and starting fluid should be done rapidly. It is generally accepted that survival after penetrating trauma with >15 min of CPR

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Fig. 68.1  This patient presented with a stab wound to the left chest. Echo did not identify pericardial fluid. Two days later he developed fever and chills, and thoracic surgery was consulted. At thoracoscopy an injured portion of the left ventricle was protruding through a hole in the pericardium, with no pericardial fluid present (see Fig. 68.3)

Fig. 68.2  Patient presented after the left parasternal knife wound (paper clip marks entry). The CXR demonstrates large pericardial effusion. The patient was tachycardic, hypotensive, had jugular venous distension, and muffled heart sounds. Just prior to intubation, the patient underwent non-ultrasound-directed pericardiocentesis, with improved vital signs. At sternotomy a 2-cm laceration to the right ventricle was found and repaired, as was a small injury from the pericardiocentesis needle at the inferior surface of the heart

and blunt trauma with >10 min of CPR is negligible and it is appropriate to withhold ERT [31]. Many centers in this scenario, especially as there is often doubt as to how long the has actually been no cardiac activity, will start with intubation and bilateral tube thoracostomy to see if there is a rapidly reversible problem and then if no response end resuscitative efforts. We utilize extended Focused Assessment

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Using Sonography for Trauma (E-FAST) to assess for pneumothorax and cardiac activity as soon as possible after arrival. The absence of any cardiac activity in any setting suggests that functional survival with ERT will be negligible, especially if no pericardial fluid is detected [35]. Evidence of extracardiac severe or non-survivable injury (such as major head trauma) is an acceptable reason for withholding ERT. The unstable patient is managed in a similar fashion. Initial steps include intubation, assuring if intubated that the tube is in place (often with capnography, which also reflects cardiac output) and product (rather than crystalloid) based resuscitation. The primary diagnostic tools should be the E-FAST and chest radiograph (CXR). Of note, a negative E-FAST in the setting of hemothorax does NOT rule out cardiac injury as the pericardium may be obscured and/or the patient may have bled out of a pericardial rent into the pleural space (Fig. 68.1) [27, 36]. If E-FAST demonstrates tamponade, ultrasound-guided pericardial drainage (we use a central line kit) can (rarely) temporarily stabilize the patient but should never be done as a “diagnostic” step and mandates operative exploration [37, 38]. Specifically for cardiac injury, the CXR may demonstrate an enlarged pericardial sac and in the case of penetrating injury give insight into the missile path (Fig. 68.2). The choice of operative exposure will be described more fully in the next section. Briefly, when ERT is performed, most centers regardless of injury perform a left antero-lateral thoracotomy [31]. Our bias is that if the patient can get to a “shock room” within minutes we perform sternotomy for penetrating injuries to the precordium and for blunt trauma. In the emergency room, we perform left antero-lateral thoracotomy for penetrating injuries on the left side, right antero-­ lateral thoracotomy for those to the right and for blunt trauma if we suspect blunt cardiac rupture. In all cases, we have a very low threshold for converting to the clamshell. Antero-­ lateral thoracotomy and clamshell are excellent for posterior and lateral injuries to the chest [32]. In patients with multiple injuries, or if in doubt, “going to the side where the blood is” is a helpful principle and avoiding the perceived need to cross-clamp the aorta mandating left antero-lateral thoracotomy in the face of evidence that the primary injury is on the right side of the sternum can avoid critical delay in repairing the injury. A simple way of determining if the right or left chest is the primary source of hemorrhage in the patient in arrest (particularly after blunt trauma) is to place bilateral chest tubes and open the side that has substantially more blood. A variable number of “unstable” patients will become “stable” with initial resuscitation. The initial assessment is still the same as for the unstable patient. However, stable patients offer the opportunity for a more deliberative approach, including advanced imaging. Computer tomographic (CT) angiography (A) is the preferred diagnostic

68 Updates in the Management of Complex Cardiac Injuries

Fig. 68.3 Same patient as in Fig. 68.1. Note how pericardial tacking sutures elevate the heart

approach for stable patients with trans mediastinal gunshot wounds and occasionally, following blunt trauma, can demonstrate pericardial fluid suggesting a contained rupture [27, 39]. Formal echocardiography (either transthoracic [TTE] or transesophageal [TEE]) might be considered. If imaging clearly demonstrates a large amount of pericardial fluid or even tamponade, we recommend exploration via sternotomy. If still in doubt, either pericardial window or thoracoscopy are reasonable approaches [32, 40]. The ECG is generally not specific in the acute setting, but if there are demonstrable ischemic changes especially in the left anterior descending region and particularly after blunt trauma, coronary angiography is reasonable [27].

68.5

Sternotomy, Thoracotomy and Pericardial Interventions

In most cases, we prefer to have the patient supine, with the arms extended in the “crucifix” position [32]. This allows wide access, including to the great vessels if these are also injured. We prefer a single lumen endotracheal tube (even with suspected airway injury) as it is easier to place and can be manipulated (e.g. left mainstem or bronchial blocker) if lung isolation is needed. Some active trauma centers are very comfortable with placing a double-lumen tube in the emergent setting, but in most cases, it takes too long to place. Since the early 1900s the standard approach to cardiac injuries has been the sternotomy and left antero-lateral thoracotomy [22, 41]. Most trauma surgeons favor antero-lateral thoracotomy as it seems “easier”, but both have their pros and cons. In the exigent circumstance of arrest or near arrest, the surgeon should choose the approach they are most comfortable with. Either approach may provide inadequate expo-

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sure and there should be no hesitancy to use additional incisions to get the exposure needed. A median sternotomy is an excellent approach to penetrating wounds that are between the anterior axillary lines (or nipples) (Fig. 68.3). This provides complete exposure to the anterior heart and great vessels, allows easy access for cardiopulmonary bypass in the rare case it is needed and is the approach of choice for more “elective” repair of more complex cardiac injuries [27, 32]. It has limited access to the posterior hemi thoraces. The midline is marked by a line from the suprasternal notch to the xiphoid. Crossing veins at the suprasternal notch and the sternal-xiphoid junction commonly cause bleeding and need to be ligated. There is a tough band of fibers just at the inferior sternal plate at the suprasternal notch that needs to be divided, which can be done with cautery, scissors or knife depending on the situation. We prefer to split the sternum from superior to inferior, as this obviates the need to dissect under the xiphoid and makes the “top down” approach quicker. A sternal retractor provides much better mobilization and stability than a standard rib retractor but either can be used. Upon entering the chest, sweeping the pleural attachments laterally will allow greater exposure. The pericardium is incised longitudinally, and then at the base extended laterally into both recesses. To gain access to the more posterior or inferior aspect of the heart, tacking up the pericardium with stay stitches will elevate the heart, as well as placing a lap sponge at the base. When closing we prefer to use cables, and there should be no motion of the sternal tables at the end. In young patients I prefer to close the upper pericardium over the aorta, in case the patient needs elective cardiac surgery later in life, the ascending aorta is not directly adherent to the sternum. We leave at least one mediastinal drain that covers the pericardium. While considered “more difficult” than antero-lateral thoracotomy, in experienced hands this approach is quicker and provides more access to the central cardiac structures and can be performed if a sternal saw/knife and sternal retractor are available, in any operative setting. Sternal retractors have different designs which can affect bone healing. The Ankeny is a sternal retractor with long arms with multiple attached c-shaped metal devices which grip the edges on each divided sternum and allows even distribution of force on the sternal halves as the Ankeny retracts the sternum to allow exposure of the middle mediastinum. Other retractors used for exposing the anterior and middle mediastinal structures are thoracotomy retractors with small metal phalanges which cause “bowing’ of the two sternal halves in the middle, and micro and macro fractures of the halves. Usually, this does not pose a problem of sternal incision healing but can increase the chances of sternal non-union. Antero-lateral thoracotomy is usually performed on the left. The incision runs in the inframammary crease (not the

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Fig. 68.4  Clamshell thoracotomy for stab wound to the heart. The entire thoracic cavity including great vessels is exposed

Fig. 68.5  Patient following clamshell thoracotomy. Note that the incision crosses nearly the midpoint of the sternum following the 4th or 5th intercostal space (staples). A common error is to make the incision to inferior, and not curling up (solid line) which often results in crossing the sternum at or near the xiphoid (triangle)

nipple line) and it is important that the medial aspect curves up following the course of the ribs. This will allow exposure in the anterior 4th or 5th intercostal space and avoids the common error of crossing the sternum too low, which limits exposure considerably. The antero-lateral thoracotomy is an excellent choice for wounds that are lateral to the anterior axillary line and/or if the mechanism suggests more poste-

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rior wounds. Upon entering the chest, the pericardium is incised anterior to the phrenic nerve longitudinally and then can be extended transversely. The left antero-lateral thoracotomy has been popularized for the following reasons: it is easier to do for some surgeons and emergency physicians; sternotomy blades and retractors are often not available in emergency departments; the perception is that the ventricles are easily seen; it is felt that open cardiac massage (OCM) can be performed better through that approach; it allows clamping of the descending thoracic aorta. As we noted before, once a surgeon is trained in median sternotomy, it is as easy or easier to get exposure with that approach for anterior wounds and the entire surface of the heart can be seen. The majority of blunt cardiac rupture injuries that are survivable (especially in the patient in arrest) occur on the right side of the heart, particularly the right atrium, atrial-caval junction and right ventricle, which are often better visualized from a right antero-lateral thoracotomy rather than a left-sided approach [27]. OCM can be performed from the right side by reaching across the midline. In addition, left antero-lateral thoracotomy for penetrating chest injuries is associated with inadequate exposure requiring extension in up to 1/5 of cases [22]. Finally, aortic occlusion, while offering improved coronary and cerebral perfusion, is not as simple as it seems. Blindly clamping the aorta can lead to esophageal and aortic lacerations, and if the operator is not facile with mobilization, can fail to clamp the aorta at all. In addition, if time is spent on aortic occlusion, the cardiac injury will keep hemorrhaging. Experimental data suggests that in uncontrolled hemorrhage, aortic occlusion is associated with impaired left ventricular function, systemic oxygenation and coronary perfusion pressure in the post-resuscitation period [41]. This is not to suggest that the antero-lateral thoracotomy is not a useful approach. However, if the injury is on the right side of the chest, or if there is evidence that the majority of hemorrhage is on the right, or in the rare case of blunt trauma undergoing immediate thoracotomy, the right antero-lateral thoracotomy in our experience is the optimal first approach. The real benefit of the antero-lateral thoracotomy is extending it into a clamshell thoracotomy. The clamshell approach provides superb exposure to the entire chest and anecdotally has become the preferred approach in the military setting (Fig. 68.4). If there is time, a towel placed longitudinally along the spine facilitates exposure. This may not be possible following blunt injury if there is the possibility of spine injury. The key is to carry the incision of the antero-lateral component high as it crosses the sternum, as we stressed above. This allows the sternum to be split in or about the 4th intercostal space (Fig.  68.5). The internal mammary arteries can be ligated in the “stable” patient, but in the unstable patient can be ligated when reperfusion occurs causing them to bleed so in the emergent

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unstable setting time does not need to be wasted in dissecting them out. The anterior pleural attachments are easily swept away, and two rib spreaders placed in the intercostal spaces bilaterally will provide exposure to the entire thorax. When closing, we make sure the bilateral internal mammary vessels (superior and inferior to the incision) are well ligated and close with two cables in the sternum and laterally intercostal sutures. Pericardiocentesis should be relegated to the rare setting where the patient is “stable” and the decision to operate has been made. It should never be done as a diagnostic tool. It has a select potential role in patients with evidence of tamponade, prior to intubation, to reduce the risk of cardiac arrest on induction [37, 42]. In the few cases we have utilized this approach, we do use a percutaneous catheter guided by ultrasound to drain the pericardial sac and all patients MUST then undergo operative exploration. A central line kit often suffices. An absolute requirement is that the pericardium and the needle MUST be clearly seen at all times during the procedure. We approach the pericardium by the window which gives the clearest view, typically the subxiphoid but occasionally from the anterior left parasternal window. Of 5 cases the authors have personally done in their experience, in all 5 the patients stabilized, and underwent successful cardiac repair. Four were after stab wounds and one after a nail gun injury. In one case, a 2 cm right ventricular laceration from the knife was repaired, as was a small needle puncture from the catheter drainage procedure (Fig. 68.2). Pericardial windows can also be used to stabilize pericardial tamponade, but usually for non-trauma causes. In the trauma setting, it is generally used to confirm or exclude cardiac injury [32]. Typically, a subxiphoid approach is used, dividing or spreading under the xiphoid, then entering the anterior-inferior pericardium. Most technical reports describe holding the pericardium with Alice clamps but often the pericardium is too thick or distended for this to work until the surgeon has made a partial incision. In patients undergoing laparotomy, some create a window directly through the diaphragm. While many surgeons feel this does not need to be closed, we have anecdotally had to operate on a colopericardial herniation after this. If blood is encountered, it is expected that formal exploration would be performed. In rare cases, after irrigating out the pericardium, the anterior surface of the heart can be inspected using a rigid scope and if no significant injury is encountered, a drain can be placed but it would take a significant degree of confidence to use this approach. An alternative in stable patients where the suspicion is low is to perform a thoracoscopic exploration. This is typically in the setting of delayed presentation or complications, and predominantly when there is another reason for thoracoscopy (retained hemothorax, pneumothorax, possible diaphragm injury etc). Video-assisted thoracic surgery (VATS)

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requires double-lung ventilation while “rigid” thoracoscopy does not but has lesser visualization [32]. Again, in the vast majority of cases, finding evidence of hemopericardium mandates formal exploration and if there is suspicion of a cardiac injury, the patient should be in the supine position with full chest prep. There can be scenarios where after massive resuscitation the chest cannot be closed due to thoracic compartment syndrome. From the heart perspective, this usually is described when there is obvious myocardial edema, aggravated by pulmonary congestion and/or abdominal compartment syndrome. It becomes clinically obvious when closing the incision leads to a significant drop in cardiac output. The basic principles of management include closing the chest loosely or not at all, until the patient's diuresis and/or any stunning myocardium recovers. Approaches have included leaving the retractors in place and covering them with sterile occlusive dressings, or, in the case of sternotomy, creating bridges out of chest tubes that keep the sternal plates separated. If laparotomy has not been performed, and there is evidence of elevated abdominal pressure, performing a decompressive laparotomy can allow thoracic closure (Fig. 68.6). Currently, we prefer to try placing a moist surgical tower over the thoracic viscera and covering it with a wound vac that is placed on low to intermediate suction. The incision can be closed in stages as the patient recovers, but it is important that the thoracic incision is closed before any abdominal closure. Our sense is that the incidence of thoracic and abdominal compartment syndrome has diminished greatly as we have shifted to a product rather than a crystalloid resuscitation strategy.

Fig. 68.6 A patient following penetrating injury to spleen, heart and lung. He developed abdominal and thoracic compartment syndrome, requiring an open abdomen and chest for a time. This is much less common with the advent of product-based resuscitation, and vacuumassisted closure devices have replaced the more crude packing/adherent drape closure methods

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Patients who have had prior thoracic procedures can be quite challenging. This is particularly true in those who have had coronary artery bypass surgery, especially with the increased popularity of sternal closure with titanium plates. The detailed approach that can be used is beyond the scope of this chapter, but it is critical to recognize the potential of adhesions of the heart, aorta and/or bypass grafts to the posterior sternal plate or lung and diaphragm to the chest wall after a thoracotomy. It is uncommon but not unheard of in the younger penetrating population to have to deal with these issues. In exigent circumstances, the optimal approach can be to do the approach NOT used prior: thus, if sternotomy, use antero-lateral thoracotomy and vice-versa. In more controlled circumstances (for example repairing in a delayed fashion a ventricular septal defect) re-operation (typically sternotomy) with cardiopulmonary bypass capability (including preemptive groin access) and using whatever technique the surgeon feels comfortable with to divide and mobilize the sternum is appropriate. One variant of re-operative surgery is managing a patient with the prior pericardial disease. One of us (M.L.) has had personal experience of managing an 85-year-old patient with a low-velocity small caliber gunshot wound to the heart that traversed from the right atrium, across the left atrium, and terminated in the left chest. The patient at surgery was found to have tamponade from the right-sided entry wound (which was repaired) but had dense posterior adhesions with no bleeding from the left atrium. The adhesions were a consequence of prior rheumatic heart disease. The adhesions were not taken down and the patient did well. Thus, prior adhesions, particularly involving the left atrium, may result in tamponade of the injury and the better part of valor would appear to be to NOT create hemorrhage by dissecting these out.

68.6 Adjuncts and Tricks There are several adjuncts, many derived from elective cases, that can be utilized to increase exposure and/or help control bleeding in the acute case. These can be performed concurrently. The first issue is exposure. Obviously, if whatever incision does not provide the exposure needed, extensions are required but typically both sternotomy and clamshell both provide wide exposure. From the sternotomy approach, tacking the pericardium up to the sternal retractor will really help exposure. Placing a lap pad at the inferior aspect of the heart beneath the apex will elevate the heart and expose the majority of the posterior inferior surface. The left lateral and posterior aspects of the heart can be difficult to visualize and if

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there is an assistant gentle retraction with a sponge that can pull the heart over will help. Other adjuncts described have been a traction suture in the apex or “suction cup” to pull the heart over and help stabilize it [27, 43]. The next issue, which practically occurs simultaneously, is the control of hemorrhage. The simplest method is direct finger compression, again easier if there is an assistant. A foley catheter can be used to control a laceration, although great care must be made to avoid excessive traction, and to clamp the non-balloon end. In our experience, this works best for small left ventricular wounds, as the right ventricle and atria tend to tear easily. Injuries at the right atrium or atriocaval junction (especially superiorly) can be controlled with blunt clamps, such as the Babcock although others describe the use of Alice clamps. Atrial appendage injuries can be controlled with curved vascular clamps. There is ongoing interest in developing other devices for the control of cardiac lacerations [26, 38, 44]. Staples have been used to temporarily control lacerations, again in our experience more optimal with the left ventricle. While offering some control they can with cardiac contraction they can lead to further myocardial tearing, especially with OCM, and generally act only as a temporizing method. Biological glues can manage small or partial thickness injuries, but again are an adjunct in most cases to definitive repair [22, 38]. A variety of biological patches, with or without adjunctive glues, have been intermittently described for complex tears that resist primary closure [45]. If there is severe hemorrhage, such that the injury(ies) cannot be adequately assessed, we have found that bicaval clamping will allow the heart to beat empty and permit suture repair. This is particularly useful for injuries at the aortic root. One effect can be fibrillation, but fibrillation will arrest hemorrhage and allow repair and should not be feared but rather taken advantage of if it happens [27, 38, 46]. Dealing with a complex injury wherein there is no concomitant catastrophic bleeding, can include adenosine to provide brief periods of slowed heart or even stand still. For anterior wounds, coronary graft stabilizers can permit delicate repairs of the coronary arteries and/or myocardial lacerations [27, 47]. Finally, if there is no or limited intravenous access, using the right atrial appendage or right atrium for access can be lifesaving.

68.7 Mechanical Circulatory Support CPB offers several theoretical advantages, although its use has been limited due to vagaries in the volume of cases and technical skills available for emergent use at different institu-

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tions. Historically, it has been touted for the repair of the coronary artery, difficult to access and/or intracardiac injuries. However, these have largely been in the controlled setting after hemorrhage has been arrested [25, 27, 48, 49]. CPB also offers an opportunity to resuscitate a patient, correcting for acidosis, hypothermia and myocardial disfunction in the emergent setting, again once the primary source of hemorrhage is controlled [25, 49, 50]. Percutaneous CPB offers a less complex method of temporizing until formal bypass can be instituted [49]. Extracorporeal membrane oxygenation (ECMO), typically also performed percutaneously, is usually utilized to support cardiac output and/or oxygenation. This is usually instituted after the repair of traumatic injuries, and its use for cardiogenic shock following trauma (which would suggest the need for veno-arterial ECMO) appears to be limited. In one large series, less than 3% of trauma patients who required ECMO had cardiac injuries [51]. If following cardiac injury, the primary problem is the poor cardiac function, without issues in oxygenation, IntraAortic Balloon Pump (and in theory the Impella device) can support perfusion and cardiac function/recovery (Fig. 68.7) [26, 50, 52, 53]. Some reports indicate that this is required in up to 10% of cases, but predominantly is used to support patients requiring other emergent surgery following cardiac injury [54, 55].

Fig. 68.7 This patient presented with a stab wound to the left precordium. He had undergone sternotomy 3 years prior for stab wound to the heart. Left anterolateral thoracotomy was performed and a laceration through the circumflex artery was ligated. He developed low cardiac output and thoracic compartment syndrome and was supported with intra-aortic balloon pump. On post-operative day 5 due to persistent low cardiac output, and ECG changes, he underwent coronary angiography which revealed a left anterior descending to right ventricular coronary fistula which was successfully stented

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68.8

Operative Repair of Specific Injuries

68.8.1 Laceration/Rupture Exposure and adjuncts to repair of ventricular and/or atrial laceration/rupture have been described previously. The principles apply to the proximal ascending aorta as well. It is important to note some anatomic features. The left ventricle is generally more robust than the right, and suturing the right ventricle is a bit more like suturing the liver, so avoiding tearing and tension is important. The right coronary artery runs in the groove between the right atrium and ventricle so if possible, care should be given to avoid inadvertent ligation of injury to the coronary artery at this site. Tears at the inferior vena cava-right atrial junction can be extraordinarily difficult to control, not the least because lifting the heart can extend the tear and the thoracic inferior vena cava is “short” and partially embedded in the pericardium making quick control difficult. This is one setting where clamping the superior vena cava and deploying a Foley into the inferior cava may provide enough control to allow sutures to be placed. Failing that, if control can be achieved by compression and there is cardiac activity, rapidly employing cardiopulmonary bypass may be lifesaving. The standard repair of a ventricular laceration is a mattress suture with pledgets. [27, 31, 32, 34, 56]. The wound can be digitally controlled (or other adjuncts as described) We favor a 3-0 double-armed long monofilament suture. If pledgets are not immediately available pericardium makes a readily available substitute. Typically, when placing a mattress suture, the operator has both needles loaded on a needle driver and the assistant has a driver or clamp to grab the needle as it passes beyond the injury site. The operator then can continue to hold pressure on the defect. It is important to try as much as possible to have the distance between the suture in the pledget be the same as the distance as it passes through the defect to avoid extra tension on the myocardium or cause misalignment of the pledget which may lead to residual gap permitting bleeding. We have found, when using pericardium, that it is easier and quicker to take a bite of the pericardium with both needles, pass the suture through the defect, then cut the pericardial wedge free then pass the suture through the opposite pericardium and similarly cut the pericardium free to create the opposite pledget. If the laceration/ rupture is near a coronary artery, it is optimal to pass the sutures deep to the artery to avoid inadvertently ligating it, although compression can occur. In more complex tears, that resist simple suture repair, the adjunctive patch may be required, which can be performed in a fashion similar to the repair of the ventricular aneurysm (usually on bypass) or with topical patches as described earlier. If the “tip of the apex” has been ruptured or lacerated, placing a number of

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pledgeted sutures through the apex while elevating the heart usually suffices. Although thin-walled, the atrium is generally more forgiving because it is relatively more pliable than the ventricle. Simple sutures often suffice. Appendage rupture can often be controlled with a vascular clamp and cava-atrial injuries can be repaired with a running suture, although if significant narrowing occurs patch repair may be required [27, 31, 32, 34, 56]. If the “tip” is blown out, vascular staples can be used.

68.8.2 Coronary Artery The incidence of coronary artery injury following penetrating trauma is roughly 5%, predominantly affecting the left anterior descending artery. Overall mortality is in the 70–80% range [25, 26]. The primary operative management has been ligation, due to the associated chamber defect, with coronary bypass reserved for cases in which there are severe arrythmias and/or obvious significant jeopardized myocardium. The most common indication is for injuries involving the proximal ½ of the left anterior descending coronary artery. While cardiopulmonary bypass has been advocated for bypass, there is data that suggests that off-pump repair is equally efficacious [57]. However, if obtuse marginal or posterior descending artery occlusion is associated with significant myocardial compromise, there may be a role for CPB [25]. Anecdotally, we have on rare occasions when the left anterior artery has a partial anterior laceration repaired the artery with interrupted fine sutures, using finger stabilization and/or adenosine to induce bradycardia to assist in stabilization. Blunt traumatic coronary occlusion requires a high degree of suspicion as the findings may be consistent with “contusion” and obscured by other injuries. As with penetrating trauma, the left anterior descending coronary artery is most commonly affected. Evidence of ischemic changes by ECG and/or TTE/TEE in a particular coronary distribution can suggest the diagnosis [56, 58, 59]. If there is significantly jeopardized myocardium, especially in a patient with cardiogenic shock, most authors recommend intervention, although mechanical support to temporize the situation is also a reasonable option. While medical management as practiced for atherosclerotic disease has been utilized, Ginzburg et  al described a 30% incidence of significantly delayed complications, suggesting that more aggressive treatment is indicated in the trauma setting [58]. Treatment can include stenting or bypass [27, 58]. A variant of coronary artery injury that can present after blunt or penetrating trauma is a coronary-ventricular fistula, with or without a pseudoaneurysm. These typically present in a delayed fashion with heart failure, angina,

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infarction and/or endocarditis. Clinically, a parasternal murmur may be detected. Echo and/or angiography (intra-arterial or dedicated cardiac CTA) can confirm the diagnosis. A variety of approaches have been utilized. Intra-cardiac repair is appropriate if there are other lesions (septal defect, valve injury) that require repair but both coronary stenting, ligation and bypass have been employed [60–63].

68.8.3 Valve Injury As noted previously, valve injury has been documented predominantly in the setting of blunt trauma, typically motor vehicle crashes, with an incidence in autopsy studies of 5%. Overall, in clinical series, aortic valve injuries predominate while in the autopsy series mitral valve injury predominates [30]. Mechanisms ascribed have included direct injury, compression and acute pressure against a closed valve, and/or delayed ischemic necrosis from hematoma or coronary injury. In the rare setting of blunt injury to the ascending aorta, some investigators have quoted up to 26% incidence of aortic valve/annulus disruption, mostly impacting the right or non-coronary cusps [64, 65]. Valve injury after penetrating trauma is even more uncommon. Typically, they are diagnosed in a delayed fashion and often with an associated septal defect [66, 67]. Rustad and associates reviewed 18 patients with stab wounds to the ascending aorta above the right coronary cusp that developed aorto-right ventricular fistula and aortic insufficiency [67]. Regardless of the mechanism, valve injury is associated with concomitant cardiac and/or great vessel injury in nearly ½ of those who survive hospital admission [27]. The diagnosis may be made acutely at exploration, with palpable thrill over the aortic valve, evidence of ventricular distention (e.g left for acute aortic insufficiency, right ventricle for acute mitral insufficiency and right atrial distension for tricuspid insufficiency). However, in the majority of cases, the diagnosis is made in a delayed fashion either because of the development of pulmonary edema, cardiac insufficiency or simply screening echocardiography [27]. TEE appears to have better visualization than TTE for the purpose of diagnosing and defining the extent of the valve injury and is particularly important intra-operatively if repair is attempted to assess competence [68]. Timing of repair depends on associated injuries and degree of cardiac compromise, but if it can be delayed until scar tissue forms, the results appear better [67–69]. Atrioventricular valve injuries can be temporized with mechanical support (predominantly intra-aortic balloon pump) but significant aortic regurgitation ends to preclude this.

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Aortic valve injury usually results in early significant regurgitation that requires repair [69]. Because of the extent of disruption, especially if the annulus is involved, the majority of patients will require aortic valve replacement. However, a small number of patients may be able to undergo valve repair. Petre and Faidutti noted that of 37 patients, 26 underwent valve replacement. Of 10 patients who underwent repair (including 4 who were operated on before valve replacement was an available option) 2 died of heart failure, and 2 subsequently required secondary valve replacement. Six patients with isolated cusp injuries that underwent repair were doing well on follow-up ranging from 6 months–17 years [69]. Li and colleagues in a review noted that typically (of the less than 100 reported cases in the literature up to 2002) one cusp was involved, the least common being the left coronary cusp, possibly because it is more posterior [70]. Of note, there is a slightly increased chance of associated left main coronary injury that may require concomitant bypass. There is a greater chance that primary valve repair will be possible after stab wounds to the aortic valve [67]. Traumatic injury to the right sinus can rarely be associated with right atrial fistulization. The cusp may be amenable to repair by closing the fistula with a patch within the aortic root [71]. Mitral valve injury involves one or both papillary muscles in 2/3 of cases, most commonly the anterior. These typically present with acute valve insufficiency. If the chordae tendinea or valve leaflet alone is injured, the course seems more indolent [68]. However, if there is evidence of progressive annular dilation and/or heart failure, the repair is recommended [72]. A rare variant is the development of subvalvular left ventricular aneurysms in conjunction with mitral insufficiency, which in turn in association with septal defects lead to left ventricular  – right atrial fistula [73, 74]. Valve repair, including papillary or chordal reattachment, leaflet repair and/or annuloplasty in stable patients. [27, 68, 69] As previously noted, repair through an area of ventricular injury may be feasible. The typical approach through the left atrium may not be feasible, as the patients are young and may have a small atrium so particularly in the acute setting replacement of repair may be better performed using a biatrial transseptal approach. In most cases replacement is performed and what data there is suggests that in the setting of concomitant septal injury, replacement is associated with better outcomes. The tricuspid valve may be more amenable to repair depending on the degree of damage, right heart failure and/ or pulmonary hypertension. Anterior leaflet prolapse, with anterior chordal rupture, with annular dilation, seems to be the most common pathology [68, 75]. As with mitral valve repair, a variety of repair techniques have been described, including ring annuloplasty, artificial chordae, and papillary reinsertion [27, 68, 75].

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68.8.4 Septal Defects Traumatic septal defects often present in a delayed fashion. The incidence after penetrating trauma is slightly less than 2% in the Ben Taub series [26]. The incidence after blunt trauma is not defined. In victims of penetrating trauma, who survive surgery, the predominant mechanism appears to be a stab wound to the right ventricle. Survival was reported to be 37.5% following stab wounds and 50% following gunshot wounds, all of whom required operative repair of the defect within 1–16 weeks [26]. The most common site of blunt trauma-related septal defects is in the muscular septum, close to the apex [27]. Initially, the majority of septal injuries are small, and as many are in the muscular septum, may actually heal. They may present in a delayed fashion due to hematoma leading to necrosis or a consequence of coronary artery injury and focal infarction [76, 77]. Indications for repair include the need for other intracardiac repair, heart failure and/or shunt > 2:1 [1, 2, 5]. Blunt injury to the atrioventricular valves can be associated with accompanying atrial and/or septal defects as their annuli form part of the septal structure. Tears under the right coronary valve in particular can be associated with significant acute shunting. Perimembranous septal tears tend to be associated with tricuspid valve injury or delayed deterioration [27, 78]. Thus, even small shunts in the infra-aortic valve septum should be considered for repair or at the least very close follow-up. Diagnosis can be made by auscultation of a new-onset systolic murmur at the left parasternal wedge, especially in the setting of persistent hypoxia and/or heart failure and can be confirmed by echocardiography (transthoracic or transesophageal) [76]. Sampling the cardiac chambers for oxygen levels can also localize the level and significance of the shut [26]. Because the defect is usually small, it may be possible to repair using interrupted pledgeted sutures. Larger defects require patches. The approach varies depending on the location and has included trans-atrial repair, through the aortic valve, via apical ventriculotomy but most recommend if possible, approaching through the area of already damaged myocardium [26, 27]. Delaying surgery will permit fibrotic tissue to build up making suturing easier. Repair of septal defects near the tricuspid valve is at higher risk of heart block requiring pacemaker insertion [79]. One of our authors (WL) took care of a 34 y.o. motorcyclist who hit a highway concrete divider at high speed with his chest. He arrived at our trauma center with hemoptysis and hypoxia from a severe right lower lobe contusion/hematocoele. He was taken directly to the OR where a right thoracotomy and right lower lobectomy was done. Postoperatively, in the Trauma ICU, he developed a holosystolic murmur heard by the ICU nurse and developed acute right ventricular

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failure. The cardiac catheterization lab confirmed the diagnosis of a ventricular septal defect measuring 4 cms x 3 cms. with a calculated 13:1 shunt. Because of progressive clinical deterioration he underwent emergent repair. On CPB, a right ventriculotomy, para LAD, was done. The defect was repaired with a velour patch secured with mattress pledgeted sutures placed in the left ventricle just lateral to the LAD coronary artery, passed under the LAD and sewn to the anterior portion of the patch. Running sutures completed the patch attachments to the inferior septal muscle leaving enough space to avoid injury to the Bundle of His. Just before the final suture of the patch, the left ventricle was de-aired, and the right ventriculotomy was closed with running sutures and two velour strips. The patient required inotropic support for several days, then he was weaned from those drugs. He was discharged home 10 days later, with an ejection fraction of 55%, and normal atrial pressures. An echocardiogram showed no ventricular shunt. He failed to follow-up in our trauma clinic. The advent of percutaneous closure devices offers a less invasive option for managing patients, although there is limited experience with this approach. The indications remain the same, and as with open repair, if possible, allowing time for fibrosis to occur helps in defining the edges of the defect during closure and may lead to a better outcome [77]. Given the limited data regarding percutaneous devices, it is hard to make specific recommendations, but the choice will be affected by the location, size and angle of the defect. Xi and associates recommended the PFO occlude device for longer, angled septal defects particularly if the defect is close to the right ventricular outflow tract. The PFO occluder has only a “left” disc and thus will not impair the right-sided outflow or valve [80]. VSD and ASD occluders have a 4 mm waist and may be best suited for small, short, straight muscular defects closer to the apex [80, 81]. Three-dimensional echocardiography can be instrumental in defining the septal anatomy and helping determine optimal device choice [81]. Given the limited experience with this approach it is hard to discuss the complications of this approach. However, there are isolated reports of hemolysis after percutaneous closure of traumatic septal defects that were significant enough to require operative removal and septal closure [82, 83]. Conversely, closure devices have been utilized to repair residual defects after surgical closure [84].

68.8.5 Retained Cardiac Missiles The most common mechanism for a retained cardiac or pericardial foreign object is direct trauma [13, 85, 86]. Typically, but not always, the patient will undergo surgery and if the missile is clearly appreciated, it will be removed at surgery.

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As with impalement injuries, it may be possible to place sutures around the object before removing it if it is embedded partially in the surface of the heart. However, the object may not be appreciated at the time of surgery, or the patient may have had minimal symptoms originally. Diagnosis can be made by plain CXR, with a blurred object suggesting that it is in contact with a pulsatile structure, although this is an unreliable sign [87]. Other diagnostic approaches in a stable patient can include CT, TTE, TEE, or even cardiac angiogram [88, 89]. Transthoracic and/or epicardial echocardiography at the time of initial surgery can be particularly helpful [89]. It is not clear if and when asymptomatic cardiac missiles should be removed nor what the incidence of complications of retained missiles from direct trauma. Symbas and colleagues have compiled an extensive review based on historical data and their own personal experiences. Briefly, it appears that increased risk of complications (ranging from 5–10% incidence) are associated with any of the following features: partially embedded missiles; those in the left-sided chambers; irregular objects; those greater than 0.38 caliber (or 2  cm in 2/3 views). Complications include arrythmias, sepsis, endocarditis, late hemorrhage and systemic embolism including to the cerebrovascular system [85, 86]. Right-sided lesions in their experience were tolerated well if they met all the other criteria. If surgery is required, especially on the left side of the heart, cardiopulmonary bypass is usually needed to permit open exploration. Of note, if imaging suggested that the missile was fully embedded then the complication rate was very low if left alone. Interestingly, in their personal experience, the incidence of cardiac neurosis was negligible compared to the historical cohort which they attribute partially to being related to wartime injuries with associated emotional strain (what is now called post-traumatic stress disorder). The management of bullet/missile embolism to the heart has undergone reevaluation with the advent of percutaneous retrieval techniques. The majority reside in the right ventricle and may be trapped by trabeculae. Some investigators feel that in these cases, asymptomatic right atrial small caliber missiles have a benign course [85, 86, 90]. Others quote a more malignant course and support retrieval [91, 92]. Alan Ellison and colleagues quoted a 6% mortality and 25% complication rate if the bullet was not removed as opposed to a mortality rate of 1–2% if the bullet was removed [91]. Endovascular retrieval has made removal more attractive [92, 93]. Yoon et al performed a literature review and found that 2/3 of bullet emboli involved the right-sided cardiac chambers, predominantly the ventricle. Endovascular retrieval was attempted in nearly ¾ with just over 50% success rate, with ¾ of these undergoing open retrievals. Of note, of those observed initially or after failed

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percutaneous removal, there were no reported complications [94]. When performing endovascular retrieval from the ventricle, it appears that using echocardiography as an adjunct is helpful in preventing tricuspid valve damage [92]. In addition, often large (24 French) sheaths are required, and while complete percutaneous access is feasible, it can be difficult to remove the missile through the sheath suggesting that venous cut down may be a safer approach. Thus, overall, in asymptomatic patients, which are “small”, smooth and/or entrapped in the right ventricle, observation is a reasonable approach as opposed to open removal. However, it is not unreasonable to consider percutaneous retrieval. All investigators agree that a missile that traversed the GI tract should be removed because of the risk of septic complications [85–87]. Free intrapericardial missiles appear to be associated with an increased risk of complications, particularly symptomatic pericarditis. Burkhart and associates described 31 cases of free intrapericardial missiles. Ten were removed acutely and had no complications. 15/21 that were observed developed symptoms (including tamponade from pericarditis) requiring an operation. Based on this experience they recommended early retrieval when feasible, which can be performed in some cases by sub xiphoid window or other minimally invasive techniques [95].

68.8.6 Impalement Injuries Impalement injuries present a unique set of issues regarding positioning and operative approach. Such injuries involving the heart are rare, representing less than 1% of patients who suffer penetrating cardiac injury [96]. If the object penetrates posteriorly, the patient may have to be intubated lying between two stretchers or if stable enough while lying on the unaffected side [87, 97]. In stable patients, there may be time to perform advanced imaging (such as CT) but typically the approach involves E-FAST and plain CXR at most following principles outlined previously (Fig.  68.8) [98]. Depending on the type of object involved, shortening the object (e.g., with metal cutters) can make the operative approach easier. In stable patients, in whom there is no direct evidence of cardiac injury, thoracoscopy offers a less invasive approach to initial exploration [97]. It is generally agreed that the impaled object should not be removed because of the concern of releasing hemorrhage [87, 98]. Our bias is that the major advantage of leaving the object in place is to actually be able to visualize what has been injured. In most cases, sternotomy or clamshell approaches offer wide exposure and greater versatility. CPB may be feasible and allow controlled removal, repairing each side of the heart in steps (Fig. 68.9) [98].

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68.8.7 Surgery for Injuries not Directly Involving the Heart Occasionally there can be a role for surgical intervention to treat cardiac decompensation when there is no specific operable cardiac injury. One uncommon but not the unheard-of scenario is cardiac tamponade secondary to retrosternal hematoma. Typically, there can be clinical evidence of tamponade, with elevated jugular pressure (which can be documented by central venous pressure), rapid heart rate and shock. Most of the case reports describing this are in patients who have undergone CT scanning which demonstrates the contained hematoma. In the majority of cases, a sternal fracture is documented but not all involve internal mammary artery injury. The patients can deteriorate suddenly, and echocardiography can be critical in detecting right ventricular compromise from extracardiac compression. When suspected, most authors recommend sternotomy, drainage of the hematoma, ligation of any vascular structures that might be the site of hemorrhage and in most cases sternal reconstruction [99–101]. Myocardial “contusion” is a nonspecific term that we have all tried to describe with more precision. Pretre and colleagues refined the term to more specifically describe structural and functional perturbations associated with blunt cardiac injury [30]. The structural injuries described earlier are much less common than what has been described as “contusion” but in rare cases, even without rupture, laceration or other operable injuries, surgery may be required. Typically, severe injuries can affect the right ventricle more than the left leading to symptoms similar to tamponade, with dilation of the ventricle, increased venous pressure, and shift of the septum to the left leading to left ventricular compromise. This low cardiac out states can be managed with pulmonary vasodilators and/or mechanical support (IABP, etc.) but if patients do not respond to these interventions, and there is a sign of right heart failure, decompressive pericardiotomy can restore perfusion, similar to managing thoracic compartment syndrome [27]. This is an extremely difficult scenario to diagnose and the surgeon may have to rely on his/ her best guess that this will benefit the patient. A more common clinical scenario is pneumopericardium, more commonly after blunt rather than penetrating trauma. The mechanism is typically ascribed to alveolar rupture with air tracking along broncho-vascular sheaths to the mediastinum. Pneumothorax does not need to be present [102–104]. In most cases, the predominant feature is extra-pericardial air, but there can be sufficient intra-pericardial air that tamponade occurs. There is probably a greater risk for patients who are mechanically ventilated. Nicol and colleagues described 27 patients (26 stab wounds) that presented with pneumopericardium. Of the six patients that went straight to surgery due to shock, one was felt to be due to tension pneumopericardium.

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Fig. 68.8  Patient presented with stable vistal signs after a nail gun injury. Echo demonstrated increasing pericardial effusion and early right ventricular collapse. After echo guided pericardial drain, the patient was intubated

68.8.8 Pericardium

Fig. 68.9  Same patient as in this figure. At sternotomy two small through and through wounds were noted. The embedded nail largely tamponaded the bleeding. Pledgeted sutures were placed around the nail before it was removed

Of 21 patients managed expectantly, 2(10%) developed delayed tension physiology [105]. They recommended early decompression, but we have felt that close follow-up is sufficient. If drainage is required, and there is no evidence of another cardiac injury, subxiphoid window, percutaneous drainage and/or thoracoscopic window usually suffices.

Pericarditis has been reported in as many as 22% of patients following penetrating cardiac injury but has been described following blunt trauma as well. The etiology appears to be an autoimmune response directed against the myocardium and/ or pericardium, but blood can also cause a vigorous inflammatory response [106–110]. The majority of cases are self-­ limiting, but some can progress to tamponade, or over a period of months or years to constrictive pericarditis. This can also be seen post cardiac repair. The diagnosis may be suspected clinically. The features described by Dressler include low grade fever and pleuropericardial pain [111]. A pericardial friction rub may become detectable but disappears if the effusion becomes large enough to potentially cause tamponade. Nonspecific diffuse ST-segment changes and elevated erythrocyte sedimentation rates are also often noted. Depending on the time course, the chest radiograph may show an enlarged heart shadow, with possibly left lower lobe atelectasis (due to left lower lobe bronchus compression). CT scan may demonstrate fluid around the heart (‘floating heart”) and /or demonstrate pericardial thickening. In the chronic stage, the pericardium may be calcified. Transthoracic echocardiography is the simplest

68  Updates in the Management of Complex Cardiac Injuries

modality to assess tamponade physiology but can also demonstrate pericardial thickening [27]. Because of its high, if sub-clinical, incidence following repair of cardiac injuries, we have tended to provide prophylaxis with nonsteroidal anti-inflammatories for about a week post-surgery. Once it occurs, nonsteroidal anti-­inflammatories in the early stages are quite effective but steroids may be used if there is evidence of a growing effusion [107, 109]. If the effusion is large enough to raise concern for tamponade, drainage is required. This can be performed by percutaneous or surgical routes. If echocardiography and/or clinical picture suggest secondary infection, then a non-rib spreading anterolateral fourth intercostal approach offers a safe approach for wide debridement with a lower risk of wound infection [112]. In acutely unstable patients, thoracotomy or sternotomy may be lifesaving [108]. Constrictive pericarditis is uncommon but has been reported both in the weeks and years following injury [29, 108]. In the longer-term follow up there may be a higher incidence of calcific pericarditis. In this latter setting, the classic approach of sternotomy, debriding the pericardium carefully starting with decompression of the left side of the heart first to avoid pulmonary edema is utilized. Pericardial lacerations are typically not a diagnostic dilemma as associated injuries prompt exploration. Blunt pericardial rupture can be a challenging diagnosis and is often found incidentally or at post-mortem [27]. The incidence is as low as 1/1000 following significant blunt trauma with an overall mortality rate due to associated injuries as high as 2/3. Left-sided rupture is more common, or at least more commonly diagnosed, and represents roughly 2/3 of reported cases [27, 113, 114]. The risk of pericardial rupture (apart from the potential for associated cardiac and extra-­ cardiac injuries) is herniation of the heart, which can occur in a delayed fashion. The pericardial defect can expand over time and once patients are extubated, positive pressure ventilation that might “keep the heart in situ” is removed. Left-­ sided defects can result in compression of the left anterior descending artery, leading to ischemia, infarction, arrythmia, and/or delayed rupture. Right-sided defects can lead to torsion of the caval-atrial junctions, creating a pseudo-­ tamponade picture [27]. There is a paucity of clinical findings. A friction rub may be heard. CXR, CT and/or ECHO might show pneumopericardium, shift or even herniating through the defect. ECG may demonstrate axis deviation to the affected side, or ST-changes or bundle branch block which might reflect blunt cardiac injury raising the suspicion of injury. Ischemic changes in the anterior descending territory should raise alarm and further investigation. Because the rupture can be occult and present in a delayed fashion if suspected exploration by thoracoscopy or subxiphoid window is reasonable if suspected [115, 116]. If detected sternotomy or thoracotomy

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(depending on the clinical setting) are all reasonable approaches. The rupture may be small enough to permit primary repair but usually is best managed by a biologic patch with care to avoid phrenic nerve injury [27]. One variant is the rupture of the inferior abdominal portion of the diaphragm, which can lead to hollow viscus herniation into the pericardial sac. This is usually repaired by a laparotomy approach due to the ease of exposure and risk of associated intra-abdominal pathology, as with other diaphragmatic injuries.

68.8.9 Follow Up Clinical suspicion must be maintained even if the initial evaluation does not identify the cardiac injury. As noted, cardiac structural injury can present in a delayed fashion. If there is a high degree of suspicion, or symptoms change, early reevaluation with echocardiography can be lifesaving. Intracardiac lesions have been documented at followup in 4–56% of patients who have undergone repair of cardiac laceration/rupture. In patients who have sustained an injury (whether it be a laceration or documented intracardiac structural injury) follow-up echocardiography in the same hospitalization is advisable with follow-up at three months. Patients who have undergone repair of cardiac surgery have up to a 40% incidence of pericarditis, which can be ameliorated with NSAIDs. If the repair has included ligation of a coronary artery, an early echo should be performed to assess myocardial function and risk of late infarct and other complications, including aneurysm formation. If the coronary repair has been performed or repair of a laceration close to the coronary artery, our bias is to closely monitor with serial ECGs, enzymes and echo and if there is suggestion of ongoing ischemia perform coronary angiography. Patients who have been diagnosed with injury (including septal, valve etc.) but in whom the defect was judged to be clinically insignificant do require regular follow-up and need to be cautioned regarding the risk of subacute bacterial endocarditis and other complications.

68.9 Conclusions As we noted at the outset, apart from penetrating cardiac lacerations, the global experience describing the management of operative cardiac injuries is based predominantly on small series and case reports. This review reflects our biases and personal experience. The overriding principles are to have a high level of suspicion, and a low level of indecision, and use the approach the surgeon is most facile with.

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The Ongoing Dilemma of Thoracoabdominal Injuries: Which Cavity and When?

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Juan A. Asensio, John J. Kessler, Parinaz J. Dabestani, and Miguel A. Cubano

Key Points 1. Thoracoabdominal injuries are uncommon even in major Trauma Centers 2. Thoracoabdominal injuries are usually due to penetrating trauma mostly gunshot wounds 3. Thoracoabdominal injuries pose great surgical challenges 4. Thoracoabdominal injuries require efficient decisions for their operative management 5. Trauma Surgeons must possess excellent surgical skills and be able to perform cardiac, thoracic, vascular, and abdominal surgical procedures. 6. Thoracic injuries have very high morbidity and mortality rates.

69.1 Introduction Thoracoabdominal injuries represent some of the most challenging injuries facing Trauma Surgeons [1]. American wartime experience has shown them to be amongst the most critical injuries incurred by battlefield casualties [2–4]. The diagnostic challenge of multiple body cavity injuries, the notorious difficulty of establishing the proper sequence for intervention, their high injury severity, frequent hemodynamic instability, and the inherent dangers of cross-cavity contamination conspire to increase morbidity and mortality for these injuries. The diagnosis of penetrating thoracoabdominal injuries is often predicated on the presence or absence of diaphragmatic penetration, which at times can be difficult to establish preoperatively [5, 6].

69.2 Definition, Perspective, Our Experience J. A. Asensio (*) Division of Trauma Surgery & Surgical Critical Care, Trauma Center & Trauma Program, Department of Surgery, Creighton University School of Medicine, Omaha, NE, USA Department of Translational Science, Creighton University School of Medicine, Omaha, NE, USA Uniformed Services University of the Health Sciences, F. Edward Hébert School of Medicine, Walter Reed National Military Medical Center, Bethesda, MD, USA Creighton University Medical Center, Omaha, NE, USA e-mail: [email protected] J. J. Kessler · P. J. Dabestani Department of Surgery, Creighton University, Medical School, Bethesda, MD, USA e-mail: [email protected]; [email protected] M. A. Cubano Uniformed Services University of the Health Sciences, F. Edward Hébert School of Medicine, Walter Reed National Military Medical Center, Bethesda, MD, USA United States Navy Medical Corp., Navy Medical Center, San Diego, CA, USA

Little has been written regarding those complex and unusual injuries. As a matter of fact, there is a great paucity of papers dealing with these injuries in the literature. Thus, in this chapter, the authors will attempt to define these injuries, present their surgical perspective and based on their vast experience, define their surgical approaches while attempting to review the literature. Errors in diagnosis often occur, as these injuries vex even the most experienced Trauma Surgeons [7]. A particularly difficult scenario presents with the unstable patient whose operative findings on one side of the diaphragm cannot account for the patient's hemodynamic instability or blood losses [8, 9]. Given the clinical challenge and large volume of these injuries, Asensio examined his institutional experience with their management. In this study, he sought to define this patient population clinically, describe the sequence of surgical interventions using combined procedures (i.e., thoracotomy and laparotomy), as well as describe the difficulties and

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pitfalls leading to inappropriate choices of surgical interventions for thoracoabdominal injuries. In this four-year study consisting of 254 patients sustaining penetrating thoracoabdominal injuries, all requiring surgical intervention were identified and studied. In patients sustaining torso injuries, violation of both the thoracic and abdominal cavities was established based on physical ­examination, location of injuries, investigative studies, chest tube output, and operative findings. In this study, data collected included demographics, Revised Trauma Score (RTS), Glasgow Coma Scale (GCS), and Injury Severity Score (ISS). Field data such as the need for intubation and cardiopulmonary resuscitation (CPR) were also recorded. Other data included preoperative investigations such as radiography (chest, abdomen, and pelvic films), echocardiography (ECHO), ultrasonography (USN), and diagnostic peritoneal lavage (DPL). In addition, the number and types of emergency department (ED) thoracotomies (left or right, anterolateral or bilateral) were recorded. Indications for the performance of thoracotomy or laparotomy were recorded. The types and combinations of surgical procedures were also tracked. Patients were grouped according to the sequence of procedures: laparotomy followed by thoracotomy (Lap + Thor) or thoracotomy followed by laparotomy (Thor + Lap). Patients subjected to laparotomy plus chest tube thoracostomy were also identified. Determination of the direction and trajectory of the injury and whether the injury crossed the thoracic or abdominal midline were recorded. Estimated blood loss (EBL), number of reoperations, and associated injuries were also examined. Further analysis of patients undergoing combined procedures was undertaken. Two patient groups were compared. Group I consisted of patients undergoing laparotomy first then thoracotomy (Lap + Thor) versus group II patients undergoing thoracotomy then laparotomy (Thor + Lap). The number of times that either of these procedures had to be interrupted to convert to the other procedure was analyzed. The reasons for these interruptions were also recorded and classified as errors or pitfalls. The outcome was measured by calculating the overall mortality with particular emphasis on the patient population who underwent combined thoracotomy and laparotomy. Over the span of this 4-year study, there were 254 patients that sustained penetrating thoracoabdominal injuries meeting the inclusion criteria. In all patients, there was confirmation of both thoracic and abdominal cavity involvement by investigative studies, operative interventions in one body cavity, or both. There were 233 males (92%) and 21 females (8%). The mean age was 27 years (range 7–69 years). The mechanism of injury was gunshot wounds (GSWs) in 187 patients (73%), shotgun wounds (STWs) in 3 (2%), and stab wounds

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(SWs) in 64 (25%). The mean RTS was 6.04 (range 0–7.84); the mean GCS was 12; and the mean ISS was 27 (range 4–75), indicating a severely injured patient population. Field data revealed the use of CPR in 33 patients (14%), and 26 patients (10%) required field intubation. Investigative studies included radiography (chest, abdomen, and pelvic films), FAST, and DPL when needed. Radiography was the most commonly used investigational procedure and DPL the least used. ED thoracotomy was performed in 51 patients (20%): 34 (67%) left anterolateral, 1 (2%) right anterolateral, and 16 (32%) bilateral anterolateral thoracotomies. Only three patients (6%) survived. All patients underwent immediate surgical intervention: 103 (41%) thoracotomy, 224 (88%) laparotomy, and 73 (29%) both. The most common indications for thoracotomy and laparotomy were resuscitation (56%) and the presence of peritoneal signs (46%). Information was available to establish the direction and trajectory of the injury for 156 (62%) of the patients. Mortality rates were consistently higher for these patients. There were multiple combinations of surgical procedures and interventions in this severely injured patient population. A total of 327 major surgical interventions (thoracotomy, laparotomy, thoracotomy + laparotomy) were performed, representing a mean of 1.3 surgical interventions per patient. Of the 103 thoracotomies, 23 (22%) revealed no thoracic pathology, including 9 of the 51 ED thoracotomies, which were considered resuscitative. Thus, resuscitation was the most frequent reason for a negative thoracotomy. If both ED and operating room (OR) resuscitative thoracotomies are excluded, negative thoracotomies decrease to 13%. Other important reasons were a misleading chest tube output and suspected cardiac tamponade. Altogether, 26 (11%) of the 224 laparotomies were also negative. The mechanism of injury (i.e., missiles or stab wounds suspected of, but not causing, intraabdominal injury) was the most important reason for performing a negative laparotomy. The mean estimated blood loss was 3004 ml (range 100–30,000 ml). Altogether, 38 patients (15%) required reoperation: 22 (58%) laparotomy, 10 (26%) other surgical interventions; 5 (13%) laparotomy and thoracotomy combined; 1 (3%) thoracotomy. Six of the reoperated patients died. There were seven missed injuries (3%), including one diaphragmatic and splenic injury and five mesenteric arterial injuries. The mortality rate among those with missed injuries was 57%. There were 462 injuries, including 179 (39%) solid organs, 116 (25%) hollow viscera, 61 (13%) pulmonary, 34 (7%) abdominal vascular, 32 (7%) cardiac, and 22 (4.8%) thoracic vascular, representing a mean of 1.8 associated injuries per patient. Altogether, 175 of 254 patients survived, yielding a 69% survival rate. Analysis of those undergoing combined procedures (laparotomy + thoracotomy) revealed a total of 73 (29%) patients, which included 70 males (96%)

69 The Ongoing Dilemma of Thoracoabdominal Injuries: Which Cavity and When?

and 3 females (4%). The mean age for this patient population was 27 years (range 14–50 years). There were 59 patients (81%) who sustained GSWs, 1 (1%) sustained an STW, and 13 (18%) sustained SWs. The mean RTS was 5.02 (range 0–7.84), the mean GCS was 10, and the mean ISS was 34 (range 9–75), revealing greater physiologic compromise and degree of anatomic injury for this subset of patients. In this group of patients, ED thoracotomy as a resuscitative procedure was performed in 21 (29%); 3 (14%) survived. All 73 patients underwent immediate surgical intervention. Altogether, 53 (73%) underwent laparotomy and thoracotomy, 17 (23%) laparotomy and median sternotomy, and 3 (4%) laparotomy, thoracotomy, and median sternotomy. The mean estimated blood loss was 6827 ml (range 500–30,000 ml). Twelve patients (16%) underwent reoperation: seven (58%) had a laparotomy, three (25%) had laparotomy and thoracotomy combined, and two (17%) had other surgical interventions. Two of the reoperated patients died. There was a total of three missed injuries (4%). All of those missed were mesenteric arterial injuries. The mortality rate among those with missed injuries was 67%. There were 196 associated injuries, representing a mean of 2.7 injuries per patient. A total of 30 of 73 patients survived, for a 41% survival rate. Among the patients who underwent combined procedures, 32 of 73 (44%) had inappropriate surgical sequencing defined by the number of times either of these procedures had to be interrupted to convert to another procedure as the patients deteriorated. In group I (Lap + Thor) the initial procedure (i.e., laparotomy) was interrupted in 18 of 34 patients (53%). In group II (Thor + Lap) the initial procedure (i.e., thoracotomy) was interrupted in 14 of 39 patients (36%). The most frequent pitfalls leading to inappropriate surgical sequencing were persistent, unexplained hypotension in 13 patients (18%) unaccounted for by surgical findings in the initial cavity accessed and misleading chest tube output (i.e., high output from abdominal injuries through diaphragmatic lacerations) in eight patients (10%).

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risk to the patient if the wrong body cavity is accessed first. Trauma surgeons dealing with these injuries should have appropriate instruments and be familiar with certain maneuvers (see Figs. 69.1, 69.2, 69.3, 69.4, 69.5, and 69.6). As well as be able to repair cardiac, pulmonary and intrathoracic vascular injuries (see Figs. 69.7, 69.8, 69.9, 69.10, 69.11, 69.12, 69.13, 69.14, 69.15, 69.16, 69.17, and 69.18). The high mortality incurred by these injuries is corroborated by both military and civilian reports, although there is a paucity of data in the literature dealing with these injuries, Brewer [2] reported World War II data on 983 thoracoabdominal injuries with a 27% mortality rate. Artz [3] reported a Korean conflict experience of 129 patients with a 13% mortality rate. In the civilian arena, both Borja and Ransdell reported 20% mortality among 44 patients who sustained thoracoabdominal injuries [11]. Similarly, Hirshberg [1] reported a 41% mortality rate for 82 patients who required combined laparotomy and thoracotomy. The incidence of thoracoab-

Fig. 69.1 Left anterolateral thoracotomy for gunshot wound in the left ventricle. Patient sustained a left thoracoabdominal gunshot wound, also required laparotomy distal pancreatectomy and splenectomy

The Dilemma: Which Cavity and When. The Rational for Surgical Approaches

Penetrating thoracoabdominal injuries pose a significant challenge to Trauma Surgeons. Involvement of the two largest cavities of the body confronts the Trauma Surgeon with a critical dilemma: Which body cavity should be accessed first, and when? This dilemma is compounded by the critical nature of these patients and the inherent hemodynamic instability that often accompanies these injuries. Establishing whether an injury trajectory has traversed the diaphragm to involve an adjacent cavity is often confusing and imposes a

Fig. 69.2 Left ventricular cardiorrhaphy requiring Teflon pledgets in the previous patient

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Fig. 69.3  Resuscitative thoracotomy on a patient that succumbed. Notice the left hemi thoracic cavity which can harbor a patient entire blood volume. Thoracic aorta is dissected. Esophagus is above

Fig. 69.4  Resuscitative thoracotomy on a patient that succumbed. Descending thoracic aorta has been clamped with Crafoord-Debakey Aortic Cross Clamp

Fig. 69.5  Ominous findings are strongly predictive of mortality

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Fig. 69.6  Cross clamping pulmonary hilum with Crafoord-Dabakey Aortic Cross Clamp

dominal injury varies depending on the patient population and the mechanism of the injury [6, 10]. It has been stated that gunshot wounds to the thorax involve the abdominal cavity approximately 30% to 40% of the time [7]. Despite the critical nature of these injuries, few data have been reported in the literature describing their management. In a series reported by Borja and Ransdell [11] Moore [12], Oparah and Mandal [13], and Hirshberg [14] there were 20 patients who underwent combined thoracotomy and laparotomy. Asensio’s study report represents a large experience with these injuries managed in a busy urban Trauma Center. This group represents a critically injured patient population who required immediate surgical intervention. The critical nature of these patients is evident by the frequent use of EDT as a resuscitative measure. Their low RTS and high ISS, the large number of surgical procedures and combinations necessary to care for these patients, elevated blood loss, and mortality rate certainly attest to the need for life-saving surgical interventions. Most of the initial diagnostic procedures include plain radiography, which is often time-consuming and yields ­suboptimal results. Although these films may be helpful, they generally do not alter indications for surgical intervention Given the advances in the field of ultrasonography, we strongly recommend the use of E-FAST as an initial evaluation tool whose use may be the first step in decreasing the number of negative explorations. The pattern of injury most frequently observed in this group of patients is in a downward direction, from the thorax to abdomen. Regardless of the direction of the missile, transdiaphragmatic injury increases the chances for cross-cavity contamination, as it permits passage of gastrointestinal contents into the affected hemi thoracic cavity, increasing the risk for empyema. The crossing of midline structures by injury patterns occurs fre-

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Fig. 69.7  Thoracic Surgical Instruments, Dr. Asensio’s tray

Fig. 69.8  Shumacker’s Maneuver for repair of lateral right atrial and ventricular injuries

Fig. 69.9  Stapled pulmonary tractotomy as described by Dr. Asensio [18–22]

quently, increasing the scope and duration of surgical exploration, which also has significant implications. The patient shown in the following figures depicts the complex surgical approaches required to manage these patients (see Figs. 69.19, 69.20, 69.21, 69.22, 69.23, 69.24, 69.25, 69.26, 69.27, 69.28, 69.29, 69.30, 69.31, and 69.32). As exploration is broadened, for instance, the opening of another body cavity drastically increases the chances for the development of hypothermia, acidosis, and coagulopathy increase; similarly, so do the chances for missed and iatrogenic injuries. The two most critical decisions that must be made during the management of these injuries are which

body cavity must be accessed first and the timing. These decisions are difficult and often wrong. In Asensio’s series, the most frequent indications for thoracotomy were resuscitation and elevated chest tube outputs, producing an overall rate of 22% negative thoracotomies. If resuscitative thoracotomies are excluded, the negative thoracotomy rate is still significant: 13%. An 11% negative ­laparotomy rate is also significant. This relatively high frequency of negative explorations is similar to those reported by Hirshberg [1]. Whom reported 11% and 22% rates for negative thoracotomy and laparotomy, respectively. These figures point to the difficulties during surgical decision-­

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Fig. 69.10  Pulmonary parenchyma is open to identify lacerated blood vessels and bronchi for selective deep blood vessel ligation [18–22]

Fig. 69.11  Argon beam coagulator is utilized as an adjunct to stapled pulmonary tractotomy to control diffuse pulmonary parenchymal bleeding. Both techniques were described by Dr. Asensio [18–22]

Fig. 69.12  Pneumonectomy for central hilar gunshot wound

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Fig. 69.13  Dissection of the extra pleural left pulmonary artery

Fig. 69.14  Left main pulmonary artery

Fig. 69.15  Saphenous vein non-reversed interposition graft between the proximal left carotid artery approximately 3 cm from its origin and the distal left common carotid artery in a patient that sustained thoracoabdominal injuries

69  The Ongoing Dilemma of Thoracoabdominal Injuries: Which Cavity and When?

Fig. 69.16  Tangential gunshot wound. Left subclavian artery Patient arrived in cardiopulmonary arrest. Required resuscitative thoracotomy. Transported to the OR for median sternotomy and left subclavicular incision. The patient also sustained abdominal injuries

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Fig. 69.18  Temporary intraluminal shunt in the left carotid artery after shotgun wounds to left zone II of neck and abdomen

Fig. 69.19  A 25-year-old male who sustained a thoracoabdominal shotgun wound admitted with evisceration and in profound shock Fig. 69.17  The same patient. Left subclavian artery clamped prior to resection and PTFE interposition graft

making. A 15% reoperation rate for unpacking/repacking and for completion of abbreviated surgical procedures (i.e., damage control) is similar to that in Hirshberg's series [1]. In Asensio’s study, the rate of missed injuries was lower (3% vs. 9%); nevertheless, the mortality rate for missed injuries was 57%. Missed injuries are generally the result of failure to explore the correct body cavity initially because of unclear indications or less than thorough explorations due to the critical nature of these patients and the need for damage control [15]. In this series, 73 patients underwent combined surgical procedures. This group of patients incurred more physiologic compromise and injury severity than the main group, as evidenced by their RTS, ISS, and greater mean

EBL (6827 vs. 3004 ml), although they experienced similar rates for reexploration, missed injuries, and mortality from missed injuries as the main group. It is in this group of patients, however, where the potential for surgical error and pitfalls is highest. Given the high potential for surgical errors in diagnosis; Asensio examined this issue by analyzing the number of times the primary surgical procedure had to be interrupted to convert to another as demanded by the patient's acuity. This situation was considered inappropriate surgical sequencing. In this group, 44% of the patients had inappropriate surgical sequencing. In the two subgroups of patients analyzed, group I (Lap + Thor) had a 53% rate of interruption of the primary procedure, and group II (Thor + Lap) had a 36% rate of interruption. The most frequent causes of inappropriate sequencing were persistent unexplained hypotension unaccounted for by the surgical

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Fig. 69.20  CXR showing a tension hemothorax and multiple shotgun pellets in previous patient

Fig. 69.21  View from abdominal revealing an extensive left hemidiaphragmatic injury in previous patient

Fig. 69.22  Hemorrhage from left lower lobe temporarily controlled with Duval lung clamps in previous patient

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Fig. 69.23  Large gastric injury with significant intragastric hemorrhage requiring partial gastric resection in previous patient

Fig. 69.24  Complex injury body and tail of pancreas in previous patient

Fig. 69.25  Distal pancreatectomy and splenectomy wit TA-55 Stapler in previous patient

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Fig. 69.26  Pancreatic Transection in previous patient

Fig. 69.27  Pointing to man pancreatic duct which has also enlarged to prevent a pancreatic fistula in previous patient

findings in the initial cavity accessed and misleading chest tube output, both of which were considered indications that the wrong body cavity had been initially accessed. Other important pitfalls included the need to access another body cavity for exposure or mobilization of the liver, as well as injuries missed during the early evaluation that later manifested during the intraoperative course. The pattern leading to inappropriate surgical sequencing usually begins during the initial assessment and resuscitation of these patients. Trauma Surgeons must be aware that abdominal examination can be unreliable in the presence of thoracic injury [14, 16]. Likewise, chest tube output can be highly unreliable for reasons such as the incomplete evacuation of the thoracic

Fig. 69.28  Massive Intraparenchymal hemorrhage left lower lobe in previous patient

Fig. 69.29  Required left lower lobectomy in previous patient

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Fig. 69.30  Complex diaphragmatic repair requiring diaphragmatic transposition to a higher level in the thoracic cavity in previous patient

Fig. 69.32  Healed thoracoabdominal incisions Fig. 69.31  Patient with Professor Asensio

cavity, clotted hemothorax, and a high output that may originate from abdominal bleeding in the presence of an associated diaphragmatic laceration that may initially go undetected. Similarly, caution must be taken when interpreting the initial set of films obtained during the resuscitation period. Often, they are unreliable and misleading. Intraoperatively, the Surgeon must be prepared for all contingencies. The patient must be prepared from neck to midthigh in the event that another body cavity must be accessed. Chest tube output must be tracked intraoperatively as well as peak airway pressures. This demands close communication with both anesthesia and nursing personnel. Intraoperatively, the Trauma Surgeon must attempt to follow injury trajectories and examine the diaphragm and pericardium for bulging or penetration. Transabdominal pericardial window, intra-operative diagnostic peritoneal lavage, reinsertion of a new chest tube, and even intraoperative chest or abdominal films are valuable tools for diagnosing an injury in an adjacent body cavity. They should be employed selectively. The wide use of these procedures or

combinations of these procedures may avoid opening another body cavity. Opening another body cavity to exclude injury (i.e., "quick" thoracotomy or laparotomy) should not be practiced indiscriminately nor routinely. The physiologic implications can be devastating and may promote hypothermia and its sequelae, increase the operating time in severely compromised patients, and place the patient at risk for iatrogenic injuries. When a thoracic cavity injury cannot be definitively excluded by employing the previously outlined procedures and strategies, thoracotomy should be undertaken. We advocate the preservation of the thoracoabdominal barrier [11] to prevent thoracic contamination and preserve diaphragmatic function. We prefer an anterolateral thoracotomy rather than a diaphragmatic incision, which is often inadequate for full exploration. In cases where damage control has been necessary, the Trauma Surgeon must entertain the possibility of missed injuries and be ready to intervene rapidly as indications develop [15, 17]. Return trips to the Operating Room impose further risk for the patient. Asensio’s study points to the difficulties in dealing with penetrating thoracoabdominal injuries. It

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defines this severely injured patient population along with the pitfalls and potential areas of inappropriate management. Clearly, a 31% mortality that increases to 59% in patients undergoing combined procedures should alert Trauma Surgeons to the complexity and the need for flexibility and surgical creativity demanded for the management of these injuries.

69.4 Conclusions Thoracoabdominal injuries are synonymous with high injury severity. They pose great challenges as accessing the wrong body cavity for hemorrhage control may lead to further physiologic compromise of these severely injured patients who often present with acidosis, hypothermia and coagulopathy. These injuries incur both high morbidity and mortality rates. Similarly, not many Trauma Surgeons or Trauma Centers have developed significant experiences with their management. As evident by the paucity of series in the literature.DisclosureAll authors declare no conflict of interest.

References 1. Hirshberg A, Wall MJ Jr, Allen MK, Mattox K. Double jeopardy: thoracoabdominal injuries requiring surgical intervention in both chest and abdomen. J Trauma. 1995;39:225. 2. Brewer, L.A., III.  Thoracoabdominal wounds. In: Ahnfeldt, A.L., editor. Thoracic surgery, vol II: Surgery in world war II. Washington, D.C.: Office of the Surgeon General, Department of the Army; 1965, pp, 101–104. 3. Artz CP, Brownwell AW, Sako Y.  Experience in the management of abdominal and thoracoabdominal injuries in Korea. Am J Surg. 1955;89:773. 4. McNamara JJ, Messermith JK, Dunn RA. Thoracic injuries in combat casualties in Vietnam. Ann Thorac Surg. 1970;10:389. 5. Merlotti GJ, Dillon BC, Lange DA, Robin AP, Barrett JA. Peritoneal lavage in penetrating thoracoabdominal trauma. J.  Trauma. 1988;28:17. 6. Asensio, J.A., Demetriades, D., Rodriguez, A. Injuries to the diaphragm. In: Feliciano DV, Moore EE, Mattox KL, editors. Trauma, 3rd ed. Norwalk, CT: Appleton & Lange, 1995; pp. 461-485.

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7. Murray JA, Berne J, Asensio JA.  Penetrating thoracoabdominal trauma. Emerg Med Clin North Am. 1998;16:107. 8. Ferrada R, Garcia A.  Penetrating torso trauma. Adv Trauma Crit Care. 1993;8:85. 9. Mattox KL. Indications for thoracotomy: deciding to operate. Surg Clin North Am. 1989;69:47. 10. Murray JA, Demetriades D, Asensio JA Penetrating left thoracoabdominal trauma: the incidence and clinical presentation of diaphragmatic injuries. J Trauma 1996;41:509. 11. Borja AR, Ransdell H.  Treatment of thoracoabdominal gunshot wounds in civilian practice: experience with forty-four cases. Am J Surg. 1971;121:580. 12. Moore JB, Moore EE, Thompson JS.  Abdominal injuries associated with penetrating trauma in the lower chest. Am J Surg. 1980;140:724. 13. Oparah SS, Mandal AK. Penetrating gunshot wounds of the chest in civilian practice: experience with 250 consecutive cases. Br J Surg. 1978;65:45. 14. Hirshberg A, Thomson SR, Blade PG, Huizinga WKJ.  Pitfalls in the management of penetrating chest injuries. Am J Surg. 1989;157:372. 15. Rotondo MF, Schwab CW, Mc Gonigal MD, Phillips GR, Fruchterman TM, Kauder DR, Latenser B, Angood PA. “Damage control”: an approach for improved survival in exsanguinating penetrating abdominal injury. J. Trauma 1993;35:375. 16. Aronoff RJ, Reynolds J, Thai ER.  Evaluation of diaphragmatic injuries. Am J Surg. 1982;144:671. 17. Burch JM, Ortiz VB, Richardson RJ, Martin RR, Mattox KL, Jordan GL.  Abbreviated laparotomy and planned reoperation for critical injured patients. Ann Surg. 1992;215:476. 18. Asensio JA, Demetriades D, Berne JD, Velmahos G, Cornwell EE, Murray J, Gomez H, Falabella A, Chahwan S, Shoemaker W, Berne TV.  Stapled pulmonary tractotomy: a rapid way to control hemorrhage in penetrating pulmonary injuries. J Am College Surg. 1997;5:486–7. 19. Asensio JA, Mazzini FN, Gonzalo R, Iglesias E, Vu T. The Argon Beam coagulator. an effective adjunct to stapled pulmonary tractotomy to control hemorrhage in penetrating pulmonary injuries. J Am College Surg. 2012;214(3):e1–4. 20. Asensio JA, Ogun OA, Mazzini F, Perez-Alonso AJ, Garcia-Nunez LM, Petrone P.  Predictors of outcomes in 101 patients requiring emergent thoracotomy for penetrating pulmonary injuries. Eur J Trauma Emerg Surg. 2018;44:55–61. 21. Petrone P, Asensio JA.  Surgical management of penetrating pulmonary injuries. Scand J Trauma Resuscit Emerg Med. 2009; 17:1–8. 22. Velmahos GC, Baker C, Demetriades D, Goodman J, Murray JA, Asensio JA.  Lung-sparing surgery after penetrating trauma using tractotomy, partial lobectomy, and pneumonorrhaphy. Arch Surg. 1999;134(2):186–9.

Subclavian Vessel Injuries: An Anatomic and Surgical Challenge to the Surgeon

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Key Points 1. Subclavian vessel injuries are uncommon even in major Trauma Centers. 2. Subclavian vessel injuries are generally caused by penetrating trauma mostly gunshot wounds. 3. Subclavian vessel injuries pose great surgical challenges to Trauma Surgeons. 4. Subclavian vessel injuries require rapid and decisive decisions for their operative management given their life-­ threatening nature. 5. Trauma Surgeons must possess excellent surgical skills and be able to perform cardiac, thoracic, and vascular surgical procedures given the number of associated injuries. 6. Subclavian vessel injuries have very high morbidity and mortality rates.

70.1 Introduction Thoracic and thoracic-related vascular injuries represent complex challenges even for very experienced Trauma Surgeons. Subclavian vessel injuries, in particular, are uncommon and highly lethal. Regardless of the mechanism of injury either penetrating or blunt, such injuries can result in significant morbidity and high mortality. Subclavian vessel injuries are also generally associated with other multiple life-threatening injuries. Over the years, the overall mortality rate has somewhat continued to improve as a result of significant advancements in resuscitation, emergency medical transport systems, and increased development of regionalized systems of Trauma Care [1–3].

70.2 Historical Perspective and Incidence

J. A. Asensio (*) Division of Trauma Surgery & Surgical Critical Care, Trauma Center & Trauma Program, Department of Surgery, Creighton University School of Medicine, Omaha, NE, USA Department of Translational Science, Creighton University School of Medicine, Omaha, NE, USA Uniformed Services University of the Health Sciences, F. Edward Hébert School of Medicine, Walter Reed National Military Medical Center, Bethesda, MD, USA Creighton University Medical Center, Omaha, NE, USA e-mail: [email protected] J. J. Kessler · P. J. Dabestani Department of Surgery, Creighton University, Medical School, Bethesda, MD, USA e-mail: [email protected]; [email protected] M. A. Cubano Uniformed Services University of the Health Sciences, F. Edward Hébert School of Medicine, Walter Reed National Military Medical Center, Bethesda, MD, USA United States Navy Medical Corp., Navy Medical Center, San Diego, CA, USA

The objectives of this chapter are to extensively present the comprehensive management of these complex vascular injuries with special emphasis on their operative management [1–3]. Halsted [4], in 1892 performed the first successful subclavian aneurysmal ligation. Given the infrequent occurrence and low incidence of subclavian vessel injuries, the vast majority of Trauma Surgeons have only minimal experience with their management in both civilian and military arenas of warfare. In the past surgical management consisted of ligation. During World War I, both American and British surgeons estimated the overall rate of subclavian vascular injuries to range from 0.4% to 1.3% [1–3]. In 1919, Makins [5] reported 45 subclavian artery injuries among British casualties during World War I. A landmark study from DeBakey and Simeone [6] in 1946 reported an incidence of less than 1%, accounting for 21 patients with 2471 arterial injuries sustained by American soldiers during World War II. During the Korean Conflict, Hughes’s [7] study of 304 major arterial vessel injuries reported only 3 subclavian arterial injuries. The relatively few cases reported throughout the history of war may be accounted by the exsanguination experienced by

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Table 70.1  Military experience with subclavian vessel injuries Conflict WWI WWII Korea Vietnam Afghanistan

Authors (Year) Makins (1919) DeBakey and Simeone (1946) Hughes (1958) Rich (1970) Sherif (1992)

Total arteries 1191 2471 304 1000 224

these patients on the battlefield prior to arrival for definitive care. Similarly, penetrating subclavian injuries accounted for less than 1% of all vascular injuries reported during the Vietnam conflict. During this conflict, 48 different surgeons treated these injuries; only two encountered this injury more than once, for a total of 68 reported cases. Rich [8], reported a total of 63 subclavian artery injuries in the original report of the Vietnam Vascular Registry describing 1000 vascular injuries during the Vietnam War [8–10]. During the recent conflicts of Iraq and Afghanistan, the overall rate of vascular injuries was reported to be greater than in previously reported conflicts. This increase in rate may be related to improved hemorrhage control, shorter evacuation times, and improved survivability [11]. High-­ velocity injuries from explosives and gunshot wounds accounted for the majority of these injuries. Interestingly, the incidence of vascular injury was higher in Iraq than in Afghanistan, 12.5% versus 9%, respectively. White identified 1570 U.S. troops, in both Iraq and Afghanistan, who presented with war-related vascular injuries. Of these, 12% resulted in vascular injuries of the torso, with subclavian vessel injuries accounting for 2.3%. Over a 24-month period, Clouse [12] identified 301 arterial vascular injuries, of which 3.7% were due to subclavian-axillary vessel injuries. Nevertheless, both the management and treatment strategies have evolved from the various wars and battlefields over the course of time (see Table 70.1).

70.3 Anatomy The subclavian arteries have different origins according to their right and left anatomic locations. On the right, the subclavian artery arises from the innominate artery behind the right sternoclavicular articulation; on the left side, it originates directly from the arch of the aorta. The subclavian artery is divided into three portions. The first portion courses from the origin to the medial border of the scalenus anterior. The second portion lies behind this muscle and the third portion courses from the lateral border of the scalenus anterior up to the lateral border of the first rib [1–58]. The first portion of the right subclavian artery arises behind the upper part of the right sternoclavicular articula-

Subclavian 45 21 3 8 Combined w/axillary

Percentage of total 3.8 0.9 1 0.8 N/A

tion and passes upward and laterally to the medial margin of the scalenus anterior. It ascends a little above the clavicle, the extent to which it does vary in different cases. It is crossed by the internal jugular and vertebral veins, by the vagus nerve and the cardiac branches of the vagus nerve, and by the subclavian loop of the sympathetic trunk, which forms a ring around the vessel. The anterior jugular vein is directed lateralward in front of the artery but is separated from it by the sternohyoid and sternothyroid strap muscles. The first portion of the left subclavian artery arises behind the left common carotid, and at the level of the fourth thoracic vertebra; it ascends in the superior mediastinum to the root of the neck and then arches lateralward to the medial border of the scalenus anterior. Its anatomic relations are as follows: in front, the vagus, cardiac, and phrenic nerves, which lie parallel with it; the left common carotid artery; left internal jugular and vertebral veins; and the commencement of the left innominate vein. It is covered by the sternothyroid, sternohyoid, and sternocleidomastoid muscles. The second portion of the left subclavian artery lies behind the scalenus anterior. It is very short and forms the highest part of the arch described by the vessel [1–58]. On the right side of the neck, the phrenic nerve is separated from the second part of the artery by the scalenus anterior, and on the left side it crosses the first part of the artery close to the medial edge of the muscle. Behind the vessel are the pleura and the scalenus medius; above are the brachial plexus of nerves; below, the pleura. The subclavian vein lies below and in front of the artery, separated from it by the scalenus anterior. The third portion of the left subclavian artery runs downward and lateralward from the lateral margin of the scalenus anterior to the outer border of the first rib, where it becomes the axillary artery. The external jugular vein crosses its medial part and receives the transverse scapular, transverse cervical, and anterior jugular veins, which frequently form a plexus in front of the artery. Behind the veins, the nerve to the subclavius muscle descends in front of the artery. The terminal part of the artery lies behind the clavicle and the subclavius muscle and is crossed by the transverse scapular vessels [1–58]. The subclavian vein is in front of and at a slightly lower level than the artery. Behind, it lies on the lowest trunk of the brachial plexus, which intervenes between it and the scale-

70  Subclavian Vessel Injuries: An Anatomic and Surgical Challenge to the Surgeon

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vertebral art. rt. subclavian vein rt. subclavian art.

ant. scalenus m. transverse art. of neck

vagus nerve left common carotid art. left subclavian art.

post circumflex art. of humerous throacoacromial art.

Fig. 70.1  Anatomy of subclavian vessels

nus medius. Above and to its lateral side are the upper trunks of the brachial plexus and the omohyoid muscle [1–58]. The branches of the subclavian artery are the vertebral, internal mammary, thyrocervical, and costocervical trunks. On the left side, all four branches generally arise from the first portion of the vessel; but on the right side, the costocervical trunk usually originates from the second portion of the vessel. On both sides of the neck, the first three branches arise close together at the medial border of the scalenus anterior; in the majority of cases, a free interval of 1.25–2.5 cm exists between the commencement of the artery and the origin of the nearest branch [1–58] (see Fig. 70.1).

70.4 Incidence Subclavian vessel injuries account for approximately 5% of all vascular injuries [8, 13, 17]. Busy urban trauma centers report admitting between two and four subclavian vascular injuries per year, although some international trauma centers have reported admitting as many as four patients per month

which is rather doubtful [1–3, 13–17]. Subclavian artery injury specifically accounts for 1–2% of all acute vascular injuries [1–3, 13, 18–21] (see Table 70.2). Although a majority of these injuries are penetrating, up to 25% occur secondary to blunt mechanisms of injury. The low incidence of subclavian artery injury is primarily explained by the anatomic location and the protective barrier provided by the clavicle and thoracic cage [1–3, 8]. In a study combining both prospective and retrospective reviews, Demetriades and Asensio [1, 3] reported 79 subclavian vessel injuries. The artery was injured in 59 patients, and the vein in 40 and 20 patients had combined injuries. On the other hand, Lin [22] reported that 24 of 54 patients presenting with subclavian artery injuries also sustained associated venous injuries. The subclavian vessels are relatively well protected by the overlying clavicle and first rib; however, fractures to these and other adjacent osseous structures may lead to serious life-threatening injury [1, 3, 8]. In one of the largest series published, Natali [23] reported a total of 10 patients with clavicle fracture-induced injury. The incidence of clavicular

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Table 70.2  Subclavian artery injury: civilian reports Cities Louisville Memphis Rochester Chicago Houston Baltimore Durban Johannesburg Johannesburg Houston Los Angeles Durban Atlanta Chicago Istanbul Houston

Year 1962 1964 1968 1969 1970 1970 1978 1987 1994 1999 1999 2000 2000 2003 2004 2008

Author Cook Pate and Wilson Matloff and Morton Amato Bricker Brawley Robbs Demetriades Degiannis Cox Demetriades and Asensio McKinley Kalakuntla Lin Aksoy Carrick

Injuries 3 12 3 14 14 11 24 127 56 56 79 260 25 54 12 15

secondary to normal physical examination findings. In other cases, patients experience a delay in symptoms after their initial injury, thereby postponing treatment [1–58].

70.5 Clinical Presentation

Patients sustaining penetrating thoracic inlet injuries presenting with hemodynamically instability should undergo early intubation, judicious fluid resuscitation, and immediate treatment of life-threatening injuries upon presentation [1– 58]. Contralateral upper extremity or lower extremity intravenous access and orotracheal intubation should be carried out in cases in which cervical or mediastinal swelling is present, resulting from expanding hematomas caused by subclavian vessel injury [1–3, 13]. In a retrospective study of subclavian vessel injury, DeGiannis [26] reported that 50% of the patients in their series presented with an initial systolic blood pressure lower fractures and associated subclavian vessel injury is estimated than 100 mmHg. Several published series confirm similar to be less than 1%. Richardson [24] identified first rib frac- hemodynamic findings consistent with hypovolemic shock ture as a useful indicator of severe upper thoracic trauma. In upon presentation [1–3, 27–32]. In Agarwal’s [33] experithis study, 55 patients with first rib fractures were evaluated, ence, the profound shock was present in 80% of those who of which 5.5% sustained associated blunt subclavian artery sustained an injury to both the subclavian artery and vein. injuries. A comparable review by Phillips [25] demonstrated The unstable patient in hypovolemic shock unresponsive to similar findings in the presence of displaced first rib frac- resuscitation should be transported immediately to the opertures, with 9% presenting with associated blunt subclavian ating room [1–58]. artery injuries. Any penetrating injury to the subclavian artery with pulThe majority of subclavian vessel injuries in the civilian satile bleeding should be controlled with infraclavicular population result from penetrating trauma [1–58]. Over the digital pressure[1, 3]. When possible, manual compression past several decades, there has been a steady rise in firearm-­ should be continued until primary vascular control in the related injuries in the United States as a result of increased operating room is achieved [1–3, 26, 35]. In cases of penecivilian use of weaponry. Several published series observed a trating retroclavicular injuries, direct pressure may not be similarly low incidence of blunt versus a relatively high inci- effective, and thus balloon tamponade may be a lifesaving dence of penetrating injury across the globe[1–58]. Graham’s option [26, 35]. [13] largest civilian series reported 93 patients sustaining In a combined retrospective and prospective study, subclavian artery injuries over a 24-year period. Of these, Demetriades reported active bleeding from the wound in only two resulted from a nonpenetrating injury. Over a period 65% of the patients upon initial evaluation, along with findof 10 years, a retrospective review by Lin [22] identified 54 ings of shock in 72%. More than 20% of patients with subpatients with penetrating subclavian artery injuries, of which clavian or axillary vascular injuries reach the hospital with 85% resulted from gunshot wounds. Conversely, McKinley no vital signs or with imminent cardiac arrest as a result of [16] reported that 82% of subclavian artery injuries resulted exsanguinating blood loss. Of note, associated intrathoracic from stab wounds and 10% from low-velocity gunshot injuries are also found in about 28% of these patients. Once wounds, a trend not appreciated in U.S. regional trauma cen- the airway is secured, these patients should undergo immediters (see Table 70.2). ate Emergency Department Resuscitative Thoracotomy On the other hand, blunt subclavian artery injuries occur (EDT) on the side of injury; if necessary, the incision may be far less frequently. Urban trauma centers report approxi- extended to the opposite side [1–3, 13, 36–40]. mately that 1–3% of all traumatic subclavian artery injuries In McKinley's [16] prospective study of 260 patients, result from blunt trauma. The relatively low incidence of approximately 25% of subclavian artery injuries had miniblunt vascular trauma is due to the subclavian vessel’s pro- mal symptoms and delayed complications, prompting tected anatomic location. Both rapid deceleration injury and patients to seek medical advice. In a series reported by Lim bony fractures are responsible for blunt injury of this artery. [15], only 24% of the patients had a pulse deficit. Apparent Not uncommonly, however, the injury remains unrecognized soft tissue ecchymosis and hematoma at the base of the neck

70  Subclavian Vessel Injuries: An Anatomic and Surgical Challenge to the Surgeon

and upper chest can be a diagnostic clue on physical examination. Other characteristic findings of brachial plexus palsy, arm swelling, pulsatile hematomas, or bruit may indicate traumatic arteriovenous fistulas [1–58].

70.6 Diagnosis Early diagnosis of subclavian vessel injury is essential [1–3]. Physical examination findings of subclavian arterial injury may be more subtle than obvious pulsatile bleeding as seen with penetrating wounds [1–58] (see Fig. 70.2). Other associated injuries in anatomic structures adjacent to the subclavian vessels are highly suspicious for the presence of branchial plexus injury. Neurologic deficits of the upper extremity; overlying bruits; decreased or absent pulses in the brachial, radial, or ulnar arteries; and ipsilateral clavicular or rib fracture are diagnostic clues. The clinical diagnosis may be obvious with a comprehensive vascular examination revealing a cool, pulseless, and pale upper extremity. Specific signs of subclavian artery injury may also include expanding or pulsatile hematomas in the supraclavicular space or the axilla, as the hematoma dissects along the neurovascular sheath [1–58]. Brachial plexopathy can also be a reliable predictor of underlying subclavian injury [39]. Radiographic investigations should only be performed in hemodynamically stable patients. In these cases, an initial plain chest radiograph is obtained without delay. Graham [13] reported that 16% of their 93 patients with penetrating subclavian injuries had radiographic evidence of mediastinal widening. Injuries to the proximal portions of the subclavian vessels may present with massive hemothorax and mediastinal widening on the chest radiograph. Other diagnostic investigations include obtaining a simple ankle-brachial index (ABI) in patients who are hemodynamically stable; an

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ABI of less than 0.9 is considered abnormal and believed diagnostic or suspicious for underlying arterial injury. However, normal ABIs may result even in the presence of a subclavian arterial injury secondary to the rich collateral circulation from this vessel [1–58]. Color flow Doppler (CFD) studies are an additional noninvasive technique in assessing subclavian vessel injury. Unfortunately, CFD studies can be suboptimal in those with a large body habitus and are limited in the views of the aortic arch, innominate vessels, and left subclavian artery [1–58]. Readily available spiral computed tomography (CT) scans with intravenous contrast (CTA’s) have become a favorable option in identifying vascular injuries. CT angiography is a potential alternative in selected cases, avoiding conventional angiography in 85% of the cases [41]. The value of emergent angiography is restricted and should be entertained only for hemodynamically stable patients after appropriate resuscitation. Ideally, the surgeon should accompany the patient to the angiography suite [1– 3]. If acute decompensation occurs, the angiogram should be aborted, and the patient rapidly transferred to the operating room. Positive studies without clinical examination findings may warrant surgical exploration of the affected segment, as in cases of intimal dissection, pseudoaneurysm, and contained transection. Many advocates the routine use of angiography with subclavian artery injuries (see Figs.  70.3 and 70.4). Precise surgical planning and the identification of additional arterial injuries support these views [1–58]. In Graham’s [13] series, 20% of associated arterial injuries were identified by angiography. Nevertheless, CFD and CT angiography are now used more frequently than conventional angiography. Angiography, however, remains the “gold standard” and should be reserved for those without any evidence of hemodynamic compromise.

Fig. 70.2  Shotgun blast, right side of thoracic inlet. Patient sustained an open clavicular fracture and right subclavian and artery injuries

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Fig. 70.3  Stab wound left subclavian artery. Patient presented with hematoma. Angiogram showing injury

Fig. 70.4  Gunshot wound left subclavian artery. Angiogram showing narrowing of the left subclavian artery. Repaired with 6 mm PTFE graft

70.7 Surgical Management The operative approach to subclavian vessel injury requires great familiarity with local anatomy. The basic vascular surgical principles of proximal and distal control are imperative. Historically, a variety of classical operative exposures have been described for the management of subclavian artery injuries [1–3]. The surgical approach is dictated by the clinical presentation and site of injury (see Fig. 70.5). The patient is initially placed in a supine position with the ipsilateral arm abducted at 30 degrees and the head turned away from the

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injury. A clavicular incision is planned, with the initial incision in the region of the sternoclavicular junction with an extension over the medial half of the clavicle, and if necessary, continued onto the deltopectoral groove (see Figs. 70.6, 70.7, 70.8 and 70.9). Adjacent muscle attachments are stripped off the clavicle to better facilitate upward retraction. Clavicular resection and disarticulation of the sternoclavicular joint are surgical techniques that offer additional exposure to proximal injuries. Henly subclavian clamps are useful in providing proximal and distal control [1–3]. A median sternotomy with cervical extension also provides optimal control of proximal right subclavian injuries [1–3] (see Figs.  70.10, 70.11, and 70.12). Steenburg and Ravitch described the “trapdoor” incision, which allows for exposure to the first and second parts of the left subclavian artery. The components of this approach include a clavicular incision, limited median sternotomy, and an anterolateral thoracotomy. This exposure was described only for left subclavian injuries, not right, because of the vessel’s posterior location. This is a very morbid incision and has been abandoned. These described surgical approaches are selected individually on a case-by-case basis and according to each surgeon’s overall experience [1–3]. Traditionally, the operative management of subclavian artery injury includes ligation, primary repair, or interposition grafts. The vascular repair chosen is influenced by the degree and level of injury. Ligation should be reserved only for those who are unstable with multiple life-threatening associated injuries, extensive shoulder trauma, or infected or ruptured aneurysms. Anatomically, extensive collateral flow through the thyrocervical trunk permits safe ligation of the subclavian arteries. Arterial reconstruction should, however, be attempted whenever feasible. Rarely, temporary shunting can be used with the intention of arterial repair at a later stage. Appropriate vascular instruments must be employed. The principal author recommends Henly subclavian clamps [1–58] (see Fig. 70.13). Stab wounds sometimes can be managed appropriately with débridement and repair. Simple lateral arteriorrhaphy is the preferred technique in the appropriate setting, but this method is able to be used only 20% of the time. Ligating multiple arterial branches may provide the additional length during primary repair, but considerable mobilization should be performed cautiously, as these branches provide an extensive collateral network to the upper extremity [1–3, 34]. On the other hand, gunshot wounds generally cause significant blast injury and usually require an interposition graft (see Figs. 70.14, 70.15, 70.16, 70.17, 70.18, 70.19, 70.20, 70.21, 70.22, 70.23, 70.24, 70.25, 70.26, 70.27 and 70.28: Multiple patients). The autogenous reverse saphenous vein or prosthetic grafts with end-to-end anastomosis following debridement is one of the conventional methods used with arterial injury, however, it is uncommon to employ these autogenous

70  Subclavian Vessel Injuries: An Anatomic and Surgical Challenge to the Surgeon

a

b

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c

Fig. 70.5  Incisions utilized for subclavian vessel exposure. (a) Supraclavicular incision, (b) median sternotomy combined with supraclavicular incision, (c) Steenburg and Ravitch trap-door incision. No longer used or recommended

pectoralis major muscle Fig. 70.7  Clavicle removal for subclavian vessel exposure. Transected clavicle at sternoclavicular junction. Subclavian vessels exposed

Fig. 70.6 Clavicle removal for subclavian vessel exposure. Periosteal elevator stripping muscular attachments off clavicle

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Fig. 70.8  Clavicle removal for subclavian vessel exposure. Utilizing Doyen costal elevator to free all muscle attachments from the clavicle

clavicle

pectoralis major muscle

manubrium

subclavian vein

Fig. 70.9  Clavicle removal for subclavian vessel exposure. Pectoralis muscle was transected and tagged for reconstruction. Complete exposure

subclavian art.

rt. subclavian rt. jugular artery vein subclavian vein

clavicle

cephalic vein pectoralis minor m. pectoralis major m.

grafts in the reconstruction of subclavian arterial injuries. Prosthetic grafts can be safely used with acceptable outcomes due to their reported low incidence of graft infection (see Figs. 70.14–70.28: Multiple patients). At the same time, prosthetic grafts offer expedient repair compared to the delay associated with autologous vein harvesting. Lateral venorrhaphy in subclavian venous injuries should be attempted if it does not cause significant luminal narrowing [1–3, 13, 14, 34] (see Figs. 70.14–70.28: Multiple patients). If not feasible, then simple ligation is acceptable with little morbidity.

Recent advancements in endovascular techniques have provided another viable option to those who are poor surgical candidates and those who meet strict selection criteria. Minimally invasive approaches to subclavian artery injuries are well documented and are promising alternatives in the management of these injuries. Carefully selected patients, such as those with arterial stenosis, false aneurysms, or arteriovenous fistulas, may be managed with catheter-based stent grafts by endovascular techniques. Definitive catheter-based repair by stent grafts is, unfortunately, not without conse-

70  Subclavian Vessel Injuries: An Anatomic and Surgical Challenge to the Surgeon

left subclavian vein

left carotid art.

left subclavian art.

innominate art.

aorta

Fig. 70.10  Combined median sternotomy and left supraclavicular extension with left clavicle removed. Forceps points to left phrenic nerve. Diagram depicting previous patient

Fig. 70.11  Patient sustaining gunshot wound, left subclavian artery injury (see arrow). Innominate vein retracted. Forceps points to left phrenic nerve

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776 Fig. 70.12  Left subclavian artery repair with PTFE graft. Left vertebral artery (see arrow)

graft

ant. scalenus muscle

left subclavian art.

Fig. 70.13  Henly subclavian clamps (arrows)

70 Subclavian Vessel Injuries: An Anatomic and Surgical Challenge to the Surgeon

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Fig. 70.14 Clavicular incision with clavicle removal to expose subclavian vessels for a gunshot wound Fig. 70.15 Thrombosed right subclavian artery post gunshot wound

Fig. 70.16 Polytetrafluoroethylene (PTFE) 8 mm graft Fig. 70.17 Doppler probe being utilized to ascertain flow and velocity postrepair

Fig. 70.18 Young female that sustained a stab wound to the left thoracic inlet. Arrived in cardiopulmonary arrest. Required left anterolateral thoracotomy and open CPR.  In the OR she required median sternotomy and supraclavicular incision to control a left subclavian arterial injury. Clamps are providing proximal and distal control

Fig. 70.19 Partial transection of the left subclavian artery in the previous patient. Required resection and interposition graft with an autogenous reserved saphenous vein graft

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Fig. 70.20  Gunshot wound: right infraclavicular area

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Fig. 70.21  Segmental resection of the injured right subclavian artery

Fig. 70.23  Gunshot wound: right subclavian artery. Vessel debridement and resection Fig. 70.22  Repaired with an autogenous reserve saphenous vein graft

Fig. 70.24  6 mm polytetrafluoroethylene (PTFE) graft inserted Fig. 70.25  Blunt injury to right subclavian artery (a) at take-off of brachiocephalic trunk (b). (c) Origin of the right common carotid artery

70  Subclavian Vessel Injuries: An Anatomic and Surgical Challenge to the Surgeon

Fig. 70.26  Resected segment of the subclavian artery. Intimal flap is seen

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Fig. 70.27  8  mm polytetrafluorethylene (PFTE) interposition graft from the origin of the right subclavian artery (a). (b) Brachiocephalic trunk

quence. At this time, however, endovascular repair does not appear to be superior to traditional surgical therapy but does remain an alternative option for very carefully selected patients, especially those patients with blunt injuries. Similarly, there are no data available reporting on their long-­ term outcome [1–3, 43, 57] (Table 70.3).

Fig. 70.28  Lacerated left subclavian vein Table 70.3  Results of subclavian artery repair Author Amato Bricker Rich Drapanas Perry Demetriades and Asensio

Year 1969 1970 1970 1970 1971 1998

Injuries 14 14 8 16 23 79

Repairs 13 11 7 0 0 59

Complications from repairs 0 0 1 0 0 0

Amputations 0 0 0 1 0 0

Deaths 0 3 0 4 1 27

J. A. Asensio et al.

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70.8 Morbidity Delays in diagnosis, complicated operative exposures, and associated injuries are all contributing factors influencing the patient’s overall morbidity at the time of admission. Hemodynamic compromise on arrival at the hospital also corresponds to higher morbidity and longer hospitalizations, as demonstrated in Kalakuntla’s 6-year retrospective review in managing subclavian artery injuries. The morbidity and mortality risks with subclavian artery injuries are greatly influenced by the number of associated injuries. In penetrating wounds, the severity of injury correlates to the location and, for cases of gunshot wounds, the velocity of the missile. Neighboring structures, particularly the subclavian vein, brachial plexus, lung, clavicle, and first rib, are most susceptible to injury [1–58]. Generally, the long-term morbidity of subclavian artery injury is closely linked to the presence of associated brachial plexus injuries. Brachial plexus symptoms have resulted in debilitating ipsilateral neurosensory deficits from contusion or crush (direct trauma) and traction injury. In Graham’s series of 65 patients, associated brachial plexus injuries were observed in 35% of the patients. Similar findings of 43% were reported by Johnson. In this series, they identified 83% of partial brachial plexus injury on follow-up, demonstrating some functional improvement, indicating neuropraxia as the initial deficit. Unfortunately, cases of complete brachial plexus transection and secondary nerve repair may only return minimal functional improvement and render the patient with permanent functional disability [1–58]. Known vascular complications such as thrombosis, graft infection, and aneurysm formation are familiar postoperative drawbacks. At the same time, postponement of medical attention following injury with symptoms of arm paralysis may occur from large false aneurysms compressing the brachial plexus. These patients, despite intervention, met with poor outcomes. In cases of venous ligation, Demetriades and Asensio observed transient swelling of the upper extremity but no significant venous-related complication. Elevation of the affected extremity over the course of several days results in considerable improvement. The clavicular division also has the potential for debilitating consequences such as osseous malunion, pseudoarthrosis, and osteomyelitis, however, patients tolerate this quite well [1–58]. Other complications of subclavian vessel injury may include the patient to local surgical wound infections, coagulopathy, massive transfusions, thoracic duct injury, and air embolism. The risk of prosthetic graft infection also exists but remains low with graft long-term patency rates of 94%. Scapulothoracic dissociation, although rare, is without question a devastating injury that results from high-energy trauma. A constellation of injuries includes clavicular frac-

ture or dislocation, avulsed shoulder muscles, and neurovascular damage. In cases of absent brachial plexus function, vascular reconstruction should not be attempted, and the arm should be amputated below the shoulder.

70.9 Outcomes and Mortality Both penetrating trauma and occasionally blunt trauma to the subclavian vessels can result in significant blood loss and hemorrhagic shock prior to presentation. Select patients who have short transport times and hemorrhage control by contained hematoma or thrombosis experience improved hemodynamic status upon arrival and thus have better survival rates. In-hospital mortality rate ranges from 5% to 35% with penetrating injuries, which is higher than in blunt trauma. The reported overall mortality rate ranges from 39% to 80%, with the majority succumbing prior to arrival at the hospital. This unfortunate statistic is directly related to exsanguination or associated Traumatic Brain Injuries (TBIs) in cases of blunt injury. McKinley [16] series confirms these findings and details postmortem evaluation on violent deaths over 4 years, documenting 135 deaths as a result of isolated injury to the subclavian artery and exsanguination [1–58]. The reported operative mortality rate in published civilian series ranges from 4.7% to 30%, with higher mortality rates seen with combined subclavian artery and vein injuries [1, 3]. In a large series of 228 penetrating subclavian vessel ­injuries, 61% of these patients were dead on arrival [19]. In these series, venous injuries experienced a higher mortality rate than arterial injuries, 82% and 60%, respectively [19]. Similar findings were found in another published series consisting of 20 patients in which isolated subclavian vein injuries resulted in a mortality rate of 50%. This high rate may be due to possible venous emboli or ongoing bleeding from venous injury without the vasocontrictive effects of arterial injuries [1–3]. The morbidity and mortality risks with subclavian artery injuries are greatly influenced by the number of associated injuries. Lin [22] reported that patients with three or more associated injuries incurred a mortality rate of 83% versus 17% for those with isolated subclavian artery injuries. At the same time, those presenting with hypotension had a much higher mortality rate of 57% versus 18% for nonhypotensive patients[1–58].

70.10 Conclusions The rarity of traumatic subclavian vessel injuries prevents many Trauma Surgeons or Trauma Centers from developing a significant experience in their management. These injuries

70  Subclavian Vessel Injuries: An Anatomic and Surgical Challenge to the Surgeon

are associated with significant morbidity and mortality rates. Patients who survive transport are subject to potentially debilitating injury and possibly death. Management of these injuries varies, depending on hemodynamic stability, mechanism of injury, and associated injuries. Despite significant advancements in Trauma Care secondary to contemporary wars the mortality rate for subclavian vessel injury remains high [1–58].DisclosureAll authors declare no conflicts of interest.

References 1. Demetriades D, Asensio JA. Subclavian and axillary vascular injuries. Surg Clin North Am. 2001;81(6):1357–73. xiii 2. Demetriades D, Asensio JA, Velmahos G, Thal E. Complex problems in penetrating neck trauma. Surg Clin North Am. 1996;76:665–83. 3. Demetriades D, Chahwan S, Gomez H, Peng R, Velmahos G, Murray J, Asensio J, Bongard F. Penetrating injuries to the subclavian and axillary vessels. J Am Coll Surg. 1999;188:290–5. 4. Halted WS. Ligation of the first portion of the left subclavian artery and excision of a subclavio-axillary aneurysm. John Hopkins Hosp Bull. 1892;24:93. 5. Makins G.  Gunshot injuries to the blood vessels. Bristol: John Wright and Sons; 1919. 6. Debakey ME, Simone FA. Battle injuries of arteries in World War II. An analysis of 2471 cases. Ann Surg. 1946;123:534–79. 7. Hughes CW.  Arterial repair during the Korean War. Ann Surg. 1958;147:555–67. 8. Rich NM, Hobson RW, Jarstfer BS, Geer TM.  Subclavian artery trauma. J Trauma. 1973;13:485–96. 9. Rich NM, Baugh JH, Hughes CW.  Acute arterial injuries in Vietnam: 1000 cases. J Trauma. 1970;10:359–69. 10. Rich NM, Spencer FC.  Subclavian artery injuries. In: Vascular trauma. Philadelphia: W.B. Saunders; 1978. p. 307–329. 11. White JM, Stannard A, Burkhardt G, Eastridge BJ, Blackbourne LH, Rasmussen TE.  The epidemiology of vascular injury in the wars in Iraq and Afghanistan. Ann Surg. 2011;253(6):1184–9. 12. Clouse WD, Rasmussen TE, Peck MA, et  al. In theater management of vascular injury: 2 years of the Balad vascular registry. J Am Coll Surg. 2007;204:625–32. 13. Graham JM, Feliciano DV, Mattox KL, Beall AC Jr, Debakey ME.  Management of subclavian vascular injuries. J Trauma. 1980;20:537–44. 14. George SM, Croce MA, Fabian TC. Cervithoracic arterial injuries: recommendations for diagnosis and management. World J Surg. 1991;15:134–40. 15. Lim L, Saletta J, Flanigan D.  Subclavian and innominate artery trauma. Surgery. 1979;86:890–7. 16. McKinley AG, Carrim AT, Robbs JV. Management of proximal axillary and subclavian artery injuries. Br J Surg. 2000;87(1):79–85. 17. McCready RA, Proctor CD, Hyde GL. Subclavian–axillary vascular trauma. J Vasc Surg. 1986;3:24–31. 18. Wall MJ, Granchi T, Liscum K, Mattox KL. Penetrating thoracic vascular injuries. Surg Clin North Am. 1996;76:749–61. 19. Demetriades D, Rabinoritz B, Pezikis A, Franklin J, Palexas G. Subclavian vascular injuries. Br J Surg. 1987;74:1001–3. 20. Fletcher JP, Little JM. Injuries of branches of the aortic arch. Aust NZ J Surg. 1988;58:217–9. 21. Pate JW, Cole FH, Walker WA, Fabian TC. Penetrating injuries of the aortic arch and its branches. Ann Thorac Surg. 1993;55:586–92. 22. Lin P, Koffron AJ, et  al. Penetrating injuries of the subclavian artery. Am J Surg. 2003;185:580–4.

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23. Natali J, Maraval M, Kieffer E, Petrovic P.  Fractures of the clavicle and injuries of the subclavian artery. J Cardiovasc Surg. 1975;16:541–7. 24. Richardson JD, McElvein RB, Trinkle JK. First rib fracture: a hallmark of severe trauma. Ann Surg. 1975;181:251–4. 25. Phillips EH, Rogers WF, Gaspar MR.  First rib fractures: incidence of vascular injury and indications for angiography. Surgery. 1981;89:42–7. 26. Gilroy D, Lakhoo M, Charalambides D, Demetriades D. Control of life-threatening, hemorrhage from the neck. A new indication for balloon tamponade. Injury. 1992;23:557–9. 27. Hoff SJ, Reilly MK, Merrill WH, et al. Analysis of blunt and penetrating injury of the innominate and subclavian arteries. Am Surg. 1994;60:151–4. 28. Abouljoud MS, Obeid FN, Horst HM, et al. Arterial injuries of the thoracic outlet: a ten-year experience. Am Surg. 1993;59:590–5. 29. Graham JM, Feliciano DV, Mattox KL.  Combine brachial, axillary and subclavian artery injuries of the same extremity. J Trauma. 1980;20(10):899–901. 30. Cheema M, Kirton O, Lukose B, Gallagher J. Ligation of the subclavian artery after blunt trauma presenting as massive hemothorax. J Trauma. 2008;64:1126–30. 31. Flint LM, Snyder WH, Perry MO, Shires GT.  Management of major vascular injuries of the base of the neck. An 11-year experience with 146 cases. Arch Surg. 1973;106:407–13. 32. Costa MC, Robbs JV. Nonpenetrating subclavian artery trauma. J Vasc Surg. 1988;8:71–5. 33. Agarwal N, Shah P, Clauss RH, Reynolds BM, Steal WM. Experience with 115 civilian venous injuries. J Trauma. 1982;22:827–32. 34. Gray H, Pick T, Holmes T.  Anatomy, descriptive and surgical. Philadelphia: Henry C. Lea’s Son & Co.; 1883. 35. Demetriades D. Balloon tamponade for bleeding control from penetrating liver injuries. J Trauma. 1998;44:538–9. 36. Katras T, Baltazar U, Rush DS, Davis D, Bell TD, Browder IW, Compton RP, Stanton PE. Subclavian arterial injury associated with blunt trauma. Vasc Surg. 2001;35(1):43–50. 37. Hawthorn IE, Rochester J, Beard JD. Treatment of combined brachial plexus and subclavian artery trauma. Injury. 1993;24(6):377–9. 38. Kalakuntla V, Patel V, Tagoe A, Weaver W.  Six-year experience with management of subclavian artery injuries. Am Surg. 2000;66(10):927–30. 39. Johnson SF, Johnson SB, Strodel WE, et al. Brachial plexus injury: association with subclavian and axillary vascular trauma. J Trauma. 1991;31:1546–50. 40. Buscaglia LC, Walsh JC, Wilson JD, Maolo NM. Surgical management of subclavian artery injury. Am J Surg. 1987;54(1):88–92. 41. Dutort DF, Strauss DC, Blaszczyk M, et al. Endovascular treatment of penetrating thoracic outlet arterial injuries. Eur J Vasc Endovasc Surg. 2000;19:489–95. 42. Shah DM, Leather RP, Corson JD. PTFE grafts in the rapid reconstruction of acute contaminated peripheral vascular injuries. Am J Surg. 1984;148:229–33. 43. Feliciano DV, Mattox KL, Graham JM. Five-year experience with PTFE grafts in vascular wounds. J Trauma. 1985;25:71–82. 44. Johnson SF, Johnson SB, Strodel WE, Barker DE, Kearney PA.  Brachial plexus injury: association with subclavian and axillary vascular trauma. J Trauma. 1991;31(11):1546–50. 45. Robbs JV, Carrim AA, Kadwa AM, Mars M. Traumatic arterovenous fistula: experience with 202 patients. Br J Surg. 1994;81:1296–9. 46. Old W, Oswaks R. Clavicular excision in management of vascular trauma. Am Surg. 1984;50:286–9. 47. Degiannis E, Velmahos G, Krawczykowski D, Levy RD, Souter I, Saadia R. Penetrating injuries of the subclavian vessels. Br J Surg. 1994;81:524–6. 48. Lee L, Miller TT, Schultz E, et al. Scapulothoracic dissociation. Am J Orthop. 1998;27:699–702.

782 49. Demetriades D, Rabinoritz B, Pezikis A, et al. Subclavian vascular injuries. Br J Surg. 1987;74:1001–3. 50. Schaff HV, Brawley RK. Operative management of penetrating vascular injuries of the thoracic outlet. Surgery. 1977;82:182–91. 51. Degiannis E, Lery R, Potoka T, Saadia R. Penetrating injuries of the axillary artery. Aust NZ J Surg. 1995;65:327–30. 52. Patel AV, Marin ML, Veith FJ, et  al. Endovascular graft repair of penetrating subclavian artery injuries. J Endovasc Surg. 1996;3:382–8. 53. Giardo E, Marston LA, Ligush J, et  al. Endovascular repair of peripheral aneurysms, pseudoaneurysms, and fistulas. Ann Vasc Surg. 1997;11:256–63.

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Management of Complex Laryngotracheal Injuries: A Challenging Surgical Emergency

71

Raja Kalaiarasi, Kushwaha Akshat, and Ramasamy Karthikeyan

Key Points 1. Laryngotracheal injuries are uncommon and can be missed in a polytrauma patient. 2. Patients can suddenly deteriorate, so meticulous clinical examination and investigations are warranted with close observation. 3. Voice change, hemoptysis, stridor, and surgical emphysema are red flag signs to alert an airway injury. 4. Quickly decide on securing the airway of the patient either with endotracheal intubation or tracheostomy/cricothyroidotomy and definitive treatment must be provided within 48–72 h. 5. A successful outcome depends on early recognition of injury, accurate evaluation, and timely appropriate treatment. 6. Always look for other associated injuries like esophageal, spine, pleural injuries, etc, and should be managed by a multidisciplinary trauma team. 7. Minor laryngotracheal injury (Grade I and Grade II) can be managed conservatively, which includes headend elevation, voice rest, use of cool humidified air, antireflux medications, and steroids to reduce edema. 8. Major laryngotracheal injury warrants surgical intervention and the extent of the injury and timing of surgical intervention correlate with the long-term outcome. 9. Long-term complications of laryngotracheal trauma include dysphonia, granulation tissue formation at the mucosal injury or repaired site, cicatricial stenosis, and vocal cord paralysis. 10. Successful management in laryngotracheal injury is without tracheostomy in long term with no/minimal dysphonia. R. Kalaiarasi (*) · K. Akshat Department of Otorhinolaryngology, Jawaharlal Institute of Postgraduate Medical Education & Research (JIPMER), Pondicherry, India R. Karthikeyan Department of ENT, Jawaharlal Institute of Postgraduate Medical Education & Research (JIPMER), Karaikal, India

71.1 Introduction Laryngotracheal injuries are life-threatening emergencies that constitute less than 1% of all trauma but constitute more than 75% of all trauma-related mortality [2]. The incidence of airway injury in polytrauma patients is only 0.5% because of its location which is protected by the mandible superiorly, spine posteriorly, and sternum inferiorly. Laryngeal injury causes severe morbidity or mortality [3]. It is the next most common cause of death after intracranial injury. Phonation is the highest level of evolution because of which humans have the ability to speak but in primates, the major function of the larynx is the protection of the lower airway from aspiration. The functionality of the larynx depends on the proper alignment of the laryngeal framework, muscles, ligaments, and mucosal integrity which is essential for its phonatory and sphincteric actions. Injury to the larynx will cause devastating morbidity of difficulty in breathing, swallowing, and inability to speak. Blunt trauma and penetrating injury are the most common types of injury. The number of Road Traffic accidents (RTA) and cutthroat injuries had been increasing during the current years [3]. Due to changes in urban lifestyle and the use of seat belts, the incidence of blunt trauma neck has reduced and that of penetrating injury neck is on the rise. The early identification and prompt management of challenging complex laryngotracheal injuries are very important for an otolaryngologist.

71.2 Aetiology RTA is the most important cause of laryngotracheal injury, although with the use of safety measures during driving like airbags, seatbelts, and many other safety features in a modern vehicle, the frequency of injury had come down. The most common cause of penetrating injury to the larynx is assault, attempted suicidal cutthroat, strangulation, near hanging, and clothesline-type injuries [4].

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 P. Aseni et al. (eds.), The High-risk Surgical Patient, https://doi.org/10.1007/978-3-031-17273-1_71

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The laryngeal injury usually happens when the head is covered with a helmet and the neck is the only exposed region. Trauma to the larynx is caused when the neck is hyperextended during RTA and the extended neck strike against the steering wheel or windshield. Whiplash type of neck injury or clothesline injury when the exposed part of the neck is impacted by fence wire or branch of a tree or shawl. When the larynx is targeted by a criminal for assault by a direct penetrating neck injury to cause strangulation or decapitation [5]. Iatrogenic injuries are exceedingly rare and may occur during percutaneous tracheostomy, traumatic incompetent intubation, and unskilled rigid bronchoscopy. Modified Schaefer classification system 2013 is used to grade the severity of laryngeal injuries [4, 6, 7]. The following figure shows common laryngotracheobronchial framework injuries (Fig. 71.1). In emergency situations, laryngotracheal injury patients are classified broadly into stable and unstable airway patients. Any unstable airway patient should get their airway secured by either intubation or by surgical interventions like an emergency tracheostomy or cricothyroidotomy. Once the airway is secured additional investigations are done. Stable patients are further assessed via fibreoptic examination and/or imaging [4, 8–10].

Modified Schaefer classification for identifying the severity of laryngeal injuries Grade Severity of airway injury 1 Minor endolaryngeal laceration or hematoma without fracture of laryngeal cartilage 2 More severe edema, hematoma, minor mucosal disruption without exposed cartilage, or non-displaced fracture 3 Massive edema, large mucosal lacerations, exposed cartilage displaced fractures, or vocal cord immobilization 4 Same as grade 3, but more severe disruption of the anterior larynx, unstable fractures, two or more fracture lines, and extensive mucosal injuries 5 Complete laryngotracheal separation

Management Conservative management

Tracheostomy Laryngoscopy & esophagoscopy Exploration Tracheostomy Laryngoscopy & esophagoscopy Exploration & stent

71.3 Pathophysiology

Hyoid fracture Linear fracture

Arytenoid dislocation

Comminuted fracture Cricoid fracture Cricotracheal membrane rupture Cervical 4% + 6.5% Tracheal wall injury Thoracic 12% + 10%

RMB 25%

1

LMB 17%

Complex 8%

LMB 0.5%

RMB 1%

Lobar 16%

Fig. 71.1  Diagram showing common sites of laryngotracheal bronchial injuries in trauma. RMB: right main bronchus, LMB Left main bronchus

71  Management of Complex Laryngotracheal Injuries: A Challenging Surgical Emergency

71.3.1 Blunt Neck Trauma Blunt trauma happens when a significant amount of force is applied to a small area of the neck like in a clothesline, or tree branch. The severity of the injury depends on the velocity of the injury. High-velocity injury may lead to fracture of laryngeal cartilages, hyoid bone, or tracheal cartilage which leads to structural damage to the larynx and trachea. In cases, with severe shearing force, laryngotracheal separation may happen. Low-velocity injury is commonly sustained during sports which can cause submucosal edema, hematoma, or laceration [11–14]. Severe blunt trauma commonly results in complex injuries like cricotracheal separation with cricoid cartilage fracture which puts recurrent laryngeal nerve at risk.

71.3.2 Penetrating Neck Trauma The severity of penetrating laryngeal injury depends on the velocity. High-velocity injuries like ballistic injury may cause devastating structural damages to the larynx and trachea. Low-velocity injury caused by a knife often may present as post-injury edema or hematoma which may again lead to a compromised airway [15–18]. The esophagus and recurrent laryngeal nerve are at more risk in penetrating injury. Penetrating neck injuries are classified based on the anatomic level with zone I from clavicle to cricoid cartilage, zone II from the cricoid cartilage to the angle of the mandible, and zone III from the angle of the mandible to the skull base [19]. Earlier all zone II wounds deep to platysma were explored surgically, but the trend has changed to more conservative management which can give good outcomes in a more selective manner.

71.4 History and Physical Examination Findings History regarding the time of injury and mode of injury is of paramount importance. Any associated injury like cervical spine injury should be ruled out. A high degree of suspicion is required in the case of polytrauma patients as these patients may be unconscious or uncooperative. Symptoms that can be secondary to laryngotracheal injury are voice changes ranging from minimal hoarseness to aphonia, dyspnoea, dysphagia, subcutaneous emphysema neck pain, and hemoptysis. Physical examination findings like skin changes over the anterior neck (ecchymosis), swelling in the neck, flattened thyroid cartilage, deviation of larynx and trachea, neck crepitus, stridor, and reduced breath sounds are looked for, some patients may not exhibit any signs. Stridor may be inspira-

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tory, biphasic, or expiratory. Stridor may not necessarily be associated with voice change. Associated cervical spine injury is to be ruled out. Palpation of the laryngotracheal framework to look for tenderness, breaks, or discontinuity. Subcutaneous emphysema indicates air dissection into the soft tissues, indicating the rupture of a hollow viscus in the neck. In penetrating trauma, through the open wound look for exposed/ fracture cartilage. Voice quality should be assessed in stable patients. External injury may be small and may lead to overseeing severe internal injury. The aim of physical examination in laryngeal injury is to identify those who require immediate airway intervention. After doing the initial examination and establishing a safe airway. Examination with fibreoptic endoscopy and computed tomography is warranted to look at the extent and to decide on the treatment options.

71.5 Evaluation 71.5.1 Flexible Laryngoscopy In blunt laryngeal injury, the initial evaluation is flexible fiberoptic transnasal laryngoscopy to directly assess internal mucosal structures of the larynx and upper aerodigestive tract. It is warranted in all stable laryngotracheal injury patients. Common findings include edema, hematoma, laceration of the mucosa, mucosal tear, congestion, restricted vocal cord mobility or vocal cord palsy, a haematoma on the aryepiglottic fold, and an avulsed epiglottis or anterior commissure. In addition to this cartilage fracture or exposed cartilage can be made out. The spectrum of possible injuries is to be considered when examining the patients [20]. Subglottic examination will be difficult to assess in an emergency. A normal fibreoptic examination may be reassuring but if the mode of injury is worrisome then further investigation might be warranted [3, 4, 21, 22]. Flexible endoscopy findings which need surgical exploration are anterior commissure disruption, major endolaryngeal lacerations with inadequate glottis chink, vocal cord tear, shortened cord or immobile cord, cartilage exposure, displaced cartilage fractures, and arytenoid displacement

71.5.2 Imaging Studies A chest radiograph is an important initial study done to rule out severe subcutaneous emphysema, pneumothorax, or pneumomediastinum. It is important to perform computed tomography (CT), after securing the airway to determine the extent of the injury and preoperative planning. CT scan helps in the identification of the underlying laryngeal or pharyn-

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or esophageal leak is anticipated as it is less irritant to body tissues [3]. If a vascular injury is suspected, then a contrast-­ enhanced CT scan or angiography is recommended for further evaluation.

71.5.3 Esophagoscopy Esophageal injury may be associated with 4-6% of laryngotracheal injuries [27]. So is always important to do a flexible/ rigid esophagoscopy under general anesthesia to rule out injury to the oesophagus. Ryle tube is inserted for all laryngotracheal injury patients this is done to avoid movement of the larynx during swallowing. If an open laryngotracheal repair is being done then the entire length of the oesophagus in the neck is to be inspected and palpated intraoperatively to rule out injury.

71.6 Anaesthesia in Laryngotracheal Trauma Fig. 71.2  Computed Tomography of the neck showing endolaryngeal injury (grade II) with subcutaneous emphysema

geal and vascular injuries. CT of the neck with or without contrast will help in assessing the laryngotracheal framework (cartilage and bone) from the hyoid bone to the trachea, it may also help in finding out even subtle or non-displaced fractures which might require stabilization [23]. Assessment of both soft-tissue and bone windows is necessary as bone windows help to identify hairline fractures on the ossified cartilages while soft-tissue windows are useful in assessing unossified cartilages and mucosal areas (Fig.  71.2) [24]. Indications for CT scans are to assess cricoarytenoid joints, study endolaryngeal tissues, and to evaluate the integrity of cricoid cartilage, hyoid bone, and thyroid cartilage. CT scan is not indicated when there is an open wound with exposed laryngeal cartilage needing definitive surgical intervention. Flexible laryngoscopy coupled with a CT scan is a reliable tool in the evaluation of traumatic larynx that fails to meet the definitive criteria for neck exploration. With its higher sensitivity, this coupled investigation helps in avoiding negative explorations [8, 25]. Magnetic resonance imaging (MRI) is rarely used for airway evaluation in an emergency setting and is reserved for stable adult patients in whom laryngeal fractures are strongly suspected clinically and in children with non-ossified cartilages when CT findings are unclear [24, 26]. Water-soluble contrast swallow studies using gastrografin are reserved for stable patients on conservative management when a pharyngeal or esophageal injury is suspected. It is preferred over barium especially if a pharyngeal

The management of laryngotracheal injury is complex as it varies on a case-to-case basis but the first and most important thing is the stabilization of the airway. Management mainly depends on the factors like mode and type of injury, site of injury, and presence of other associated injuries. For patients with worsening stridor or impending respiratory distress, the airway should be secured with intubation but should have a low threshold to intubate when partial cricotracheal separation is suspected. Mostly a tracheostomy or cricothyroidotomy under local anesthesia might be required during the initial airway stabilization in such situations as intubation might cause a partial cricotracheal separation into complete laryngotracheal separation or creating a false passage [14]. In complete tracheal transection or laryngotracheal separation, the surrounding tissues in the gap between proximal and distal ends form “neotrachea” attempting intubation is dangerous because endotracheal tube may pass into a false track causing complete airway obstruction [28]. False tracking of the endotracheal tube may worsen mediastinal or pleural air leak. Minor mucosal injuries and endolaryngeal hematomas should be observed meticulously. Tracheostomy is done under local anesthesia. In laryngotracheal trauma, tracheostomy is indicated to provide controlled ventilation distal to the damaged airway, for protecting the airway from bleeding, in patients who require prolonged ventilation and to rest the repaired larynx hastening faster healing. Cricoid pressure while attempting intubation can displace a subtle fractured cricoid cartilage. In airway injury, spontaneous ventilation with inhalational agents is preferred as positive pressure ventilation can make partially fractured segments into complete disruption.

71  Management of Complex Laryngotracheal Injuries: A Challenging Surgical Emergency

If airway injury distal to the carina is suspected, then bronchoscopic guided endotracheal intubation to undamaged main bronchus should be attempted to give single lung ventilation [6]. In an open neck wound, an endotracheal tube can be passed through the open wound. The other entity which gives a real challenge to anesthetists is the tracheoesophageal fistula when there is a traumatic tear in the posterior tracheoesophageal party wall. Unless the trachea below the fistula is intubated, there will be an aspiration of gastric contents with massive lung injury. Spontaneous ventilation is preferred for the unsecured airway in a tracheoesophageal fistula. An endotracheal tube or tracheostomy tube should be placed below the fistula under the guidance of fiberoptic scope and it is preferable to have the inflated cuff distal to the fistula to prevent the enlargement of the fistulous opening. Management protocol will be based on modified Schaffer’s grading of traumatic laryngeal injury at the time of presentation. In Schaffer’s grading, partial laryngotracheal separation was not graded separately but included as grade IV for management [10, 29]. Proper communication between the anesthesiologist and surgeon is crucial. While induction, the ENT surgeon should be prepared to do an emergency tracheostomy and rigid bronchoscopy if needed. Pan endoscopy including micro-laryngoscopy, bronchoscopy, and esophagoscopy must be performed to rule out associated injuries.

71.7 Protocol for Different Grades of Injury 71.7.1 Grade I and II Neck laceration alone with no or minimal airway injury will undergo a flexible laryngoscopic assessment. Depending on the severity of injury in the flexible endoscopic assessment, a contrast-enhanced CT scan can be done to rule out any associated injury to great vessels, oesophagus. Conservative management is apt for patients with stable airway and minor injuries which includes administration of humidified air, and headend elevation to improve lymphatic drainage and reduce airway edema. Factors like trauma, infection, and gastroesophageal reflux disease which might cause airway stenosis should be addressed. Broad-spectrum antimicrobials are indicated to treat and prevent infection in the damaged airway mucosa, as late can lead to stenosis [9]. Antireflux medical therapy should be considered to reduce reflux-induced injury to damaged airway mucosa. There is no supporting data on the use of steroids but should be considered to decrease edema. Ryles tube feeds to provide rest to the larynx by avoiding swallowing may be indicated in grade II injury.

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71.7.2 Grade III An emergency tracheostomy will be done to secure the airway. Most of the Grade III patients (71%) required neck exploration with esophagoscopy in addition to emergency tracheostomy. These patients have large endolaryngeal mucosal lacerations and displaced cartilage fractures (Fig.  71.3). During neck exploration and laryngeal repair, wound swab/ tissue bits from exposed laryngeal cartilage framework are to be sent for culture sensitivity. Cartilage pieces without any viable mucosa need to be debrided. Cut ends of the mucosa, membrane and muscles are sutured with 3-0 vicryl. Fractured cartilages are kept in approximating position using 2-0 prolene sutures taken in the perichondrial plane connecting the two cartilages sometimes mini plating with titanium plate and screw might be required [17, 18, 25, 30].

71.7.3 Grade IV Comminuted fractures of laryngeal cartilage or partial cricotracheal separation patients have a compromised airway (Figs. 71.4, 71.5 and 71.6). Emergency tracheostomy should be performed bedside under local anesthesia in the emergency room following which these patients need neck exploration and esophagoscopy under general anesthesia in the operating room (Fig. 71.7). Patients with extensive mucosal injury and anterior larynx damage need debridement to remove non-viable cartilage pieces. Anterior commissure if injured is sutured using 3-0 vicryl by taking a bite from one true cord anterior end to another true cord anterior end and taking a bite in the thyroid cartilage inner or outer perichondrium. The mucosa of the remaining larynx is then sutured using 3-0 vicryl followed by cartilage repair and membrane repair. The laryngeal cartilages are sutured with 3-0 prolene in a perichondrial or extra mucosal cartilaginous plane. Tension release at the suture site is done by taking a bite through the cartilage above and below the suture line with 2-0 Prolene sutures in a perichondrial plane. In patients with partial laryngotracheal separation after primary suturing, the thyroid gland is mobilized and brought in front of the defect. Strap muscles are sutured using 3-0 vicryl. These measures are made in an attempt to aid the healing of the defect. Some of these patients may need laryngeal stents. An intraoperative nasotracheal endotracheal tube is also preferred over other stenting materials, positioned at the level of the suture line. The stent is removed on postoperative day 4 or 5. Hammock sutures using 1-0 silk are taken to maintain the neck in flexion and to release tension in suture lines. Hammock sutures were removed on Postoperative day-6.

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a

b

Fig. 71.3 (a) Computed Tomography (CT) of the neck showing displaced cricoid cartilage; (b) CT neck showing displaced thyroid cartilage (Grade III injury)

a

b

Fig. 71.4 (a, b) Intraoperative image showing shattered anterior larynx (Grade IV) injury

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71.7.4 Grade V

Fig. 71.5  Computed Tomography of the neck showing grade IV injury with damaged anterior larynx with extensive subcutaneous emphysema

a

Complete cricotracheal (laryngotracheal) separation commonly happens with high shearing force injury. The separation happens at the cricothyroid membrane or cricotracheal junction. Most of these patients will have severe respiratory distress and may require emergency tracheostomy. Recurrent laryngeal nerves may be injured temporarily or permanently [2, 31, 32]. But tracheostomy might be difficult in this case because the larynx may get retracted toward the hyoid bone and the trachea gets retracted towards the sternum. In this condition, a tracheostomy has to be done in the lower part of the neck. An associated pneumothorax is common in laryngotracheal separation and should be identified and ­ treated appropriately. After initial airway stabilization patient should be taken under general anesthesia for oesophagoscopy, direct laryngoscopy, and tracheal repair. Suprahyoid and infra hyoid release maneuvers are done to reduce tension on the anastomotic site. Separated end of larynx and trachea are identified and sutured with 3’0 prolene and knots are placed extraluminal. A nasotracheal intubation tube or Montgomery T tube is placed as a stent.

b

Fig. 71.6 (a) Clinical picture of a patient with penetrating neck injury showing partial cricotracheal transection with endotracheal tube insitu. (b) Intraoperative picture showing approximated cricoid and tracheal segment with 2-0 prolene

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Fig. 71.7 (a) Penetrating neck injury with the plane of transection passing through thyrohyoid membrane level opening the supraglottis with tilted thyroid cartilage (white arrow) and open wound showing

oedematous arytenoids (white arrow). (b) Intraoperative picture showing repaired thyrohyoid membrane

Laryngotracheal separation either partial or complete commonly occurs between the cricoid cartilage and the first tracheal ring along the anterior wall of the trachea leaving the posterior wall intact, thus, if the endotracheal tube is introduced following the posterior tracheal wall, intubation of the separated tracheal segment can be achieved. If complete separation occurs, still the surrounding soft tissues will hold the larynx for some time, and still, the airway can be secured by tracheostomy. The level of tracheostomy depends on the level of neck injury which can be detected clinically by palpating the neck in emergency conditions. If the injury is at a higher level airway is secured by cricothyrotomy. Low tracheostomy usually in the third or fourth tracheal ring is preferred when there is fractured thyroid and cricoid cartilage [2, 31, 33]. Correct insertion of the tracheostomy at the third or fourth rings is a must to prevent the late rate complication of tracheobrachiocephalic artery fistula [34–36]. It is advisable to use a soft tracheostomy tube and avoid sharp-­ angled tracheostomy tubes and overinflation of tube cuffs.

transference of massive external trauma forces directly to the mediastinum. This saves the integrity of the chest wall and prevents rib fractures. Thus, rib fractures which are present in 90% of adults with laryngotracheobronchial trauma are much less common in children. The incidence of rib fractures associated with tracheobronchial injury in children is closer to 24% [37]. This concludes the fact that children and young adults may have suffered major intrathoracic injuries even in the absence of rib fractures, thus tracheobronchial injury should be actively looked for in such patients [38]. It is likely that a rapid spike of intrabronchial pressure against the closed glottis, or rapid deceleration of forces can produce airway injuries. Tracheobronchial injuries are more common in lower tracheal regions and the spectrum manifested can range from minor horizontal tears to complete transection of the trachea. The thoracic trachea can undergo tears either anteriorly or posteriorly commonly originating from the carina and running upwards. Anterior tears tend to run through the tracheal cartilages and posterior tears along the membranous walls. These lower tracheal injuries are commonly accompanied by complete or partial shearing of one or both bronchi. Most of the previous literature reviews and case series have reported a predilection towards transverse ruptures more commonly in the right main bronchus. As per Symbas and colleagues in a review of 183 patients with laryngotra-

71.8 Thoracic Trachea and Bronchial Injury Any closed chest injury can lead to injury of the thoracic trachea, carina, or main bronchi. As the cartilaginous chest wall in children and young adults is more pliable, it allows

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71  Management of Complex Laryngotracheal Injuries: A Challenging Surgical Emergency Suspected laryngotracheal injury

Airway status

Stable airway

Impending airway obstruction

Flexible fibreoptic laryngoscopy

• Normal endolarynx • Minimal mucosal injury

ETT/intubation through open wound

Moderate to severe endolaryngeal injury

Direct laryngoscopy/esophagoscopy

• Undisplaced fracture • Normal vocal cord mobility

Awake tracheostomy

CT with/without contrast Repair of laryngotracheal injury

Observation for 24 hours

Surgical intervention

No progression of symptoms

Discharge and follow up

Flowchart 71.1  Algorithm for early treatment of acute external laryngotracheal trauma CT computed tomography, ETT Endotracheal tube intubation

cheal injury, nearly three fourth of the total transections were transverse ruptures most commonly occurring in the right main bronchus (25%) [39]. Other areas involved were the left main bronchus, lobar bronchi, thoracic trachea, and cervical trachea in that order. Most injuries occur within 2.5 cm of the carina. Similarly, Kiser and colleagues, reviewed 265 patients with blunt tracheobronchial trauma, reported similar findings with a greater predilection toward right-sided injuries. They found that around 76% of patients who suffered bronchial rupture had ruptures within 2 cm proximal to the carina and that 43% occurred in the right main bronchus [40]. Recurrent laryngeal nerve injuries are not so common in thoracic tracheal trauma but should always be actively looked for. Although rare, hollow viscus injury is also a possible manifestation of blunt trauma chest. Its early identification and management are equally important as is the management of trauma per se. Most concurrent injuries occur as lacerations of the esophagus which are more longitudinal than transverse. An esophageal injury should be ruled out in every posterior laceration of the trachea.

Since esophageal injury is unlikely to occur in the absence of a penetrating injury, the most common mechanism postulated is sudden forceful compression of the trachea and esophagus against a rigid vertebral column as it occurs when the chest is struck against the steering wheel during road traffic accidents. The injury occurs more often in young patients due to the transmission of force across the pliable structures. Flowchart 71.1 showing the approach to suspected laryngotracheal injury.

71.9 Esophageal Injury Traumatic esophageal perforations are injuries of rare occurrence but are associated with significant morbidity. The primary mechanisms of esophageal injury are penetrating trauma accounting for 70% of the cases followed by blunt trauma [41]. Total mortality is estimated to be around 20–30% mostly due to the associated severe injuries [38]. Furthermore, a delay in identification and management adds to the morbidity and mortality [39].

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Early recognition of esophageal injury helps to avoid catastrophic mediastinitis or mediastinal abscess. An esophageal injury should be suspected when there is a laceration of the posterior tracheal membrane [30, 40]. In severe blunt trauma, forceful compression of the trachea and vertebrae on the esophagus damages the wall. It is more common in young patients with an elastic rib cage. Tracheoesophageal fistula can happen immediately or delayed when the necrosed part sloughs out. General symptoms of esophageal trauma are not organ-­ specific and can include pain or difficulty during swallowing, retrosternal pain radiating to the back, tachycardia, and fever. The clinical examination may reveal subcutaneous emphysema, neck hematoma, and neck tenderness. Thoracic esophageal injuries may be associated with a mediastinal crunch on auscultation known as Hamman’s sign. Associated cervical and thoracic spine injuries should be actively looked for. An initial diagnostic workup should include a plain x-ray chest and abdomen. The presence of air within the soft tissue planes of the neck, pneumomediastinum, or pneumoperitoneum may suggest a ruptured esophagus. Stable patients should be assessed with a water-soluble contrast esophagogram. An esophagoscopy with a contrast esophagogram compliments the diagnosis with 100% specificity. CT scans have limited capacity in diagnosing esophageal tears. Initial management includes keeping the patient nil by mouth and internal drainage by using a nasogastric tube, fluid resuscitation, and broad-spectrum antibiotics. Unstable patients may require an emergent surgical exploration. Esophageal tears requiring surgical repair may be done by an open or an endoscopic approach. The principles involved in surgical repairs are : 1. Rigid or flexible esophagoscopy is performed and the thoracic area for access is identified. 2. Adequate debridement of necrotic tissues. 2. Insertion of chest tubes for drainage of pleural space and mediastinum. 3. Anastomotic repair is always done in two layers. 4. Neighboring tissues are used to strengthen and reinforce the suture line. 5. Lung tissue decortication may be required for expansion. 6. Patient to be kept nil per oral and enteral feeds to be initiated by feeding gastrostomy or jejunostomy. Although primary surgical repair yields good results, the rate of leak is considerably high at around 30%. Around 40% of these patients may require additional procedures for esophageal repair [42]. Under such circumstances, the length of hospital stays increases. Some surgeons now prefer to use

R. Kalaiarasi et al.

nonsurgical procedures including endoscopic repairs [43, 44]. The principles of repair for an endoscopic approach comprise of insertion of covered self-expandable stents, use of clips, and the injection of fibrin glue. Endoscopic repair using the hemoclip device has recently been tried and is considered to be safe and effective. Endoscopic procedures may be advantageous over open procedures as they include pain reduction, speed of hospital discharge, and cost–benefits [45, 46]. Posterior tracheal membranous injury is treated by suturing primarily and reinforcement with pleura or pericardium to promote faster healing and prevent tracheoesophageal fistula [33–35].

71.10 Laryngotracheal Injury with Vascular Injury Vascular injuries associated with laryngotracheal trauma are fairly common mostly including the subclavian vessels External trauma can damage the brachiocephalic artery resulting in a false aneurysm or, rarely causing tracheobrachiocephalic artery fistula. In patients with penetrating neck injuries in zones I and III who are hemodynamically stable and have a secure airway, an angiographic evaluation is indicated to look for any leaking vessels. In case of a vascular injury, angiographic embolization can be attempted [47]. This approach is particularly useful in injuries involving vertebral vessels, which are technically difficult to expose and repair. In zone II injuries, in the absence of clinical findings suggestive of vascular injury, the yield of angiography is low and the decision to perform angiography must be individualized [21]. Emergent surgical exploration is necessary for patients with hard signs of vascular injury such as hemodynamic instability, exsanguinating hemorrhage, or expanding hematoma [48]. The mortality associated with vascular injuries is much higher and thus requires aggressive management.

71.11 Long-Term Complications of Laryngotracheal Trauma Granulation tissue formation at the mucosal injury site (Fig. 71.8), cicatricial restenosis formation, vocal cord paralysis, trachea or laryngocutaneous fistula, esophageal injury, dysphonia, aspiration, prolonged tracheostomy dependence.

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References

Fig. 71.8  Postoperative endoscopic assessment showing granulation tissue in the repaired site (white arrow) Checklist for laryngotracheal injuries documentation based on endoscopic and radiological findings and the need for surgical intervention External laryngotracheal framework

Endolaryngeal mucosal findings

Vocal cord status

Laryngotracheal continuity

Stable  1. No radiological evidence of fracture line  2. Single undisplaced fracture line Unstable  1. Displaced fractures  2. Comunited fractures  3. Cricoid cartilage fracture   4. Tracheal cartilage fracture Normal/minimal injury   1.  No mucosal injuries  2. Small submucosal hematoma within one quadrant  3. Linear mucosal laceration without exposed cartilage Massive injury  1. Significant mucosal loss  2. Exposed cartilage  3. Multiple hematomas/ large hematomas  4. Devitalized mucosa Intact Damaged   1. Anterior commissure avulsion   2. Arytenoid dislocation Intact Any degree of separation

Vocal cord mobility

Mobile Restricted Palsy

Conservative management

Surgical intervention

Conservative management

Surgical intervention

Conservative management Surgical intervention

Conservative management Surgical intervention Conservative management

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794 25. Atkins BZ, Abbate S, Fisher SR, Vaslef SN. Current management of laryngotracheal trauma: case-report and literature review. J Trauma Acute Care Surg. 2004;56(1):185–90. 26. Sofferman RA. Management of laryngotracheal trauma. Am J Surg. 1981;141(4):412–7. 27. Vassiliu P, Baker J, Henderson S, Alo K, Velmahos G, Demetriades D. Aerodigestive injuries of the neck. Am Surg. 2001;67(1):75–9. 28. Baumgartner M, Fritz J, Ayres M.  Bruce, Theuer M.  Charles. Danger of false intubation after traumatic tracheal transection. Ann Thorac Surg 1997;63(1):227–228. 29. Shaker K, Winters R, Jones EB.  Laryngeal injury. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2021 [cited 2021 Jul 7]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK556150/ 30. Symbas PN, Hatcher CR, Boehm GAW. Acute penetrating tracheal trauma. Ann Thorac Surg. 1976;22(5):473–7. 31. Smith DF, Rasmussen S, Peng A, Bagwell C, Johnson C III. Complete traumatic laryngotracheal disruption—a case report and review. Int J Pediatr Otorhinolaryngol. 2009;73(12):1817–20. 32. Deshpande S. Laryngotracheal separation after attempted hanging. Br J Anaesth. 1998;81(4):612–4. 33. Chagnon FP, Mulder DS. Laryngotracheal trauma. Chest Surg Clin North Am. 1996;6(4):733–48. 34. Donaldson L, Raper R.  Successful emergency management of a bleeding tracheoinnominate fistula. BMJ Case Rep. 2019;12(12):e232257. 35. Grewal HS, Dangayach NS, Ahmad U, Ghosh S, Gildea T, Mehta AC. Treatment of tracheobronchial injuries: a contemporary review. Chest. 2019;155(3):595–604. 36. Wright CD. Management of tracheoinnominate artery fistula. Chest Surg Clin N Am. 1996;6(4):865–73. 37. Grant WJ, Meyers RL, Jaffe RL, Johnson DG.  Tracheobronchial injuries after blunt chest trauma in children—hidden pathology. J Pediatr Surg. 1998;33(11):1707–11.

R. Kalaiarasi et al. 38. Asensio JA, Chahwan S, Forno W, MacKersie R, Wall M, Lake J, et  al. Penetrating esophageal injuries: multicenter study of the American Association for the Surgery of Trauma. J Trauma. 2001;50(2):289–96. 39. Patel MS, Malinoski DJ, Zhou L, Neal ML, Hoyt DB. Penetrating oesophageal injury: a contemporary analysis of the National Trauma Data Bank. Injury. 2013;44(1):48–55. 40. Feliciano DV, Bitondo CG, Mattox KL, Romo T, Burch JM, Beall AC, et  al. Combined tracheoesophageal injuries. Am J Surg. 1985;150(6):710–5. 41. Sudarshan M, Cassivi SD.  Management of traumatic esophageal injuries. J Thorac Dis. 2019;11(Suppl. 2):S172–6. 42. Eroglu A, Turkyilmaz A, Aydin Y, Yekeler E, Karaoglanoglu N. Current management of esophageal perforation: 20 years experience. Dis Esophagus. 2009;22(4):374–80. 43. Kiev J, Amendola M, Bouhaidar D, Sandhu BS, Zhao X, Maher J. A management algorithm for esophageal perforation. Am J Surg. 2007;194(1):103–6. 44. Sung HY, Kim JI, Cheung DY, Cho SH, Park S-H, Han J-Y, et al. Successful endoscopic hemoclipping of an esophageal perforation. Dis Esophagus. 2007;20(5):449–52. 45. Shimamoto C, Hirata I, Umegaki E, Katsu K. Closure of an esophageal perforation due to fish bone ingestion by endoscopic clip application. Gastrointest Endosc. 2000;51(6):736–9. 46. Blocksom JM, Sugawa C, Tokioka S, Williams M. The hemoclip: a novel approach to endoscopic therapy for esophageal perforation. Dig Dis Sci. 2004;49(7–8):1136–8. 47. Rao PM, Ivatury RR, Sharma P, Vinzons AT, Nassoura Z, Stahl WM.  Cervical vascular injuries: a trauma center experience. Surgery. 1993;114(3):527–31. 48. Tan Z, Tian R, Yu Z.  Surgical management of penetrating cervical vascular trauma. Zhonghua Yi Xue Za Zhi. 2012;92(27):1905–8.

Complex Duodenal Injuries

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Areg Grigorian, Kazuhide Matsushima, and Demetrios Demetriades

Key Points • The second part of the duodenum shares a common blood supply with the head of the pancreas and dissection of the space between the two organs may cause duodenal ischemia. • Isolated duodenal injuries due to blunt trauma often present with subtle clinical signs and the diagnosis may be delayed. • CT with intravenous contrast and in the appropriate cases oral contrast remains the cornerstone of early diagnosis in patients with subtle clinical signs. Delayed diagnosis and treatment are associated with a high incidence of severe complications and mortality. • Duodenal wall hematomas after blunt trauma diagnosed with CT scan may be safely managed conservatively. However, all duodenal hematomas diagnosed at exploratory laparotomy should be explored to rule out an underlying perforation and avoid prolonged postoperative recovery due to obstruction. • Adequate exposure of the descending and proximal third part of the duodenum can be achieved with the Kocher maneuver, while the distal third and fourth segments require an additional Cattell–Braasch maneuver. • Minor or moderate (Grades I–III) injuries can safely be managed with debridement of the edges of the wound to healthy tissue and tension-free transverse repair to avoid stenosis of the lumen. The management of severe duodenal injuries (Grades IV–V) has undergone significant

A. Grigorian Division of Trauma, Burns and Surgical Critical Care, University of California, Irvine, Orange, CA, USA e-mail: [email protected] K. Matsushima · D. Demetriades (*) Division of Trauma, Emergency Surgery, and Surgical Critical, LAC+USC Medical Center, University of Southern California, Los Angeles, CA, USA e-mail: [email protected]; [email protected]

changes over the past decade, with a shift from major complex operations to simple procedures, when feasible. • The current trend in the management of severe duodenal injuries favors an approach with simpler techniques and avoidance of complex procedures, such as pyloric exclusion or major resections. • In the presence of severe hemodynamic instability, a damage control operation at the index operation and definitive reconstruction at a second semi-elective operation, after patient stabilization, should be considered.

72.1 Surgical Anatomy The duodenum is approximately 25–35 cm long and is anatomically divided into four parts. • The superior or first part is intraperitoneal along the anterior half of its circumference. Superiorly, it is attached to the hepatoduodenal ligament, which contains the portal triad (common bile duct, proper hepatic artery, portal vein). Its posterior wall is associated with the gastroduodenal artery, common bile duct, and portal vein. • The descending or second part lies on the inferior vena cava and the right renal vessels. Anteriorly, it is covered by the hepatic flexure and transverse colon. Medially, it shares a border with the head of the pancreas. The common bile duct and pancreatic duct drain into its medial wall. • The transverse or third part posteriorly lies on the inferior vena cava and the aorta. The superior mesenteric vessels cross anteriorly. • The ascending or fourth part is approximately 2.5 cm in length and continues as the jejunum and is suspended by the ligament of Treitz. • The common bile duct lies posterior to the first part of the duodenum and pancreatic head and is partially invested by the pancreatic head. It joins the main pancreatic duct to drain into the ampulla of Vater in the medial aspect of the

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 P. Aseni et al. (eds.), The High-risk Surgical Patient, https://doi.org/10.1007/978-3-031-17273-1_72

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Table 72.1  Duodenal organ injury scale by the American Association of the Surgery of Trauma Grade Type I Hematoma Laceration II Hematoma Laceration III Laceration

Fig. 72.1  The second portion of the duodenum and the head of the pancreas receive their blood supply from the anterior and posterior pancreaticoduodenal arcades. Attempts to separate the two organs at this site may cause ischemia of the duodenum (with permission, Atlas of Surgical Techniques in Trauma, 2019, Cambridge University Press, editors Demetriades, Inaba, Velmahos)

second part of the duodenum. The ampulla of Vater is located approximately 7  cm distal to the pylorus. The accessory pancreatic duct of Santorini drains approximately 2 cm proximal to the ampulla of Vater. • The duodenal blood supply is provided by the gastroduodenal artery and the superior mesenteric artery. The head of the pancreas and the second part of the duodenum share their blood supply from the anterior and posterior pancreaticoduodenal arcades, which branch off the gastroduodenal (superiorly) and superior mesenteric arteries (inferiorly). These arcades lie on the pancreas near the medial aspect of the duodenal C-loop. Dissection of the space between the medial aspect of the second part of the duodenum and the head of the pancreas usually results in ischemia of the duodenum (Fig. 72.1).

72.2 Epidemiology A majority of duodenal injuries are due to penetrating trauma, usually gunshot wounds [1]. Duodenal injury following blunt trauma is rare due to its protected location deep within the retroperitoneum [2]. In a National Trauma Data Bank (NTDB) study of 388,137 patients with blunt abdominal trauma, the overall incidence of duodenal injury was 1.0% and isolated duodenal injury was 0.6% [3]. Blunt duodenal trauma usually occurs after direct trauma to the abdomen, resulting in compression of the duodenum

IV

Laceration

V

Laceration Vascular

Description Involving single portion of duodenum Partial thickness, no perforation Involving more than one portion Disruption 75% of D2 Involving ampulla or common bile duct Massive disruption of duodenopancreatic complex Devascularization of duodenum

against the vertebral column or after deceleration injuries in high-speed accidents. In abdominal trauma due to a steering wheel or handlebar injury impacting the anterior abdomen, an associated flexion/distraction fracture of L1–L2 vertebrae (Chance fracture) may be seen [4, 5]. In children, blunt trauma leading to duodenal injury is more common, due to the more horizontal costal margin and pliable abdominal musculature, offering less protection from high impact forces to the abdominal wall [6]. Duodenal injuries are graded by the American Association of the Surgery of Trauma (Table 72.1) [7]. Grades I or II are considered as minor injuries, Grade III as moderate, and Grades IV or V as severe injuries. More than 80% of patients with duodenal trauma have either Grades I, II, or III injuries. In the military setting with higher velocity bullet or blast injuries, trauma victims experience higher grade trauma with about 40% having Grades IV or V duodenal injuries [8].

72.3 Clinical Presentation In penetrating trauma, due to the anatomic proximity of the duodenum to numerous organs, there are often multiple associated abdominal injuries. The initial clinical examination usually reveals peritonitis or signs of hypovolemia and the need for emergency operation is obvious. In blunt trauma, the injury often involves the retroperitoneal part of the duodenum, and the initial clinical examination may be unreliable due to subtle signs. The initial presentation may include minor epigastric tenderness [9]. Clinical signs of peritonitis may appear a few hours or even days later. Delayed diagnosis of isolated duodenal injury following blunt trauma is not uncommon. Duodenal hematomas without perforation due to blunt trauma occur more commonly in children and are often the result of non-accidental trauma [10]. Since the hematoma is localized to the submucosal and subserosal layer, peritonitis is not frequently seen. As the hematoma evolves over the next few hours or days, the resultant breakdown of hemoglo-

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bin induces a hyperosmotic fluid shift and enlargement of the hematoma, leading to symptoms of mechanical obstruction [11].

72.4 Imaging Studies Penetrating duodenal injuries are more likely to prompt immediate surgical exploration, and the diagnosis is usually made intraoperatively. Blunt duodenal injuries are more difficult to diagnose clinically and rely more heavily on imaging studies. Computed tomography (CT) scan with intravenous contrast remains the cornerstone of diagnosis of blunt duodenal injuries and provides important information about the presence of associated pancreatic or other injuries [12]. Administration of oral contrast enhances the diagnostic yield and provides valuable information regarding the nature, size and location of duodenal injuries [13, 14]. However, oral contrast is rarely used in the initial evaluation of the acute trauma because of time constraints and risk of aspiration. CT scan findings suspicious of duodenal injury include wall thickening (>4 mm), hyperdense hematoma in the duodenal wall, intramural gas (pneumatosis), periduodenal fluid or stranding, discontinuity of the duodenal wall, and paraduodenal extraluminal gas [12]. In selected cases with suspicious CT scan findings, imaging studies with administration of oral contrast can provide the definitive diagnosis (Fig. 72.2). Diagnostic laparoscopy is a poor method of evaluating for duodenal or pancreatic injury due to its retroperitoneal location [15].

72.5 Laboratory Studies Laboratory studies are seldomly helpful in the early diagnosis of duodenal trauma. Serum amylase or lipase may be elevated in some patients, but this finding is non-specific and may be normal in the first 24–48 h [16–18].

72.6 Nonoperative Management Duodenal wall hematomas after blunt trauma may be safely managed conservatively, provided that the oral contrast radiological studies exclude an underlying perforation. These patients can be managed with serial clinical examinations, nasogastric decompression, and parenteral nutrition. The resolution of the hematoma might take several days or even weeks. If the patient fails to improve with conservative management, open surgery evacuation of the hematoma may be required. Minimally invasive interventions, such as drainage under either ultrasound or CT guidance, have been reported [19, 20]. There are also rare reports of laparoscopic incision and drainage of intramural duodenal hematomas after trauma [21–23].

72.7 Operative Management 72.7.1 Duodenal Wall Hematomas Preoperative diagnosis of a duodenal wall hematoma is not an indication for an operation if the oral contrast study does not show a duodenal perforation. However, all duodenal wall hematomas secondary to blunt or penetrating trauma, discovered during exploratory laparotomy, should be explored to rule out an underlying duodenal perforation and avoid the risk of duodenal obstruction, which could complicate and prolong the postoperative recovery (Fig. 72.3).

72.7.2 Exposure of Duodenal Injuries

Fig. 72.2  Abdominal CT scan demonstrating oral contrast extravasation (arrows) from duodenal perforation following blunt trauma

During exploratory laparotomy, any periduodenal hematoma, emphysema, or bilious staining, should raise the suspicion of duodenal injury and mobilization and inspection of the duodenum should be performed. Injuries involving the posterior first part of the duodenum are almost always due to penetrating trauma and pose significant challenges because of the close anatomical relationship with the common bile duct, the gastroduodenal artery, and the portal vein. Adequate exposure of this part of the duodenum can be achieved with the Kocher maneuver and medial rotation of the C-loop of the duodenum and head of the pancreas.

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Similarly, injury to the medial wall of the second part of the duodenum is almost always due to a penetrating mechanism and is often associated with trauma to the head of the pancreas. The common bile duct and pancreatic duct drain into this part of the duodenum and their integrity should be evaluated intraoperatively, by direct visualization. If intraoperative exposure of these structures is not possible due to a hematoma or edema, postoperative evaluation by magnetic

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resonance cholangiopancreatography (MRCP) should be considered. Evaluation and repair of duodenal and associated injuries in this area can be done from within the lumen via a lateral duodenotomy in selected cases. Dissection of the space between the duodenum and the head of the pancreas should be avoided because of the high risk of devascularization and necrosis of the duodenum or injury to the pancreatic or common bile duct. Exposure of the third and proximal fourth parts of the duodenum can be achieved with a combination of a Kocher maneuver (Fig.  72.4) and a Cattell–Braasch maneuver (Fig. 72.5). Exposure of the distal fourth part of the duodenum requires division of the ligament of Treitz. The superior mesenteric artery is located to the right of the ligament of Treitz, and care should be taken to prevent injury.

72.7.3 Management of Minor or Moderately Severe Duodenal Injuries

Fig. 72.3  Hematoma involving the second portion of the duodenum during exploratory laparotomy, following blunt trauma. These hematomas should always be explored to rule out an underlying perforation and avoid the risk of duodenal obstruction, which could complicate and prolong the postoperative recovery

Almost all minor or moderate (Grades I–III) duodenal injuries can safely be managed with debridement of the edges of the wound to healthy tissue and transverse repair to avoid stenosis of the lumen. A longitudinal injury with a length less than 50% of the circumference of the duodenum can easily be closed transversely. However, transverse closure of bigger longitudinal wounds is usually not possible, and in this situation, a longitudinal repair may be necessary with the addition of a gastrojejunostomy if there is significant stenosis.

Fig. 72.4  Kocher maneuver for exposure of the first, second, and proximal third parts of the duodenum: The ascending colon and hepatic flexure are mobilized and retracted medially to provide exposure of the anterior surface of the second and third portions of the duodenum (Left). The lateral peritoneal attachment of the first, second, and proxi-

mal third parts of the duodenum is incised, and the C-loop of the duodenum is rotated medially. Care should be taken to avoid injury to the superior mesenteric vein (Right) (with permission, Atlas of Surgical Techniques in Trauma, 2019, Cambridge University Press, editors Demetriades, Inaba, Velmahos)

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Fig. 72.5  Cattell–Braasch maneuver for exposure of the third and fourth parts of the duodenum: Following a Kocher maneuver, the right colon and small bowel are retracted cephalad and to the left. An incision is made on the visceral peritoneum in an oblique fashion from the ileocecal junction toward the ligament of Treitz (Left). The superior mesen-

teric vessels are retracted with the small bowel and are no longer crossing the duodenum. The third and proximal fourth parts of the duodenum are now fully exposed (Right). (with permission, Atlas of Surgical Techniques in Trauma, 2019, Cambridge University Press, editors Demetriades, Inaba, Velmahos)

The repair of these injuries is performed in one or two layers with 3-0 absorbable sutures. If a second seromuscular layer is used, care should be taken to avoid excessive inversion, which could narrow the duodenal lumen. In pediatric patients, the repair is usually done in one layer to prevent stenosis. The repair may be buttressed using omentum, and a closed drain should always be placed. A serosal patch over the repaired duodenum, using a loop of jejunum, may be used in rare cases with concerns about the quality of the repaired duodenal tissues. Overall, in minor or moderate severity injuries of the duodenum, there is no need for complex procedures such as pyloric exclusion or major resections. Also, a gastrojejunostomy should be considered only in cases with significant lumen stenosis after repair. In addition, a feeding jejunostomy catheter should rarely be used because of the risk of complications associated with the procedure.

injuries requiring a complex repair or a repair with tenuous blood supply. The current trend in the management of severe duodenal injuries is “less is better” [24]. In the late 2000s, a 10-year retrospective analysis demonstrated that patients with a duodenal injury that underwent primary repair with pyloric exclusion were more likely to experience a higher postoperative complication rate and longer hospital length of stay, compared to those that only underwent primary repair [25]. In another NTDB study, which included severe duodenal injuries (Grade III or higher), pyloric exclusion was performed in only 15.9% of Grade III and 34.0% in Grades IV–V injuries. Despite similar demographics, pyloric exclusion was associated with a longer hospital stay and was not associated with a mortality benefit. Multivariable analysis showed no significant differences in mortality or occurrence of septic abdominal complications between patients undergoing primary repair only or repair with pyloric exclusion. A more recent NTDB study which included 2163 patients who underwent an operation for a traumatic duodenal injury, during the 2007–2014 period, there was a progressive trend toward less invasive procedures for duodenal injury during the later study period, which was associated with improved mortality [26]. In the latest iteration of consensus guidelines from the Western Trauma Association, simple techniques for repair of even large duodenal injuries using a tension-free primary closure is the recommended approach [27]. This paradigm shift occurred at a time where damage-­ control surgery and damage-control resuscitation were

72.8 Management of Severe Duodenal Injuries The management of severe duodenal injuries (Grades IV–V) has undergone significant changes over the past decade, with a shift from major complex operations to less complex procedures when feasible (Fig. 72.6). Pancreaticoduodenectomies (Whipple procedure) are very rarely performed, duodenal diverticulization has been completely abandoned, and pyloric exclusion is performed only in selected cases with severe

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Fig. 72.6  Near-complete transection of the second part of the duodenum following a low-velocity gunshot wound. The duodenum can be repaired primarily after debridement of the wound edges. A gastrojejunostomy may be needed if there is significant stenosis of the repair. There is no need for pyloric exclusion

tomy may be necessary. Segmental resection of the second part is challenging because of the presence of the ampulla of Vater and the common blood supply with the pancreas, which make the mobilization difficult. In this situation, or if a tension-free anastomosis is not possible, a Roux-en-Y duodenojejunostomy may be indicated. Alternatively, a direct Roux-en-Y loop anastomosed over the duodenal defect may be considered. Pyloric exclusion should be considered in rare cases with tenuous repairs. The technique of the procedure is shown in Fig. 72.7a–c. Closed-suction drains should always be placed adjacent to the area of repair of severe duodenal injuries. Destructive injuries to the duodenum involving the ampulla of Vater or the head of the pancreas may require pancreaticoduodenectomy. These patients are often hemodynamically unstable and are best managed with damage control techniques, with completion of the resection and delayed reconstruction at a planned second operation.

72.9 Outcomes gaining popularity and proven to provide clear survival benefits for critically injured trauma patients. Avoiding complex duodenal operations coupled with damage-control approach in patients with severe duodenal trauma likely has a synergistic role in the improved outcomes seen in the modern era [28, 29]. The principles of primary repair in severe duodenal injuries are similar to the ones described above: debridement of the wound, adequate blood supply, tension-free anastomosis, and buttressing with omentum. Destructive injuries may not be amenable to primary repair, and in these cases, segmental resection and duodenoduodenostomy or duodenojejunos-

Prompt diagnosis and surgical intervention are critically important for patients with severe duodenal trauma. Delay of the operation by more than 24 h increases mortality rates by nearly four times [30]. Immediate mortality after duodenal trauma is usually the result of hemorrhagic shock from associated injuries. Mortality due to duodenal trauma is often a result of intra-abdominal sepsis, secondary to suture line dehiscence [31]. Duodenal leaks may occur in up to 8% of patients, and these patients usually have a complicated postoperative course, including the development of an intra-­ abdominal abscess and duodenal fistula [32].

Fig. 72.7 (a–c) Technique of pyloric exclusion for duodenal injury: A 6–8 cm anterior gastrotomy is performed along the greater curvature of the stomach, near the pylorus (a Left). The pylorus is identified through the gastrotomy, grasped with a Babcock clamp and pulled out through the gastrotomy (a Right). A purse-string suture using absorbable sutures is placed and tied to occlude the pylorus (b Left). The pyloric exclusion is completed with a gastrojejunostomy, utilizing the previous gastrotomy (b Right). An alternative to the purse-string is stapling of the post-pyloric duodenum with a non-cutting linear stapler (c). (with permission, Atlas of Surgical Techniques in Trauma, 2019, Cambridge University Press, editors Demetriades, Inaba, Velmahos)

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References 1. Santos EG, Sanchez AS, Verde JM, Marini CP, Asensio JA, Petrone P. Duodenal injuries due to trauma: review of the literature. Cirugía Española (English Edition). 2015;93(2):68–74. 2. Asensio JA, Feliciano DV, Britt LD, Kerstein MD. Management of duodenal injuries. Curr Probl Surg. 1993;30(11):1023–93. 3. Siboni S, Benjamin E, Haltmeier T, Inaba K, Demetriades D. Isolated blunt duodenal trauma: simple repair, low mortality. Am Surg. 2015;81(10):961–4. 4. Clarnette TD, Beasley SW. Handlebar injuries in children: patterns and prevention. Austr New Zealand J Surg. 1997;67(6):338–9. 5. Vandersluis R, O'Connor HM.  The seat-belt syndrome. Can Med Assoc J. 1987;137(11):1023–4. 6. Terreros A, Zimmerman S. Duodenal hematoma from a fall down the stairs. J Trauma Nurs. 2009;16(3):166–8. 7. Moore E, Cogbill T, Malangoni M, Jurkovich G, Champion H, Gennarelli T, et  al. Organ injury scaling, 11: pancreas, duodenum, small bowel, colon, and rectum. J Trauma Acute Care Surg. 1990;30(11):1427. 8. Antón J.  Management of duodenal trauma. J Trauma Acute Care Surg. 2019;87(3):739. 9. Pandey S, Niranjan A, Mishra S, Agrawal T, Singhal BM, Prakash A, et al. Retrospective analysis of duodenal injuries: a comprehensive overview. Saudi J Gastroenterol. 2011;17(2):142–4. 10. Wisner D, Hoyt D.  Definitive care phase: abdominal injuries. Surgery: scientific principles and practice. Philadelphia: Lippincott Williams & Wilkins; 1997. p. 331–41. 11. Kunin JR, Korobkin M, Ellis J, Francis I, Kane N, Siegel S.  Duodenal injuries caused by blunt abdominal trauma: value of CT in differentiating perforation from hematoma. AJR Am J Roentgenol. 1993;160(6):1221–3. 12. Melamud K, LeBedis CA, Soto JA. Imaging of pancreatic and duodenal trauma. Radiol Clin. 2015;53(4):757–71. 13. Carrillo EH, Richardson JD, Miller FB.  Evolution in the management of duodenal injuries. J Trauma Acute Care Surg. 1996;40(6):1037–46. 14. Hofer GA, Cohen AJ.  CT signs of duodenal perforation secondary to blunt abdominal trauma. J Comput Assist Tomogr. 1989;13(3):430–2. 15. Brooks AJ, Boffard KD. Current technology: laparoscopic surgery in trauma. Trauma. 1999;1(1):53–60. 16. Ashi M, Saleh A, Albargi S, Babkour S, Banjar A, Ghazawi M.  Isolated duodenal injury following blunt abdominal trauma. Radiol Case Rep. 2020;15(7):939–42. 17. Flint LM Jr, McCoy M, Richardson JD, Polk HC Jr. Duodenal injury: analysis of common misconceptions in diagnosis and treatment. Ann Surg. 1980;191(6):697. 18. Olsen WR.  The serum amylase in blunt abdominal trauma. J Trauma Acute Care Surg. 1973;13(3):200–4.

A. Grigorian et al. 19. Lloyd GM, Sutton CD, Marshall LJ, Jameson JS. Case of duodenal haematoma treated with ultrasound guided drainage. ANZ J Surg. 2004;74(6):500–1. 20. Hanish SI, Pappas TN.  CT guided drainage of a duodenal hematoma after trauma. J Trauma Acute Care Surg. 2007;63(1):E10–E2. 21. Nolan GJ, Bendinelli C, Gani J. Laparoscopic drainage of an intramural duodenal haematoma: a novel technique and review of the literature. World J Emerg Surg. 2011;6(1):1–5. 22. Banieghbal B, Vermaak C, Beale P.  Laparoscopic drainage of a post-traumatic intramural duodenal hematoma in a child. J Laparoendosc Adv Surg Tech. 2008;18(3):469–72. 23. Maemura T, Yamaguchi Y, Yukioka T, Matsuda H, Shimazaki S. Laparoscopic drainage of an intramural duodenal hematoma. J Gastroenterol. 1999;34(1):119–22. 24. Ordonez C, García A, Parra MW, Scavo D, Pino LF, Millán M, et al. Complex penetrating duodenal injuries: less is better. J Trauma Acute Care Surg. 2014;76(5):1177–83. 25. Seamon MJ, Pieri PG, Fisher CA, Gaughan J, Santora TA, Pathak AS, et al. A ten-year retrospective review: does pyloric exclusion improve clinical outcome after penetrating duodenal and combined pancreaticoduodenal injuries? J Trauma Acute Care Surg. 2007;62(4):829–33. 26. Aiolfi A, Matsushima K, Chang G, Bardes J, Strumwasser A, Lam L, et  al. Surgical trends in the management of duodenal injury. J Gastrointest Surg. 2019;23(2):264–9. 27. Malhotra A, Biffl WL, Moore EE, Schreiber M, Albrecht RA, Cohen M, et  al. Western trauma association critical decisions in trauma: diagnosis and management of duodenal injuries. J Trauma Acute Care Surg. 2015;79(6):1096–101. 28. Roberts DJ, Ball CG, Feliciano DV, Moore EE, Ivatury RR, Lucas CE, et  al. History of the innovation of damage control for management of trauma patients: 1902–2016. Ann Surg. 2017;265(5):1034–44. 29. Cannon JW, Khan MA, Raja AS, Cohen MJ, Como JJ, Cotton BA, et al. Damage control resuscitation in patients with severe traumatic hemorrhage: a practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2017;82(3):605–17. 30. Clendenon J, Meyers R, Nance M, Scaife E. Management of duodenal injuries in children. J Pediatr Surg. 2004;39(6):964–8. 31. Ferrada P, Wolfe L, Duchesne J, Fraga GP, Benjamin E, Alvarez A, et al. Management of duodenal trauma: a retrospective review from the Panamerican Trauma Society. J Trauma Acute Care Surg. 2019;86(3) 32. Phillips B, Turco L, McDonald D, Mause A, Walters RW. Penetrating injuries to the duodenum: an analysis of 879 patients from the National Trauma Data Bank, 2010 to 2014. J Trauma Acute Care Surg. 2017;83(5):810–7.

Abdominal and Peripheral Vascular Injuries: Critical Decisions in Trauma

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Alfredo Lista, Pierantonio Rimoldi, Erika De Febis, Nicola Monzio Compagnoni, Giulia Lerva, and Valerio Tolva

Key Points • Precocity of diagnosis is critical in vascular injuries of the abdomen and extremities. • Options for management of abdominal vessel injuries include nonoperative (intimal flap on computed tomography angiogram), endovascular (hostile abdomen, delayed diagnosis, or failed prior repair), and operative. • Ligation of the infrarenal inferior vena cava after a severe injury is more commonly practiced in the modern era and is usually well tolerated in young patients. • In the absence of palpable peripheral pulse, an arterial injury must be suspected. • Palpable pulse means patency of the vessel at that moment but does not mean the absence of arterial injury, which could be evident later. • Tissue contusion, the severity of ischemia, and infection are most responsible for revascularization procedure failure. • Functional prognosis of the revascularized limb is often better than amputation, despite sequelae. • The adoption of different prognostic scoring systems cannot replace multidisciplinary discussion among orthopedic, vascular, and plastic surgeons.

A. Lista (*) · P. Rimoldi · E. De Febis · N. Monzio Compagnoni V. Tolva S.C. Chirurgia Vascolare, Dipartimento Cardiotoracovascolare, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected] G. Lerva Università degli Studi di Milano, Milan, Italy e-mail: [email protected]

73.1 Abdominal 73.1.1 Introduction Abdominal vessel injuries are among the most lethal injuries encountered by trauma surgeons because the vast majority of these patients arrive at trauma centers in profound hemorrhagic shock. Patients sustaining abdominal vessel injuries best exemplify the lethal vicious cycle of shock, with secondary hypothermia, acidosis, and coagulopathy. The major sites of hemorrhage in patients sustaining blunt or penetrating abdominal trauma are the viscera, the mesentery, and the major abdominal vessels [1]. The abdominal vessel injury is classified into four zones described as follows and shown in Table 73.1: Zone 1: Midline retroperitoneum • Supramesocolic region • Inframesocolic region Zone 2: Upper lateral retroperitoneum Zone 3: Pelvic retroperitoneum Zone 4: Porta hepatis/retrohepatic inferior vena cava Since most of the vessels in these areas are in the retroperitoneum, they are difficult to access via a midline laparotomy incision quickly. Therefore, a systematic operative approach is required to diagnose and manage these potentially devastating injuries adequately. The abdominal vessel injury is classified into five grades by AAST (American Association for the Surgery of Trauma) as shown in Table 73.2.

73.1.2 Epidemiology Major abdominal vascular injury (AVI) is the leading cause of non-compressible torso hemorrhage (NCTH) accounting for 40% of all bleeding locations and 8% to 25% of vascular trauma cases among adults and children.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 P. Aseni et al. (eds.), The High-risk Surgical Patient, https://doi.org/10.1007/978-3-031-17273-1_73

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Table 73.1  Classification of abdominal vessel injury Zone 1 Supramesocolic

Major arterial branches Suprarenal aorta Celiac axis Su. mesenteric artery Proximal renal artery

Major venous branches Superior mesenteric vein

Operative maneuvers Left medial visceral rotation Midline suprarenal aortic exposure

Table 73.2  AAST (American Association for the Surgery of Trauma) Organ Injury Scale Grading AVI (Abdominal Vascular Injuries) Grade Injury I Non-named mesenteric arterial/venous branches, phrenic artery/vein, lumbar artery/vein, gonadal artery/vein, ovarian artery/vein, other nonnamed small artery/vein requiring ligation II Right, left, or common hepatic artery; splenic artery/vein; right or left gastric; GDA (gastroduodenal artery); IMA/IMV (Inferior Mesenteric Artery/Vein); primary named branches of SMA/SMV (Superior Mesenteric Artery/Vein) III SMV trunk, renal artery/vein, iliac artery/vein, hypogastric artery/vein, infrarenal IVC (Inferior Vena Cava) IV SMA trunk, celiac axis, suprarenal or infrahepatic IVC, infrarenal aorta V Portal vein, extraparenchymal hepatic vein, retrohepatic or suprahepatic IVC, suprarenal aorta

Abdominal vascular injuries are caused by penetrating injury in 60% to 95% of patients, although the proportion is slightly less in pediatric populations, and males are affected more frequently than females. Arterial and venous injuries are encountered more or less equally among all abdominal vascular injuries. Among arterial injuries, the iliac artery, renal artery, and abdominal aorta (AA) are the most frequently damaged, followed by the superior mesenteric artery (SMA) and celiac artery (CA). Inferior vena cava and iliac vein injuries represent the majority of venous AVIs, while renal, mesenteric, and portal vein (PV) injuries are encountered less frequently. Among major portal-venous injuries, superior mesenteric vein (SMV), PV, and hepatic vein injuries are distributed equally. In the pediatric population, inferior vena cava (IVC), iliac, and renal vessels are injured most commonly.

73.1.3 Pathophysiology 73.1.3.1 Blunt Trauma A rapid deceleration in motor vehicle collisions may cause two different types of vascular injuries in the abdomen. The first is the avulsion of small branches from major vessels with subsequent hemorrhage. A common example of this is

the avulsion of intestinal branches from either the proximal or distal superior mesenteric artery at sites of fixation. The second type of vascular problem seen with deceleration injury is the development of an intimal tear with secondary thrombosis of the lumen, such as is seen in patients with renal artery thrombosis, or a full-thickness tear with a secondary traumatic false aneurysm of the renal artery. Crush injuries to the abdomen, such as by a lap seat belt, posterior blows to the spine, and any mechanism that causes significant anterior-to-posterior compression may cause two different types of vascular injury, also. The first is an intimal tear or flap with secondary thrombosis of a vessel, such as the superior mesenteric artery, infrarenal abdominal aorta, or iliac artery. Direct blows can also completely disrupt exposed vessels, such as the left renal vein over the aorta or the superior mesenteric artery or vein at the base of the mesentery, leading to massive intraperitoneal hemorrhage, or they may even partly disrupt the infrarenal abdominal aorta, leading to the development of a traumatic false aneurysm.

73.1.3.2 Penetrating Trauma In contrast, penetrating injuries create the same kinds of abdominal vessel injuries as seen in the vessels of the extremities, producing blast effects with intimal flaps and secondary thrombosis, lateral wall defects with hemorrhage or pulsatile hematomas (early false aneurysms), or complete transection with either free hemorrhage or thrombosis. On rare occasions, a penetrating injury may produce an arteriovenous fistula involving the portal vein and hepatic artery, renal vessels, iliac vessels, or superior mesenteric vessels. Iatrogenic injuries to major abdominal vessels are an uncommon but persistent problem.

73.1.4 Clinical Presentation and Diagnosis An abdominal vessel injury may present in one of four ways, including free intraperitoneal hemorrhage; a contained mesenteric, retroperitoneal, or portal hematoma; thrombosis of the vessel; or some combination of these. As such, patients can be quickly divided into two major groups: those with ongoing hemorrhage and those without ongoing hemorrhage (contained hematoma or thrombosis). Thus, the presenting symptoms are variable based on both presentation and the involved vessel (Fig. 73.1). Penetrating truncal wounds between the nipples and the upper thighs remain the most common cause of abdominal vessel injuries. Major AVI is typically characterized by massive intraabdominal or retroperitoneal blood loss and profound shock. Patients with ongoing hemorrhage deteriorate rapidly, require life-saving interventions for hemorrhage control and massive transfusion, and have high prehospital and in-­

73  Abdominal and Peripheral Vascular Injuries: Critical Decisions in Trauma Fig. 73.1  Diagnosis and management of abdominal vascular injuries

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Hemodynamically stable

YES

NO

Exploratory Laparotomy

Multi-detector CT

Grade 1 injury

Grade 3 injury

Grade 4 or 5 injury

Blunt with low suspicion for other injuries?

Blush?

NO

Grade 2 injury

YES

YES

Consider endovascular repair

NO

Iliac

Renal

SMV or IVC

Aorta, CA, SMA

Blunt injury? YES

Low suspicion for other injuries?

NO

YES NO NOM

Low Grade Renal Injury

Consider endovascular repair

Exploratory Laparotomy

hospital mortality. To characterize complex severe torso injuries, the term “non-compressible torso hemorrhage” has been recently proposed and introduced into civilian and military practice. Patients with NCTH are defined as axial torso vascular injury, solid organ injury Abbreviated Injury Scale score of ≥4, or pelvic fracture with ring disruption. A patient with NCTH is physiologically compromised and unstable and requires immediate hemorrhage control. On physical examination, the findings in patients with abdominal vessel injury will depend on whether a contained hematoma or active hemorrhage is present. Patients with contained hematomas at the base of the mesentery, in the retroperitoneum, or in the hepatoduodenal ligament, particularly those with injuries to abdominal veins, may be hypotensive in transit but often respond rapidly to the infusion of fluids. They may remain remarkably stable until the hematoma is opened at the time of laparotomy. Conversely, patients with active hemorrhage, particularly those with injuries to abdominal arteries, generally have a rigid abdomen and unrelenting hypotension. These patients should obviously undergo immediate laparotomy without further evaluation (Fig. 73.2).

The other major physical finding that may be noted in patients with abdominal vascular injury is loss of the pulse in the femoral artery in one lower extremity when the ipsilateral common or external iliac artery has been transected or is thrombosed. In both stable and unstable patients, a rapid surgeon-­ performed ultrasound (focused assessment for the sonographic evaluation of the trauma patient [FAST]) is useful in ruling out an associated cardiac injury with secondary tamponade or an associated hemothorax mandating the insertion of a thoracostomy tube. In a stable patient with an abdominal gunshot wound, a routine flat-plate X-ray of the abdomen is of diagnostic value, so that the track of the missile can be predicted from markers placed over the wounds or from the position of a retained missile. In patients with blunt abdominal trauma, hematuria, modest hypotension, and peritoneal signs in the emergency department, computed tomography (CT) scanning of the abdomen has documented that the absence of renal enhancement and excretion and the presence of a cortical rim sign are diagnostics of thrombosis of the renal artery.

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Fig. 73.2 Intraoperative management of abdominal vascular injuries

Grade 2

Gastric Hepatic IMA

NO - Ligate

Stable?

YES - Repair NO - Splenectomy

Splenic

Stable?

YES

YES – splenic injury?

NO - Ligate

NO - Ligate Infrarenal IVC

Stable?

YES - Repair NO - TIVS

Intra-operative management

Iliac

Stable?

YES - Repair NO - Observe

Grade 3 Renal

Expanding hematoma?

YES – Nephectomy Contralateral Kidney intact?

SMV

Stable?

NO - Repair

YES - Repair NO – TIVS vs ligate + TC

SMA

Stable?

NO

Grade 4

YES - Repair Aorta

Repair

YES - Repair Celiac

Aorta/IVC

Grade 5

Stable?

Repair

YES – Ligate if unstable Portal Vein HA intact?

In other patients with blunt trauma, CT angiography is used to diagnose and treat deep pelvic arterial bleeding associated with fractures and to diagnose unusual injuries such as the previously mentioned intimal tears with or without thrombosis in the infrarenal aorta, the superior mesenteric artery, the renal artery, or the iliac artery. As the technology of CT scanning has advanced, many surgeons and radiologists are comfortable making therapeutic decisions based on data acquired from multiplanar scanning and formal CT angiography. Most of the positive scans involved branches of the internal iliac artery with a concomitant pelvic fracture or injuries to solid organs and thus were not necessarily diagnostic of true abdominal vessel injury.

NO - Ligate

NO - Repair

Still, in the stable patient with blunt trauma, findings on CT that are suggestive of injury to the retroperitoneal great vessels mandate nonoperative management with CT angiographic follow-up, endovascular management, or operation [2]. In summary: • Hemodynamically unstable trauma patients with signs of abdominal or pelvic trauma and peritonitis should be suspected to have major abdominal vascular injuries until proven otherwise. • Bilateral femoral pulses should be examined to exclude possible aortic and iliac artery injuries in patients with abdominal and pelvic trauma.

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• Ultrasound imaging is a simple and noninvasive method for the detection of intra-abdominal fluid but has poor accuracy related to major abdominal vascular injuries. • Computed tomography angiography (CTA) assessment is recommended for screening stable trauma patients who do not require immediate laparotomy but who have signs of intra-abdominal injury. • Computed tomography angiography and angiography can be useful for renal artery injury detection. • Preperitoneal pelvic packing supplemented with angiography is recommended for hemodynamic instability associated with severe pelvic fractures without another significant source of bleeding. • The presence of pelvic contrast extravasation seen on CTA may also indicate the need for angiography and pelvic embolization. • Patients with venous abdominal or pelvic injuries should be monitored for possible development of deep venous thrombosis (DVT).

peritonitis, or evisceration, a time limit of less than 5 min in the emergency department is mandatory. Figures  73.3 and 73.4 show the diagnostic and management algorithms for blunt and penetrating abdominal vascular injury.

73.1.5 Treatment

73.1.5.4 Options for Management of Injuries to Abdominal Vessels: Endovascular Management Endovascular approaches for injuries to abdominal vessels are particularly appealing in patients without another indication for laparotomy in the following circumstances: associated injury to the brain, associated extensive burns, or early organ failure; “hostile” abdomen from prior laparotomies; delayed diagnosis; or patient returns with a failed operative repair or chronic missed vessel injury. There has been extensive experience with the insertion of endostents for intimal flaps, intramural hematomas, and luminal thromboses in major named abdominal vessels after trauma. Interventional vascular surgeons routinely embolize bleeding vessels in solid organs and the pelvis.

73.1.5.1 Prehospital Resuscitation Resuscitation in the field in patients with possible penetrating or blunt abdominal vessel injuries should be restricted to basic airway maneuvers such as intubation or cricothyroidotomy and decompression of tension pneumothorax at the scene. Insertion of intravenous lines for infusing crystalloid solutions and blood products is best attempted during transport to the hospital. Restoration of blood pressure to reasonable levels is critical to neurologic recovery in patients with associated blunt intracranial injuries and possible abdominal injuries. 73.1.5.2 Emergency Department Resuscitation In the emergency department, the extent of resuscitation clearly depends on the patient’s condition at the time of arrival. In the agonal patient with a rigid abdomen after penetrating or blunt (if the admission chest X-ray is not suggestive of an injury to the descending thoracic aorta) trauma, resuscitative endovascular balloon occlusion of the aorta (REBOA) is now performed in trauma centers around the world in preference to emergency department thoracotomy. A REBOA device mimics a cross-clamp on the descending thoracic aorta in the following ways: preserves available blood supply to the coronary and carotid arteries; decreases arterial bleeding from injuries to the abdomen, pelvis, and lower extremities; and possibly decreases bleeding from abdominal venous injuries. In the patient arriving with blunt abdominal trauma, significant hypotension, and a positive surgeon-performed FAST or penetrating abdominal trauma and hypotension,

73.1.5.3 Options for Management of Injuries to Abdominal Vessels: Non-Operative Management Much as in trauma to cervical, thoracic, and peripheral vessels, an intimal flap or mural hematoma that is not flow limiting may be observed in selected patients. The risk is the progression of the wall injury and secondary thrombosis of the artery. Should observation be chosen, one option is to perform an early (48 h) repeat CT angiogram to see if there has been a further progression of the injury. Otherwise, a repeat CT angiogram should be performed in the asymptomatic patient before discharge. With either repeat CT angiogram, evidence of progression of the injury and a decrease in arterial flow mandate choosing an endovascular or operative approach.

73.1.5.5 Options for Management of Injuries to Abdominal Vessels: Operative Management Hemodynamically unstable trauma patients with suspicion of AVI should be taken immediately to the operating room for exploration, hemorrhage control, and resuscitation. • Where available, REBOA with zone 1 deployment should be considered in unstable patients with a positive FAST to achieve elevation of blood pressure before emergent operative intervention. • During laparotomy, all retroperitoneal hematomas resulting from penetrating trauma should be explored. • All zone 1 hematomas regardless of the mechanism of injury should be explored.

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Fig. 73.3  Blunt abdominal vascular injury algorithm. CT, computed tomography

Supramesocolic Perform left medial visceral rotation. Zone 1

Divide left crus of aortic hiatus. Obtain proximal control of dital descending thoracic aorta or diaphragmatic aorta. Inframesocolic Obtain exposure at base of transverse mesocolon. Obtain proximal control of infrarenal abdominal aorta.

Zone 2 Expose ipsilateral renal vessels at base of transverse mesocolon. Open hematoma. Obtain proximal control of renal vessels. Zone 3 Expose bifurcation of infrarenal arta and junction of inferior vena cava with iliac veins. Obtain proximal control of common iliac vessels and distal control of external iliac vessels. Portal area Perform Pringle maneuver for proximal control. Apply distal vascular clamp or forceps, if possible. Dissect common bile duct away from common hepatic artery and portal vein. Retrohepatic area Do not open hematoma unless it is rupured, pulsatile, or rapidly expanding.

• Zone 2 hematomas due to blunt mechanisms of injury should undergo operative exploration only if expanding. • Stable zone 3 hematomas after blunt trauma should be observed. Expanding hematomas due to blunt trauma associated with a pelvic fracture should undergo preperitoneal packing, angioembolization, or both in sequence.

• Where available, REBOA with zone 3 deployment should be considered in transient responders and HD unstable patients with pelvic injury to augment the effect of preperitoneal packing and allow resuscitation before definitive operative or endovascular control.

73  Abdominal and Peripheral Vascular Injuries: Critical Decisions in Trauma Fig. 73.4 Penetrating abdominal vascular injury algorithm

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Supramesocolic Zone 1

Proceed as for penetrating injury. Inframesocolic Proceed as for penetrating ulcer.

Zone 2 Do not open hematoma if kidney appears normal on preoperative CT or arteriography. If kidney does not appear normal, still do not open hematoma unless it is ruptured, pulsatile or rapidly expanding.

Open hematoma.

Zone 3 Do not open hematoma unless it is ruptured, pulsatile, or rapidly expanding or unless ipsilateral iliac pulse is absent. Portal area Proceed as for penetrating injury.

Retrohepatic area Proceed as for penetrating injury.

• In patients who remain unstable and in those with significant physiological derangements, damage-control techniques should be used including vessel ligation, temporary intravascular shunts (TIVSs), and temporary abdominal closure. • After initial vascular control, it is reasonable to consider definitive repair, including primary repair, patch angioplasty, resection with primary anastomosis, and resection with interposition graft in stable well-resuscitated patients. • During operative exploration, all aortic injuries should be repaired or shunted, and then repaired after resuscitation is completed. • In unstable patients, destructive injuries to the infrarenal IVC that cannot be repaired primarily may be ligated. Suprarenal IVC injuries must be repaired or shunted to prevent renal failure.

• Destructive injuries to the CA and/or its branches may undergo ligation without significant morbidity, unless there is a replaced hepatic artery (present in 4–11% of patients). • Injuries to the inferior mesenteric artery (IMA)/inferior mesenteric vein (IMV) may undergo ligation without significant morbidity unless there is advanced atherosclerosis of the mesenteric arteries. • Destructive injuries to the SMA in HD unstable patients should undergo vascular shunting with delayed reconstruction; however, ligation may be tolerated in some patients. • Destructive injuries to the PV or SMV can be managed with ligation, although temporary shunting with delayed repair may be appropriate. Temporary abdominal closure, to monitor for bowel edema and ischemia, should be con-

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sidered, and aggressive resuscitation for the syndrome of splanchnic hypervolemia and systemic hypovolemia is recommended. • The common and external iliac arteries should be repaired in stable patients or shunted in unstable patients. Internal iliac artery injuries may be repaired if possible or ligated without significant morbidity, but bilateral ligation should be avoided. • In the stable patient with isolated Grades 1–4 injuries without associated injuries, endovascular repair may be considered (Fig. 73.2).

73.1.6 Summary Abdominal vessel injuries are most commonly seen in patients with penetrating wounds to the abdomen but occur after blunt abdominal trauma as well. When tamponade is present, proximal and distal vascular control should be obtained before opening the hematoma causing the tamponade. If active hemorrhage is present, direct compression of the bleeding vessels with a finger, hand, laparotomy pad, or sponge stick at the site of injury is necessary until proximal and distal vascular control can be obtained. Vascular repairs are generally performed with polypropylene sutures and can range from simple arteriorrhaphy or venorrhaphy to the insertion of substitute vascular conduits. Overall, if hemorrhage can be rapidly controlled and distal perfusion restored, many patients with major abdominal vessel injuries can be salvaged with the techniques described. Survival rates after abdominal arterial injuries are as follows: suprarenal aorta, 8–24%; infrarenal aorta, 34–58%; superior mesenteric artery, 40–61%; and iliac artery, 60–80%. Survival rates after abdominal venous injuries are as follows: infrarenal inferior vena cava, 46–76%; superior mesenteric vein, 35–71%; iliac vein, 74–91%; and portal vein, 50% [3].

73.2 Peripheral 73.2.1 Introduction The majority of arterial trauma (90% in most records) involves limb arteries, and vascular trauma of the limbs is associated with injury to other organs. Furthermore, in recent years, due to the increasing numbers of endovascular procedures, there has been a growth in iatrogenic injuries, and drug addiction injuries are also considered classic vascular trauma.

A. Lista et al.

73.2.2 Epidemiology Vascular injuries of the extremities are uncommon. In civilian urban trauma centers, peripheral vascular injuries are present in 1% to 5% of admissions; in rural centers, they are even less common, occurring in less than 1% of admissions. Most are penetrating, due to either gunshot or stab wounds, and occur predominantly in males in their third and fourth decades. Blunt trauma sufficient to produce fractures or dislocations is a much less frequent cause. Explosive and high-­ velocity projectiles are the predominant wounding agents in the recent military experience. Iatrogenic arterial injuries occur in approximately 0.6% of patients undergoing endoluminal therapies, and they appear to be specialty related. Iatrogenic vascular injuries can also occur during open operations on the extremities, such as during total joint procedures, intramedullary and external fixation, and plate osteosynthesis. Iatrogenic arterial injuries are definitely not benign. Limb-threatening complications have occurred and recent reports have documented a 5% to 7% all-cause mortality following iatrogenic arterial injury.

73.2.3 Pathophysiology The typical classification of vascular trauma is divided into penetrating and blunt injuries (Fig.  73.5). In penetrating trauma, the vascular lesion consists of a partial or complete section of the vessel, independently from the agent. In blunt trauma, instead, the mechanism is an indirect compression, deceleration, or stretching of the vessel often associated with osteoarticular injuries. Gunshot wounds have different mechanisms. The bullet forms a temporary cavity along its trajectory and a permanent cavity filled by tissue debris, causing a sudden shift of tissues. Complete transections of the artery consist of adventitia, media, and intima laceration; such injuries are circumferential, causing a retraction of arterial extremities, followed by obstruction of the arterial lumen with temporary hemostasis. Partial lesions, instead, lead to a pulsating hematoma formation and a pseudoaneurysm thereafter as often happens in the iatrogenic trauma due to arterial catheterization. Arteriovenous fistula could form when a lateral arterial lesion involves the nearby vein. Arterial contusions are often met in blunt trauma due to stretching, deceleration, or cavitation. A broken intima or media can occur. The intimal layer is by far less extensible compared to media or adventitia. Therefore, it could be torn along with the formation of dissecting flap leading to secondary thrombosis. The exposition of the medial layer, after intimal rupture, has a thrombogenic effect. The adventitial

73  Abdominal and Peripheral Vascular Injuries: Critical Decisions in Trauma

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Fig. 73.5  Algorithm for limb trauma

LIMBS TRAUMA

RESUSCITATION

CLINICAL EXAMINATION

PENETRATING TRAUMA

• Delayed observation • Associated bone injuries • PAOD • Associated soft tissues injuries • Hunting rifle wounds • Localization at thoracic outlet

EVENTUAL REALIGNMENT OF BONES

HARD SIGNS of vascular lesions

BLUNT TRAUMA

ABSENCE OF vascular lesions or SOFT SIGNS DOPPLER ULTRASONOGRAPHY

POSITIVE

NEGATIVE

ARTERIOGRAPHY/ ANGIOGRAM CT

YES

NO

SURGICAL EXPLORATION

layer, instead, is more resistant and can often stop blood spilling. The mechanism of iatrogenic complications due to percutaneous sealing systems in endovascular procedures is different: in these cases, thrombosis is due to posterior intimal detachment, associated with the presence of an intra-­ arterial component of the percutaneous sealing system. In the most critical arterial trauma, rupture of three layers is observed with the formation of pseudoaneurysm (PSA). Arterial spasms determine a reduction in caliber of the vessel: they are typical in small- caliber arteries and more frequent in young people with normal vessels [4].

73.2.4 Clinical Presentation and Diagnosis We can distinguish between “hard” signs, in which arterial injury is almost always present, thus leading to mandatory surgical exploration, and “soft” signs, in which arterial lesion is suspected, leading, at least initially, to noninvasive diagnostic tests. Hard Signs • Active hemorrhage –– Pulsatile or expanding hematoma

POSITIVE

NEGATIVE OR WITH MINIMAL/NON OCCLUSIVE INJURIES

–– Bruit or thrill –– Absent or diminished pulses –– Distal ischemia Soft Signs • –– –– –– ––

Stable hematoma Trauma close to major nervous or vascular structures Bone fractures Unexplained hypotension Limb paresis or paresthesias Clinical signs of arterial injury can be furtherly distinguished as hemorrhagic or ischemic.

73.2.4.1 Hemorrhagic Signs The most commonly encountered sign of arterial injury is a hematoma. It can be compressive or expanding, rarely pulsating. If it is localized in a closed space, it can worsen ischemic and neurologic complications. External pulsating hemorrhage allows determining the location of the arterial injury. Most of the time, it is a self-­ limiting blood loss due to arterial stump spasm. A thrombus is evident in the lumen.

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73.2.4.2 Ischemic Signs –– The classical description of patients with acute limb ischemia is represented by the “six Ps”: pain, pallor, paralysis, pulse deficit, paresthesia, and poikilothermia. Pain may be either constant or elicited by passive movement of the involved extremity. History should include relation to trauma, duration, location, intensity, and suddenness of the onset of pain and changes over time. –– More frequently, however, subacute ischemia is encountered. The extremity is cold and pale; pulses are absent, and neurological examination is normal. –– Compartment syndrome appears most of the time after revascularization: absence of a peripheral palpable pulse is first noticed, followed by painful muscular swelling causing progressive neurological sensory deficit first, and ultimately, also motor. –– Muscular ischemia is due to revascularization edema. –– Diagnosis is easier if edema is localized in the anterior, lateral, or superficial posterior compartment of the foreleg, more difficult if in the deep posterior lower limb. –– Compartment syndrome requires urgent fasciotomies: different studies limit the pressure to 45 mmHg. Fasciotomies in forearms can be performed anteriorly and posteriorly. –– Arteriovenous fistula is characterized by the presence of a continuous systolic–diastolic bruit and palpable thrill, although its formation in trauma is rare. 73.2.4.3 Hidden and in Development Clinical Pictures Hidden clinical pictures are common in polytrauma with multilevel bone injury leading to swelling for tissue ischemia and contusion. In-development clinical pictures are sneaky: pulses, initially palpable, can later disappear due to intimal tear leading to thrombus formation. Hence it is necessary to check pulses after the reduction of fracture or dislocation in any major joint (shoulder, elbow, hip, knee, etc.). 73.2.4.4 Doppler Ultrasound Scan Advantages of Doppler ultrasound scan are as follows: –– Point of care at patient’s bedside –– Noninvasive procedure –– Easily repeatable, allowing to detect the evolution of the injury –– Screening methods in asymptomatic lesions Disadvantages of Doppler ultrasound scan are as follows: –– Operator dependent –– Lack of detection of injuries to side branches and isolated intimal tears –– Troublesome performance in painful limb Different authors studied the diagnostic value of ankle-­ brachial index (ABI), showing that a value 10 mm and dangerous if 10, no concurrent surgery with a general or orthopedic surgeon is recommended because of the length of such procedures, blood loss, and intraoperative hypothermia [5]. Only concomitant multi-professional operative procedures of a shorter duration are allowed, such as the position

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of maxillomandibular fixation in preparation for the definitive treatment of facial injuries [5]. Isolate severe facial injuries can be treated within 24 h, using an “early total care” philosophy, before the onset of soft tissue swelling, especially if wide wounds are useful as a surgical approach.

74.4.2 Intraoperative Airways Management Surgical reconstruction of complex craniofacial injuries characteristically requires intraoperative maxillo-mandibular fixation, free access to nasal cavities for nasal and maxillary fractures mobilization and reduction, and often a wide “vertex-­to-chin” surgical field to permit simultaneous neurosurgical and maxillofacial procedures (Fig. 74.6). So traditionally, alternatives to managing airways are switching from orotracheal-nasotracheal intubation or performing a tracheotomy. The former is contraindicated in concomitant skull base fractures and this solution leads to a “blind time frame” in which the definitive airway is lost. Tracheotomy has a complication rate of 14–45% and is reserved only for patients that will need a prolonged period of ventilation support because of associated injuries, regardless of the facial injury severity [2, 92]. Submental orotracheal intubation is an easy way to solve the problem of airways management of these cases; proposed at the end of the nineteenth century by Altemir, it involves a temporary deviation of orotracheal intubation going through a tunnel, created with blunt dissection in the a

b

Fig. 74.6  Surgical treatment of severe craniofacial injury requires free exposure from the cranial vault to the mandible (a, b), maxillomandibular fixation, and free access to nasal cavities (c). Intraoperative diver-

floor of the mouth through a submental skin incision [2, 93– 97] (Fig. 74.6). A contraindication of this type of intubation is anterior and bilateral comminuted mandibular fractures, in which the tube could interfere with proper reduction. Unilateral cases allow contralateral submental intubation. Complications of a right Altemir intubation are extremely rare and could include bad skin scars, bleeding, damage to the lingual nerve and the marginal mandibular branch of the facial nerve, damage to the duct of the submandibular gland, damage to the sublingual gland, salivary fistulae, and damage to the tube and skin infections [95, 96, 98, 99].

74.4.3 General Principle, Surgical Approaches, and Sequencing The main reconstructive goal in severe craniofacial injuries is to restore the morphology of the face (anteroposterior projection, height, width, and facial symmetry) together with the re-establishment of functions (dental occlusion, ocular motility, nasal breathing, sensory and motor nerve function, lacrymal and salivary drainage, mouth opening, and mandibular movements) and avoid communication between airways and intracranial space [89, 100]. All of these results must be sought in a single and comprehensive procedure. The facial skeleton is founded on horizontal and vertical buttresses, which are the focus areas of force resistance and reconstruction [7, 89] (Fig. 74.7). c

sion to submental endotracheal intubation is a simple and less invasive way to get each of these necessities

74  Updates in the Management of Complex Craniofacial Injuries

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H. Orbital walls fractures have to be reconstructed at the end of the procedure to restore orbital volume and shape with a careful manipulation of soft tissues content I. Closed nasal reduction or primary bone grafting with rigid fixation J. Medial palpebral canthos, if detached, need an overcorrected reposition with medial canthopexy K. Craniotomies, frontal sinus cranialization, and cranial base reconstruction with pericranial flap are performed with the neurosurgeon team L. Redraping of the soft tissues skeletonized during surgical access or as a consequence of trauma M. Soft tissues wound in layer reconstruction, with neurorrhaphy/nerve grafts of facial and trigeminal nerve injuries, salivary or lacrimal duct stenting

Fig. 74.7  Vertical (nasomaxillary, zygomaticomaxillary, pterygomaxillary) and horizontal (zygomatic arches, lower and upper orbital rims, hard palate, and maxillary alveolus) midfacial bone buttresses (Brainlab Elements™)

Vertical midfacial buttresses are nasomaxillary, zygomaticomaxillary an pterygomaxillary ones. The horizontal buttresses are the zygomatic arches, the lower orbital rims, the hard palate and maxillary alveolus for the midface, and the supraorbital rims for the upper face. The horizontal buttresses are supported by vertical struts such as columns or pillars [2, 79, 100, 101]. When trauma force magnitude is sufficient, these facial struts fail. Preoperative manipulation of diagnostic images, with proper identification of these standardized structures, is crucial to organize a sequence of treatments to restore the facial bio-architecture [100]. Guiding treatment principles are: A. To expose all fractures that require rigid fixation (titanium plates and screws) B. Mobilization of grossly displaced fragments with rudimentary bone reduction C. Use maxillomandibular fixation to restore premorbid dental occlusion D. Displaced condyle fractures are treated before other mandibular fractures E. Palatal fractures must be early reduced and stabilized F. To proceed with sequential and meticulous reduction and rigid fixation of each fracture to reconstruct principal buttresses G. Comminuted fractures of principal buttresses have to be reconstructed, eventually with primary autologous bone grafts

The most widely used approach for complex middle/ upper facial third fractures is coronal flap combined with lower lid/transconjunctival and maxillary vestibular incision [89, 102] (Fig. 74.8); in this way, a wide area from the vertex to the maxillary dentoalveolar arch is exposed. Treatment of mandibular fractures requires an intraoral approach for many injuries of the tooth-bearing horizontal branch; extraoral approaches are reserved for comminuted, complicated, or atrophic bone fractures, requiring load-­ bearing fixation. Mandibular vertical branches and condyles are generally approached via extraoral surgical incisions, especially in severe craniofacial injuries, to achieve a rigid fixation and obtain a proper posterior facial height and width. General organization of repair philosophies is a centripetal “Outside-In,” starting from zygoma toward central midface [103], or centrifugal “Inside-Out,” starting from naso-orbital-ethmoid toward zygoma reconstruction sequence [3, 104, 105]. Other approaches are “Top-to-Bottom,” from vertex toward the mandible [106], or “Bottom-to-Top,” starting from the mandible and going on toward the cranial vault [1]. None of these approach philosophies is demonstrated to be the best solution, and an individualized treatment plan, with first reduction and reconstruction of the least damaged region, usually provides a precise and most stable bone reference which can be used to proceed in a sequential manner [1, 7, 9, 89, 105]. Surgeons may use a combination of sequences as each patient will have a unique pattern of injury [2]. Condyle and mandible are well-recognized starting points in the Bottom-to-Top philosophy [1, 6, 88] and are recommended to ensure a good reference for the maxilla through occlusion [6]. Then the zygomatic arch is a critical buttress whose reconstruction allows simultaneous restoration of projection and facial width. It is considered “the outer facial frame” and is identified as the starting reconstruction point

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b

c

Fig. 74.8  Coronal (a), intraoral maxillary vestibular (b), and transconjunctival lower lid (c) approaches allow to expose a wide field, extending from the vertex to the upper dentoalveolar arch. These are the most used approach for the surgical treatment of severe craniofacial injuries

a

b

c

Fig. 74.9  Preoperative CT-3D reconstruction (a), intraoperative (b), and postoperative CT-3D reconstruction (c) of bilateral zygomatic arch reconstructed as the “Outer facial frame,” to restore middle facial third projection and width

by Outside-In and Top-to-Bottom philosophies [6, 89, 103] (Fig. 74.9). Starting from mandible (and condyle) reconstruction, we create a stable occlusion reference and go on from the upper facial third toward the maxilla, with a lateral to medial direction, realizing a true centripetal reconstruction which usually confers the best anatomical landmarks [7, 9]. The Top-to-Bottom approach could be preferred when there are cranial vault/base injuries, in which an emergency intervention is required [9].

74.5 Innovations and Technology The use of technology in craniofacial traumatology represents an essential aid for surgeons, especially in complex cases. Most of the technology developed and introduced in clinical practice during the past years allowed to perform increasingly complex surgical procedures with higher safety and result predictability.

The innovations and the technologies that are currently the gold standard for correct diagnosis and adequate surgical planning in complex cases of face traumatology, are represented by thin-layer CT scan, image elaboration software, surgical navigation, rapid prototyping models, and Patient-Specific Implants (PSI).

74.5.1 CAS in Acute Care Setting The introduction of new technologies in clinical practice through the years led to the development of the computer-­ assisted surgery (CAS) concept. CAS represents an excellent chance for the maxillofacial surgeon to combine firm surgical techniques and up-to-date technologies through different ways of development. The main target should always be the rational use of technological tools to “assist” the operator through different surgical steps to improve the results, with no replacing clinical examination and reasoning.

74  Updates in the Management of Complex Craniofacial Injuries

The CAS in maxillofacial trauma has been developed during the past twenty years. Firstly used in oncological surgery, it has been applied to complex reconstructions such as correction of orbital deformities, orbital-zygomatic complex repositioning, and primary and secondary reconstruction after complex craniofacial trauma. The same technologies are regularly used in oncology, orthognathic surgery, malformative surgery, and dental implantology. The correct workflow for complex facial trauma begins with an appropriate acquisition of preoperative CT images, which have to be necessarily characterized by high quality. The most common CT method is represented by spiral TC, based on a thin X-rays beam rotating several times around the patient; the X-rays beam is then captured by detectors, while the supine patient proceeds inside the machinery. One of the main advantages of spiral CT is represented by the possibility of obtaining reformatted data that can be manipulated to generate reconstructions in different planes. The eventual integration through MRI can be exploited in order to identify clinical conditions that may require urgent surgical treatment or, furthermore, to investigate pathological alterations of orbital content, such as hematomas, muscle/nerve injuries, or bulbar affections. Raw data of radiological examinations can be then elaborated through dedicated software that allows to implement the diagnostic process and to individualize the preoperative surgical planning and the consequent therapeutic path. Several surgical planning software is currently available and the most modern ones are associated with optic navigation systems; this software, in addition to preoperative planning, can perform other functions, such as bone segmentation, orbital volume calculation, mirroring procedures, image fusion of preoperative and postoperative scans for the control of the surgical results, and the possibility to import/export STL (STereoLithography) data [107, 108] (Fig. 74.10). The correct workflow is represented by the following steps: A. High-resolution CT images acquisition; B. Image elaboration through a planning software, which can be integrated with navigation systems; C. Skull prototyped model production; D. Virtualization of the surgical procedure; E. Customization of reconstruction through PSIs production or implant shaping on the stereolithographic model; F. Surgical navigation checking; G. Post-surgical CT scan, intra/postoperative; H. Image fusion and final checking. The target of preoperative surgical planning is to elaborate a virtual model which could match with the outcome that is expected to be obtained with surgical intervention, raising its predictability. These tools may be applied to selected patients

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to customize reconstruction in case of loss of substance or massive bone dislocation: virtual reconstructions will be commuted by biotechnological companies into patient-specific prosthetic devices that could be implanted in the patient. Once the surgical procedure has been planned, the next step is represented by intraoperative surgical navigation, followed by a postoperative radiological check. Surgical navigation, which is considered the evolution of stereotaxic surgery, is a technique that allows a three-­ dimensional localization of anatomical landmarks of the skull. The method was introduced in maxillofacial surgery in 1994 by Hassfeld for the resection of skull base tumors, representing a fundamental turning point for both planning and checking steps: this is a central feature of surgical navigation since it could be even used in the intraoperative phase, working as a valid surgical instrument for real-time checking of reconstruction previously planned [107, 109]. During preoperative planning, 3D images for virtual representation of the skull are generated. Other ancillary technological tools that can be applied to improve surgical outcomes are image amplifiers, such as the exoscope, microscope, and endoscope, which may be even used as operative tools.

74.5.2 Secondary Reconstruction The secondary treatment of the outcomes of complex craniofacial injuries is a demanding challenge for the maxillofacial surgeon because of reconstructive issues that often have to be faced. The bone matrix loss, the inveterate dislocation of bone fragments, and the anatomical/volumetric modification of the structures (especially the orbits) appear to be hard to correct without technological aid and would depend only on the “artistic” skills of surgeons. Computer-assisted surgery offers undoubted advantages in predictability and reproducibility of outcomes. Preoperative planning allows the surgeon to comprehend and personalize the reconstructive steps fully. Several protocols of integration between different technologies have been previously described: the common trait for every protocol is virtual planning through appropriate software. The following step is virtual customization, which leads to the realization of patient-specific implants. A valuable tool for orbital or orbital-zygomatic reconstruction is represented by Virtual Surgery Simulation (VSS) [109]. This protocol implies the production of a high-­definition rapid prototyping model that is used to customize titanium plates and grids straight on the model (Fig. 74.11a). Later, surgical navigation on the model completes the planning phase (Fig.  74.11b). The intraoperative surgical navigation on the

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Fig. 74.10  Manipulation of preoperative images during the planning of computer-assisted surgery; tridimensional analysis of bone fractures allows to organize a better reconstruction sequence (a). The possibility

a

of importing an STL file of preformed orbital mesh is useful to verify its size and positioning as a reference for a highly accurate surgical reconstruction (b) (Brainlab Elements™)

b

Fig. 74.11  Customize titanium plates and grids straight on the model (a). Preoperative surgical navigation simulated on the model (b)

patient is then performed, and lastly, postoperative CT scan acquisition inside the operating room completes CAS configuring three levels of control and checking for reconstruction (preoperative, intraoperative, and postoperative). Future development prospects are focusing on the refinement of image processing software, associating them with augmented and mixed reality.

These procedures may introduce a further advantage for the surgeon in terms of quality of intraoperative visibility, based on the concepts of real 3D vision, holograms, and depth of operative field. Even the production of alternative reconstructive materials may lead to important innovations, such as the introduction of new materials and alternative synthesis procedures.

74  Updates in the Management of Complex Craniofacial Injuries

74.6 Multidisciplinary Management of Facial and Skull Base Injuries Fractures of the anterior skull base are frequently associated with meningeal lesions and cerebral contusions. The basal bone is generally thin and relatively delicate so the injury may easily result in multiple fractures with the formation of bony spiculae that may lacerate the overlying meningocerebral structures [110, 111]. Otherwise, the meningeal layers may be torn off or lacerated by fractures with bone diastasis. When the arachnoid is injured, pneumocephalus and/or CSF leaks may occur through the nose or the pharynx. From a practical point of view, communication exists between the paranasal sinuses and the subarachnoid space, which may be maintained by a persistent, continuous CSF leakage [111]. In these conditions, the infective risks (abscess, meningitis, ventriculitis, and so on) are relatively high. Indeed, in most cases, mucosal and pial adherences soon occur, thus sealing the osteo-dural defects. Often, a more or less amount of injured brain protrudes through the osteo-dural breaks contributing to creating adherences and sealing the CSF leakage Subsequently, such adherences evolve into a fibrous scar, and the patient may be theoretically considered healed [112].

74.6.1 Diagnosis and Preoperative Management Appropriate diagnosis requires the following: 1. Brain CT scan to evaluate the presence and the severity of the brain contusion. If no infection is suspected, an enhanced CT scan has no indication. 2. The skull base must be studied by a high-resolution (1  mm slices) CT scan with bone window and coronal and sagittal reconstruction. 3. Cervical radiograms to rule out spinal lesions since facial trauma may be easily associated with hyperextension cervical injuries. 4. Angio-CT scan is indicated when the fractures extend to the carotid canal, the anterior clinoid process, and/or the clivus. MRI is required when an abscess is suspected or when a large encephalocele has to be evaluated. Differential diagnosis of CSF-leak may be sometimes difficult. Fluid collection and analysis of β-2 transferrin may be diriment.

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74.6.2 Treatment Indications Cerebral contusions may require timely surgical treatment depending on the size, the mass effect, and the intracranial pressure [111]. In these cases, the skull base repair is usually postponed owing to brain edema and swelling. Anyway, most frontal lobe lesions may be conservatively managed [111, 112]. Addressed treatment of the skull base lesions is generally required in the following cases: 1. CSF leaks/pneumocephalus that persist for more than one week [110, 112]. These are usually massive and unlikely to heal spontaneously. 2. CSF leaks/pneumocephalus that cease but recur [110, 112]. Recurrences may occur even years after injury and are often associated with abscess formation. 3. Multiple, comminute, and compound fractures with large bone lacunae on CT scan (the so-called “fracas de la base du crâne”), extending to the whole anterior cranial fossa [110, 111, 113]. In these conditions, the mucosal and pial adherences cannot be able to provide adequate support for healing. Portions of the brain may protrude through the osteo-dural defect (encephaloceles). Accordingly, sneezing, coughing, and straining may activate or reactivate the fistula at any time. There are patients who require surgical treatment of brain abscess even decades after injury [114]. That means surgical indication may be considered even if no CSF leak is evident [110, 114]. 4. Another indication might be represented by a maxillofacial procedure which is expected to require significant bone traction for fracture reduction, that could be dangerous for the skull content. In all surgical cases, the surgical timing has to be agreed with the maxillofacial surgeon that usually favors relatively early procedures [115]. This early attitude is usually counterbalanced by the neurosurgeon who prefers a delayed procedure to avoid the retraction of contused frontal lobes. In general, a period of a couple of weeks represents a good compromise between the requirements of the two specialists [112]. Spinal CSF drainage might be used to dry the CSF leakage. In the writer’s opinion, this maneuver should be reserved for very selected cases. It may be dangerous in the early phases of injury when the intracranial pressure could be higher than expected. Furthermore, it creates a negative ­pressure gradient, thus favoring the entrance of germs from the nose. Finally, it induces arachnoido-mucosal adherences that may arrest the CSF leak but that may not represent true (and effective) healing.

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74.6.3 Surgical Technique Surgical repair is generally accomplished through a bilateral subfrontal approach [110, 111]. Selected cases with limited derangement may be managed through a unilateral subfrontal approach. A coronal flap is fashioned taking care to elevate a periosteal flap with an intact anterior vascular pedicle, which will be used to cover the whole cranial fossa at the time of closure, according to Derome’s technique. A basal bifrontal craniotomy through the frontal sinus is then performed. The possible bone fragments are carefully collected for subsequent reassembling with titanium plates and screws. The posterior wall of the frontal sinus is completely abolished (cranialization). The entire sinus mucosa is cauterized and toileted, up to Behcet's foramina; the nasofrontal ducts are prepared for subsequent obliteration by bone chips and/or autologous temporal muscle grafts. The dural sac is incised parallel to the skull. The superior sagittal sinus is ligated and sectioned close to the crista galli, which is then completely removed. In this way, the whole anterior cranial fossa can be accessed by gentle frontal lobe retraction. Possible basal contusions, encephaloceles, and/or arachnoid/pial-mucosal adherences are microsurgically repaired. The olfactory nerves are usually deranged since the injury; however, there may exist cases where one or both the nerves appear more or less intact. In these cases, attempts at nerve preservation may be accomplished provided that possible posterior lesions to the sphenoid plane can be adequately handled and that the nerves do not appear atrophic or severely injured. The progressive degeneration of the olfactory bulbs and the fila olfactoria may be responsible for late CSF leakage. Furthermore, reconstructing the basal dural sac around the

pedunculated pericranial flap ready to be folded backwards

a pericranial graft already sutured over the skull base, ready to be sutured with the convexity dura

subraorbital ridge

olfactory nerve may not be easy. Accordingly, the option of nerve sacrifice may have its rationale allowing wider exposure and more accurate reconstruction. The posterior limit of exposure (and reconstruction) is represented by the lesser sphenoid wings and the optic nerves chiasm [111]. Lesions extending beyond this limit have to be faced through either a lateral (i.e., pterional) approach or better through transnasal endoscopic access [113]. The exposure should be extended as far as the intact posterior dural plane. A pericranial graft can be sutured to the intact dura (otherwise, it may be sealed by fibrin glue) [111]. Alternatively, an autologous graft of fascia lata may be used. In this way, the sphenoid plane and the cribriform plate can be repaired by covering the whole injured area with the pericranial graft, which should be large enough to allow water-tight repair of the dural sac (Fig. 74.12a). Afterward, the anterior bone breakages are repaired by flat structural autologous calvarian bone grafts to reconstruct a plane floor of the anterior cranial fossa. Then, the anteriorly pedunculated pericranial flap is folded back to cover the orbital roofs and the cranialized frontal sinus. Fibrin glue is used to adequately seal the flat to the reconstructed floor (Fig. 74.12b). Finally, the cranial vault is repaired by reassembling the possible bone fragments by means of titanium micro-plates and screws (Fig. 74.13). Superficial layers are usually closed in layers. Two subgaleal drainages are usually left in aspiration.

74.6.4 Postoperative Management Patients are well hydrated and treated with analgesics for approximately a week. Prophylactic antibiotics are debated

pedunculated pericranial flap folded back over the supraorbital ridge and the cranialized frontal sinus

b

cranialized frontal sinus skull base dura repaired convexity dura

convexity dura

dural suture

dural incision parallel to the skul base

brain retractor

hemostatic material over the Superior Sagittal Sinus bifrontal craniotomy

bifrontal craniotomy

Fig. 74.12  Schematic drawing of anatomical structures prepared for obtaining frontal sinus cranialization and dura repair with pericranial graft (a). The surgical field at the end of dura repair, bone grafting of the cranial base, and rotation of anterior pedicle pericranial flap (b)

74  Updates in the Management of Complex Craniofacial Injuries

Fig. 74.13  Sagittal postoperative CT scan of a craniofacial injured patient who sustained cranialization of frontal sinus; note the ablation of posterior sinus wall (Green line), occlusion of nasofrontal ducts with multiple bone chips (Green arrows), dural reconstruction with pericranial graft (Blue line), rotation of anterior pedicled pericranial flap, to cover bone grafts and anterior cranial base reconstruction (Red line). The pericranial flap is incised behind the coronal suture during dissection and skeletonization (red dashed line), then passed through the inferior margin of the frontal craniotomies before the frontal bone flap is repositioned and stabilized with plates and screws

since they could select resistant germs [112]. Sedation, corticosteroids, and anti-epileptic drugs are just used in selected cases. Subgaleal drainages are generally removed within 24 h. Ambulation is allowed as soon as possible based on the general conditions. Each effort is made to avoid coughing and sneezing. CT scan is obtained within 24 h to rule out possible surgical complications. Another CT scan is generally performed around the 7th postoperative day. Discharge occurs as soon as possible, depending on neurological and general conditions. Postoperative controls are generally planned at one, three, and six months. Long-term radiological follow-up is recommended to verify the functional exclusion of frontal sinus mucosa.

74.7 Special Part: Gunshot Injuries 74.7.1 Definition and Epidemiology Gunshot injuries are a very complex part of maxillofacial traumatology that often requires the application of reconstructive microsurgery compared to blunt trauma. This is

831

because in blast injuries there is the destruction or ablation of soft tissues and bone, resulting in defects due to the loss of tissues (Fig. 74.14). This type of injury is particularly rare, especially in developed countries and in the absence of wars, and epidemiological data are uncertain [116]. In economically developed countries and in peaceful conditions, the main causes are self-inflicted injuries, armed robbery, attempted murder, and accidental conditions. Cases of attempted suicide are generally linked to psychiatric pathology, illegal substances, and poor socio-economic conditions. These are all high-energy trauma, but the severity of the injuries varies depends on several factors including the type of weapon, the type of bullet, and the distance from the blast. In a suicide attempt, generally, the firearm is placed in the submental region or directly into the mouth. Gunshot wound oriented in the sagittal plane demonstrating vast facial hard and soft tissue injury with relative sparing of the neurocranium and reduced fatality compared to the coronal plane [117] (Fig. 74.14). The extent of the injuries also depends on the type of bullet. Those of small caliber generally have a limited entry hole with minor damage to the skin, but a high energy distribution to the bone tissue causing complex fractures with comminution. The bullets of large caliber have greater kinetic energy, so they create more significant damage, especially in the case of "fragmentation bullets” that explode after they have penetrated, creating enormous damage with large tissue deletions. The characteristics of the injuries are also different in injuries caused by shotguns loaded with shots; the kinetic energy of the small shots is lower than the single bullets, but they create a major external burst with extensive burns and soft tissue loss. Traditionally, gunshot injuries can be divided into penetrating, perforating, avulsive, blast, and "Chop off" injuries [118]. In penetrating injuries, the bullet has a low velocity, while in "Chop off" injuries, the bullet is faster and transmits high amounts of kinetic energy to the tissues, resulting in extensive destruction and avulsion [119].

74.7.2 General Management and Priorities In the pre-hospital setting, primary lifesaving and organ preservation procedures must be performed following ATLS protocols. Airway control is achieved as usually with intubation or alternatively with surgical airways if intubation is not possible due to the degree of upper airway compromise. Stabilization of the bloodstream occurs with hemostasis through direct pressure and packing and hemodynamic stabilization.

832

a

G. Canzi et al.

b

Fig. 74.14  Clinical picture (a) and angio-CT-3D reconstruction (b) of a self-inflicted gunshot injury with a rifle. Note the wide ablation of facial hard and soft tissues and the preserved anatomy of the neurocranium

In hospital radiological diagnostics, surgical damage control and definitive treatment are performed. Multiplanar CT scans with 3D reconstruction and angio­CT are performed in all maxillofacial ballistic injury patients [120]. Diagnostic angiography with superselective embolization may be necessary for the definitive treatment of life-­ threatening hemorrhages, especially in cases involving the middle facial third. When the patient has been stabilized, an interdisciplinary assessment of the lesions and treatment priorities is carried out. As far as the maxillofacial surgeon is concerned, these are bleeding, airways safety, and visual-threatening injuries.

74.7.3 Timing and Surgical Treatment The possibility of performing a primary definitive treatment rather than a secondary one has been much debated over time [121]. Each case must be evaluated individually based on its characteristics, but overall the literature reports better results and fewer complications in cases where primary definitive treatment is performed [122, 123]. In wide avulsive and more complex injuries, tracheotomy and percutaneous gastrostomy are performed at the first sur-

gical time in the operating room. At the same time, extensive debridement of all not vascularized tissues and foreign bodies removal must be performed. One of the most frequent complications is infection. At this point, the surgeon has to decide how to reconstruct, based on the residual tissues and the extent of the bone and soft tissue defects. Primary early reconstruction requires that these patients are managed in a center with high technical skills [123]. Composite vascularized free flaps are the first choice over the use of local or regional soft tissues flaps and bone grafts. The most used microvascular flaps are the fibula flap for the mandible reconstruction (Fig.  74.15), the iliac flap for the middle third, the latissimus dorsi flap, and the radial forearm or ALT (Antero-Lateral Thigh) flap for soft tissue reconstruction [124, 125]. The goals of reconstructive surgery are to restore basal bone of upper and lower jaws, normal motility of the mandible, a tight diaphragm between oral and nasal cavities and between airways and cranial base, to cover all defects with an adequate amount of well-vascularized soft tissues and to confer the most socially acceptable aesthetics results. Vascularized free flaps have the main advantage of allowing inset of large quantities of composite tissues (bone, skin,

74  Updates in the Management of Complex Craniofacial Injuries

833

a

b

c

d

Fig. 74.15  Axial CT of right mandibular bone comminution and avulsion, due to large caliber gunshot injury (a). Intraoperative early reconstruction, after proper debridement, with vascularized free fibula flap

and reconstructive titanium plate (b). Postoperative panoramics (c) with free bone flap inserted and final results after titanium plate removal and occlusal rehabilitation with titanium dental implants (d)

muscles, tendon) and with autonomous vascularization. They are free from the risk of progression of local tissue suffering due to burns, progressive demarcation and cavitation, and ultimately reduce the risk of infection and dehiscence. Postoperative management relies on long-term coverage with broad-spectrum antibiotics, daily wound dressings, and eventual progressive and further not vital tissue debridement. In some cases, hyperbaric oxygen therapy and negative pressure wound therapy help to promote healing and reduce complications due to dead space cavities.

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G. Canzi et al. the face. Plast Reconstr Surg. 1991;87(3):436–50. https://doi. org/10.1097/00006534-­199103000-­00008. PMID: 1998014 124. Gurunluoglu R, Gatherwright J.  Microsurgical reconstruction of complex maxillofacial gunshot wounds: outcomes analysis and algorithm. Microsurgery. 2019;39(5):384–94. https://doi. org/10.1002/micr.30418. Epub 2019 Jan 24. PMID: 30676662 125. Sokoya M, Vincent AG, Joshi R, Kadakia S, Kohlert S, Lee TS, Saman M, Ducic Y.  Higher complication rates in self-­ inflicted gunshot wounds after microvascular free tissue transfer. Laryngoscope. 2019;129(4):837–40. https://doi.org/10.1002/ lary.27391. Epub 2018 Sep 24. PMID: 30247763

Non-Operative Management of Blunt Traumatic Injuries

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Stefania Cimbanassi, Roberto Bini, and Osvaldo Chiara

Key Points 1. Non-operative management (NOM) is an initial non-­ surgical management strategy used extensively to treat solid organ injuries after blunt trauma. 2. The risk of NOM failure (fNOM) increases proportionally with the grade of organ injury. 3. Interventional radiology and endoscopy are techniques that may help improve the success rate of NOM. 4. Essential requirements to attempt initial NOM are patient’s haemodynamic stability, absence of other indications to exploratory laparotomy, precise grading of organ injury by CECT, availability of continuous patient monitoring and operating/hybrid room 24/7. 5. NOM reduces open surgery-related complications but it is not without drawbacks.

75.1 What Is NOM? Non-operative management (NOM) of solid organ injury is an initial non-surgical management strategy, which usually consists of clinical observation of the patient, but may include early or late use of ancillary tools, such as interventional radiology (IR) and/or endoscopy to improve the healing of injuries (i.e. treating active bleeding or pseudoaneurysms (PSAs)/arteriovenous fistula (AVF) or to treat complications (i.e. biliary leaks, abscesses), avoiding intervention [1]. Nowadays, it represents the gold standard

S. Cimbanassi (*) · O. Chiara Department of Pathophysiology and Transplantation, General Surgery and Trauma Team, University of Milano, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy e-mail: [email protected]; [email protected] R. Bini General Surgery and Trauma Team, ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy e-mail: [email protected]

of treatment of parenchymal injuries, particularly in paediatric patients, provided the haemodynamic stability and the absence of other indications for exploratory laparotomy.

75.2 Why Perform NOM? In the last 30 years, the awareness of the high rate of negative or nontherapeutic laparotomies, which carry themselves high morbidity due to both intra- and extra-abdominal complications, together with the improvement of accuracy of diagnostic imaging, intensive care and IR techniques, favoured the shift from surgical management of parenchymal injuries towards NOM. Particularly, in the case of splenic injuries, NOM reduces the risk of overwhelming post-­ splenectomy infections (OPSI), notwithstanding concerns that exist about immunocompetence of a traumatized spleen, mostly if a variable portion of tissue is devascularized.

75.3 General Principles Conditions that in the past prompted mandatory surgical management, as age older than 55 years, neurologic impairment, severe extra-abdominal associated injuries, large blood requirement, a huge amount of hemoperitoneum, high-grade parenchymal injury or contrast medium extravasation, today are no longer considered as contraindications for NOM [2], provided some cornerstones for a successful non-operative strategy: -accurate patient selection: the feasibility of NOM depends on the patient’s haemodynamic stability. A patient who is unstable on the scene, during transport and/or initial emergency department evaluation and does not respond to resuscitation, in the presence of a positive abdominal window of the Extended-Focused Assessment Sonography for Trauma (E-FAST), requires intervention according to damage control principles. On the other hand, a patient who is three-times stable or responder, having one or

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more of the emergency departments tests positives (clinical evaluation, E-FAST, lab tests) mandates further diagnostic evaluation, by contrast-enhanced torso computed tomography (CECT) [3]. Tomography allows the detection and characterization of parenchymal and vascular solid organ injuries, besides injuries that require surgical repair (i.e. diaphragmatic laceration, hollow viscus injury and high-grade pancreatic trauma), precluding any possibility of NOM. -accurate grading of parenchymal injury, estimating the risk of NOM failure: Parenchymal injuries must be characterized and graded according to the American Association for the Surgery of Trauma (AAST) grading system because the risk of NOM failure (fNOM) increases proportionally to the severity of the injury itself. For example, for splenic injury, fNOM increases from 19.6% for grade III to 75% in grade V, respectively [4]. Moreover, active contrast extravasation (blushing) detected at CECT is widely accepted as risk factor for fNOM, mandating angioembolization (AE), where feasible, or surgery if IR is not available. After contrast medium injection, the evaluation of CT images in different phases (arterial, portal, venous) allows precise visualization of vascular injuries, through indirect signs as vessel truncation, non-bleeding vascular injuries PSAs or AVF which are at risk of delayed bleeding, mandating pre-­ emptive AE or active bleeding. Classification of signs of vascular involvement to be detected at CECT is listed below. The risk of fNOM increases from type A to type D. • • • • •

Venous bleeding. Thrombosis or dislocation (type A). Pseudoaneurysm or AV fistula (type B). Intraparenchymal blushing (type C). Intraperitoneal blushing (type D).

-availability of an operating room (or hybrid) and of clinical monitoring 24/7: Interventional radiology, by AE, improves the outcomes of NOM when clinical or imaging findings indicate a high risk of continued or delayed haemorrhage. Moreover, even for low-grade injuries, a sudden change in patient’s clinical conditions may happen, which mandates a prompt re-evaluation, both clinical and instrumental, and a potential shift from NOM to operative management. For these reasons, NOM should be considered feasible and safe only if continuous clinical and instrumental monitoring and operating room are available at any moment. Institutions without these capabilities should transfer the patient to a higher level facility. -sound considerations about the mechanism of trauma: While NOM is extensively applied for blunt injuries, after penetrating trauma it should be employed selectively, only provided the possibility of a patient’s reliable clinical (re) evaluation and after the trajectory of the wound has been

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accurately assessed by CECT.  This last concern is of the utmost importance, mostly in case of wounds of the lateral abdominal wall or flank, due to the high risk of retroperitoneal involvement, which may carry a delayed peritoneal irritation due to missed injuries. Several reports are available about the safety and feasibility of NOM after gunshot wounds of the anterior abdominal wall with an isolated trajectory to the right upper quadrant, if the patient is alert, stable, reliable, without significant abdominal tenderness [5]. If it is not possible to settle the peritoneal penetration or potential diaphragmatic laceration by CECT, a diagnostic laparoscopy is mandatory to assess potential intraperitoneal injuries not to be missed. How to do NOM of Specific Injuries. Approaching NOM, several organ-specific considerations have to be done: 1. Which are the success rate and advantages of NOM in a given setting? 2. Are there indications to NOM? 3. How to improve successful NOM? 4. How to manage potential complications? 5. How to follow the patient?

75.3.1 NOM for Spleen Injuries Non-operative management is the gold standard for any AAST grade of spleen injuries if the patient is haemodynamically stable, without peritonitis or other contraindication to NOM. In this case, the success rate is near 95% [6]. It represents the treatment of choice, especially for AAST grades I–II, where the risk of bleeding and delayed rupture is low. In higher grades, NOM should be considered only if continuous monitoring is possible and operating/room is always available. The main advantage of NOM after spleen injury is the avoidance of OPSI, particularly in paediatric patients for whom complete immunocompetence may not be already accomplished. Because a contrast medium extravasation is detected at CECT in 15–19% of the stable patients undergoing NOM, and the associated risk of fNOM ranges from 67% to 93% if observed without intervention [7], AE represents a useful tool to improve splenic salvage rate. It must be performed early in any AAST grade of injury if active bleeding is detected, and strongly considered in AAST grades IV–V, regardless the presence or absence of contrast extravasation, due to the higher risk of delayed bleeding in high-grade splenic injury. Angioembolization should be performed proximally, occluding the splenic artery after the origin of the dorsal pancreatic artery, in order to preserve the collateral circulation, limiting the risk of infarction of the spleen parenchyma. The proximal spleen artery embolization (PSAE) improves tissue healing allowing a reduction of intraarterial pressure, favouring clot formation. On the other hand, distal

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splenic artery embolization (DSAE) allows a selective bleeding control, creating limited portions of ischemia, because of the segmental distribution within the parenchyma of splenic artery branches. However, DSAE does not induce ischemia in the non-embolized area whereas it does not prevent other vascular injuries. In patients at high risk of delayed bleeding, regardless of whether they have had AE, follow-up imaging is required within 48–72 h from trauma. Several authors have reported the risk of PSAs formation in 30.4% of ASST grade II and 18.4% of AAST grade III [8, 9]. The persistence of PSAs after AE has been reported in 20.8% of patients [10]. The follow-up may be performed by contrast-enhanced ultrasound (CEUS), to be preferred in paediatric patients, keeping in mind that its use should be tailored to local expertise or by CECT. Laboratory and close clinical monitoring is mandatory to timely detect possible complications of AE (i.e. abscess, collections and cystic evolution). Such complications, occurring in 20% of cases, are easily managed by antibiotics or with percutaneous drainage. Concerns exist about recovery of splenic immune function after splenic trauma and AE. In general, if more than 50% of parenchyma is involved, and AE performed, patients should be treated as though to be asplenic, requiring vaccination against encapsulated germs that cause OPSI (S. Pneumoniae in 57% of cases, H. Influenzae 6% in of cases, N. Meningitis in 3.7% of cases, respectively). The risk of OPSI after splenic trauma, even if managed non-operatively, is due to a reduction in opsonizing antibodies, impaired clearance of opsonized germs by the reticuloendothelial system, impaired mechanical filtration, loss of macrophages and changes in B-lymphocytes subpopulations. Trivalent vaccination should be administered on the day of discharge or after 14  days from trauma, whichever comes first, in the absence of contraindications. Two-month follow-up after the initial vaccination is needed, and lately every 5 years [11].

75.3.2 NOM for Liver Injuries Non-operative management is feasible in any AAST grade of liver injury, provided the patient’s haemodynamic stability, the absence of other indications to surgery and the institution ability to correctly diagnose and grade the hepatic injury and to intervene in case of change in a patient’s haemodynamic status due to bleeding [12]. Because the risk of (re)bleeding is high in AAST grades IV and V, requiring intervention in 25–75% of cases initially managed by NOM [13], the availability of clinical monitoring and operating room 24/7 is mandatory to try NOM in these cases. If all the criteria to approach NOM are respected, the success rate is higher than 90%, notwithstanding the fNOM carries poor outcomes and high mortality. The benefits of NOM are represented by the reduction of laparotomy-related complications and blood

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transfusion requirements and the decrease in overall mortality. The possibility to improve NOM is associated with timely detection of direct and indirect signs of vascular injuries, favoured by CECT, together with a prompt AE of active bleeding and PSAs. Angioembolization is effective in more than 83% of cases to achieve haemostasis at once, despite in 13–20% of patients it should be necessary to repeat the procedure to obtain sound bleeding control [14]. In a transient responder patient, primary AE should be attempted only if a hybrid room is available, in order to proceed with a damage control laparotomy if AE is unsuccessful. NOM is not without complications, which approach 63% in grade V. Delayed haemorrhage, biliary leak, biloma, haemobilia, hepatic necrosis and abscesses represent the most frequent complications. The last two are related to ischemia induced by AE [15]. Hepatic necrosis of a huge amount of parenchyma may require surgical debridement, whereas abscesses, occurring in at least 4% of liver trauma, may easily be managed by percutaneous drainage. Biliary complications, due to the association of direct parenchymal damage and AE, are usually observed lately in 3.2% of hepatic injuries. Signs and symptoms are jaundice, pain, increased liver enzymes and sepsis. Biliary leaks occur in 4.9% of liver trauma. Endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy, stenting or nasobiliary drain is the treatment of choice for the persistent biliary leak [16, 17]. In the case of biliary peritonitis, the peritoneal cavity wash out has to be performed. If not contraindicated, laparoscopy is a viable tool. A routine CECT follow-up is unnecessary if clinical and/or laboratory signs (sudden and unexplained drop in haemoglobin levels, worsening of liver function tests) of complications are absent [12].

75.3.3 NOM for Pancreas Injury Non-operative management of pancreatic injuries is possible and safe for low AAST grade, I or II, where the involvement of the major pancreatic duct is excluded if the patient is stable and without other indications of exploratory laparotomy [18]. The ductal integrity is the cornerstone to try to attempt NOM because if missed at the initial diagnosis it induces leakage of pancreatic enzymes which triggers both local and systemic inflammatory responses, with high morbidity and mortality rates, from 66% to 100% and 11.1–14%, respectively. On the other hand, operative management is recommended for AAST grades III to IV [19], in order to avoid pancreatic juice leak-related complications, which are the causes of fNOM in 10–50% of high-grade pancreatic injuries, being the major fistula the commonest drawback [18]. In AAST grade IV injury NOM could not be possible because of the associated injury of the duodenum, while in ASST grade V, the patient is usually unstable because the massive

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disruption of the pancreatic head is associated with major vascular injuries. Clinical and laboratory signs of pancreatic injury are subtle, making difficult a timely diagnosis only on these bases. CECT has a sensitivity of 25–54% and a specificity of 90–94% [18], allowing the visualization of the pancreatic duct by multiplanar reformation and minimum intensity projections [20]. The portal venous phase is the most accurate CECT phase to diagnose duct injury. If this one cannot be completely settled or it is suspected according to an increase in lipase/amylase levels, magnetic resonance cholangiopancreatography (MRCP) and endoscopic ­retrograde cholangiopancreatography (ERCP) may improve the diagnosis. The advantages of MRCP are non-invasivity, the ability to detect the integrity of the pancreatic duct distally to the site of injury, visualization of eventual peripancreatic collections and other organ damages. On the other hand, MRCP reaches its maximum sensitivity after a few days from trauma, and it may be wise in the emergency setting because of associated conditions. ERCP provides either diagnosis and simultaneous treatment of duct injury, by sphincterotomy, stenting, transpapillary drainage, improving successful NOM. Limitations are represented by its invasivity, risk of complications, lack of availability of the technique and trained personnel to perform the procedure in the emergency setting. The commonest complications of NOM are pancreatic fistula, collections, pseudocyst and, lately, duct stricture. Tomography-guided-percutaneous drainage is effective to manage the vast majority of fistula and collections at the parietocolic gutters, while ERCP is used for stenting persistent fistula, or to perform transgastric or transduodenal drainage of pseudocyst or retrogastric collections using plastic stents. After complication resolution, diagnostic follow-up is indicated by CECT if obstructive symptoms (epigastric pain, delayed gastric emptying) or sepsis are present.

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active bleeding, or by discontinuation of the Gerota’s fascia and the presence of huge perirenal haematoma, with a positive predictive value for AE of 92% [22]. Notwithstanding that the majority of urinary leaks heal spontaneously, persistent urinary extravasation, urinoma formation are possible and may indicate major injury to the collecting system or ureter. For this reason, if a urinary leak has been detected at the initial CECT, a follow-up imaging must be obtained after 48–72 h to rule out the need for intervention to minimize the risk of sepsis, ileus and fistula [23]. Possible options to manage complications are represented by open surgery, nephrostomy and stenting. As a general rule, the less invasive local treatment should be attempted first, while maintaining a urinary catheter in place reducing the pressure of the collecting system. Another possible complication of a high-grade renal trauma managed non-operatively is the dissection or thrombosis of the renal artery. In this case, revascularization may be attempted with endovascular stenting within 4–6  h from trauma, notwithstanding this procedure does not guarantee successful recovery of function of the reperfused kidney. This will be checked at follow-up DMSA scintigraphy at least one month later [24].

75.4 Particular Concerns About NOM Some concerns are represented by the long-term outcomes of this type of management and the appropriate timing of venous thromboembolism (VTE) prevention in patients who underwent NOM.

75.4.1 Long-Term Outcomes

Data on long-term outcomes after successful NOM are scarce and the effects of variable amounts of hemoperitoneum and different gradings of parenchymal injuries are not 75.3.4 NOM for Kidney Injury yet completely understood. Moreno and co-workers [25] recently performed a questionnaire-based survey on 138 In a stable patient, without other indications of exploratory patients who successfully underwent NOM for hepatic and laparotomy, any AAST grade of renal injury may be initially splenic trauma. The median follow-up time was 4 years. A treated by NOM, once a four-phase CECT (including non-­ vast majority of patients were asymptomatic, but in 33.8% of contrast, arterial, nephrographic and pyelographic images) cases, chronic abdominal pain (53%), irregular bowel movehas been obtained [21]. The pyelographic phase is manda- ments (41%) and recurrent infections (25%) requiring antitory to identify urinary extravasation consistent with col- biosis have been complained. No statistically difference was lecting system injury, which if persistent at follow-up observed between asymptomatic and symptomatic patients mandates operative procedures. The success rate of NOM regarding the amount of hemoperitoneum or AAST grade of for AAST grades I–III is higher than 82.9%, allowing the injury, but interestingly, symptomatic patients were younger advantages of reducing the nephrectomy rate which than asymptomatic ones. Among patients complaining of approaches 64% when renal injuries are explored surgically, irregular bowel movements, 16% reported episodes of conto decrease complications and hospital length-of-stay. In stipation, probably due to peritoneal adhesions. This finding higher grades, NOM can be improved by early use of AE of was more frequent in those patients having had associated renal vessels, which is dictated in 10–40% of cases due to severe pelvic fractures and neurogenic dysregulation, which

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may contribute to irregular bowel movements. Among patients who suffered from splenic injury, the rate of recurrent infections was higher compared to that observed in a patient with different injuries, raising doubts about immunocompetence after splenic injury even if treated by NOM.

75.4.2 Timing of Venous Thromboembolism (VTE) Prevention The exact timing of deep venous thromboprophylaxis is unknown, whereas it is well established that major trauma patients, even if managed by NOM, experience a shift from a hypocoagulable state due to Acute Trauma Coagulopathy (ACT) to an eventual hypercoagulable state within 25% of the spleen AAST grade (IV); (b) the angiography shows reduction in vascularization of the superior splenic pole without signs of active bleeding; (c) contrast

injection after deployment of a vascular plug in the intermediate part of the splenic artery (see arrow). Note the absence of flow beyond the plug; (d) CT control at 48 h after TAE shows the plug in the correct site (see arrowhead) and the absence of arterial bleeding

tomically, end-arteries, which means that there is no collateralization between vessels: this is why superselective TAE coincides with more kidney salvage (Fig. 77.6). Microcoils are useful in renal TAE because they are safer than other agents (low risk of non-target embolization) and effective (in the absence of collaterals, there is no risk of reperfusion from other vessels). Some authors observed how total renal loss may be lower with TAE than with operative management [36]. Another setting where interventional radiology may be used is the traumatic lesion of the main renal artery: a renal artery dissection may be treated with uncovered stenting of the artery [37]; a renal artery lesion may be treated with the placement of a covered stent [38]. This procedure may be challenging and time-consuming, so that it could be an alternative in the case of stabilized patients and high-risk surgical patients. In both cases, a dual antiplatelet therapy followed by a single antiplatelet therapy lifelong is necessary for stent patency.

77.3.5 Pelvis Pelvis traumas are mainly due to blunt traumas causing pelvic fractures. A major injury of the pelvis can be observed in 9% of blunt traumas [39]. The mortality rate from pelvic trauma ranges from 5.6– 15% to 36.4–54% if associated with hemorrhagic shock [40]. Unstable pelvic ring injuries are more frequently associated with high blood losses because of the absence of the tamponade effect on pelvic bones and ligamentous structures and its increasing capacity to hold a great volume of blood. In most cases, bleedings are of venous or bony origin, but in 10–20% of cases, bleedings are of arterial origin [41]: this condition is more frequently associated with hemodynamic instability. Pelvic binders and external fixation are useful maneuvers to reduce venous or bony bleeding but are not sufficient to stop arterial bleeding. Operative management is based on

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b

a

c

d

Fig. 77.6 (a) CT showing a complete renal rupture (AAST grade V) with a large active bleeding (see arrow). Despite the vascular lesion, confirmed at angiography (figure b, see arrowheads), the patient was a

transient responder and, because of the young age (20 y.o.) was submitted to the angio suite. The bleeding was embolized with coils (figure c, see arrow); (d) CT control after TAE. No bleedings can be observed

pelvic packing, but open surgical procedures may bring the loss of the tamponade effect of fixation/binders and have a high risk of failure [42]. The correct management of pelvic fractures with or without hemodynamic instability requires, when feasible, a CT evaluation of the patient. Contrast-enhanced CT has a high sensitivity, specificity, and accuracy (respectively, 60–90%, 85–90%, 87–98%) for the detection of arterial sources of bleeding [43]. Indications for angiography include any type of vascular injury seen at CT: active blushing, pseudoaneurysm, and arteriovenous fistula [44, 45]. Some authors suggest that patients with hemodynamic instability and pelvic hematomas should be submitted to the angio suite even in the

absence of an arterial source of bleeding at CT [46]. This indication is controversial because many studies observed a mismatch between CT findings and angiographic findings. Angiography can be negative despite signs of arterial bleeding at CT; on the other side, angiography can be positive after no signs of arterial bleeding at CT [47]. Technically, angiography starts with a femoral approach. Pelvic binder can cause trouble during femoral puncture so that it should be removed or shifted from the groin. Arterial bleedings usually arise from internal iliac branches, less frequently from inferior epigastric arteries: an accurate evaluation of CT images is fundamental to reduce operative times during angiography. A preliminary high-flow aortography can also aid in determining which artery should be studied

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F. Morelli et al.

a

b

c

d

Fig. 77.7 (a) CT showing a hematoma with active bleeding anterior to the bladder (see arrow); (b) left femoral puncture, catheterization of the right internal iliac artery and injection from a microcatheter in the right inferior vesical artery which confirms the active bleeding (see arrow-

head); (c) angiographic control after injection of cyanoacrylate with complete embolization of the vessel (see arrow); (d) CT control showing hyperdense cyanoacrylate in the pelvis (see arrowhead) without active bleeding

before. Then, a superselective study with a microcatheter must be performed to confirm and treat the bleeding. A detailed knowledge of the arterial pelvic supply is fundamental to treat pelvic bleedings. Almost all the embolic agents can be used to treat pelvic bleedings, but the appropriate material depends on the artery affected. Pudendal artery embolization can bring impotence in males: in this case, coils are less ischemic than particles or glue and should be preferred. Gluteal artery embolization can bring tissue necrosis: even in this case, coils are better to use than particles or glue. In the case of bleeding from other branches (obturator artery, vesical artery, and inferior epigastric

artery) particles and glue can be used as an alternative to coils (Fig. 77.7): moreover, they are faster to release, so that especially in the case of bleeding from the inferior epigastric artery (a muscular branch with low risk of ischemic complications after embolization), glue should be the embolic agent to use. In those cases where CT shows an arterial bleeding but angiography is negative, a nonselective embolization with gelfoam of the iliac artery involved can be an effective treatment: gelfoam induce hemostasis with a low risk of consequences in the long term thanks to their temporary nature. Another indication to proximal gelfoam embolization is the

77  Current Perspectives of Interventional Radiology in Trauma

presence of multiple arterial bleedings in the unstable patient in order to reduce operative time. Angiography of the contralateral internal iliac artery or the ipsilateral inferior epigastric artery should be always performed because of the complex arterial network of the pelvis. Clinical success of TAE is high, ranging from 84 to 100% [48, 49]. Recurrent bleeding rate is quite low (0–23%) and mainly depends on a new bleeding from another branch not seen at CT or at previous angiography. It should be considered in the case of persistent hypotension or transfusion requirement of >2 U/h of packed red blood cells after first angiography [50]. Mortality rate in these patient remains high despite effective TAE; higher mortality rates are observed in elderly patients, in patients in whom TAE was delayed, and in patients with greater hemodynamic compromise [51].

77.3.6 Extremities The extremities can be affected by penetrating or blunt injuries which can lead to acute limb ischemia. Symptoms of acute limb ischemia include the “six P’s”: pain, pallor, paresthesia, perishingly cold, pulselessness, and paralysis. These are signs of neurovascular lesions which need to be promptly treated. In this setting, an operative management is usually preferred for many reasons: surgery can treat a compartment syndrome; moreover, because osseous fixation of associated bone fractures is often necessary, a concomitant surgical repair of the vascular lesion is more appropriate. In the absence of hard signs of acute limb ischemia or if a concomitant operative management is not necessary, endovascular treatment can be evaluated. Aspects that should be taken into consideration are the type and localization of vascular lesions together with the age of the patient. Arterial dissections may be treated with uncovered stenting; arterial transactions can be treated with covered stenting; arterial occlusion may be treated with thromboaspiration; arterial bleeding from collateral branches can be treated with coil embolization (Fig. 77.8). Stenting of anatomic locations with relative flexibility (axillary artery, common femoral artery, and popliteal artery) should be avoided for the high risk of unfolding and crushing of the stent. On the other side, deep anatomic locations where surgery can be challenging like the subclavian artery or the iliac artery are good candidates to endovascular or combined treatments [52].

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The main concern of stent-grafts placement in these patients is the lack of long-term data on patency and safety: it means that special attention should be paid to younger patients’ candidates to the endovascular approach. A combined approach can be another alternative: the placement of an occlusion balloon proximal to an arterial lesion can be associated with surgery in order to avoid massive intraoperative bleeding [53]. As a general rule, lack of robust data in this field makes necessary a careful evaluation of each case by a multidisciplinary team [54].

77.4 Other Organs Other abdominal organs like adrenal gland, pancreas, and intestine are by far less prone to traumatic lesions and even less to endovascular treatments. These organ injuries are almost ever associated with other organ injuries like spleen or liver. Adrenal glands can be rarely injured in the case of blunt thoracoabdominal trauma. The adrenal gland is supplied by three different little arteries: the superior, middle, and inferior adrenal artery, which usually originate from the phrenic artery, the aorta and the renal artery, respectively [55]. Few data regarding endovascular treatment are present in the literature, so a careful evaluation by a multidisciplinary team is mandatory. If indicated, TAE can be performed with the use of microcoils in the affected artery. No cases of adrenal gland of ischemia have been observed in literature thanks to the triple arterial supply of the gland [56]. Pancreatic trauma is rare, occurring in