Office Based Anesthesia Complications: Prevention, Recognition and Management 3030614263, 9783030614263

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Office Based Anesthesia Complications Prevention, Recognition and Management Gary F. Bouloux Editor

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Office Based Anesthesia Complications

Gary F. Bouloux Editor

Office Based Anesthesia Complications Prevention, Recognition and Management

Editor Gary F. Bouloux Division of Oral and Maxillofacial Surgery Department of Surgery Emory University School of Medicine Atlanta, GA USA

ISBN 978-3-030-61426-3    ISBN 978-3-030-61427-0 (eBook) https://doi.org/10.1007/978-3-030-61427-0 © Springer Nature Switzerland AG 2021 This work is subject to copyright. All rights are reserved 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

Preface

The simultaneous provision of anesthesia and surgery by the oral and maxillofacial surgeon creates many challenges. However, a robust education and training in anesthesia during residency equips the surgeon with the skill set and experience to manage patients. The use of local anesthesia, conscious sedation, deep sedation, and general anesthesia allow the surgeon to perform invasive and painful procedures with relative ease. However, the provision of anesthesia is not without risk. It remains the responsibility of the oral and maxillofacial surgeon to ensure that both the anesthesia and surgery are completed in a safe and efficient manner. There is no room for complacency in the provision of anesthesia, rather a healthy paranoia is needed. Despite adequate risk stratification and careful preparation, complications can and will occur. It remains paramount that the surgeon approach each and every anesthesia with a mantra to initially prevent, then recognize, and finally manage all complications. This will ensure that the risk associated with the provision of anesthesia is mitigated for every patient. This text and the contents within it are based on the most common anesthesia-related complications that have been documented over more than 20 years of data collection for oral and maxillofacial surgery. This book is dedicated to our specialty, the providers who administer anesthesia and perform surgery, and the patients who choose to place their lives firmly in our hands. Atlanta, GA, USA

Gary F. Bouloux

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Contents

1 Risk Stratification for Office-Based Anesthesia��������������������������������������   1 Stuart Lieblich and Marissa R. Shams 2 Basic Life Support and Advanced Cardiac Life Support����������������������  13 Jeffrey Bennett 3 Laryngospasm��������������������������������������������������������������������������������������������  23 Jeffrey A. Elo 4 Aspiration ��������������������������������������������������������������������������������������������������  35 Vincent J. Perciaccante 5 Asthma��������������������������������������������������������������������������������������������������������  41 Jeffrey A. Elo and Marissa R. Shams 6 Anaphylaxis������������������������������������������������������������������������������������������������  53 William Chung 7 Bronchospasm��������������������������������������������������������������������������������������������  59 William Chung 8 Obesity��������������������������������������������������������������������������������������������������������  65 Robert C. Bosack 9 Obstructive Sleep Apnea ��������������������������������������������������������������������������  73 Martin B. Steed and Austin Lyman 10 Trismus��������������������������������������������������������������������������������������������������������  79 Martin B. Steed and Kacy Wonder 11 Cardiac Arrhythmias��������������������������������������������������������������������������������  85 Steven M. Roser and Dimitri Cassimatis 12 Myocardial Infarction����������������������������������������������������������������������������   101 Dimitri Cassimatis and Gary F. Bouloux 13 Pulmonary Embolism�������������������������������������������������������������������������������� 109 Lisa Bernstein and Gary F. Bouloux

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Contents

14 Pediatric Emergencies ������������������������������������������������������������������������������ 113 Erin Rosenberg 15 Emergent Airway Management���������������������������������������������������������������� 125 Deepak G. Krishnan and Vincent J. Perciaccante 16 Prescription Opioid Abuse��������������������������������������������������������������������   137 Gary F. Bouloux and Deepak G. Krishnan Index�������������������������������������������������������������������������������������������������������������������� 147

Contributors

Jeffrey Bennett, DMD  Oral and Maxillofacial Surgery, Indianapolis, IN, USA Lisa  Bernstein, MD  Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA Robert C. Bosack, DDS  Private Practice, Oral and Maxillofacial Surgery, Orland Park, IL, USA Gary F. Bouloux, DDS, MD, MDSc, FRACDS(OMS), FACS  Division of Oral and Maxillofacial Surgery, Department of Surgery, Emory University School of Medicine, Atlanta, GA, USA Dimitri  Cassimatis, MD  Emory University Hospital Midtown, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA William  Chung, DDS, MD  Department of Oral and Maxillofacial Surgery, University of Pittsburgh School of Dental Medicine, Pittsburgh, PA, USA Jeffrey A. Elo, DDS, MS, FACS, FACD, FICD  Division of Oral and Maxillofacial Surgery, College of Dental Medicine, Western University of Health Sciences, Pomona, CA, USA Department of Oral and Maxillofacial Surgery, Loma Linda University, Loma Linda, CA, USA Deepak G. Krishnan, DDS, FACS  Division of Oral and Maxillofacial Surgery, Department of Surgery, University of Cincinnati, Cincinnati, OH, USA Stuart  Lieblich, DMD  University of Connecticut School of Dental Medicine, Farmington, CT, USA Private Practice, Avon Oral and Maxillofacial Surgery, Avon, CT, USA Austin Lyman, DMD, MS  Department of Oral and Maxillofacial Surgery, Medical University of South Carolina, Charleston, SC, USA Vincent  J.  Perciaccante, DDS, FACS  Oral and Maxillofacial Surgery, Emory University School of Medicine, Atlanta, GA, USA Private Practice, South Oral and Maxillofacial Surgery, Peachtree City, GA, USA

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Contributors

Erin Rosenberg, MD  Childrens Healthcare of Atlanta, Emory University School of Medicine, Atlanta, GA, USA Steven M. Roser, DMD, MD, FACS  Division of Oral and maxillofacial Surgery, Department of Surgery, Emory University School of Medicine, Atlanta, GA, USA Marissa R. Shams, MD  Department of Internal Medicine, Division of Pulmonary, Allergy, Critical Care & Sleep Medicine, Emory University School of Medicine, Atlanta, GA, USA Martin  B.  Steed, DDS, FACS  Department of Oral and Maxillofacial Surgery, Medical University of South Carolina, Charleston, SC, USA Kacy  Wonder, DMD  Department of Oral and Maxillofacial Surgery, Medical University of South Carolina, Charleston, SC, USA

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Risk Stratification for Office-Based Anesthesia Stuart Lieblich and Marissa R. Shams

Introduction The care of the patient involves two considerations: the planned surgical procedure and the appropriate management of the discomfort and anxiety that will accompany that procedure. The provision of these separate aspects of patient care makes our profession unique. The office-based surgery is planned to be minimally invasive with a low potential for significant blood loss and hemodynamic changes. However, the provision of local anesthesia, deep sedation, or general anesthesia, all involve the administration of agents with systemic effects. The responsibility of the oral and maxillofacial surgeon (OMS) is to ensure that the patient can tolerate not only the surgical procedure but also more importantly the local and general anesthesia. The provision of local anesthesia, deep and general anesthesia in any patient is not without risk. The very essence of risk stratification is to identify patients with varying degrees of anesthesia risk and adjust the anesthesia plan accordingly. Most patients are relatively healthy and will require no particular modification to the anesthesia plan. Other patients will require modification to the anesthesia plan. This may include the choice of local anesthetic, anesthesia medications, drug doses, duration of anesthesia, and post anesthesia recovery. On occasion, it will also necessitate that a patient be treated in an ambulatory surgical center or hospital operating room. The five key elements to enable appropriate risk stratification for office-based anesthesia include the following: S. Lieblich (*) University of Connecticut School of Dental Medicine, Farmington, CT, USA Private Practice, Avon Oral and Maxillofacial Surgery, Avon, CT, USA e-mail: [email protected] M. R. Shams Department of Internal Medicine, Division of Pulmonary, Allergy, Critical Care & Sleep Medicine, Emory University School of Medicine, Atlanta, GA, USA e-mail: [email protected] © Springer Nature Switzerland AG 2021 G. F. Bouloux (ed.), Office Based Anesthesia Complications, https://doi.org/10.1007/978-3-030-61427-0_1

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• • • • •

S. Lieblich and M. R. Shams

American Society of Anesthesiology physical status Functional status (METs) Mallampati classification Body mass index (BMI) Airway access

Patient Evaluation Patient evaluation begins with a thorough medical history that includes specific questions about previous surgical and anesthetic experiences. The initial consultation with a patient provides the opportunity to obtain a thorough medical, social, and surgical history as well as perform a physical examination. This allows the OMS to identify the appropriate surgical plan as well comorbid medical conditions that allow risk stratification prior to determining the most ideal anesthetic technique. On occasion, this will require that the OMS consult with the patients other healthcare providers and/or request additional diagnostic testing to appropriately risk stratify the patient. It is ideal if patients can complete their medical history intake forms at home prior to presenting to the office. This allows the patient to gather the information at home prior to the consultation. Furthermore, the documents can be submitted electronically ahead of time facilitating an initial review of the patient’s medical history. The initial office visit should include obtaining vital signs including blood pressure and heart rate. It may also be advantageous to record the oxygen saturation (SaO2) that serves as a good surrogate monitor of cardiopulmonary function. Staff who record these vital signs should have basic training in the recognition of abnormal rhythms including bradycardia, tachycardia, and irregular rhythms. All abnormal values should be flagged for review by the OMS. A review of the patient’s past medical and surgical history will allow the patient to be classified using the American Society of Anesthesiologists (ASA) physical status guidelines (Table 1.1). In an ideal setting, patients within ASA I and II classes are the best candidates for office-based anesthesia as they most likely have acceptable cardiovascular and pulmonary reserves to withstand deep sedation and general anesthesia. Office-based deep sedation and general anesthesia should be approached with caution for ASA III patients. This may require significant modifications to the anesthesia plan to further reduce the potential risk of adverse cardiovascular and pulmonary complications. Contemporary pre-anesthetic evaluation has greatly reduced the need for routine laboratory testing. Significant information about pulmonary and cardiovascular reserve can be obtained by determining the patient’s metabolic equivalents (METs). This reflects the patients exercise tolerance with one MET equivalent to 3.5 mL of oxygen per kilogram consumed per minute (3.5  mL O2/kg/min). METs offer the best insight into a patient’s ability to withstand changes in pulmonary and cardiovascular function that may occur during anesthesia. Low METs or a recent decline

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Table 1.1  American Society of Anesthesiology Physical Status guidelines ASA PS classification ASA I

Definition Normal healthy patient

ASA II

Patient with mild systemic disease

ASA III

Patient with severe systemic disease

ASA IV

Patient with severe systemic disease that is a constant threat to life

ASA V

Moribund patient who will not survive without the operation Brain dead patient having organs harvested

ASA VI

Explanation No smoking and moderate alcohol Mild disease without functional limitations Severe disease with functional limitations Severe disease, e.g., recent MI, CVA, or TIA ACS, severe valvular heart disease, and sepsis NA NA

MI myocardial infarction, CVA cerebrovascular accident, TIA transient ischemic attack, ACS acute coronary syndrome Table 1.2  Functional status assessment (MET) examples Excellent (>7 METs) Squash Tennis Jogging Cleaning floors

Moderate (4–7 METs) Cycling Climbing a flight of stairs Walking 4 mph Yardwork

Poor (≤4 METs) Walking 2 mph Activities of daily living

Adapted from: Hlatky MA, Boineau RE, Higginbotham MB, Lee KL, Mark DB, Califf RM, et al. A brief self-administered questionnaire to determine functional capacity (the Duke Activity Status Index). Am J Cardiol. 1989;64:651–4

in METs should alert the OMS to the potential for adverse anesthesia-related complications that require further work-up and risk stratification. Patients that report a functional status of less than 4 METs are not candidates for an office-based deep sedation or general anesthesia due to their lack of cardiac and respiratory reserve (Table 1.2). The ability to establish an airway remains critical to office-based anesthesia. The Malampati classification remains a robust tool for predicting difficulty related to establishing and maintaining an airway in addition to intubating patients. Although it is not possible to adjust a patient’s Malampati score, the anesthesia plan should be modified according to the relative airway risk associated with different scores (Fig. 1.1). The BMI is a useful parameter to help predict anesthesia-related complications. It is calculated by dividing the patient’s weight (kg) by their height (m2). Patients that fall into a normal or overweight category pose little anesthetic risk. A BMI that places a patient in the underweight category increases the anesthesia risk due to electrolyte abnormalities and cardiac arrhythmias. A BMI that places a patient in the obese and morbidly obese categories also places the patient at increased risk due to the potential for loss of airway; decrease functional residual capacity (FRC) and

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Fig. 1.1  Mallampati classification (1–4) Table 1.3  Body mass index

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Underweight Normal Overweight Obese Morbidly obese

difficulty with establishing an airway or intubation. Adjusting the anesthesia regime by avoiding apnea-producing drugs maybe beneficial (Table 1.3). Challenges related to maintaining a patent airway or establishing one when it is lost are compounded not only by the BMI but also the length and diameter of the neck. The sternomental distance extends from the sternal notch to the menton with a distance of less than 12.5 cm having a positive predictive value of 82% for a difficult intubation (Fig. 1.2). The checklist for a patient evaluation for office-based anesthesia should include the following: • • • • • • •

Blood pressure, heart rate, and rhythm Height and weight (body mass index) Past medical, social, surgical, and anesthesia history Current medications including recent changes in medications Allergies Risk factor evaluation for obstructive sleep apnea Salient laboratory results review (a) ECG for patients with cardiac disease (within 6–12 months) (b) Blood glucose levels and hemoglobin A1C for diabetics (type I and type II) (c) INR reports for patients taking warfarin (within 7 days of planned surgery) or suspected hepatic disease (d) SaO2 on room air for patients with respiratory disease • Recording of ASA status • Recording of functional status There are specific aspects of the patient physical examination that are critical for office-based anesthesia. These include the following:

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Fig. 1.2 Sternomental distance

• Focused airway examination (a) Mallampati score recorded (b) Maximum incisal opening (c) Risk factors that contribute to difficulty with positive pressure ventilation including facial hair, edentulism, short and thick neck, increased BMI • Auscultation of lungs • Observation of extremities for venipuncture sites It remains controversial whether pregnancy testing is appropriate for females of childbearing age who undergo office-based deep sedation or general anesthesia. The American Association of Oral and Maxillofacial Surgeons (AAOMS) Parameters of Care does not endorse routine testing for pregnancy. Exceptions may be indicated if there is an equivocal history of sexual activity with a possibility of pregnancy due to an uncertainty regarding the time of the last menstrual period. A point of care (POC) urine testing kit for pregnancy is available and usually positive within 14 days of conception. Minors (12 years old) Components of severity Symptoms

Intermittent 80%

Some limitation 60–80%

Extremely limited

0–1/year

>2× per year

>2× per year

>2× per year

SABA as needed

Low-dose ICS, LTRA

Medium-­ dose ICS, +/− LABA, LTRA

High-dose ICS + LABA or LAMA, LTRA, daily oral corticosteroids, biologic agentsa

>80%

Mild >2 days per week but not daily 3–4× per month

Several times per day

2 days/ week Daily

< 60%

≥2/day

≥ 80%

Interference with activity None

Use of oral steroids in the prior 12 months 0–1

Minor

a

Some

a

Extremely limited

a

2 or more 2 or more 2 or more

Adapted from: Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2020. Available from: www.ginasthma.org FEV1 forced expiratory volume in 1 second; SABA short-acting β-agonist a Not including prevention of exercise-induced bronchospasm

airway obstruction on spirometry, especially if acutely reversible with a bronchodilator, strongly supports the diagnosis of asthma. Peak flow meters can also be used to monitor asthma and diagnose asthma exacerbations at home by measuring a decline in peak flow with respect to a previously determined baseline. The traditional approach to the classification of asthma described asthma as extrinsic or intrinsic. Extrinsic asthma occurs as a result of sensitization to a specific antigen. Intrinsic asthma occurs without identifiable antigen or prior sensitization. Current guidelines suggest that asthma is better classified as allergic, non-allergic, eosinophilic, and adult onset. Furthermore, asthma can be classified based on the severity and control (Table 5.1). The severity and control when assessed are based on the worst/most severe marker. For example, if a patient has FEV1 > 80% (intermittent), nighttime symptoms 3 times in the past 12 months Nocturnal dry cough Recent upper respiratory infection (2 hospitalizations in the past year for asthma-related illness >3 emergency room visits for asthma-related illness >2 metered-dose inhaler usages of short-acting β2-agonists in the past month Obesity Low socioeconomic status Illicit drug use An FEV1 < 1 L with spirometry

Several important factors should be considered in patients with a history of asthma to help reduce the likelihood of developing an asthmatic attack during an intravenous sedation or general anesthesia. General guidelines include the following: • Never induce a wheezing patient. • Defer elective oral and maxillofacial surgical sedation/anesthesia treatment until the patient’s asthma is controlled and wheezing is no longer present. • Recent upper respiratory infection ( 35 kg/m2, age > 50, neck circumference, and male gender that predict the likelihood of OSA. The risk for having undiagnosed

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OSA is proportional to the score. Other screening questionnaires include the Epworth Sleepiness Score (ESS), Berlin questionnaire, Sleep Apnea Clinical Score, NoSAS Score, and the Multivariable Apnea Prediction Instrument (MVAP). There are various phenotypes of OSA patients, so physical examination is essential for diagnosis as well as predicting a difficult airway. Increased body mass index (BMI), neck circumference (>17″ in men or >16″ in women), and a reduced thyromental distance are all frequently seen in OSA. There are multiple potential sites for obstruction in patients with OSA.  The physical examination should evaluate for adequacy of the nasal valve (Cottle test), deviated septum, turbinate hypertrophy, rhinitis, elongated soft palate, enlarged tonsils or tongue, and the skeletal structure as it pertains to the anteroposterior position of the maxilla and mandible. Mandibular hypoplasia is frequently associated with OSA. If the history and physical exam suggest the possibility of OSA in an otherwise undiagnosed patient, consideration should be given to referring the patient for polysomnography prior to office-based sedation or general anesthesia. Patients with a diagnosis of OSA are generally poor candidates for office-based sedation due to the anesthetic issues including challenges with maintaining an airway and the ability of the provider to establishing a patent airway when difficulty is encountered. Several approaches can be adopted to reduce the likelihood of anesthesia complications in the patient with OSA.

Pre-operative • Avoid preoperative prescriptions of anxiolytic or sedatives. • Consider preoperative prophylaxis with proton-pump inhibitors, antacids, or histamine-­2 blockers to reduce the potential for gastric aspiration. • Use ideal body weight for loading dose of medications. • Use ideal body weight to calculate maintenance doses. • Position patient semi-upright or sitting. • Have patient bring home CPAP mask and/or mandibular reposition splint to appointment for use.

Operative • Monitor vital signs closely with end-tidal CO2, precordial auscultation, pulse oximetry, ECG, and blood pressure. • Use local anesthesia alone. • Use local anesthesia in addition to conscious sedation with nitrous oxide. • Moderate sedation with a benzodiazepine (midazolam) and an opioid (fentanyl) alone. Dose conservatively with 0.05–0.1  mg/kg midazolam and 0.5–1  μg/kg fentanyl. While apnea is less likely with this regimen, jaw support via chin lift or jaw thrust may be needed given soft tissue redundancy. • Consider opioid alternatives for analgesia including ketamine, acetaminophen, ketorolac, dexmedetomidine, and corticosteroids.

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• Avoid irreversible medications that are likely to result in apnea such as propofol or methohexital. • Avoid long-acting opioids with active metabolites such as hydromorphone or morphine. • Have reversal agents immediately available including flumazenil (0.5 mg) and naloxone (0.4 mg). • Ensure appropriately sized oral and nasal airways are immediately available. • Ensure the ability to provide two-person positive pressure ventilation (PPV). • Utilize high flow supplemental oxygen at rate of 4 L/min to improve oxygenation. • Ensure an adjunctive airway such as a laryngeal mask (LMA) is readily available. • Intubation is likely to be challenging; have appropriately sized endotracheal tube, tube catheter, and a video laryngoscope available.

Postoperative • Avoid or minimize postoperative opioid prescriptions. • Consider weak mu-receptor agonists such as Tramadol with less respiratory depression. • Consider the use of long-acting liposomal bupivacaine to further reduce the need for postoperative opioids. • Utilize postoperative analgesic opioid alternatives such as ibuprofen, celecoxib, ketorolac, acetaminophen, gabapentin, or pregabalin. • Consider a longer postoperative monitored recovery with the use of CPAP if needed. • Recommend lateral sitting or semi-upright recovery position. The American Society of Anesthesiology recommends that patients with OSA undergoing ambulatory receive at least 3  h of postoperative recovery before discharge to ensure adequate recovery and minimize the potential for airway loss. It may also be beneficial in those patients being treated with continuous positive airway pressure (CPAP) to have the device available for use in the post anesthesia care unit (PACU).

Recognition Complications related to OSA and office-based sedation generally relate to loss of the airway and the challenges related to reestablishing an airway. It remains imperative to immediately recognize any complication and initiate treatment quickly. This remains a recurrent theme for all office-based procedures whether under local or general anesthesia. Early recognition is facilitated by the following: • Monitor end-tidal CO2 for changes in the waveform that suggest apnea, decreased respiratory rate, and obstruction. • Monitor precordial sounds to identify any decline in the respiration or obstruction.

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• Monitor the ECG and recognize any changes in rhythm that may reflect hypoxemia (tachycardia, bradycardia, premature ventricular contractions (PVC), and junctional escape). • Monitor pulse oximetry but realize that there is a lag time between clinical apnea and saturation values depicted on monitors. Early recognition of airway difficulties allows the surgeon to initiate treatment early. In order to successfully initiate corrective action, it is imperative to reestablish a patent airway within a short time frame, which may be as short as 1–2 min for complete apnea or somewhat longer in cases of partial apnea.

Management Partial or complete loss of the airway requires urgent treatment. The following stepwise algorithm should be considered. Reevaluate the patient’s response to each maneuver before advancing to subsequent steps. • Stop the procedure and pack wounds with gauze attached to ligature/string that exits at the corner(s) of the mouth. • Head tilt up, chin lift, or jaw thrust maneuver. • Suction oropharynx with Yankauer high volume suction. • Pull the tongue forward with Russian clamps or suture. • Consider insertion of a lightly lubricated nasal airway early. • Consider insertion of an oral airway as needed. • Begin two-person bag–valve-mask ventilation with 100% supplemental oxygen at flow rate of 15 L/min. • Consider drug reversal with IM/IV flumazenil (0.5 mg) or naloxone (0.4 mg). These drugs may need to be re-dosed depending on the response and patient size. • Consider an additional airway such as LMA. • Consider intubation, but appreciate the difficulty associated with intubating many patients with OSA due to their BMI, neck size, thyromental distance, and mandibular hypoplasia. • Consider rapid sequence intubation if need to establish a secure airway. • Consider a needle cricothyroidotomy (with jet ventilation).

Suggested Reading 1. Abuzaid AS, Al Ashry HS, Elbadawi A, et al. Meta-analysis of cardiovascular outcomes with continuous positive airway pressure therapy in patients with obstructive sleep apnea. Am J Cardiol. 2017;120:693–9. 2. Oksenberg A, Gadoth N. Positional patients (PP) and non positional patients (NPP) are two dominant phenotypes that should be included in the phenotypic approaches to obstructive sleep apnea. Sleep Med Rev. 2018;37:173–4.

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3. Carberry JC, Amatoury J, Eckert DJ.  Personalized management approach for OSA.  Chest. 2018;153:744–55. 4. American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: an updated report by the American Society of Anesthesiologists Task Force on perioperative management of patients with obstructive sleep apnea. Anesthesiology. 2014;120:268–86. 5. Halle TR, Oh MS, Collop NA, Quyyumi AA, Bliwise DL, Dedhia RC. Surgical treatment of OSA on cardiovascular outcomes: a systematic review. Chest. 2017;152:1214–29. 6. Javaheri S, Barbe F, Campos-Rodriguez F, et al. Sleep apnea: types, mechanisms, and clinical cardiovascular consequences. J Am Coll Cardiol. 2017;69:841–58. 7. Martinot JB, Le-Dong NN, Crespeigne E, et al. Mandibular movement analysis to assess efficacy of oral appliance therapy in OSA. Chest. 2018;154:1340–7. 8. Yuan I, Sinha AC.  Chapter 6: Obesity and nutrition disorders. In: Fleisher LA, editor. Anesthesia and uncommon disorders. Philadelphia: Elsevier; 2012. 9. Pardo MC, Miller RD. Basics of anesthesia. 7th ed. Philadelphia: Elsevier; 2018. p. 849–56. 10. Reutrakul S, Mokhlesi B. Obstructive sleep apnea and diabetes: a state of the art review. Chest. 2017;152:1070–86. 11. Senaratna CV, Perret JL, Lodge CJ, et al. Prevalence of obstructive sleep apnea in the general population: a systematic review. Sleep Med Rev. 2017;34:70–81.

Trismus

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Martin B. Steed and Kacy Wonder

Introduction Trismus is broadly defined as a restricted opening of the oral cavity. There are a myriad of causes for trismus. Mild to moderate trismus should be considered relative to the patient’s baseline or preoperative opening as a normal maximum incisal opening (MIO) varies between individuals. The lower limit of a normal is considered to be 35  mm for females and 40  mm for males. The Diagnostic Criteria/ Temporomandibular Disorders (DC/TMD) defines trismus as a maximum assisted opening (including vertical incisal overlap) of less than 40 mm. An MIO of 40 may be too high, and for the purposes of this chapter, trismus will be defined as an MIO of ≤30 mm. Severe trismus is probably best defined as trismus that prevents the use of direct laryngoscopy, video laryngoscopy, or the insertion of a supraglottic airway (SGA). The severity of the trismus is often helpful in determining the diagnosis and potential treatment modalities. Trismus may be secondary to pain or due to a mechanical obstruction within the temporomandibular joints, coronoid process, masticatory muscles, or soft tissues. Distinguishing between pain and mechanical obstruction is crucial as the latter is unlikely to allow any additional opening despite a deep sedation or general anesthesia. This requires a very directed examination of the MIO as part of a routine physical examination. It is helpful to determine if the limited MIO has a soft or hard end feel. Asking the patient to open maximally and then using the thumb and middle finger to further stretch the opening is helpful. Patients should be warned that this might provoke pain. Inability to further increase the opening suggests that the limitation is mechanical. The ability to open further would suggest that pain is the predominant limiting factor. M. B. Steed (*) · K. Wonder Department of Oral and Maxillofacial Surgery, Medical University of South Carolina, Charleston, SC, USA e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2021 G. F. Bouloux (ed.), Office Based Anesthesia Complications, https://doi.org/10.1007/978-3-030-61427-0_10

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The choice of anesthesia technique (local anesthesia versus deep sedation/general anesthesia) must in part be based on the MIO. It should also influence the decision between an office-based or Ambulatory Surgical Center (ASC)/hospital-based location. Patients with trismus who lose their airway present a significant challenge to establishing and maintaining an airway. Two-person bag valve mask ventilation (BMV) and the use of head tilt, chin lift, and jaw thrust when combined with a nasal or oral airway will often suffice. When these interventions are not adequate, it should be noted that direct laryngoscopy (DL) typically requires an MIO of 40 mm rendering it inadequate in patients with trismus. Indirect laryngoscopy with video-­ laryngoscopy requires less MIO, but may still be very challenging. This makes intubation very challenging and unlikely to be successful in an emergent situation. The use of a SGA should be considered, as this does not require DL or indirect laryngoscopy. However, trismus is also a known risk factor for SGA failure. The airway challenges with patients with trismus will ensure that most office-based procedures are completed under local anesthesia alone or in an ASC/hospital environment.

Etiology There are a number of causes of trismus. The oral and maxillofacial surgeon may encounter any of these. The surgical plan may be relatively simple, but the plan for anesthesia should be very carefully considered (Table 10.1). Table 10.1  Etiology of trismus Possible etiology for trismus Infectious  Odontogenic fascial space abscess  Osteomyelitis  Tetanus  Parotid abscess  Septic TMJ arthritis Neoplastic  Pharyngeal carcinoma  Masticator space extension of malignancy  Status post radiation therapy for head and neck cancer  Status post ablative and reconstruction for head and neck cancer Inflammatory  TMJ ankylosis  Osteoarthritis  Rheumatoid arthritis  Scleroderma/systemic sclerosis  Ankylosing spondylitis  Myositis ossificans  Coronoid hypertrophy

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Table 10.1 (continued) Possible etiology for trismus Traumatic  Mandible fracture  Zygoma or zygomatic arch fracture  TMJ traumatic hemarthrosis or condyle/middle cranial fossa perforation  Masticator space hematoma  Hematoma within medial pterygoid following IAN block injection Congenital malformations  Pierre-Robin sequence  Trismus-pseudocamptodactyly syndrome  Crisponi syndrome  Distal arthrogryposis 2A and 2B  Van der Woude syndrome  Trismus pseudocampylodactly (TPS) Neurogenic  Status epilepticus  Parkinsonism TMD  Internal derangement (anterior disc reduction without reduction [Wilkes III])  Orofacial dystonia Malignant hyperthermia

Prevention Preoperative Assessment Trismus that is likely to affect the establishment and maintenance of an airway is critically important. The OMS must have several plans should an anesthetic emergency develop. The initial plan will include supplemental oxygen via two-person BVM combined with head tilt, chin lift, or jaw thrust combined with a nasal and/or oral airway. It remains paramount that the OMS prepare for an additional airway should the above not be successful. The MIO must allow for intubation or insertion of a SGA depending on the surgeon’s preference and/or experience. If the trismus does not permit intubation or a SGA, it behooves the OMS to choose between local anesthesia alone or surgery in an ASC/hospital environment. The latter allows for flexible awake fiber optic bronchoscope-guided nasal intubation that is the most trusted technique for managing trismus and an anticipated difficult airway. One of the challenges in the preanesthetic deliberations of the patient with fascial space/odontogenic infection is will the patient be able to open their mouth more fully when they are sedated? It is a mistake to assume so unless the physical exam suggests that pain is a major factor. Furthermore, infections of the floor of mouth, medial, and lateral masticator spaces typically result in significant challenges with MIO and intubation.

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Choice of Drugs Deep sedation and general anesthesia represent the spectrum of anesthesia that can occur following drug administration. The OMS may plan for a lighter sedation and end up with a deeper plane of anesthesia than originally anticipated. Although apnea can often be managed with two-person bag valve mask ventilation (BMV) and the use of head tilt, chin lift, and jaw thrust when combined with a nasal or oral airway, it is prudent to assume that a minority of patients will require an airway (SGA, intubation, or cricothyroidotomy). It is important to consider the choice of anesthetic drugs to reduce the risk of apnea. The drug dosage to produce a lighter sedation for any given patient varies considerably. The ideal body weight, body mass index (BMI), age, and prior exposure to anesthetic drugs must all be considered. Drugs that are likely to produce apnea include propofol and methohexital, which should be avoided. Benzodiazepines and narcotics when used together at moderate doses are very unlikely to produce apnea. If they do result in apnea, it should be remembered that they are reversible. This is not the case with propofol and methohexital. The use of ketamine should also be considered as this dissociative anesthetic is a respiratory stimulant at moderate doses. The following conservative loading doses may be a starting point: • Midazolam 0.05 mg/kg IV • Fentanyl 0.5 μg/kg IV • Ketamine 0.5 mg/kg IV

Recognition The time to recognize trismus is not when an anesthesia emergency develops. It remains critical to identify trismus during the preanesthetic assessment. This allows the anesthesia plan and location to be modified. However, as with all office-based anesthesia, apnea should be readily identified using standard monitoring. A decline in end-tidal carbon dioxide (ETCO2) and a reduction in airway sounds (precordial stethoscope) should immediately alert the OMS to the presence of apnea. Most episodes of apnea are brief and require no intervention. The time from apnea onset until intervention should not exceed 30 seconds. A decline in pulse oximetry, tachycardia/bradycardia, and blood pressure will occur with the passage of time (minutes) unless the airway is reestablished.

Management The surgical procedure should be terminated and wounds packed with gauze attached to string that exists the corners of the mouth. Supplemental oxygen should be administered with two-person bag valve mask ventilation (BMV) and the use of head tilt, chin lift, and jaw thrust when combined with a nasal or oral airway. If these

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maneuvers are not successful, consideration should be given to drug reversal and/or establishing an airway with a SGA or cricothyroidotomy. Drug reversal is possible when midazolam and a narcotic are used alone or in combination. • Midazolam can be reversed with 0.5 mg flumazenil (IV). • Fentanyl can be reversed with 0.4 mg naloxone (IV). Careful patient assessment after reversal is important as additional or repeat doses may be needed even in the post anesthesia care unit (PACU).

Suggested Reading 1. Beddis HP, Davies SJ, Budenberg A, Horner K, Pemberton MN. Temporomandibular disorders, trismus and malignancy: development of a checklist to improve patient safety. Br Dent J. 2014;217:351–5. 2. Estabrooks L. Morbidity and mortality. In: Bosack B, Liebleich S, editors. Anesthesia complications in the dental office. Oxford: Wiley; 2015. p. 293–8. 3. Rosenblatt WH. Development of an airway management plan. In: Hagberg C, editor. Benumof and Hagberg’s airway management. 3rd ed. Philadelphia: Saunders; 2012. p. 197–202. 4. Saito T, Liu W, Chew ST, Ti LK. Incidence of and risk factors for difficult ventilation via a supraglottic airway device in a population of 14,480 patients from South-East Asia. Anaesthesia. 2015;70:1079–83. 5. Jain U, McCunn M, Smith CE, Pittet JF. Management of the traumatized airway. Anesthesiology. 2016;124:199–206. 6. Jaskolka MS, Eppley BL, van Aalst JA. Mandibular coronoid hyperplasia in pediatric patients. J Craniofac Surg. 2007;18:849–54. 7. Wallender A, Ahson I, Steinberg B. Neonatal coronoid hyperplasia: a report of a case and concepts to promote early diagnosis and treatment. J Oral Maxillofac Surg. 1615;2015(73):e1–7.

Cardiac Arrhythmias

11

Steven M. Roser and Dimitri Cassimatis

Introduction Major adverse cardiac events (MACEs) are reported to account for one-third of the postoperative deaths in surgical patients. However, the incidence of MACE during and after office-based oral surgery under deep sedation/general anesthesia is exceedingly low. This is in part because the population of patients that undergo oral surgery under deep sedation/general anesthesia are generally healthy and usually fall into an ASA Class I or II status. Additionally, the significant training in anesthesia undertaken by the oral and maxillofacial surgeon and the office staff provides a safe environment for office-based sedation/general anesthesia. In order to manage arrhythmias that occur during office-based surgery, the oral and maxillofacial surgeon must be familiar with the cardiac conduction system; the mechanisms of the various arrhythmias; and the prevention, recognition, and management of the arrhythmias. Major adverse cardiac events including myocardial infarction or new cardiac arrhythmias are relatively common in patients undergoing noncardiac surgery with an incidence of 5% being reported. The incidence of cardiac arrhythmias during office-based deep sedation/general anesthesia for oral surgery is not known. Deep sedation and general anesthesia both obtund respiratory drive, but they may also result in cardiovascular changes including hypotension, hypertension, tachycardia, bradycardia, myocardial ischemia, myocardial infarction, and arrhythmias. S. M. Roser (*) Division of Oral and Maxillofacial Surgery, Department of Surgery, Emory University School of Medicine, Atlanta, GA, USA e-mail: [email protected] D. Cassimatis Emory University Hospital Midtown, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA e-mail: [email protected] © Springer Nature Switzerland AG 2021 G. F. Bouloux (ed.), Office Based Anesthesia Complications, https://doi.org/10.1007/978-3-030-61427-0_11

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Fig. 11.1  Normal electric representation of the cardiac conduction cycle. PR interval: atrial contraction, QRS: ventricular contraction. (https://www.pngwave. com/png-clip-art-dfwxp)

QRS complex

R ST segment

PR segment

T

P

PR interval

Q S QT interval

The normal cycle of cardiac chamber contractions is generated by electrical activity that starts in the sino-atrial (SA) node and spreads through the atria, producing the P wave on an electrocardiogram and resulting in atrial contraction. The impulse is then transmitted to the atrioventricular (AV) node and down the Purkinje fibers to depolarize the ventricles resulting in the QRS complex and ventricular contraction. Myocardial repolarization occurs during the ST interval. The end result is a normal ventricular rate typically between 55 and 85/min in people 12 years and older (Fig. 11.1). The genesis of arrhythmias falls into three categories: (1) increased automaticity, (2) triggered activity due to after-depolarization reaching the threshold of the action potential, or (3) circus movement or re-entry. Some arrhythmias will not produce any significant symptoms while others result in significant brady-arrhythmias or tachy-arrhythmias that can result in symptoms including dizziness, palpitations, shortness of breath, and chest pain. Patients can experience significant hemodynamic instability leading to cardiac ischemia, heart failure, and death. Treatment of acutely occurring arrhythmias is focused on establishing a heart rate that allows for adequate cardiac output and identifying and treating the underlying arrhythmia. The management of arrhythmias may include the application of electricity to the heart, use of pharmacological agents that block sodium, calcium, and/or potassium channels or attenuate sympathetic nervous system activity. Certain groups of patients, types of surgeries, and anesthetic agents will result in a higher incidence of intraoperative arrhythmias. These include patients with preexisting cardiac disease, intracranial disease, and elderly patients. Although much less common than the oculo-cardiac reflex, the trigemino-cardiac reflex can also result in cardiac arrhythmias when the sensory branches of the trigeminal nerve are stimulated. Certain anesthetic agents also have the potential to produce intraoperative arrhythmias including inhalational agents such as sevofluorane, which can prolong

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Table 11.1  Arrhythmias with a pulse Sinus arrhythmias  Sinus tachycardia  Sinus bradycardia

Atrial arrhythmias  Premature atrial contraction  Supraventricular tachycardias  Atrial fibrillation  Atrial flutter

Ventricular arrhythmias  Premature ventricular contractions  Ventricular tachycardia (when fast may have no pulse)

the QT interval. Electrolyte abnormalities, particularly those related to potassium and magnesium, can also result in arrhythmias. Arrhythmias can be grouped in various ways. A common grouping method includes brady-arrythmias and tachy-arrythmias, sinus arrhythmias, and atrial and ventricular arrhythmias. Rhythms that are typically pulseless include fast ventricular tachycardia, ventricular fibrillation, and pulseless electrical activity (PEA). Severe heart block (atrioventricular nodal block) may slow conduction from the atria to the ventricle and ranges from clinically insignificant (a prolonged PR interval) to severe (complete loss of conduction to the ventricle). Asystole is a special case in which there is no electrical activity in the ventricle (Table 11.1).

Prevention For patients undergoing office-based procedures under deep sedation/general anesthesia, a thorough medical history and focused physical examination is required. The resulting risk assessment and classification may help identify those patients at risk for an arrhythmia. Patients with some chronic arrhythmias (e.g., atrial fibrillation), cardiac pacemakers, or automatic intracardiac defibrillators (AICDs) should be identified. Careful discussion with the patient’s primary care physician or cardiologist is paramount to risk stratify the patient and determine the most ideal location to perform the surgical procedure (office versus hospital). It remains important to determine what hemodynamic impact any particular arrhythmia will have in any patient even if they are currently in a normal sinus rhythm. Patients with pacemaker or AICD should be managed in an outpatient ambulatory facility if deep sedation/ general anesthesia must be used, with perioperative guidance from the patient’s cardiologist or arrhythmia device specialist. Similarly, patients with existing significant cardiac disease and an arrhythmia history are not candidates for office-based deep sedation/general anesthesia. The occurrence of the arrhythmia can quickly precipitate cardiac ischemia further impacting on the patient’s hemodynamic stability. Monitoring for all patients undergoing office-based surgery under deep sedation/ general anesthesia must include continuous ECG monitoring and noninvasive blood pressure monitoring set at an interval of 5 min or less, pulse oximetry, and end-tidal expired CO2 monitoring. For all patients, a designated trained individual must be present to monitor the patient and administer the medications. For the person monitoring the patient under deep sedation/general anesthesia, the appearance of the

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arrhythmia is most often first noted on the ECG monitor. The procedure should be stopped and the following questions asked: 1 . Is the patient hemodynamically stable with an adequate blood pressure and pulse? 2. What is the heart rate? 3. Is the rhythm regular or irregular? 4. Is there a P wave for every QRS complex? 5. Is the QRS complex normal in appearance?

Recognition and Management

Sinus Tachycardia. (Adapted from: www.practicalclinicalskills.com)

• • • •

Rate: Typically less than 150/min but can be high as 200/min in younger patients Rhythm: Regular P-QRS ratio: 1:1 QRS: Normal width

Management Sinus tachycardia is usually self-limiting and does not require treatment. However, older patients may not tolerate a rapid heart rate that can result in hypotension, reduced cardiac output, and angina. Treatment should focus on looking for an underlying cause of the tachycardia (e.g., pain, anxiety, hemorrhage, hypoxia, or medication allergy). Rate-slowing medications to treat sinus tachycardia should be avoided, as often the sinus tachycardia is compensatory, and slowing the rate could lead to severe hypotension. Rather, the primary cause should be elucidated and directly treated (Fig. 11.2).

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AHA ACLS adult tachycardia algorithm (with a pulse) Tachyarrhythmia typically seen when the heart rate is ≥ 150/min Is the tachyarrhythmia causing the symptoms?

Synchronized cardioversion doses Initial recommended doses: • Narrow regular: 50–100 J • Narrow irregular: 120–200 biphasic or 200 J Monophasic • Wide regular: 100 J • Wide irregular: defibrillation dose (not synchronized)

The priority should be to identify and treat the underlying cause • • •

Maintain patent airway ; assist breathing if necessary Apply oxygen (if hypoxemic); monitor pulse oximetry Apply cardiac monitor; monitor blood pressure

Adenosine IV dose: First dose 6 mg rapid IV push and NS flush Second dose: 12 mg if needed

Is the tachyarrhythmia causing: • • • • •

Hypotension? Altered mental status? Signs of shock? Ischemic chest discomfort? Acute heart failure?

Synchronized cardioversion

Yes

• •

Consider sedation May use adenosine for regular narrow complex tachyarrhythmia

No

Is the QRS wide ≥0.12 s

Yes

• • • •

Start IV and 12 lead ECG if possible May use adenosine only if regular and monomorphic Consider antiarrhythmic infusion Consider expert consultation

No

• • • • •

Start IV and obtain 12-lead ECG if possible Vagal maneuvers Adenosine (if rate is regular) β-blocker or calcium channel blocker Consider expert consultation

Antiarrhythmics that may be considered Amiodarone Procainamide Sotalol

Fig. 11.2 AHA/ACLS tachycardia algorithm. (©2016. Jeffery Media Productions, with permission)

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Sinus Bradycardia. (Adapted from: www.practicalclinicalskills.com)

• • • •

Rate: Less than 50–60/min Rhythm: Regular P-QRS ratio: 1:1 QRS: Normal width

Management If the patient is hemodynamically stable, no immediate treatment is necessary. If the bradycardia results in hypotension, angina or altered mental status treatment should be instituted (Fig. 11.3).

Premature atrial contractions. (Adapted from: www.practicalclinicalskills.com)

• • • • •

Rate: Variable Rhythm: Irregular P-QRS ratio 1:1 P wave: PAC P wave may be normal or abnormal QRS: Normal width

Management Intermittent PACs are not treated.

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AHA ACLS adult bradycardia algorithm Bradyarrhythmia typically seen when the heart rate is 2 weeks preoperatively • Most other antihypertensive medications that are part of a stable regimen Patients with a prior MI who have received percutaneous coronary angioplasty (PCA) are typically treated with dual antiplatelet therapy (DAPT). This involves the use of a glycoprotein IIb/IIIa inhibitor (e.g., abciximab or eptifibatide given intravenously) or an ADP antagonist (e.g., clopidogrel, ticagrelor, or prasugrel, given orally) in addition to low-dose aspirin. Aspirin should always be continued in the perioperative period. The glycoprotein IIb/IIIa inhibitor or ADP antagonist should be continued without interruption for a minimum period of 14 days, 30 days, and 3  months for balloon angioplasty, bare metal stents, and most current-generation drug-eluting stents, respectively. That said, dual antiplatelet therapy is usually continued for a full year after any acute coronary syndrome, with allowed interruptions within the year once the minimum time has passed. The American College of Cardiology (ACC) recommends waiting a minimum period of 6 months after an MI before proceeding with elective surgery. As the urgency for surgery increases, the interval may need to decrease, and the timing should be individualized to the patient, with a multidisciplinary discussion of risks and benefits taking place between the

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patient’s cardiologist and surgeon. In general, the longer the time between MI and subsequent non-cardiac surgery, the lower the risk for an additional MI. Prior to an elective surgery in any patient with known CAD, especially in a patient who has had an acute coronary syndrome within the past year, it is advised that the patient obtain a preoperative risk assessment from their cardiologist, along with detailed and individualized recommendations on perioperative medication management. Additional perioperative strategies that are beneficial for office-based OMFS involve modifications to both the local and general anesthesia.

Local Anesthesia Provide adequate and profound local anesthesia using the least volume of local anesthesia to minimize the epinephrine content. The recommendations for the maximum dose of any local anesthetic in healthy patients are driven by the potential for cardiac and central nervous system toxicity secondary to the local anesthetic. The recommendations for the maximum dose in cardiac patients are driven by the potential for arrhythmias and ACS (Table 12.1).

General Anesthesia The goals of providing conscious, moderate, or deep sedation in patients with CAD is to minimize the risk of ACS including MI. This requires adequate oxygen delivery via a nasal hood or nasal cannula. The adequacy of oxygen delivery must be measured continuously using pulse oximetry and end-tidal CO2. The use of medications that are the least likely to produce changes in cardiovascular parameters is crucial. Benzodiazepines and opioids, such as midazolam and fentanyl, are ideal choices and less likely to produce significant fluctuations in blood pressure, heart rate, or respiratory rate when titrated appropriately. Many factors influence the response to these medications and therefore the appropriate dosing. The following dose recommendations are considered relatively conservative: • Midazolam 0.05–0.1 mg/kg • Fentanyl 1 μg/kg

Table 12.1  Local anesthesia doses in healthy and cardiac patients Local anesthetic Lidocaine Bupivacaine Mepivacaine Articaine a

1.8 mL cartridge

Max dose without Epi (healthy) 4 mg/kg 2 mg/kg 5 mg/kg NA

Max dose with Epi (healthy) 7 mg/kg 2 mg/kg NA 7 mg/kg

Max dose with Epi (cardiac) 2.2 cartridgesa 4.5 cartridgesa NA 2.2 cartridgesa

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The use of propofol, and barbiturates such as methohexital, while considered routine in healthy patients, may result in changes to cardiovascular parameters that have the potential to increase myocardial oxygen demand and the risk for ACS including MI.  These drugs should only be used with extreme caution in these patients in an office setting.

Recognition The ability to recognize an MI in an office setting depends on many factors including the presenting symptoms, signs, cardiovascular changes (blood pressure and heart rate) as well as changes on an electrocardiogram (ECG). Classic symptoms include chest pain or tightness that may radiate to the left arm, neck, and/or jaw. Patients may also experience light-headedness, anxiety, fatigue, shortness of breath, nausea, and vomiting. Signs include clammy skin, perspiration, and palpitations. These are more likely to be recognized during procedures performed under local anesthesia. It can more challenging to recognize an MI when patients are sedated as the sympathetic response to an MI is blunted. Patients with diabetes mellitus present an additional challenge as the autonomic neuropathy may also mask the sympathetic response and the pain may be atypical or absent, resulting in a silent infarct. An acute change in heart rate and blood pressure may be the result of multiple local anesthesia, sedation, and procedural-related interventions. It would behoove the surgeon to keep the diagnosis of MI and pulmonary embolism on the differential diagnosis when faced with unexplained changes in cardiovascular parameters. An ECG remains an excellent modality to recognize cardiac ischemia or MI. A 12-lead ECG provides the greatest sensitivity and is able to identify most MIs but is typically not available in an office setting. The standard 3-lead ECG provides less information but can identify most rhythm changes in leads I, II, and III. Lead II is typically the default lead on most monitors, and this will also allow recognition of most inferior and some lateral MIs.

Rhythm Strip Interpretation The ability to interpret ischemic changes in a rhythm strip requires a basic understanding of a normal PQRST complex (Fig. 12.1). The ability to recognize myocardial ischemia or infarction (MI) depends on recognizing dangerous rhythms (e.g., ventricular tachycardia) or changes in the appearance of the ST and T wave segments. Although a 12-lead electrocardiogram (ECG) will provide much greater sensitivity and specificity to detect MI, the routine use of lead II for monitoring during deep sedation and general anesthesia will allow many MIs to be appreciated. Changing the monitor selection to view leads I and III may also facilitate the process if MI is suspected. The key electrocardiographic changes that should be sought include ST segment elevation and depression, and inverted T waves. Q waves may also be present but

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R

P

ST segment

PR segment

PR interval

Q

T

J-point

S QT interval

Fig. 12.1  Basic PQRST wave. (Adapted from ECGs in Acute Myocardial Infarction, ACLS Medical Training at https://www.aclsmedicaltraining.com/ecg-in-acute-myocardial-infarction/)

may represent a previous MI rather than an acute MI as they typically take several hours to develop following an MI. Changes in a single lead rhythm strip will depend on several factors including the anatomical location of the ischemia/infarct, the leads that are being monitored, and whether the ischemia/infarct is subendothelial or transmural. The diagnosis of MI by ECG requires that the changes be present on two contiguous leads (Fig. 12.2). This is challenging for patients under a deep sedation or general anesthesia. The presence of any change on a single lead rhythm strip should be considered highly suggestive in this situation, and should urgently prompt further evaluation.

ST Segment Depression or Elevation ST segment depression or elevation suggests ischemia or MI. ST segment depression may have a horizontal or sloping pattern (Fig. 12.3). ST segment elevation may also have a varied pattern (Fig. 12.4).

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Fig. 12.2  12-lead ECG with an acute inferior-posterior MI as seen on leads II, III, aVF, V2, V3. (Adapted from Myocardial Infarction, E Learning Center. Available at https://ecg.utah.edu/ lesson/9)

a

b

c

d

e

Fig. 12.3  ST segment depression. (a). Horizontal ST depression. (b, c) Downsloping ST depression. (d) Upsloping ST depression. (e) Normal variant QRS. (Adapted from Acute Myocardial Infarction. Available at http://www.medicine-on-line.com/en/detail_ecg.php)

Fig. 12.4  Varying patterns of ST elevation. (Adapted from Acute Myocardial Infarction. Available at http://www.medicine-on-line.com/en/detail_ecg.php)

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The definitive diagnosis of an MI requires the use of blood tests to identify cardiac enzymes including troponin and CK-MB (MB isoenzyme of creatine kinase).

Management Once acute coronary syndrome is recognized or suspected, the procedure should be terminated immediately. Current evidence supports the use of low-dose aspirin (81 mg) that has been shown to reduce mortality. It can be administered by mouth in a non-sedated patient or via the sublingual route when sedated. Nitrates should be used in the presence of persistent ischemic pain lasting more than 5–10 min, as well as for hypertension and for acute pulmonary edema from heart failure. Although the use in acute coronary syndrome is well accepted, nitrates have not clearly been shown to reduce mortality. Nitrates must be titrated to blood pressure and are contraindicated in the presence of hypotension when systolic blood pressure is less than 90 mmHg. Oxygen should only be used when oxygen saturation is less than 90% on room air as it has been shown to increase the infarct size. Opiates may mask ischemic symptoms without relieving the ischemia, and have been associated with worse outcomes, and thus are not recommended for use in acute coronary syndrome. Emergency Medical Services (EMS) should be summoned immediately to facilitate urgent transport to a hospital setting, preferably to a center with a cardiac catheterization lab and interventional cardiology on call. The administration of antiplatelet drugs combined with emergent percutaneous angioplasty (PCA) can dramatically reduce mortality and morbidity. Thrombolytic medications may also be used in select patients with lower bleeding risk when there is an expected delay for PCA; however, in a recent postoperative patient, they are generally avoided. Patients may also benefit in the post-MI period from the use of beta-blockers, angiotensin converting enzyme inhibitors, and statins. If multi-vessel CAD is found, or severe left main CAD, then coronary artery bypass grafting may be considered.

Suggested Reading 1. de Alencar Neto JN. Morphine, oxygen, nitrates, and mortality reducing pharmacological treatment for acute coronary syndrome: an evidence-based review. Cureus. 2018;10:e2114. 2. Maddox TM. Preoperative cardiovascular evaluation for noncardiac surgery. Mt Sinai J Med. 2005;72:185–92. 3. Garg PK.  Preoperative cardiovascular evaluation in patients undergoing vascular surgery. Cardiol Clin. 2015;33:139–50. 4. Chaudhry W, Cohen MC. Cardiac screening in the noncardiac surgery patient. Surg Clin North Am. 2017;97:717–32.

Pulmonary Embolism

13

Lisa Bernstein and Gary F. Bouloux

Introduction Acute pulmonary embolism (PE) is a potentially life-threatening condition characterized by obstruction of the pulmonary artery or its branches. Most PEs arise from a thrombus in a proximal deep vein (DVT) of the lower extremities or the pelvis potentially resulting in leg pain and swelling. Risk factors include genetic polymorphisms that predispose patients to hypercoaguability as well as acquired factors such as recent surgery, cancer, pregnancy, and immobility. The severity of the PE depends on the size and location of the embolus. Smaller peripheral emboli are less symptomatic than larger, more central, clots (saddle emboli) that can result in significant right ventricular strain, vascular collapse, or immediate death.

Prevention A thorough preoperative risk stratification allows patients with increased risk of developing PE to be identified and risk reduction strategies employed. Risk factors for DVT/PE include the following: • Hypercoaguability (e.g., factor V Leiden or prothrombin gene mutation) • Heart failure • Malignancy L. Bernstein Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA e-mail: [email protected] G. F. Bouloux (*) Division of Oral and Maxillofacial Surgery, Department of Surgery, Emory University School of Medicine, Atlanta, GA, USA e-mail: [email protected] © Springer Nature Switzerland AG 2021 G. F. Bouloux (ed.), Office Based Anesthesia Complications, https://doi.org/10.1007/978-3-030-61427-0_13

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• • • • •

Prolonged immobilization Recent major surgery Smoking Obesity Supplemental estrogen (oral contraceptives or postmenopausal hormone replacement therapy) • Pregnancy If possible, the use of local anesthesia alone for oral surgery procedures will substantially mitigate the risk of PE.  General anesthesia and moderate/deep sedation increase the risk of DVT as a result of the anesthetic agents and immobility, although the risk remains exceedingly small. DVT and PE have rarely been reported during office-based procedures under sedation, and those reported were most commonly in women of childbearing age on oral contraceptives and in those patients undergoing procedures of longer duration. Consideration should be given to the use of sequential calf compression devices (SCDs) or compression stockings during the procedure to mitigate the risk in both of these higher risk groups. Early ambulation after surgery will further reduce the likelihood of developing a PE in the postoperative period.

Recognition It is important to maintain a high level of suspicion for acute PE as its presentation can range from an asymptomatic presentation to circulatory collapse with a larger clot burden. Patients most commonly present with shortness of breath, chest pain (usually pleuritic), and cough. Some patients will have leg swelling from a DVT or present with wheezing or hemoptysis. The most common physical signs include tachypnea, signs of DVT such as calf or thigh swelling, and tachycardia, but patients may also have clammy skin, a low-grade fever, sweating, arrhythmia, and hypotension. Patients who receive moderate and deep sedation may present additional challenges in recognizing PE as the sympathetic response may be dampened and mask many of the classic signs and symptoms. When a PE is suspected, assessment of hemodynamic stability is paramount. An acute change in heart rate and blood pressure should raise suspicion for PE, though these signs may also be the result of multiple local anesthesia, sedation, and procedural-­related interventions. The classic ECG presentation that is often suggested as being pathognomonic of PE includes a prominent S wave in lead I and both a Q and T wave in lead III (Fig. 13.1a, b). Sinus tachycardia remains the most common abnormal initial ECG presentation, and it can be readily identified using the default lead II on the heart monitor (Fig. 13.2). Additional findings may include a right bundle branch block (RBBB) or ST segment elevation. A reduction in the end-tidal CO2 is also common due to ventilation-perfusion mismatch. Additionally, an acute decrease in the oxygen saturation on pulse oximetry may also support the diagnosis of PE. As the majority of PEs arise from a DVT in the lower extremity, physical examination of the legs, looking for unilateral swelling or a palpable cord would increase

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a

b

Fig. 13.1 (a) Lead I with prominent S wave. (b) Lead III with prominent Q and T waves

Fig. 13.2  Sinus tachycardia

pretest probability for PE. Homans sign (calf pain with dorsiflexion of the foot) is unreliable in the diagnosis of PE.  The initial diagnostic test for suspected PE, if signs point to a possible concurrent DVT, is a duplex ultrasound scan (U/S) of the deep veins of the leg. The sensitivity of U/S to detect a DVT approaches 95% when veins above the knee are involved, but this drops to 70% for veins below the popliteal fossa. A D-dimer blood test is not helpful in someone with a high likelihood of a PE, but in someone with low or intermediate probability for a thrombus, a normal result effectively rules out a PE. The patient for whom there is a high suspicion for PE should be transferred to an emergency setting as the definitive diagnosis requires additional tests which may include the following: • • • •

Arterial blood gas (ABG) revealing an arterial-alveolar O2 gradient Spiral computed tomography of the chest Ventilation-perfusion scan Pulmonary angiogram

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Management The management of PE within an office setting is limited. Patients should receive supplemental oxygen via a non-rebreather mask in an attempt to compensate for the ventilation-perfusion mismatch and hypoxemia. The administration of intravenous fluids (IVFs) using normal saline or lactated Ringers to increase preload is encouraged, particularly in the face of hypotension. Emergency Medical Services (EMS) should be summoned immediately to facilitate urgent transport to a hospital setting for further diagnostic studies and treatment, which can include anticoagulation, thrombolysis, or other interventions.

Suggested Reading 1. Casazza F, Pacchetti I, Rulli E, et al. Prognostic significance of electrocardiogram at presentation in patients with pulmonary embolism of different severity. Thromb Res. 2018;163:123–7. 2. Qaddoura A, Digby GC, Kabali C, Kukla P, Zhan ZQ, Baranchuk AM. The value of electrocardiography in prognosticating clinical deterioration and mortality in acute pulmonary embolism: a systematic review and meta-analysis. Clin Cardiol. 2017;40:814–24.

Pediatric Emergencies

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Erin Rosenberg

Introduction The provision of moderate/deep sedation and general anesthesia in pediatric patients presents many additional challenges. The pediatric patient should not be viewed as a dimuitive adult. There are significant anatomical and physiological differences between pediatric and adult patients that need to be understood and appreciated.

Airway and Respiratory System The most important differences in respiratory physiology between the pediatric patient and adults are related to the growth of the chest wall in the first several years of life [1]. In infancy, the orientation of the ribs predisposes them to inefficient inspiration because they are situated in a more horizontal plane compared to adults. This leads to a relatively fixed tidal volume that is difficult to overcome. Additionally, this also causes elevation of the diaphragm and reduces the functional residual capacity (FRC) resulting in an increased chance of reflux and aspiration (Fig. 14.1). The cartilaginous nature of the the chest wall of neonates and infants makes it more compliant than adults with a tendency to collapse inwards, resulting in the use of accessory muscles of respiration to maintain a negative intrathoracic pressure. Infants and neonates depend on the tonic muscular contraction of the accessory muscles to preserve their FRC. Sedatives and anesthetics cause a decrease in muscle tone that predisposes them to rapid oxygen desaturation and hypoxemia. Tidal volumes are relatively the same for both infants and adults; however, infants have a much higher rate of oxygen consumption 6–7 mL/kg (infants) compared to adults (3  mL/kg). The increased rate of oxygen consumption, along with the decreased E. Rosenberg (*) Childrens Healthcare of Atlanta, Emory University School of Medicine, Atlanta, GA, USA e-mail: [email protected] © Springer Nature Switzerland AG 2021 G. F. Bouloux (ed.), Office Based Anesthesia Complications, https://doi.org/10.1007/978-3-030-61427-0_14

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Newborn

Adult

Fig. 14.1  Differences in the pediatric and adult chest. (Adapted from Litman RS. Pediatric anesthesia: the requisites in anesthesiology. Philadelphia: Elsevier Mosby; 2004. p. 8)

FRC, leads to hypoxemia at a much faster rate in infants than adults during periods of apnea.

Pediatric Airway Anatomy Providers should have knowledge and understanding of the key differences between the adult and pediatric airway for clincal management (Fig. 14.2).

Occiput Neonates and infants have larger occiputs, which affects head and neck positioning during airway management. The occiput places the head and neck in a more flexed position that can predispose to airway obstruction. This can be overcome by placing a shoulder roll underneath the infant’s shoulders. Tongue An infant’s tongue is disproportionately large compared to the rest of the oral cavity making it much easier to obstruct the airway. In older children, the presence of hypertrophied lymphoid tissue may also lead to airway obstruction with sedation and general anesthesia. Larynx The infant larynx is located at the 3rd and 4th cervical vertberae (C3/C4), which is more cephalad than the location within an adult (C4/5). This higher position results in a more acute angle making visualization and intubation more difficult during laryngoscopy.

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Anatomy of adult airway

Anatomy of pediatric airway

Tongue

Tongue

Epiglottis (shorter)

Epiglottis (floppier, u-shaped)

Cylinder Funnel

Hyoid bone

Hyoid bone

Vocal cords (narrowest)

Airway (more anterior and higher)

Thyroid cartilage

Trachea

Vocal cords Thyroid cartilage Cricoid ring (narrowest)

Cricoid ring

Posterior

Anterior

Trachea (more flexible)

Posterior

Anterior

Fig. 14.2  Pediatric and adult anatomy. (Adapted from Zeretzke-Bien CM.  Airway: pediatric anatomy, infants and children. In: Zeretzke-Bien C, Swan T, Allen B, editors. Quick hits for pediatric emergency medicine. Cham: Springer; 2018)

Epiglottis The epiglottis of a neonate and infant is described as omega (Ώ) shaped and angles away from axis of the trachea, while the adult epiglottis is flat and broad with its axis parallel to the trachea. The angle and shape of the infant epiglottis makes it longer and less rigid leading to increased difficulty when lifting an infant’s epiglottis with a laryngoscope blade. This may also increase the likelihood of obstruction when prone. Subglottis Classic teaching is that in children younger than 10 years of age, the narrowest portion of the airway is at the level of the cricoid cartilage, while in an adult the narrowest part is the level of the rima glottidis [2]. This anatomic difference may make placing an endotracheal tube in an infant more challenging after it passes through the vocal cords.

Cardiovascular System The left ventricle (LV)of the neonate and infant exhibits less compliance than the adult LV.  Maintaining cardiac output is more dependent on heart rate, as stroke volume remains relatively fixed. They are more prone to the development of

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Table 14.1  Age-related changes in heart rate and blood pressure Age Premature 0–3 months 3–6 months 6–12 months 1–3 years 3–6 years 6–12 years >12 years

Heart rate range 120–170 100–150 90–120 80–120 70–110 65–110 60–95 55–85

Mean systolic blood pressure (mmHg) 55–75 65–85 70–90 80–100 90–105 95–110 100–120 110–135

Mean diastolic blood pressure (mmHg) 35–45 45–55 50–65 55–65 55–70 60–75 60–75 65–85

Adapted from: Mathers LH, Frankel LR. Pediatric emergencies and resuscitation. In: Nelson textbook of pediatrics. 17th ed. Philadelphia: WB Saunders; 2004

congestive heart failure during periods of fluid overload, and one must be judicious with fluid management. Additionally, the parasympathetic nervous system predominates in neonates and young infants resulting in exaggerated vagal responses with minor stimuli, which can lead to bradycardia. However, the sympathetic nervous system becomes increasingly active with age (Table 14.1).

Fasting Times Prevention of perioperative (or preprocedural) pulmonary aspiration is part of the process of preoperative evaluation and preparation of the patient. Guidelines published by the American Society of Anesthesiologsists are intended for use by anesthesiologists and other anesthesia providers. They also may serve as a resource for other healthcare professionals who advise or care for patients who receive anesthesia care during procedures. •  •  •  • 

Solids (fried, fatty, meat) Non-human milk, formula, light meal Breast milk, formula Clear liquids

8 h 6 h 4 h 2 h

Establishing the Pediatric Airway Intubation Pediatric intubation can be challenging for the anatomic reasons stated above with perioperative complications occurring more commonly than with adults. Direct laryngoscopy (DL) can be performed with the use of a Macintosh or Miller blade. The Miller blade is straight and directly elevates the epiglottis when the tip of the blade is placed over the tip of the epiglottis. The Macintosh blade is designed to

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a

b

c

Fig. 14.3 (a) Progressive elevation of the epiglottis utilizing the hyoepiglottic ligament. (Adapted from Miller KA, Nagler J. Advances in emergent airway management in pediatrics. Emerg Med Clin North Am. 2019;37:473). (b) C-MAC® with Macintosh and Miller blades. (c) C-MAC® in use

indirectly elevate the epiglottis when placed into the vallecula. The inherent floppiness of the epiglottis in young children may result in the epiglottis falling back and obstructing the laryngeal inlet when this blade is used. This can to some degree be mitigated by having the tip of the Mac blade engage the hyoepiglottic ligament (Fig. 14.3a). The growth of videolaryngoscopy (VL) has been a natural progression from DL. Videolaryngoscopy provides the operator of the device with indirect visualization of anatomic structures. These devices tend to be smaller than traditional DL instruments and can additionally be used when the oral opening is more limited. It is generally accepted that VL improves glottic visualization although the time to first-pass intubation may be longer. The latter may be due to inexperience with these devices and the more cephalad larynx. The C-MAC®1 and Glidescope®2 are examples of the traditional indirect nondisposable laryngoscopes. They are both inserted into the oropharynx in a similar

 C-MAC, Karl Storz, Tuttlingen, Germany.  Glidescope, Verathon Medical, Bothell, WA.

1 2

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b

Fig. 14.4 (a) Glidescope®. (b) Glidescope® in use

manner to DL but both utilize a remote viewing screen to visualize the larynx (Figs. 14.3b, c and 14.4a, b). Several newer devices such as the Airtraq®3 are available, which differ in that they are inserted in the midline, disposable, and utilize any eye piece or small viewing screen. Additionally, the endotracheal tube is inserted into a channel within the device to facilitate rapid and seemless intubation (Fig. 14.5a, b).

Endotracheal Tube Size The selection of the appropriate-sized endotracheal tube (ETT) is dependent on the age of the pediatric patient. It has also been customary to use uncuffed ET tubes in pediatric patients. Recent evidence suggests that the use of smaller cuffed tubes in all pediatric ages is acceptable. Several formulas exist to help calculate the correct size of the endotracheal tube. Uncuffed tube size = 4 + (age/4) while cuffed tube size = 3.5 + (age/4). This correlates with the following tube sizes (Table 14.2). Laryngeal Mask An alternative to intubation is the use of a laryngeal mask (LMA). Multiple sizes exist that allow placement in newborns through adults. They are technically simple to place with few complications. Second-generation devices allow increased seal pressures and provide esophageal lumens for gastric decompression. The advantages over the use of an endotracheal tube include improved hemodynamic stability and reduced complications including laryngospasm, coughing, laryngeal edema, and soft tissue trauma. The size of the pediatric LMA depends on the weight of the pediatric patient (Table 14.3).

 Airtraq® Prodol Meditec, Vizcaya, Spain.

3

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a

b

Fig. 14.5 (a) Airtraq. (b) Airtraq in use

Table 14.2  ETT sizes

Table 14.3  LMA sizes

Age 1–2 3–4 5–8 8–10 10–14

LMA size 1 1.5 2 2.5 3

Internal diameter (mm) 4.0 4.5 5.0 5.5 6.0

Weight (kg) ≤5 5–10 10–20 20–30 30–50

Depth (cm) 10 12 14 15 16–18

Maximum inflation volume (mL) 4 7 10 14 20

Insertion The cuff should be deflated or partially inflated during insertion. There are several techniques for insertion including the following: • Insert LMA laterally at 45° against the tongue, advance until resisance is met, and then rotate back to midline. • Insert LMA in the midline against the hard and soft palate until the posterior pharyngeal wall is encountered. • Insert the LMA in the midline with the cuff facing the palate until the posterior pharyngeal wall is encountered then rotate 180°.

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Pediatric Complications Anesthesia-related complications are not common but require immediate attention and management. The most common complications include laryngospasm, aspiration, bradycardia, and anaphylaxis.

Laryngospasm Airway and respiratory events are the most common perioperative complications in pediatric patients with laryngospasm being the most common cause of respiratory-­ related cardiac arrest. Laryngospasm is the spontaneous partial or complete closure of the vocal cords. It results in a partial or complete obstruction of the airway with resultant hypoexemia. Laryngospasm can occur during induction, maintenance, or emergence from anesthesia. Risk factors include airway instrumentation during light anesthesia, vocal cord irritation (by inhalational anesthetics, secretions, mucus, or blood), young age, recent upper respiratory infection (URI), and airway procedures. It requires immediate attention.

Prevention Several strategies can be used to reduce the likelihood of developing laryngospasm. • Delay elective surgery for children with current or recent URIs • Suction secretions, if present • Use of inhalational agents that are not irritating to the airway such as Sevoflurane or Desflurane • Allow patients who undergo inhalational induction to pass Stage II of anesthesia before any type of stimulation is provided including intravenous access • Consider use of an LMA rather than endotracheal intubation • Minimize salivary secretions perioperatively with the use of glycopyrolate 0.01  mg/kg, which can be administered intramuscularly (IM) or intravenously (IV)

Recognition • Respiratory stridor on inspiration • Retractions and rocking chest wall movement • Loss or reduction of ETCO2 waveform • Decrease in pulse oximetry • Tachycardia • Bradycardia Management • Stop stimulation/surgery • Administer 100% oxygen • Two-person bag valve mask positive pressure ventilaton with head tilt, jaw thrust, or chin lift

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• Deepen the anesthesia with sevoflurane or propofol • Succinylcholine 0.25–0.5 mg/kg IV and atropine 0.02 mg/kg IV for resultant bradycardia OR • Succinylcholine 3–4 mg/kg IM and atropine 0.02 mg/kg IM for resultant bradycardia when no IV access

Bronchospasm Bronchospasm is a reversible reflex spasm of the smooth muscle in the bronchi, which is vagally mediated and caused by histamine or noxious stimuli (e.g., inhaled irritants and instrumentation). Bronchospasm may appear as an entity in its own right or be a component of another problem such as anaphylaxis. The majority take place during induction and maintenance of anesthesia.

Prevention • Encourage patients to continue all asthma medications until the time of surgery • Preoperatively assess patients with asthma for any exacerbation • Consider postponing procedure if child has had an upper respiratory tract infection in the prior 2 weeks • Pretreatment with an inhaled/nebulized short-acting beta agonist (SABA) 30 min prior to surgery can be considered in the asthmatic child • Make sure adequate depth of anesthesia is attained before instrumenting the airway • If procedure allows, use of an LMA in suitable patients has been shown to reduce the incidence of bronchospasm Recognition • Wheezing on auscultation • Slow or incomplete expiration • Decrease ETCO2 • Upsloping waveform (Fig. 14.6) • Decreased or absent waveform Fig. 14.6 Capnograph during bronchospasm

Normal 45 0

Bronchospasm 45 0

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• Decreased tidal volume • High inspiratory pressures • Decreasing oxygen saturation

Management • Stop stimulation/surgery • Administration of 100% oxygen • Two-person bag valve mask positive pressure ventilaton with head tilt, jaw thrust, or chin lift • Consider allergy/anaphylaxis and stop administration of suspected drugs • Deepen the anesthesia with propofol, ketamine, and/or volatile anesthetic • Administer IV epinephrine 0.005–0.01 mg/kg depending on severity • Consider either: –– 1. EpiPen Jr. (0.15 mg epi) intramuscular (IM) for patients >30 kg –– OR –– 2a. Calculate total dose of epinephrine needed (0.01 mg/kg) –– 2b. In a 10 cc syringe, draw up 0.1 mL of epinephrine from a standard 1.0 mL (1 mg) vial. Dilution with 9.9 mL normal saline then results in an epinephrine concentration of 0.01  mg/mL. More than one syringe may be necessary depending on the patients weight.

Aspiration Aspiration is a rare complication in pediatric airway management. It is considered to be the inhalation of oropharyngeal or gastric contents into the larynx, trachea, and lungs. Aspiration can lead to immediate obstruction or result in pneumonitis. The normal physiological mechanisms that protect against aspiration include the vocal cords, upper esophageal sphincter, and lower esophageal sphincter. Several factors are thought to increase the risk of aspiration: • ASA III or IV • Emergency procedures • Inadequate NPO status • Delayed gastric emptying • Use of first-generation LMA • Light anesthesia • Increased oral secretions or blood

Prevention • Appropriate preoperative fasting • Cricoid pressure (Sellick maneuver) • Tracheal intubation or second-generation LMA Recognition • Visualized aspiration of blood or object

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• • • •

123

Presence of vomitus Coughing, wheezing, or laryngospasm Loss or reduction of ETCO2 waveform Decrease in pulse oxymetry

Management • Removal of supraglottic airway (SGA) • Suction oral cavity and hypopharynx • Administer 100% oxygen • Two-person bag valve mask ventilation as needed • LMA or intubation as needed • Consider postoperative chest X-ray • Observe patient for 2  h postoperatively for new pulmonary symptoms (i.e., cough, wheeze, need for oxygen) • Patient may be discharged home after 2 h if no new pulmonary sequelae develop

Bradycardia Bradycardia is typically defined as a heart rate that is below 60 beats per minute (BPM) for children older that 3 years of age. However, in patients under 3 years of age bradycardia is defined as a HR under 100 BPM. It may be tolerated in an adult but is very concerning in a pediatric patient. Cardiac output is primarily driven by heart rate in the pediatric population, which mandates that bradycardia be treated.

Prevention • Administer glycopyrolate at 0.1 mg/kg IV when succinylcholine is administered • Maintain adequate oxygenation as monitored through ETCO2 and pulse oximetry Recognition • HR