Review of Surgery for Students 9811156083, 9788184451672

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Review of Surgery for Students AUTHORS Dr. Krishna Adit Agarwal, MBBS Alumnus of Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India Founder, I-MediSTAR Innovation in Medical Science, Technology and Research www.IMediSTAR.com AND

Dr. Avantika Singh, MBBS Alumna of Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India Founder, I-MediSTAR Innovation in Medical Science, Technology and Research www.IMediSTAR.com

PEEPEE PUBLISHERS AND DISTRIBUTORS (P) LTD.

Review of Surgery for Students Published by Pawaninder P. Vij and Anupam Vij Peepee Publishers and Distributors (P) Ltd. Head Office: 160, Shakti Vihar, Pitam Pura Delhi-110034 (India) Correspondence Address: 7/31, First Floor, Ansari Road Daryaganj, New Delhi-110002 (India) Ph: 65195868, 23246245, 9811156083 e-mail: [email protected] e-mail: [email protected] e-mail: [email protected] www.peepeepub.com

© 2014 Peepee Publishers and Distributors (P) Ltd. All rights reserved No part of this publication may be reproduced or transmitted in any form or by any means, electronic, mechanical, photocopy, recording, translated, or any information storage and retrieval system, without permission in writing from the editor and the publisher.

This book has been published in good faith that the material provided by authors/contributors is original. Every effort is made to ensure accuracy of material, but publisher and printer will not be held responsible for any inadvertent errors. In case of any dispute, all legal matters to be settled under Delhi jurisdiction only.

First Edition : 2014 ISBN: 978-81-8445-167-2

FOREWORD

Dr. Devi Prasad Shetty Chairman and Founder Narayana Health

Healthcare delivery in India is at a tipping point requiring major interventions. Even if investments are made available to create the necessary infrastructure, the big challenge of creating skilled manpower remains an uphill task. For a country with a population of 1.21 billion, we might have the largest number of medical colleges producing 50,000 doctors, yet, today we have only 18,000 surgeons in the country, i.e., one surgeon for 67,000 people! Due to the vast gap in demand and supply of post-graduate seats, entry into higher medical education has remained elusive to majority of MBBS graduates. In spite of large number of medical graduates, we are contending with only 2,030 post-graduate seats in General Surgery. With the scenario tough and competitive, the aspirants for General Surgery course need well-organized material for preparation and better outcomes in the entrance tests. In this direction, the book ‘Review of Surgery for Students’ by Dr. Krishna Adit Agarwal and Dr. Avantika Singh should come handy. With well classified and clearly laid out content, the effort of the young authors in their maiden publication deserves admiration. I am sure they will be able to enrich subsequent editions with valuable feedback from students and faculty alike. I wish the authors as also the students a resounding success.

Dr. Devi Prasad Shetty

PREFACE Review of Surgery for Students is aimed at providing the most concise and high-yielding information to undergraduate students preparing for their surgery final professional examination in India and abroad. There are a lot of surgery textbooks available in the market but no review book was so far available to help the students properly revise what they have learnt at their medical school. Our book is based on the Indian examination pattern and features a point-wise approach to topics. It is a book that has been written keeping in mind the last minute examination stress faced by students and it strives to help them retain the matter and answer well in the examinations. Only the must-know line diagrams have been included in the book. These diagrams are easy to remember as well as draw in the exam and will help achieve higher scores. We have consulted the standard surgery textbooks, Bailey and Love’s Short Practice of Surgery (26th Ed.) and Manipal Manual of Surgery (3rd Ed.) alongwith various online resources in preparing this review book. Although, we have tried our best to include the latest guidelines and management protocols but these guidelines are continuously being updated and we encourage our readers to keep themselves up-to-date with the future advances in surgery. Being the first edition, there might be some inadvertent errors in the book. We request our readers to kindly email us any corrections, suggestions and contributions in the form of latest protocols, line diagrams, newer topics asked in exams etc. to [email protected] . We welcome your feedback and will surely incorporate it in the next edition of this book. “Let the young know they will never find a more interesting, more instructive book than the patient himself.” —Giorgio Baglivi

Most importantly, attend your clinics and listen to the patient, for the patient teaches you far more than any book ever can!

Dr. Krishna Adit Agarwal Dr. Avantika Singh New Delhi, India

INTRODUCTION TO THE AUTHORS Dr. Krishna Adit Agarwal

Dr. Avantika Singh

Krishna is a recent medical graduate of Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi. He aspires to specialize in the field of Renal Medicine and has been offered a position at the prestigious Beth Israel Deaconess Medical Center (a teaching affiliate of Harvard Medical School) as a Research Fellow from August 2014.

Avantika is a recent medical graduate from Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi. She aspires to specialize in the field of Neonatal Medicine and has been offered a position at the prestigious Boston Children’s Hospital (a teaching affiliate of Harvard Medical School) as a Research Fellow from August 2014.

He has consistently performed well in his medical school examinations and displayed the ability to approach academic and practical problems in a logical, analytical and systemic manner.

Avantika has excelled in her medical school, winning numerous accolades. She topped the University in the third and final professional examinations. She was awarded gold medals in Community Medicine and Obstetrics and Gynecology, silver medals in Pediatrics, Surgery, Ophthalmology and ENT, and bronze medal in Internal Medicine besides a distinction in Pharmacology.

He has also undertaken several initiatives for the medical students like envisioning and organizing the Medical Students’ International Conference (MEDSICON) at VMMC. As the founder of the first MEDSICON conducted in 2011, Krishna aimed at providing undergraduate (bio) medical students an opportunity to showcase their research potential and take their research ideas forward. It has grown over the past three years and now receives a handsome international and national participation. Krishna has also been a co-founder of Innovation in Medical Science, Technology and Research (I-MediSTAR) which is an organization providing medical students and graduates with various opportunities to hone their clinical and research skills. He has also been instrumental in setting up of the ‘Journal of Young Medical Researchers’ (JYMR), an open access journal providing an exclusive avenue for young researchers to publish their work. Krishna is a highly intellectual, dedicated and practical thinking doctor who excels in thinking beyond the boundaries of the fixed academic curriculum.

Besides excelling in academics, she has founded an organization – Innovation in Medical Science, Technology and Research (I-MediSTAR). The organization provides mentorship to medical students and graduates seeking to sharpen their clinical and research skills. It conducts various skill-based hands-on workshops to help students learn the science and art of medicine. Avantika has also been the co-founder of Medical Students’ International Conference (MEDSICON) and organized it at VMMC for the past three years. The conference provided the much-needed platform to young researchers to share their research ideas with the medical community. She is also the Student Editorial Board Coordinator at the Journal of Young Medical Researchers (JYMR). Avantika is a brilliant doctor, who strives to excel in life. She is compassionate and caring towards her patients and has the ability to make the best possible medical decisions.

Prof. Dr. Renuka Sharma Professor, Dept. of Physiology VMMC and SJH, New Delhi

ACKNOWLEDGEMENTS

We are thankful to… Gods in Heaven Gods on Earth, Our Parents Our Gurus, Guides and Mentors Dr. Jayashree Bhattacharjee Dr. Chintamani, Dr. Harish Chellani Dr. Renuka Sharma, Dr. Rajeev Tiwari Dr. Sugandha Arya, Dr. Harpreet Singh Our great friends, especially Manmohan for igniting the spark to write this book Our Dear Readers and The awesome team at Peepee Publishers and Distributors (P) Ltd. for their wonderful work with this book.

CONTRIBUTING AUTHORS Joyutpal Biswas Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi Arteries, Veins and Lymphatics and Burns Akriti Sinha Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi Miscellaneous Questions Asked in Exams Arushi Devgan Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi Paediatric Surgery Aditya Ranot Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi Oral Cavity and Oropharynx and Salivary Glands Nayan Agarwal University College of Medical Sciences and G.T.B. Hospital, New Delhi Trauma Care Shivani Sharma Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi Fluid and Electrolyte Balance, SIRS and MODS

CREATIVE TEAM

Shashank Singh Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi Vinay Kumar Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi Kaveri Pandit Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi Sachin Goel Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi

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Review of Surgery for Students

REVIEWERS Dr. Rohan Khandelwal MS, MRCS (Edin.), FIBD Oncoplastic Breast Surgeon Editor-in-Chief: Journal of Young Medical Researchers Dr. Megha Tandon MS, DNB, MRCS Ed.,FICS,FIAGES Instructor for ATLS (American College of Surgeons) Dr. Mayank Mehrotra MBBS, MD Anaesthesiology (Gold Medallist) Senior Resident, Department of Anaesthesiology VMMC and Safdarjung Hospital, New Delhi

CONTENTS

Section 1: Gastrointestinal Surgery Chapter 1.

Hernias

1

Chapter 2.

Oesophagus

6

Chapter 3.

Stomach and Duodenum

15

Chapter 4.

Liver and The Biliary System

26

Chapter 5.

Pancreas and Spleen

46

Chapter 6.

Small and Large Intestines

57

Chapter 7.

Intestinal Obstruction

73

Chapter 8.

Rectum and Anal Canal

81

Chapter 9.

Bariatric Surgery

90 Section 2

Chapter 10.

The Breast

93 Section 3

Chapter 11.

Thyroid and Parathyroid Glands

111 Section 4

Chapter 12.

Adrenal Gland

129 Section 5

Chapter 13.

Oral Cavity and Oropharynx

131 Section 6

Chapter 14.

Salivary Glands

137 Section 7: Urology

Chapter 15.

Kidney and Ureter

142

Chapter 16.

Urinary Bladder and Urethra

153

Chapter 17.

The Prostate Gland

161

Chapter 18.

Penis, Testis and Scrotal Sac

167

xii Review of Surgery for Students Section 8: Arteries, Veins and Lymphatics Chapter 19.

Arterial Disorders

177

Chapter 20.

Venous Disorders

186

Chapter 21.

Lymphatic Disorders

191 Section 9: Trauma Care and Burns

Chapter 22.

General Principles

193

Chapter 23.

Head Trauma

195

Chapter 24.

Chest Trauma

201

Chapter 25.

Abdominal Trauma

204

Chapter 26.

Burns

208 Section 10

Chapter 27.

Paediatric Surgery

213 Section 11

Chapter 28.

General Surgery

222 Section 12

Chapter 29.

Fluid and Electrolyte Balance, SIRS and MODS

242

Section 13 Chapter 30.

Post-Operative Fever

247 Section 14

Chapter 31.

Principles of Anaesthesiology

250 Section 15

Chapter 32.

Miscellaneous Questions Asked in Exams

260

Section 16 Chapter 33.

Surgical Instruments

268

Chapter

SECTION 1 : GASTROINTESTINAL SURGERY

1 HERNIAS reinforced in the lateral one-thirds by the internal oblique muscle.

A hernia results from protrusion of a viscus through a weakness in its containing wall.

INGUINAL HERNIA Inguinal hernias occur when abdominal contents pass through the inguinal canal. They usually occur above the inguinal ligament and medial to the pubic tubercle.

SURGICAL ANATOMY OF THE INGUINAL CANAL

2. Posterior: Formed by the fascia transversalis, reinforced in the medial one-thirds by the conjoint tendon. 3. Floor: Formed by the inguinal ligament and lower border of external oblique aponeurosis. It is continuous medially with the lacunar ligament and gives attachment to the fascia lata on its inferior border. 4. Roof: Formed by the arched fibres of the conjoint tendon.

Openings

Contents of Inguinal Canal

1 . Deep Inguinal Ring: It is an opening in the fascia transversalis, 1 cm above the inguinal ligament, midway between the anterior superior iliac spine (ASIS) and the symphysis pubis. The inferior epigastric vessels lie medial to this opening.

• Males: Spermatic cord and ilioinguinal nerve.

2. Superficial Inguinal Ring: It is a triangular defect in the external oblique aponeurosis, overlying the pubic crest which forms the base of the triangle.

• Females: Round ligament of uterus and ilioinguinal nerve.

Coverings of Spermatic Cord •

From within outwards the coverings are derived as follows: o Internal spermatic fascia from fascia transversalis.

Boundaries

o Cremasteric fascia from internal oblique.

1 . Anterior: Formed by the external oblique aponeurosis,

o External spermatic fascia from external oblique.

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Contents of Spermatic Cord •

Vas deferens.

•

Artery to vas deferens (branch of inferior vesical artery).

•

Testicular artery (branch of abdominal aorta).

•

Testicular vein (drains into the IVC on the right and the renal vein on the left).

•

Testicular lymphatics.

•

Testicular nerve fibres.

•

Processus vaginalis.

•

Cremasteric artery (branch of inferior epigastric artery).

•

Nerve to cremaster muscle (genital branch of genitofemoral nerve).

contents can be felt distinctly from the testis, which lies below the sac. o Complete: The processus vaginalis is patent throughout here and the hernia sac is continuous with the tunica vaginalis of the testis. Therefore, the contents of the hernial sac reach the very bottom of the scrotum and are indistinguishable from the testis. •

Direct Inguinal Hernia •

Cause: Weakness in the abdominal wall, increased intra-abdominal pressure.

•

Peritoneum does not traverse the deep inguinal ring. It enters the inguinal canal through the posterior wall from a defect in fascia transversalis.

•

More common in older age groups and males (four times more common than in females).

•

The hernial sac originates from the Hesselbach’s triangle, medial to the inferior epigastric vessels.

•

The hernial sac has a broad neck and therefore, lesser chances of strangulation than in an indirect inguinal hernia.

Hesselbach’s Triangle •

Boundaries o Base: Medial half of inguinal ligament. o Medial Border: Linea semilunaris (lateral border of rectus abdominis). o Lateral Border: Inferior epigastric artery.

•

Significance: This area is potentially weak because it is not reinforced by the conjoint tendon and therefore most of the direct inguinal hernias protrude through it.

TYPES OF INGUINAL HERNIAS Indirect Inguinal Hernia •

Indirect hernias can also occur in females (4% as common as in males) and when they do occur, they can eventually reach the ipsilateral labium majus.

Classification of Hernia Nyhus Classification

Cause: Failure of embryonic closure of the deep inguinal ring after the descent of testes.

Table 1.1: Nyhus classification of hernias

•

Peritoneum traverses the deep inguinal ring to come into the inguinal canal.

Type 1

Indirect inguinal hernia with a normal ring; sac in the canal

•

More common in younger age groups.

Type 2

•

The origin of hernial sac is lateral to the inferior epigastric artery.

Indirect inguinal hernia with an enlarged internal ring but the posterior wall is intact; inferior deep epigastric vessels not displaced; sac not in scrotum

•

The hernial sac has a narrow neck and higher chances of strangulation than in a direct inguinal hernia.

Type 3a

Direct hernia with a posterior floor defect only

Type 3b

Indirect hernia with enlargement of internal ring and posterior floor defect

Type 3c Type 4

Femoral hernia Recurrent hernia: A-direct, B-indirect, C-femoral, D-combinations of A-B-C

•

Subtypes: o Bubonocoele: Hernia limited to the inguinal canal. o Funicular: The processus vaginalis closes at its lower end just above the epididymis and the

Hernias

Complications of Inguinal Hernia 1. Irreducible hernia: Formation of adhesions between the sac and its contents. 2. Obstructed hernia: Occurs when the inguinal rings/ constrict, thereby occluding the lumen of the bowel contained within the sac. But the blood supply to bowel wall is intact. 3. Strangulated hernia: The constriction is so severe that it occludes the bowel wall blood supply, therefore causing ischemia of the bowel loop. It is a surgical emergency.

10. Laugier’s hernia: A hernia arising from the lacunar ligament defect.

TREATMENT OF INGUINAL HERNIA 1. Herniotomy – used only for congenital hernias. 2. Herniorrhaphy – uses the tissue present in the body. a. Bassini’s repair – used silk for approximation of tissues. b. Shouldice repair – used stainless steel wire for approximation of tissues. 3. Hernioplasty – uses foreign objects like prosthetic meshes

Other Types of Inguinal Hernias

Lichtenstein’s mesh repair

1. Hernia en W a.k.a Maydl’s Hernia: Two bowel loops in a single hernial sac, causing gangrene at the apex of the double loop which lies inside the abdomen. 2. Sliding hernia a.k.a Hernia en Glissade: Occurs when extra-peritoneal structures like the sigmoid colon (most common) descend with the hernial sac, forming its wall. 3. Richter’s hernia: Occurs when the lumen of the bowel loop contained in the sac is not obstructed but only a part of the bowel wall is being constricted by the neck of the sac. 4. Litter’s hernia: A hernia containing Meckel’s diverticulum. 5. Pantaloons’ hernia: Contains both the direct and indirect hernias, one on either side of the inferior epigastric artery. 6. Phantom hernia: Occurs when a weak abdominal muscle bulges and produces a visible protrusion, without any abdominal contents being involved. It can occur with poliomyelitis and hypokalemia in children. 7. Amyand’s hernia: A hernia containing the appendix which becomes incarcerated. 8. Spigelian hernia: A hernia developing at the arcuate line through the Spigelian’s fascia, which is the aponeurosis between the rectus abdominis muscle medially and semilunar line laterally. 9. Berger’s hernia: A hernia in the Pouch of Douglas.

3

•

Tension-free repair.

•

Variety of meshes can be used.

•

Fibrosis occurs on the mesh and provides support to the floor of the canal.

•

The mesh per-say does not provide support.

4. Laparoscopic hernia repair a. Intraperitoneal onlay mesh (IPOM). b. Transabdominal pre-peritoneal repair (TAPP). c. Totally extra-peritoneal repair (TEP). *Post-Herniorrhaphy pain syndrome or inguinodynia: Upto 20% of patients can experience a chronic groin pain lasting for more than three months after surgical or laparoscopic repair of inguinal hernias. It is a type of neuropathic pain due to insult to the nerve supplying the operative site like the genitofemoral nerve. It is mostly described as burning or stabbing pain. Triple neurectomy including the genitofemoral nerve has shown some benefit in studies.

FEMORAL HERNIA Femoral hernias occur when abdominal contents pass through a naturally-occurring defect known as the femoral canal. They usually occur below the inguinal ligament and lateral to the pubic tubercle. They point towards the pubic tubercle and bear a shape known as the Retort shape. •

Account for only 3% of all hernias.

•

Can occur in both males and females, but occur more commonly in females (M:F = 1:4) due to the wider bony pelvis.

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Review of Surgery for Students

•

More common in adults than children.

•

The complications are similar to inguinal hernias.

•

Treatment options:

over the diaphragmatic defect. The baby must be mechanically ventilated during the procedure and may also require respiratory assistance postoperatively to expand the lungs. ECMO (Extra-Corporeal Membrane Oxygenation) is also a useful option in these babies.

1. Lockwood’s infra-inguinal approach (preferred for elective surgeries). 2. Lotheissen’s trans-inguinal approach. 3. McEvedy’s high approach.

Umbilical Hernia •

These hernias usually occur in the newborn and involve a protrusion of abdominal contents at the site of the navel due to a congenital defect in the umbilicus.

•

Usually resolve without any treatment by the age of 2-3 years.

•

Categories.

Congenital Diaphragmatic Hernia •

In the foetus, pleuroperitoneal membranes exist between the thorax and abdomen.

•

These membranes have openings known as the pleuroperitoneal canals, which normally get obliterated and disappear by the ninth or tenth week of intrauterine life.

•

•

Table 1.2: Different types of umbilical hernia

Diaphragmatic hernia results when these canals persist beyond that time and abdominal contents protrude through them into the thorax.

Minor •

Since the position of these canals is fixed, the position of diaphragmatic hernias is also fixed.

•

1. Canal of Bochdalek – Left posterior (posterolateral diaphragmatic hernia).

•

2. Canal of Morgagni–Right anterior (retrosternal or parasternal diaphragmatic hernia).

•

Bulge becomes prominent when the child cries Common in low birth weight babies May be associated with Beckwith-Wiedemann syndrome Resolves spontaneously in most of the children by the age of 2-3 years, otherwise surgery may be required Surgery is also indicated if the neck of the sac is narrow, although this is very rare

Major • OMPHALOCOELE • It is a big defect with a peritoneal sac containing a major part of the bowel outside the abdominal cavity • Surgical emergency

•

Diaphragmatic hernias are more common in boys.

•

More commonly, hernias protrude through the canal of Bochdalek.

•

Upto fifty percent of patients with Bochdalek’s hernia have an associated cardiac anomaly.

•

Morgagni’s hernia is more common in females.

•

Presentation: Respiratory failure owing to pulmonary hypertension and pulmonary hypoplasia due to compression by the abdominal contents.

GASTROSCHISIS

Diagnosis:

•

Protrusion of intestinal contents freely outside the abdomen, through a defect on the right side of the umbilical cord is known as Gastroschisis.

•

The contents are not covered by any hernial sac, rather a gelatinous substance covers them.

•

The size of the congenital abdominal defect is usually less than 4 cm in size.

•

•

•

1. X-Ray: Shows bowel gas in the thorax. 2. Barium swallow: Confirms plain X-ray findings. 3. Endoscopy. •

Treatment: Surgery is required to reduce the abdominal contents back into the abdomen and place a mesh

Treatment: Mayo’s operation, which involves overlapping the rectus muscles on either side of the midline.

Hernias

•

Many hypotheses have been formed to explain this defect. These theories involve a failure of mesoderm to form in the abdominal wall, rupture of amnion around the umbilical ring, abnormal involution of the right umbilical vein, disruption of the right vitelline artery and abnormal folding of the body wall.

5

•

This condition is a surgical emergency.

•

Surgery involves reduction of contents back into the abdomen and application of a pressure band until the wall defect heals itself.

•

Multiple surgeries may be required to correct the defect.

Chapter

SECTION 1 : GASTROINTESTINAL SURGERY

2 OESOPHAGUS lying below the inferior constrictor muscle and above the cricopharyngeus muscle.

ZENKER’S DIVERTICULUM A.k.a. Pharyngoesophageal diverticulum, hypopharyngeal diverticulum, pharyngeal pouch. •

A diverticulum arises by two mechanisms: o Pulsion diverticulum: Push from inside the lumen increases intraluminal pressure and results in an outpouching, e.g., Upper and lower oesophageal diverticuli. o Traction diverticulum: Pull from outside results in an outpouching, e.g., Middle oesophageal diverticulum.

•

Diverticuli can be of 2 types: o Congenital diverticuli: Full thickness, mucosa to serosa, e.g., Meckel’s diverticulum. o Acquired diverticuli: Partial thickness, muscles are not involved, e.g., Zenker’s diverticulum.

•

•

Zenker’s diverticulum results from an uncoordinated swallowing associated with cricopharyngeal muscle spasm and delayed muscle relaxation which cause increased intrapharyngeal pressure and outpouching of the mucosa at the weakest point of the pharyngeal wall – Killian’s dehiscence. Killian’s dehiscence is a weak area of the pharynx

Fig. 2.1: Zenker’s diverticulum

•

Clinical Presentation: o Dysphagia. o Lumpiness. o Regurgitation of swallowed food. o Halitosis. o Cough.

Oesophagus

•

•

Diagnosis:

•

Causes:

o Barium swallow.

1. Idiopathic.

o Water soluble contrast and CT.

2. Obesity.

o Endoscopy is usually not performed for the risk of perforation.

3. Hiatal hernia.

Treatment:

5. Zollinger-Ellison syndrome.

o Diverticulectomy and cricopharyngomyotomy: Excise the diverticulum and reduce the tone of cricopharyngeus muscle to prevent recurrence.

6. Scleroderma or systemic sclerosis.

o Diverticulopexy: Reverse the direction of diverticulum and fix it so that it can drain and gradually reduce in size.

4. Hypercalcemia.

7. Visceroptosis a.k.a. Glenard syndrome. 8. Chronic steroid use. •

Clinical Presentation: 1. Heartburn (retrosternal burning pain).

o Botulinum toxin injection into the cricopharyngeus: Maximum relief of 6 months.

2. Regurgitation.

o Dohlman’s procedure: Double-lipped oesophagoscope is used for cutting and stapling.

4. Water brash.

o Medical management in patients unfit for surgery: Can use calcium channel blockers or nitrates.

7

3. Pain while swallowing (odynophagia). 5. Coughing (due to laryngeal irritation). •

Diagnosis: 1. 24-hour ambulatory monitoring of pH is the investigation of choice.

GASTRO-OESOPHAGEAL REFLUX DISEASE (GERD)

o pH is measured 5 cm above and below the gastro-oesophageal junction.

GERD is a chronic condition characterized by reflux of acidic stomach contents back into the oesophagus, causing damage to the mucosal lining of the oesophagus.

o Patient maintains a symptom diary also.

•

•

Pathophysiology: The most important factor causing reflux is abnormal lower oesophageal sphincter.

2. Manometry. 3. Upper GI endoscopy. •

Treatment: 1. Lifestyle modification

Normally, this sphincter stays closed and relaxes only during swallowing. In acid reflux disease, this

o Weight reduction.

sphincter loses its tone and remains open, allowing acidic contents of the stomach to go back into the oesophagus and damage its mucosal lining.

o Avoidance of heavy meals before lying down.

Other Important Factors: 1. Lower oesophageal sphincter. 2. Oesophageal motility.

o Sleep hygiene. o Stopping smoking and alcohol. o Moderate exercise. 2. Medications o Proton Pump Inhibitors (PPI), e.g., Pantoprazole, Rabeprazole, Omeprazole.

3. Gastric emptying.

o H2-Receptor blockers, e.g., Ranitidine, Famotidine.

4. Angle between the stomach and oesophagus (Angle of His).

o Antacids, e.g., hydroxide etc.

Sucralfate,

Aluminium

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Review of Surgery for Students

dislocation of the upper stomach into the posterior mediastinum.

3. Surgery o Nissen’s fundoplication: The upper stomach is wrapped around the oesophagus to strengthen the lower oesophageal sphincter and prevent reflux. It is a 360 degree wrap.

2. Type II a.k.a. Rolling or Paraoesophageal Hernia: Occurs when the fundus of the stomach herniates alongside a normal oesophagus.

o Belsey’s fundoplication: Partial 270 degree wrap.

3. Type III: Mixed variety.

o Hill’s repair.

(See Fig. 2.2)

o Laparoscopic fundoplication. •

•

Complications:

1. Increased intra-abdominal pressure due to violent coughing, chronic constipation, pregnancy, obesity etc.

1. Oesophageal stricture. 2. Oesophageal ulcer. 3. Barrett’s oesophagus: Metaplasia of the normal stratified squamous epithelial lining of the lower oesophagus to the intestinal simple columnar epithelium with goblet cells. It is a pre-malignant condition, strongly associated with the development of adenocarcinoma of the oesophagus.

2. Congenital diaphragmatic weakness. 3. Smoking. •

Clinical Presentation: 1. Rolling hiatal hernia usually presents with dysphagia or symptoms of obstruction. 2. Sliding hiatal hernia usually presents with symptoms of heartburn and regurgitation.

HIATUS HERNIA It is an abnormal protrusion of the stomach into the thorax through a weakness or defect in the diaphragm. •

Associated Risk Factors:

•

Diagnosis: 1. Upper GI endoscopy.

Types of hiatal hernias:

2. Barium swallow in erect position.

1. Type I a.k.a. Sliding Hernia: Occurs due to a laxity of the phrenico-oesophageal ligament resulting in

3. Plain X-rays – Might show an abnormal air fluid level in the thorax.

Fig. 2.2: Hiatus hernia

Oesophagus

•

Treatment 1. Lifestyle modification. 2. PPIs, H2-blockers, antacids to reduce acid production.

oesophageal junction due to retching or vomiting. The initial vomitus does not contain blood, but the subsequent vomitings contain blood from the bleeding laceration. •

4. Laparoscopic fundoplication.

o May also present as melena. •

BOERHAAVE SYNDROME It is a full-thickness tear in the left distal oesophagus (a few centimetres away from the stomach) due to forceful vomiting or retching against a closed glottis. •

o Odynophagia, tachycardia, tachypnoea, cyanosis and shock may develop. o Mackler’s triad: Classical presentation seen in less than 20% of cases comprises chest pain, vomiting and subcutaneous emphysema. o Subcutaneous emphysema may be audible as Hamman’s crunch or Hamman’s sign. •

•

o Endoscopic cauterization may be used to stop the bleeding if it persists.

TRACHEO-OESOPHAGEAL FISTULA A fistula is defined as a tract open at both ends, connecting two epithelial lined cavities. The trachea-oesophageal fistula refers to an abnormal communication between the trachea and oesophagus. It is generally a congenital abnormality but it may also occur following laryngeal surgeries. •

During the development of the trachea and oesophagus, normally a septum divides them in a cranio-caudal direction. But if the septum develops in a cranio-dorsal direction then a trachea-oesophageal fistula results.

•

Pressure necrosis due to an indwelling tracheostomy tube might also cause an abnormal communication between the trachea and oesophagus.

•

Types:

o Gastrograffin oesophagogram (water soluble contrast). o CT scan. •

Treatment: o IV rehydration. o Antibiotics to prevent mediastinitis. o Surgery – Left thoracotomy with lavage and primary repair within 48 hours. o Controlled fistula may be otherwise used.

Treatment: o Bleeding usually stops within 2-3 days.

Investigations:

o Plain X-ray.

Investigations: o Upper GI endoscopy is the investigation of choice.

Clinical Presentation: o Usually patient has a history of severe retching or vomiting followed by severe abdominal or chest pain.

Clinical Presentation: o Usually presents as hematemesis following a severe episode of vomiting or retching.

3. Nissen’s fundoplication. 5. Hill’s repair.

Table 2.1: Types of tracheo-oesophageal fistula Type

Remarks

Type A

Second-most common type

Type B Type C

It is a partial thickness mucosal tear at the gastro-

Most common type Seen in 80-87% of the cases

MALLORY-WEISS SYNDROME A.k.a. Gastro-oesophageal laceration syndrome.

9

Type D Type H

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Review of Surgery for Students

Fig. 2.3: Tracheo-oesophageal fistula

•

TOF is commonly associated with Down’s syndrome.

•

Other congenital anomalies often present in association with TOF–VACTERL anomalies:

1. A right posterolateral thoracotomy is done from the 4th intercostal space to repair the defect.

1. Vertebral anomalies.

2. Waterston’s criteria takes into account the birth weight (BW) and presence or absence of pneumonia into account while deciding on surgery:

2. Anorectal anomalies (Most common association). 3. Cardiac anomalies (PDA, VSD, Tetralogy of Fallot). 4. Tracheo-oesophageal fistula. 5. Renal anomalies. 6. Limb anomalies (Radial hypoplasia being the most common). •

Polyhydramnios is seen in 50% of the mothers with a TOF-afflicted foetus.

•

Clinical Presentation:

•

•

Treatment:

o BW>5.5 lbs and pneumonia absent – Surgery can be performed immediately. o BW55-60 years.

Oesophagus

•

It is commonly seen in China (due to some nonspecific nutritional deficiency, e.g., riboflavin).

•

The squamous variety can arise almost anywhere in the oesophagus, but commonly arises in the upper half of the oesophagus whereas the adenocarcinoma variety has a propensity to arise in the distal half.

•

o CT scan abdomen – To assess the liver metastasis. o Trans-oesophageal ultrasonography – Most sensitive investigation to assess the depth of involvement and node status and stage the disease. o PET scan – Staging.

Risk factors for squamous variety:

o Bronchoscopy – To rule out invasion into the respiratory structures.

o Smoking.

o MRI scan.

o Alcohol.

o Barium swallow – A “Filling defect” or an “AppleCore defect” may be seen. But this is usually not performed nowadays.

o Deficiency of molybdenum, zinc, Vit. C, riboflavin. o Smoked fish. o Hot beverages. o Zenker’s diverticulum.

•

TNM Staging: o T staging Tx

Tumour cannot be assessed

T0

No primary tumour

T1

Tumour invades lamina propria, muscularis mucosae or submucosa

T1a

Tumour invades lamina propria or muscularis mucosae

Clinical Presentation:

T1b

Tumour invades submucosa

o Constitutional symptoms – significant weight loss, appetite loss, cachexia, lethargy, asthenia.

T2

Tumour invades muscularis propria

T3

Tumour invades adventitia

o Local symptoms – Dysphagia (more for solids initially, then progressing to liquids), bleeding, retrosternal chest pain, hoarseness and cough.

T4

Tumour invades adjacent structures

T4a

Resectable tumour invading pleura, pericardium or diaphragm

T4b

Unresectable tumour invading other adjacent structures like aorta, vertebral body, trachea etc.

o Achalasia cardia. o Plummer-Vinson syndrome. o Caustic injuries. o Tylosis. o Human papilloma virus (HPV). •

o Metastatic symptoms – Enlarged lymph nodes, bone pains etc. o Examination is mostly normal except for enlarged supraclavicular nodes and hepatomegaly in case of metastasis. •

•

13

Patients are usually asymptomatic until approximately 70-75% of the oesophageal lumen is occluded, therefore most of them present late at the metastatic stage and are hence unfit for surgery. Investigations: o Upper GI endoscopy – For direct visualisation and biopsies for tissue diagnosis. o CT scan chest – To stage the disease and see involvement of adjacent structures.

o N staging Nx

Regional lymph nodes could not be assessed

N0

No regional lymph node metastasis

N1

Metastasis in 1-2 regional lymph nodes

N2

Metastasis in 3-6 regional lymph nodes

N3

Metastasis in >=7 regional lymph nodes

o

M staging

M0

No distant metastasis

M1

Distant metastasis present

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Review of Surgery for Students

o Staging Stage IA

T1

N0

M0

Stage IB

T2

N0

M0

Stage IIA

T3

N0

M0

Stage IIB

T1,T2

N1

M0

Stage IIIA

T4a

N0

M0

T3

N1

M0

T1,T2

N2

M0

Stage IIIB

T3

N2

M0

Stage IIIC

T4a

N1,N2

M0

T4b

Any N

M0

Any T

N3

M0

Any T

Any N

M1

Stage IV

o Ivor-Lewis oesophagectomy is a type of transthoracic oesophagectomy done for middle and lower third oesophageal carcinomas. o McKeown oesophagectomy a.k.a. Three-Hole oesophagectomy is a type of trans-thoracic procedure performed for upper third oesophageal carcinomas. o Chemoradiation includes both chemotherapy and radiotherapy. o Drugs used for chemoradiation include Cisplatin, Adriamycin and Methotrexate for the squamous variety and 5-fluoro-uracil for the adenocarcinoma type. o Palliative procedures are done for Stage IV patients who are otherwise unfit for surgery and cannot tolerate Chemoradiation. These procedures help relieve dysphagia and provide comfort to the patient. Some examples include:

• Treatment: o General considerations Tis and T1aN0

Endoscopic mucosal resection or Endoscopic submucosal dissection

T1b and Any N

Surgery can be the initial choice

T2 and beyond

Trimodal (Chemoradiation + Surgery) therapy if the patient can tolerate

2. Radiotherapy. 3. Chemotherapy. 4. Oesophageal stenting. •

Prognosis: TNM Stage

5-year survival (%)

0

100

I

80

IIA

40

1. Trans-thoracic oesophagectomy.

IIB

30

2. Trans-hiatal oesophagectomy.

III

15

3. Endoscopic mucosal resection.

IV

0

Stage IV (M1) o

1. Laser therapy.

Chemotherapy or Palliation

Surgical options include:

Chapter

SECTION 1 : GASTROINTESTINAL SURGERY

3 STOMACH AND DUODENUM MENETRIER’S DISEASE

o Serum gastrin is normal.

•

o Chromium-labelled albumin test might reveal enhanced GI protein loss.

It is an autoimmune disease characterised by large gastric rugosities, decreased acid production and increased mucous secretion (rich in proteins).

•

More common in females.

•

It is a premalignant condition.

•

The proximal part of the stomach is predominantly involved and all cells like the chief and parietal cells are destroyed and replaced my mucous producing cells.

•

Therefore, it is a.k.a Hypertrophied protein losing gastropathy.

•

The disease is associated with overexpression of the TGF-Alpha.

•

Clinical Presentation: o Mean age of presentation is 30-60 years.

•

ATROPHIC GASTRITIS Table 3.1: Types of atrophic gastritis Type A

Type B

•

Autoimmune condition

•

Caused by H. pylori infection

•

Antibody is present against the parietal cells

•

Involves the distal stomach (antrum)

•

Involves the proximal • stomach (fundus and cardia)

•

Premalignant condition

•

Hypergastrinemia

•

Also results in a deficiency of Vit. B12 and pernicious anaemia because the same parietal cells secrete the intrinsic factor which is required to absorb Vit. B12 distally

o Upper abdominal pain, nausea, vomiting. o Loss of appetite and weight loss. o Hypoalbuminemia and oedema. •

Diagnosis: o Barium meal study. o Upper GI endoscopy. o Oesophageal pH hypochlorhydria.

monitoring

reveals

Treatment: Total gastrectomy is the definitive treatment. Cetuximab is a novel monoclonal antibody against EGFR, being tried in this condition.

No associated nutritional deficiencies

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PEPTIC ULCER DISEASE •

•

A peptic ulcer is a discontinuity of the gastric mucosal lining as a result of imbalance between the injuring and protecting mechanisms of the lining. Table 3.2: Injuring and protecting mechanisms of gastric mucosa Injuring

mechanisms

Protecting mechanisms (Gastric barrier)

•

Modified Johnson’s Classification of peptic ulcers Type I

At lesser curvature of the stomach

Type II

Combined gastric and duodenal ulcer

Type III

Isolated duodenal or pyloric ulcer

Type IV

Proximal gastro-oesophageal ulcer

Type V

Diffuse ulcer (e.g. NSAID use)

Clinical Presentation:

1. Gastric acid

1.

Mucosal lining

1. History of GERD.

2. Helicobacter pylori

2.

Bicarbonate secretion

2. Retrosternal or epigastric burning pain.

3. Prostaglandin inhibitors e.g. NSAIDs

3.

Prostaglandins

4. Steroids

4.

Mucous cover

3. Regurgitation. 4. Water brash. 5. Loss of appetite and weight (alarming symptom). 6. Hematemesis and melena (alarming symptom).

5. Smoking

7. Duodenal perforation leading to acute peritonitis. •

6. Alcohol

Peptic ulcers can occur at mainly two locations:

1. Peptic ulcer is usually a clinical diagnosis, but tests can be ordered in case of persistent symptoms to rule out development of carcinoma.

1. Gastric ulcer – occurs in the stomach.

2. Barium swallow can show the edges of the ulcer.

2. Duodenal ulcer – occurs in the duodenum.

3. Upper GI endoscopy allows direct visualisation of the ulcer and taking biopsies.

7. Bile salts

•

Investigations:

Table 3.3: Differences between gastric and

4. H. pylori infection can be detected by:

duodenal ulcers Gastric ulcer o Occurs most commonly along the lesser curvature of the stomach o Primary cause is a decrease in the mucosal defence mechanisms o Gastric acid levels are normal or decreased o Pain of gastric ulcer occurs immediately after taking a meal o Hematemesis is more common than melena

o Urea breath test.

Duodenal ulcer o Occurs at the junction of acid producing and nonacid producing mucosa, i.e., just distal to the pylorus

o Rapid urease test on the biopsy specimen. o Stool antigen test. •

Differentials: 1. Inferior wall MI.

o Primary cause is hyperacidity, most commonly due to H. pylori infection

2. Acute cholecystitis.

o Gastrin and gastric acid levels are increased

4. Acute cholangitis.

o Pain of duodenal ulcer occurs 2-3 hours afterwards a meal

6. Gastritis.

o Melena is more common than hematemesis

3. Acute pancreatitis. 5. Oesophageal rupture or tear. 7. Acute gastroenteritis. •

Medical management: 1. Treatment options include empiric therapy or endoscopy followed by appropriate therapy.

Stomach and Duodenum

2. In the Indian setting, the empiric therapy with antisecretory drugs or empiric triple therapy is the first line treatment. 3. Triple therapy consists of a proton pump inhibitor, amoxicillin and clarithromycin given for a period of 7-14 days, longer period being more effective in eliminating H. pylori infection.

1. Vagotomy + drainage procedure 2. Gastrectomy. (See Table 3.4) •

Sample Triple Therapy Regimen Drug

Dose

Duration

Omeprazole

20 mg PO bid

14 days

Amoxicillin

1g PO bid

Clarithromycin 500 mg PO bid 4. Amoxicillin should be replaced with metronidazole in penicillin-allergic patients. 5. Prophylactic therapy for patients requiring intake of NSAIDs over a long period involves the use of prostaglandin analogue like misoprostol and PPIs like omeprazole, pantoprazole etc. 6. Long-term PPIs for 4-8 weeks may be used in patients who have otherwise non-complicated ulcers but do not respond to the 14-day therapy. •

Surgical Options (For patients who fail triple therapy or have complicated ulcers):

Vagotomy o Truncal vagotomy – This involves cutting of the main trunk of the vagus nerve which supplies the parietal cells. This stops all stimulation for gastric acid release and results in achlorhydria. o Selective vagotomy – This involves cutting of the trunk beyond the point where it gives off the hepatic and coeliac branches. Therefore, the complications of cholelithiasis and postvagotomy diarrhoea are avoided. o Highly selective vagotomy – This involves section of only the small branches of the vagus nerve which go towards the stomach, leaving intact the branches of the last 6 cms (Nerve of Latarjet). It is a.k.a. parietal cell vagotomy. A drainage procedure is not required after this procedure. o The truncal and selective types of vagotomies result in damage to the Nerve of Latarjet, which supplies the pylorus. This makes the pylorus go into spasm and therefore a drainage procedure is required with these vagotomies. Drainage procedures can be of two types – Pyloroplasty (opening up the pylorus) or Gastrojejunostomy (anastomosis of stomach with jejunum).

Table 3.4: Surgical options for peptic ulcer disease Vagotomy

Partial Gastrectomy

Rationale

The vagus nerve stimulates production of gastric acid by direct action on the parietal cells and indirect action on the gastrin secreting G-cells. Vagotomy abolishes these stimuli and help control the gastric acid release

Partial gastrectomy or antrectomy helps by reducing the number of gastrin secreting G-cells and thereby reduce the acid production

Use

Primarily useful for duodenal ulcers

Primarily useful for gastric ulcers

Types

1. Truncal Vagotomy

1. Billroth I

2. Selective Vagotomy

2. Billroth II

3. Highly Selective Vagotomy

3. Polya gastrectomy

1. Anastomotic leak 2. Postvagotomy diarrhoea

1. Anastomotic leak 2. Stomal ulcer

3. Biliary gastritis

3. Iron deficiency anaemia (Billroth II)

4. Gallstones

4. Duodenal blow out

5. Delayed gastric emptying 6. Anastomotic site ulcer

5. Afferent loop syndrome (jejunojejunostomy can prevent this)

7. Ulcer recurrence in case of incomplete vagotomy

6. Dumping syndrome

Post-op complications

17

7. Weight loss 8. Diarrhoea

18

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Review of Surgery for Students

Partial Gastrectomy

4. Sweating and flushing.

o Billroth Type I gastrectomy – Two-thirds of the stomach near the ulcer is removed and an end to end anastomosis is performed.

5. Seizures, fainting or passing out. o

1. Frequent and low quantity meals.

o Billroth Type II gastrectomy – A small part of the stomach near the ulcer is excised and a gastrojejunostomy is performed by taking the duodenum from infront of the colon and anastomosing it on the anterior wall of the stomach. This procedure is more commonly done than Type I. o Polya gastrectomy – It is a modification of Billroth Type II gastrectomy where the duodenum is taken from behind the colon (retrocolic) through the mesocolon and anastomosed to the posterior wall of the stomach. •

Treatment of dumping syndrome: 2. No water intake with meals. 3. Intake of complex polysaccharides more than simple carbohydrates. 4. Decreasing intake of carbohydrate-rich food like sweets etc. 5. Octreotide (somatostatin analogue). 6. Roux-en-Y surgery.

•

Complications of peptic ulcers: o Bleeding. o Perforation.

Dumping Syndrome

o Penetration.

o Partial gastrectomy involves the pylorus. Therefore, after the procedure, all the hyperosmolar food ingested directly goes into the intestine rather than being slowly absorbed through the stomach. This results in drawing out of fluid from the blood stream into the intestines. Hence, the early phase of dumping syndrome presents as:

o Gastric outlet obstruction.

1. Occurs 30-60 minutes after a carbohydrate-rich meal. 2. Sudden bloating, fullness and abdominal discomfort. 3. Nausea, vomiting, severe diarrhoea.

o Tea-Pot stomach. o Hourglass stomach. o Gastric carcinoma.

BLEEDING PEPTIC ULCER •

Most common complication of peptic ulcer disease.

•

It is a medical emergency.

•

A peptic ulcer bleed may present as coffee-ground hematemesis or melena (black tarry stools).

•

Upper GI endoscopy can be performed to visualize the bleed and use appropriate therapies.

•

Treatment:

4. Light-headedness, sweating and flushing. 5. Tachycardia. o Dumping of carbohydrate-rich meal into the intestines results in rapid absorption of all the glucose and resultant hyperglycaemia. This causes insulin production, which leads to the late phase of dumping syndrome later due to hypoglycaemia: 1. Occurs 1-3 hours after the meal.

o Intravenous proton pump inhibitors: Several studies have suggested the use of a high dose regimen of IV PPI, e.g., 80 mg of omeprazole bolus and then 20 mg infusion over 8 hours. o Oral PPIs can also be used. o Endoscopic haemostatic therapy:

2. Loss of consciousness or mental confusion.

1. Epinephrine injection (diluted to 1:10,000).

3. Fatigue and weakness.

2. Electrocoagulation (Cauterization).

Stomach and Duodenum

19

3. Laser coagulation.

PEPTIC ULCER PERFORATION

4. Haemoclips.

•

A perforation of the peptic ulcer is a serious condition and should be considered as a surgical emergency.

•

Duodenal ulcers are more prone to perforation than gastric ulcers.

•

Most perforations occur on the anterior aspect of the duodenum. (See Table 3.5)

o Usually a combination therapy including PPIs and endoscopic procedures are used in conjunction with the usual resuscitation measures like rehydration, blood transfusion etc. *Forrest’s classification of gastrointestinal haemorrhage: Class

Description

Forrest I

Active bleeding

Ia

Arterial spurter

Ib

Oozing vessel

Forrest II

Evidence of recent bleeding but no active bleeding

IIa

Ulcer with visible open vessel at base

IIb

Ulcer with adherent clot

IIc

Ulcer with a coffee-brown coloured base

Forrest III

No stigmata of active bleeding

CONGENITAL HYPERTROPHIC PYLORIC STENOSIS •

Incidence: 3 per 1000.

•

Common in the first born male child (reason not known).

•

Bottle feeding has been shown to increase the risk for this condition.

•

Presents after 2 weeks of age, usually in the 4th to 6th week of life.

•

Clinical presentation: o Initially, the child presents with infrequent episodes of non-bilious vomiting.

Table 3.5: Differences between anterior and posterior ulcer perforations Anterior perforation

Posterior

perforation

Relative occurrence

More common

Less common

Presentation

•

Features of peritonitis

•

Presents with torrential hematemesis because

•

The most important presentation is with sudden excruciating epigastric pain

•

of erosion of ulcer into the gastroduodenal artery Pain

•

Obstipation

•

Lying still in bed

•

Diffuse tenderness

•

Diffuse guarding and rigidity

Location of leaked contents

Gastric contents go into the peritoneal cavity Gastric contents go into the lesser sac

Diagnosis

•

Treatment

•

X-ray abdomen in the erect position shows gas under the diaphragm Upper GI endoscopy

•

Exploratory laparotomy

Graham-Steele repair or omental patch repair

•

Upper GI endoscopy is the preferred investigation because it can be used as a therapeutic aid also

Epinephrine can be injected endoscopically to stop bleeding but the definitive procedure consists of an anterior duodenotomy with closure of the vessel and ulcer and a pyloroplasty

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Review of Surgery for Students

o Gradually, the vomiting becomes projectile and occurs after every feed. o The child remains hungry and feeds well in the early phase of the disease, but delayed diagnosis may result in the child becoming weak, malnourished and lethargic.

GASTRIC VOLVULUS •

It is a rare condition where the stomach rotates around its axis for more than 180 degrees.

•

The gastric axis is formed by joining the gastrooesophageal junction and pylorus.

o On examination, a palpable lump of the hypertrophied pylorus can be felt in the right upper quadrant of the abdomen or in the epigastrium. •

Investigations: o Serum electrolytes – Hypochloremic hypokalemic metabolic alkalosis is the classical picture in these patients. They also show a paradoxical aciduria. Please see the diagram for the underlying mechanism. Fig. 3.1: Gastric axis H + & Cl- lost in the vomitus

Hypochloremic hypokalaemic metabolic alkalosis

Na+ conservation and K + & Mg+ excretion

Hyponatremia stimulates aldosterone release

•

Volvulus can occur in 2 ways: o Organoaxial – Rotation occurs along the gastric axis. o Mesenteroaxial – Rotation occurs along a line perpendicular to the gastric axis.

Hyponatremia

Table 3.6: Different types of gastric volvulus Organoaxial volvulus

Mesenteroaxial volvulus

It is more common than the mesenteroaxial variety

Less common

Associated congenital anomaly is present more commonly

Less commonly present

o Ultrasound abdomen – Investigation of choice.

Presents acutely

o Barium upper GI study – Might show the “double track” sign when barium is flowing between the thick pyloric mucosal folds.

This is more commonly chronic in nature

Ischemia, necrosis and gangrene of the stomach loop occur more commonly

These complications are less common in this variety of volvulus

K+

exchanged with H+ in the renal tubules

•

H+exchanged with Na + in the kidney tubules

Paradoxical aciduria

Treatment: o Correct any fluid and electrolyte imbalance.

•

o Borchardt’s triad is the classical presentation.

o Ramstedt Pyloromyotomy – Standard treatment of choice. It involves cutting of the pyloric muscle without breaching the mucosa. o Laparoscopic pyloromyotomy. o Endoscopic pyloromyotomy. o Endoscopic balloon dilation.

Clinical Presentation: o The triad consists of acute epigastric pain, retching without vomiting and inability to pass a nasogastric tube.

•

Investigations: o Plain X-ray abdomen (erect) – May show an upside down stomach in the organoaxial type.

Stomach and Duodenum

•

o Barium study. o CT scan. o Upper GI endoscopy. Treatment: o Surgery is the only treatment for this condition. o Surgical principles include decompression, derotation (reduction) and fixation (gastropexy) to prevent recurrence. o Laparoscopic repair can be attempted by trained surgeons.

CARCINOMA OF THE STOMACH • • • • •

•

It is an adenocarcinoma pathologically. Gastric cancer is the second-most common cause of cancer related deaths worldwide. It is the fourth-most common cancer worldwide with wide regional variations. It is more common in males than females. Risk Factors Associated with Gastric Cancer: o Dietary – Vit. C deficiency, smoked fish, nitrosamine compounds etc. o Blood group A. o Pernicious anaemia. o Partial gastrectomy done previously. o Premalignant conditions: 1. Atrophic gastritis. 2. H. pylori infection and ulcer. 3. Adenomatous polyp. 4. Type III intestinal metaplasia. Clinical Presentation: o Early gastric cancer is usually asymptomatic and is diagnosed in patients having non-specific complaints. o Physical signs developing in a patient with gastric cancer indicate late stage of the disease and any curative intervention is usually ruled out in these cases. o Symptoms include: 1. Indigestion. 2. Dysphagia. 3. Anorexia. 4. Asthenia. 5. Weight loss.

•

21

6. Hematemesis. 7. Nausea and vomiting. 8. Abdominal pain and fullness. o Signs include: 1. Tenderness on palpation. 2. Palpable mass. 3. Palpable enlarged lymph nodes like the Virchow node (left supraclavicular node) and Irish node (anterior axillary node). 4. Succussion splash. 5. Hepatomegaly in case of liver metastasis. 6. Signs of peritonitis in case of a perforation. o Complications of gastric cancer include: 1. Cachexia. 2. Gastric outlet obstruction. 3. GI bleeding. 4. Perforation. 5. Ascites. Investigations: o Upper GI endoscopy a.k.a Oesophagogastroduodenoscopy – Useful to directly visualise the lesion and obtain biopsies for a tissue diagnosis. A minimum of 6-7 biopsy samples from around the ulcer should be obtained. o Double contrast barium studies – The surface of the ulcer can be seen. It is agreed upon my radiologists that if the mucosal folds of the stomach are seen away from the ulcer, then the lesion is most probably malignant. Also, ulcers at the greater curvature are mostly malignant and those at the lesser curvatures are mostly benign. o Carmen Meniscus sign on barium study is a feature of malignancy. o CT scan and MRI of abdomen, chest and pelvis – Done to evaluate the spread of the disease. o Endoscopic ultrasound – Can help in better staging the disease. o Chest X-ray – For lung metastasis. o Haemogram – Can show an anaemic picture. o Tumour markers – Not specific for gastric cancer. 1. CEA – Increased in 40-50% of cases. 2. CA 19-9 – Increased in 15-20% of cases.

22

Review of Surgery for Students Table 3.7: Classification of stomach cancer

Classification of gastric adenocarcinoma

Lauren's classification (microscopic)

Intestinal

Related to environmental risk factors Associated with chronic atrophic gastritis, retains the glandular structure Metastatises to liver and nodes Better prognosis

Diffuse

Related to genetic factors Poorly differentiated, invades larger areas Metastasises to nodes, ovaries and serosa Poor prognosis

Borrman's classification (gross)

I - Polypoid II - Fungating, ulcerated with sharp raised margins III - Ulcerated with poorly defined infiltrating margins IV - Infiltrative, intramural and poorly demarcated lesion

•

Metastasis of gastric carcinoma can occur as following:

Flowchart 3.1

Stomach and Duodenum

•

23

TNM staging of gastric carcinoma: Primary Tumour (T)

Tx- Primary tumour could not be assessed T0- No evidence of primary tumour Tis- Carcinoma in situ, intraepithelial neoplasm with no invasion of lamina propria T1- Tumour invades lamina propria or submucosa T2- Tumour invades muscularis propria or subserosa T3- Tumour penetrates serosa (visceral peritoneum) without invasion of adjacent structures T4- Tumour invades adjacent structures

Regional Lymph Nodes (N)

Nx- Regional lymph nodes could not be assessed N0- No regional lymph node metastasis N1- Metastasis in 1-6 regional lymph nodes N2- Metastasis in 7-15 regional lymph nodes N3- Metastasis in more than 15 regional lymph nodes

Metastasis (M)

Mx- Distant metastasis could not be assessed M0- No distant metastasis M1- Distant metastasis present

•

•

Prognostic factors: o Depth of invasion of stomach wall.

3. Subtotal or Partial gastrectomy with lymph node dissection (for distally located tumours).

o Regional lymph node involvement.

o A tumour-free margin of 5 cm is ideally required.

Treatment: Essentially surgical. o Level of nodes 1. Level 1 – Perigastric nodes. 2. Level 2 – Nodes along the coeliac trunk branches including hepatic, left gastric and splenic as well as the lymph nodes in hilum of spleen. 3. Level 3 – Para-aortic lymph nodes. o Options 1. Total gastrectomy with lymph node dissection. 2. Oesophagogastrectomy with lymph node dissection (for proximally located tumours).

o Procedures: 1. D1 Gastrectomy = Partial gastrectomy + Resection of level 1 lymph nodes. 2. D2 Gastrectomy = Partial gastrectomy + Resection of level 1 and 2 lymph nodes. o Earlier, D2 gastrectomy involved distal pancreatectomy and splenectomy but the National Comprehensive Cancer Network now recommends a pancreas and spleen sparing D2 gastrectomy over D1 gastrectomy for better longterm results and low recurrence rates. o Reconstruction of stomach after a total gastrectomy is done by a Roux en Y oesophagojejunostomy.

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Review of Surgery for Students

o Adjuvant chemotherapy with 5-fluorouracil and leucovorin have been used in some clinical trials and found to have little effect if at all. o Chemoradiation using the above regimen with 40 Gy radiation can also be used as suggested by some trials.

•

Studies have shown linkage to presence of C-kit protooncogene which acts through the tyrosine kinase enzyme. Therefore, tyrosine kinase inhibitors like imatinib and sunitinib are used for its treatment.

•

Clinical presentation: o Usually presents with vague abdominal discomfort and fullness.

MALT LYMPHOMA

o Malaise, fatigue, weight loss. a.k.a MALToma •

Mucosa-associated lymphoid tissue lymphoma.

•

Derived from B cells of the marginal zones of the MALT.

•

Most commonly occurs in the stomach in association with the presence of Helicobacter pylori and chronic inflammation.

o Palpable mass is rare. o Oesophageal GIST may cause dysphagia. o Colorectal GIST may cause constipation. o Duodenal GIST may cause obstructive jaundice. •

Investigations: o Barium studies.

•

CagA protein of the bacterium has been strongly linked to the development of MALToma.

•

The patient can present with pain, obstruction or bleeding.

o MRI.

•

MALToma is diagnosed by biopsy on doing an upper GI endoscopy.

o Endoscopy – Useful for biopsy also.

•

Treatment involves eradication of H. pylori and use of chemotherapy (CHOP/MOP regimens) if the disease spreads beyond the stomach.

•

o Double contrast studies. o CT abdomen. o PET – For malignant disease. o Endoscopic ultrasound. •

o Surgery – Wide local excision of the GIST is the only curative option.

Surgery is indicated in case of haemorrhage, perforation or for residual disease after chemotherapy.

o Chemotherapeutic agents – Tyrosine kinase inhibitors like Imatinib and Sunitinib can be used as neoadjuvant or adjuvant therapy.

GASTROINTESTINAL STROMAL TUMOUR (GIST) •

Treatment:

o Sorafenib, Dasatinib and Nilotinib are second line agents.

GIST is the most common mesenchymal tumour of the GIT but it constitutes less than 1% of all GIT tumours.

o Regorafenib – Latest drug to get the FDA approval for use in metastatic or unresectable GIST.

•

Most commonly presents in the stomach and small intestines but can occur anywhere along the GI tract.

•

Cell of origin: Interstitial Cell of Cajal.

•

These tumours have a potential for local infiltration and vascular metastasis.

•

They have overexpression of the CD117 and CD34 molecules.

Complete occlusion or a congenital absence of a segment of duodenum.

•

Incidence – 1:2500.

•

•

5-year survival ranges from 30-70% depending upon the grade and stage of the disease.

DUODENAL ATRESIA

Stomach and Duodenum

•

More common in male babies than female babies.

•

50% of the pregnant mothers carrying a foetus with duodenal atresia have polyhydramnios because of the inability of the foetus to swallow the amniotic fluid and absorb a part of it.

•

Duodenal atresia can be associated with Down’s syndrome (Trisomy 21), annular pancreas and other GI atresias.

•

25

Treatment: o Fluid and electrolyte maintenance. o Orogastric/Nasogastric tube stomach decompression. o Duodenostomy is the surgical procedure to be performed.

SUPERIOR MESENTERIC ARTERY SYNDROME A.k.a. Cast Syndrome / Wilkie’s Syndrome / Mesenteric Root Syndrome •

Normally, the superior mesenteric artery originates at an angle of 40-50 degrees to the abdominal aorta and lies anterior to the duodenum and uncinated process of pancreas.

•

In cast syndrome, the angle between the SMA and abdominal aorta is less than 25 degrees, which causes compression and obstruction of the third part of the duodenum.

•

It can be of 2 types: o Chronic/Congenital – This is present since birth and patients have lifelong history of vague abdominal discomfort or pain. It is associated with a lean body build and precipitating factors like anorexia, cachexia, sudden weight loss etc.

Fig. 3.2: Duodenal atresia

•

o Acute/Induced – This usually occurs as a consequence of prolonged supine position, scoliosis or scoliosis surgery, nephrectomy etc. It presents with an acute abdomen and can be treated with medications after initial stabilisation.

Clinical Presentation: o Baby born with a scaphoid abdomen (rarely the abdomen may be distended due to a distended stomach). o Bilious vomiting within few hours of birth.

•

o Dehydration, weight loss and electrolyte abnormalities.

o Plain abdominal X-ray. o Barium upper GI studies.

o Hypokalemic/Hypochloremic metabolic alkalosis with paradoxical aciduria. •

o Contrast enhanced CT scan – Investigation of choice.

Investigations:

o Upper GI endoscopy.

o Plain X-ray abdomen (erect)

o Ultrasound.

– “Double Bubble” appearance. – The upper bubble corresponds to the gastric air. – Lower bubble corresponds to the prestenotic dilated duodenal loop. – Double bubble appearance is also seen in annular pancreas and malrotation of gut (Ladd’s band).

Investigations:

o Angiography. •

Treatment: o Fluid and electrolyte maintenance. o Nasogastric tube decompression of the stomach and duodenum. o Total parenteral nutrition might have to be offered. o Definitive surgery – Duodenojejunostomy.

Chapter

SECTION 1 : GASTROINTESTINAL SURGERY

4 LIVER AND THE BILIARY SYSTEM SURGICAL ANATOMY OF THE LIVER •

Couinaud’s division of the liver into 8 segments. (See Flowchart 4.1 and Fig. 4.1)

•

The right and left lobe of the liver receive their blood supply from their respective vessels.

Liver (divided by Cantlie’s line into)

Left lobe

Right lobe

Posterior sector

VII (Superior)

VI (Inferior)

Medial sector (Quadrate lobe)

Anterior sector

VIII (Superior)

V (Inferior)

Flowchart 4.1

Lateral sector

IV a (Superior)

II (Superior)

IV b (Inferior)

III (Inferior)

Liver and The Biliary System

27

o Does not drain into the hepatic veins, drains directly into the inferior vena cava. •

Some important types of hepatectomy: o Left extended hepatectomy – removal of segments II, III, IVa, IVb, V, VIII. o Right extended hepatectomy – removal of segments VII, VI, VIII, V, IVa, IVb. o Left hepatectomy – removal of the left lobe of the liver. o Right hepatectomy – removal of the right lobe of the liver.

PORTAL HYPERTENSION (Fig. 4.2) Anterior surface Fig. 4.1: Couinaud’s segments of the liver

•

80% of the hepatic blood supply is through the portal vein and the rest 20% is from the hepatic arteries. All of this blood drains via the hepatic veins into the inferior vena cava.

•

The “Portal Triad” (misnomer) consists of:

•

Normal portal pressure is around 5-10 mmHg.

•

Portal hypertension is defined as an elevation of portal pressure above 12 mmHg.

•

Causes: (See Table 4.1)

o Hepatic artery. o Portal vein. o Bile duct. o Lymph vessels. o Branch of the vagus nerve. •

Segment I: o A.k.a. caudate lobe. o Lies behind the gallbladder. Fig. 4.2: Portal venous system

o Derives blood supply from both the sides.

Table 4.1: Causes of portal hypertension Causes of Portal Hypertension

Pre-hepatic

Congenital portal vein atresia Portal vein thrombosis Portal cavernoma

Hepatic

Cirrhosis Chronic active hepatitis Schistosomiasis

Post-hepatic

Budd-Chiari syndrome Constrictive pericarditis IVC obstruction

28

•

Review of Surgery for Students

– Draw samples for basic haemogram and coagulation profiles alongwith LFTs.

Clinical Presentation: o Bleeding oesophageal/gastric varices. o Caput medusa – dilated peri-umbilical veins.

– Associated thrombocytopenia should be treated with PRP infusion and coagulopathy by FFP infusion.

o Massive splenomegaly.

– Administer Vit. K 10 mg IV stat.

o Rectal varices.

– Vasopressin or Octreotide (Vasopressin is drug of choice).

o Ascites.

o Features of liver failure – spider nevi, asterixis, hyperestrogenism etc. •

– After initial stabilisation of the patient, perform an urgent upper GI endoscopy to visualise the bleeding vessel and treat it:

Child-Pugh classification of severity of liver failure

Table 4.2: Child-Pugh classification of severity of liver failure

•

1 point

2 points

3 points

Bilirubin (mg/dL)

3

Albumin (g/dL)

>3.5

2.8-3.5

5 cm in size 2. Left lobe abscess for the fear of rupture into the pericardium

1. 2.

Abscess > 5cm in size Abscess which cannot be percutaneously drained due to its location

3. Impending rupture

3.

Coexisting intra-abdominal disease which requires surgical management

4. No response to medications within 5-7 days

4.

Failure of antibiotic therapy

1. Sympathetic pleural effusion

1.

Pleurisy

2. Rupture into the lung – lung abscess

2.

Pleural effusion

3. Empyema

3.

Bronchohepatic fistula

4. Rupture into the pericardium

4.

Subphrenic abscess

5. Intraperitoneal rupture

5.

Intraperitoneal rupture

6. Rupture into the stomach or colon

6.

Rupture into stomach, colon, kidney etc.

7. Bacterial superinfection

7.

Haematogenous spread to the brain – brain abscess

8.

Rupture into the pericardium

5. Failure to differentiate from pyogenic abscess Complications

HYDATID LIVER DISEASE

•

Clinical Presentation: o Pain – In the right upper quadrant. A large hydatid cyst might cause a dragging type of pain.

•

Caused by the tapeworm echinococcus granulosus.

•

Right lobe is more often involved than the left.

•

Unilocular space occupying lesion.

o Jaundice – Obstructive jaundice can be caused by compression of the CBD at the hilum.

•

The cyst wall consists of 3 layers (from inside out):

o Hepatomegaly.

o Endocyst – germinal layer – giver rise to daughter cysts.

o Rupture of the cyst may lead to anaphylactic reactions. o Signs of liver failure – in long standing hydatid liver disease.

o Ectocyst. o Pericyst – compressed liver tissue. •

Surgical cyst removal involves the endocyst and ectocyst only.

•

Rate of growth of hydatid cyst is 1.5 cm every year.

•

Investigations: o Eosinophilia (25% of cases), hypogammaglobinemia (30% cases), elevated bilirubin and alkaline phosphatase levels.

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Review of Surgery for Students

o ELISA test.

– Minimally invasive procedure.

o Abdominal Plain X-ray: A cyst delineated by a thin white rim of calcification.

– A special cannula is used to drain the cyst percutaneously, then a scolicidal agent like 20% hypertonic saline or cetrimide is instilled and left for 15 minutes. Then the cyst is reaspirated.

o USG Abdomen: Hypoechoic lesion with smooth walls, daughter cysts and hydatid sand. o CT Scan Abdomen: Best investigation to differentiate between the various different liver cysts.

– This is repeated till the draining fluid is clear. – Finally, normal saline is instilled in the clear cyst and cannula taken out.

o MRI scan. o Casoni’s Test: Not done anymore (but it was a hypersensitivity test). •

o Surgery

Treatment:

– Simple tube drainage.

o Mebendazole – 40-50 mg/kg/d orally for a period of 3-6 months.

– Open cystectomy with use of scolicidal agents.

o Albendazole, Praziquantel.

– Partial liver resection.

o PAIR – Percutaneous Aspiration, Instillation of scolicidal agent and Re-aspiration.

– Total pericystectomy.

LIVER MALIGNANCY (Flowchart 4.3)

Liver Malignancy

Primary

Secondary

Hepatocellular carcinoma Metastasis

Fibrolamellar carcinoma

Cholangiocarcinoma

Flowchart 4.3

Liver and The Biliary System

HEPATOCELLULAR CARCINOMA •

It is a primary cancer of the liver.

•

Arises on a background of liver cirrhosis and chronic liver failure.

•

Commoner in males than females.

•

Common in elderly.

•

Common in Africa and Asia due to the high prevalence of chronic hepatitis A and B.

•

Risk Factors:

o Hemoperitoneum – Advanced stage and poor prognosis. •

Investigations: o Anemia, thrombocytopenia, hyponatremia, elevated serum creatinine (hepatorenal syndrome), coagulopathy, altered LFTs. o Viral serologies for HBV and HCV. o Hemochromatosis - >50% iron binding capacity. o Alpha-1 antitrypsin levels. o Tumour markers.

o Hepatitis virus – HBV, HCV.

– Alpha fetoprotein

o Liver cirrhosis. o Aflatoxin. o Alpha-1 antitrypsin deficiency. o Hemochromatosis. o Anabolic steroids. •

33

♦

Non-specific.

♦

Can’t be used for screening.

♦

Levels more than 400 ng/mL are considered diagnosed in the presence of other suitable imaging studies.

o Alcohol and tobacco.

– Vit. B12 binding protein.

Pathophysiology (See Flowchart 4.4)

– Soluble IL-2 receptor. o Ultrasound abdomen – Best procedure for screening. o Triple phase CT scan with contrast (arterial phase, portal venous phase and washout phase). – Primary malignancies are characteristically hypervascular, therefore hyperattenuating lesion with arterial phase enhancement and rapid portal venous phase washout. – Secondary malignancies or metastases are hypovascular and therefore hypoattenuating. o MRI scan. – Best modality to characterise the lesion.

Flowchart 4.4

•

Clinical presentation:

– Tumours are hyperintense on both T1 and T2 images.

o Usually discovered on routine Investigations for other reasons.

– Well-differentiated tumours are more hyperintense on T1-weighted images.

o Anorexia, weight loss. o Hepatomegaly. o Jaundice – Late feature. o Abdominal pain – Late feature, when the liver capsule is stretched.

o PET-CT. •

Treatment: o Trans-Arterial Chemo-Embolization (TACE) – The hepatic tumours receive 80% of their blood supply from the hepatic artery, as opposed to

34

Review of Surgery for Students

– Then the first lobe is resected.

the normal liver parenchyma receiving 80% supply from the portal vein.

– This procedure requires an otherwise healthy liver.

– Therefore, the branch of the hepatic artery supplying the tumour can be cannulated by an interventional radiologist, who then delivers high dose chemotherapy locally. – Chemotherapeutic drugs include doxorubicin, mitomycin-C and cisplatin. These drugs are coated on microspheres which stay in the peripheral branches of the artery supplying the tumour and occlude them while also delivering the drug. – The feeding artery is then embolized with gel foam or coils to occlude the lumen and prevent systemic toxicities of these drugs. – TACE is done in patients who are not suitable for a resection or a liver transplant. – Post-embolization syndrome is an important complication which presents with abdominal pain, fever and raised ALT levels. o TheraSphere.

o Partial hepatectomy. – Lobectomy. – Extended lobectomy. o Orthotopic liver transplantation.

FIBROLAMELLAR HEPATOCELLULAR CARCINOMA •

Very rare malignancy.

•

Occurs in young patients (20-30 years).

•

No background of chronic liver disease required.

•

Commoner in females than males.

•

No risk factors as with hepatocellular carcinoma.

•

Alpha fetoprotein is not elevated.

•

Tumour markers include Neurotensin and Vit. B12 binding protein.

•

Has a better prognosis than HCC because it is more resectable.

•

Histology: Laminated fibrous layers interspersed between tumour cells.

•

Diagnosed upon CT/MRI scan.

•

Surgical resection is the treatment of choice.

•

It is a recurrent tumour, therefore regular follow-up imaging studies should be done.

– Latest modality of low dose brachytherapy – Small glass beads are inserted into the tumour angiographically and then radiotherapy is targeted directly to the tumour, avoiding the surrounding liver parenchyma. o Radiofrequency ablation. o Injection of absolute alcohol into a single cancerous nodule. o Microwave therapy.

BENIGN TUMOURS OF THE LIVER

o Systemic chemotherapy with 5-fluorouracil, oxaloplatin and folinic acid have been tried but not found to be as effective as other modalities.

Adenoma •

Rare tumours.

o Nimura Surgery.

•

Epithelial cell origin.

•

Most common in females of child bearing age taking OCPs.

•

Can be single or multiple.

•

Risk factors:

– Done in patients requiring a lobectomy or extended lobectomy. – The portal vein of the lobe to be resected is blocked. – This leads to a compensatory hypertrophy of the other lobe.

o Oral contraceptive pills – Strongest association. o Anabolic steroid.

Liver and The Biliary System

o Androgenic steroids.

FOCAL NODULAR HYPERPLASIA

o Tyrosinemia.

•

Second most common liver tumour after hepatic haemangioma.

o Barbiturate intake.

•

It is a firm tumour.

o Clomiphene intake.

•

Low malignant potential.

o Hemochromatosis.

•

Consists of hepatocytes, proliferated bile ducts and malformed vessels.

•

It has a central stellate-shaped fibrous scar.

•

Diagnosed by a positive 99mTc sulphur colloid scan alongwith other imaging studies.

•

Symptomatic tumours can be resected.

o Type I DM.

o Glycogen storage diseases – Multiple liver adenomas. •

Gross: Smooth, well circumscribed, fleshy, tan coloured, 1-30 cm in size, large blood vessels on the surface. Central necrosis may occur in large tumours.

•

Histology: Sheets of hepatocytes with no bile ducts and reduced Kupffer cells.

•

These tumours classically have a tendency to rupture, thereby leading to peritoneal disease.

•

Clinical presentation:

SURGICAL ANATOMY OF THE BILIARY SYSTEM •

Gallbladder is a pear shaped organ lying on the under surface of the liver.

•

It might be embedded in the liver tissue or attached by a mesentry.

•

The normal capacity of the GB is 25-30 mL.

•

GB is divided into a fundus, a body, a neck and an infundibulum.

•

The muscle coat of the GB consists of criss-crossing fibres which help in its contraction while secreting bile.

•

The mucosa dips into the muscle coat to form Crypts of Luschka (inflammation of the mucosa and stones in these sinuses can lead to Cholesterosis or Strawberry GB).

•

The infundibulum is the distal portion of the neck known as the Hartmann’s pouch. It is a common site of impaction of stones.

•

Cystic duct

o Pain right upper abdomen. o Palpable mass or hepatomegaly. o History of chronic OCP or steroid use. o Features of hemoperitoneum and shock – If the tumour ruptures into the peritoneum. •

Investigations: o Abnormal LFTs. o Ultrasound abdomen – Hypoechoic lesion. o CT scan – Well circumscribed hypoattenuating lesion with central necrosis and calcification. o MRI scan. o HIDA scan – positive. o

99mTc

sulphur colloid scan.

– Negative in adenomas because of the lack of Kupffer cells. – Positive in FNH because increased number of Kupffer cells result in increased uptake of the colloid. •

35

Treatment:

o 3 cm in length and 1-3 mm in diameter.

o Stoppage of OCPs.

o Joins the supraduodenal portion of the common hepatic duct usually.

o Yearly ultrasounds and alpha fetoprotein levels to monitor for development of HCC. o Resection of symptomatic adenomas.

o Mucosa arranged a spiral folds known as spiral valves of Heister.

36

•

•

Review of Surgery for Students

Common Hepatic Duct

o Medial border – Common hepatic artery.

o Formed by the union of right and left hepatic ducts.

o Contents:

o Joined by cystic duct to form the common bile duct.

1. Caterpillar turn/Moynihan’s hump.

Common Bile Duct (CBD)

3. Fibrofatty stroma.

2. Lund’s lymph node. o Calot’s triangle is the most important surgical landmark in cholecystectomy and it needs to be identified before dissection to avoid injury to the bile duct and vessels.

o Divided into 4 parts: 1. Supraduodenal part – In the free edge of lesser omentum. 2. Retroduodenal part.

•

Moynihan’s hump – This is a variation of the normal anatomy of the Calot’s triangle where either the common hepatic artery or the right hepatic artery is tortuous and becomes a content of the Calot’s triangle.

•

Lymphatic Drainage

3. Infraduodenal part – On the posterior surface of the pancreas. 4. Intraduodenal part – Passes obliquely into the wall of the second part of duodenum and is surrounded by the sphincter of Oddi. Terminal opening on the summit of Ampulla of Vater. • •

o The subserosal and submucosal lymph vessels drain into the Lund’s lymph node at the junction of cystic duct with the common hepatic duct.

Cystic artery – Arises from the right hepatic artery behind the common hepatic duct.

o The efferents from this lymph node drains to the hilar lymph nodes and the coeliac lymph nodes.

Calot’s Triangle (Fig. 4.3)

o The subserosal lymphatic vessels also communicate with the subcapsular lymphatics of the liver, thereby being an important route of spread of gallbladder carcinoma to the liver.

o Superior border – Cystic artery. o Inferior border – Cystic duct. •

Histology of the GB: It is lined by simple columnar epithelium with mucous secreting cells being present in the neck region.

EXTRAHEPATIC BILIARY ATRESIA

Fig. 4.3: Calot’s triangle

•

Complete occlusion or discontinuity of the extra hepatic biliary tract due to an inflammatory process of the tract.

•

Most common surgically correctable cause of neonatal jaundice.

•

Untreated, EHBA may result in biliary cirrhosis and portal hypertension.

•

May be associated with situs inversus, polysplenia, cardiac lesions and an absent vena cava in 10-30% of cases.

•

Types of EHBA: o Type I – Atresia limited to the common bile duct only.

Liver and The Biliary System

done when the proximal bile duct is patent (Type I).

o Type II – Atresia of the common hepatic duct. o Type III – Atresia of the right and left hepatic ducts upto the level of porta hepatis. •

o Kasai portoenterostomy.

Clinical presentation:

– Radical excision of all extrahepatic biliary tissue till the surface of the liver.

o Jaundice by the end of first week of life and progressive.

– Anastomosis of a Roux-en-Y loop of jejunum to this exposed area.

o Meconium is bile stained.

o Liver transplantation.

o Later on the stool becomes pale and urine becomes dark. o Steatorrhoea – May give rise to osteomalacia (biliary rickets) and weight loss. o Severe pruritus. o Hepatosplenomegaly – Progressive in nature. •

Differentials of neonatal cholestatic jaundice o Alpha 1 antitrypsin deficiency.

o The surgeries have to be performed by the age of 8 weeks for good results.

CAROLI’S DISEASE •

It refers to the ectasia or dilation of the intrahepatic bile ducts with normal segments in between.

•

Types: o Simple Caroli’s disease–Involves the larger intrahepatic ducts.

o Jaundice due to parenteral feeding. o Choledochal cyst.

o Caroli’s disease with periportal fibrosis–Associated with biliary stasis, stone formation and cholangitis.

o Inspissated bile syndrome. o Caroli’s disease.

•

It can occur in a sporadic form (Caroli’s disease) or maybe associated with autosomal recessive variant of polycystic kidney disease (Caroli’s syndrome).

•

Clinical presentation:

o Cystic fibrosis. •

Investigations: o Serum bilirubin – Conjugated bilirubinemia (>2 mg/dL or >20% of total bilirubin).

o Vague, recurrent abdominal pain.

o LFTs – Elevated alkaline phosphatase and gamma glutamyl transpeptidase (GGT).

o Cholangitis – Pain, fever and jaundice (Charcot’s triad).

o Serum alpha-1 antitrypsin levels.

o Portal hypertension and its sequalae.

o Sweat chloride test. o Ultrasound abdomen – Absence of GB and bile ducts in type III. o Hepatobiliary scintiscan with technetium labelled diisopropyl iminodiacetic acid (DISIDA) – If it shows excretion into the GI tract, then the extrahepatic biliary tract is patent.

•

37

o Associated liver and kidney diseases. •

Investigations: o Abnormal LFTs, coagulopathy, abnormal renal function. o Ultrasound. o CT scan.

o Percutaneous liver biopsy.

o MRI scan.

o Intraoperative cholangiography.

o Hepatobiliary scintiscan.

Treatment:

o ERCP – Can be therapeutic also in stone removal and biliary stenting etc.

o Direct Roux-en-Y hepaticojejunostomy can be

38

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Review of Surgery for Students

Treatment:

o Pancreatitis.

o Ursodeoxycholic acid to decrease the complications of cholestasis.

o Increased risk of Cholangiocarcinoma. •

Investigations:

o Fat soluble vitamin supplementation.

o Abnormal LFTs.

o Antibiotics for cholangitis and septicaemia.

o USG.

o Screening for development of cholangiocarcinoma.

o CT scan.

o Removal of stones, biliary stenting.

o MRI scan.

o Lobectomy – Can be done if the disease is limited to only one lobe.

o MRCP – for evaluating the pancreaticobiliary junctions.

o Liver transplantation – In refractory cases.

•

CHOLEDOCHAL CYST

Treatment: Surgical Management of Choledochal Cysts

•

Congenital dilations of the extrahepatic and intrahepatic bile ducts.

•

Classification:

Type I

Complete excision of the extrahepatic dilated segment and a Roux-en-Y hepaticojejunostomy

Type II

Complete excision of the diverticulum and closure of CBD with a T-tube insitu

Type III

3 cm–Surgical transduodenal excision

Type IV

Complete excision of the extrahepatic dilated segment and a Roux-en-Y hepaticojejunostomy alongwith hepatic lobectomy if required for intrahepatic disease

Type V

Mentioned previously

Todani’s Classification of Choledochal Cysts Type I (True Choledochal cyst)

Fusiform dilation of the extrahepatic bile ducts

Type II (Bile duct diverticulum)

Diverticulum arising from the supraduodenal biliary system

Type III (Choledochocoele)

Protrusion of dilated terminal segment of common bile duct into the duodenum

Type IV

Multiple communicating intra- and extra-hepatic bile

Type V

ducts

CHOLELITHIASIS

Caroli’s disease – Only

•

A.k.a. gall stone disease.

•

Causes:

intrahepatic bile duct dilation

•

Clinical Presentation: o Jaundice. o Fever. o Abdominal pain. o Right upper quadrant mass.

o Increased serum cholesterol – Normally the cholesterol : bile acid ratio in GB is 1:25. This ratio is required to keep the cholesterol in the liquid form as micelles. An increase in this ratio to 1:13 or beyond results in precipitation of cholesterol crystals. o Stasis of bile – Vagotomy, somatostatin, octreotide, prolonged starvation or parenteral nutrition may result in stasis of bile in the GB.

Liver and The Biliary System

o Infection – Infection can be a cause as well as effect of cholelithiasis.

•

o Haemolysis – Increase bilirubin produced as a result of haemolysis combines with calcium to form calcium bilirubinate stones (pigment stones) in the biliary ducts. o Infestation – Infestation of the bile duct with Ascaris lumbricoides can result in stasis of bile and stone formation. •

Types of gall stones: (Flowchart 4.5)

•

39

Clinical Presentation: o Mostly asymptomatic. o Dyspepsia. o Biliary colic. o Acute cholecystitis. o Chronic cholecystitis. o Mucocoele. The stone might reach the bile duct – choledocholithiasis (described later) or it may rarely reach upto the intestine causing obstruction (gall stone ileus).

Flowchart 4.5

40

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Review of Surgery for Students

Investigations:

4. Post-operative pain in the right shoulder – Due to accumulation of CO2 under the diaphragm which irritates the phrenic nerve.

o Blood – Leucocytosis, elevated ESR in acute cholecystitis. o Plain abdominal X-ray (erect) – Only 10% of the stones are radio-opaque and visible on plain films.

o Open cholecystectomy – Unusual nowadays. o Conservative management – Acute cholecystitis can be managed conservatively with fluids and antibiotics and an elective cholecystectomy can be done 6 weeks later.

o Ultrasound abdomen – Gall stones cast a posterior acoustic shadow. o HIDA scan – For diagnosis of acalculous cholecystitis. •

•

Treatment: o Laparoscopic cholecystectomy treatment of choice: – View the complete www.endosurgeon.org.

–

Surgical

procedure

at

– Indications for ‘lapchole’ include:

ACUTE CHOLECYSTITIS •

It is defined as an acute bacterial infection of the GB with or without the presence of a stone.

•

Types: o Calculous cholecystitis – Most common variety. Caused by gall stones obstructing the outflow of bile or by oedema caused by the stones.

1. Any symptomatic gall stones. 2. Large stone (>3 cm). 3. Multiple small stones. 4. Complicated cholelithiasis, gangrenous GB.

Long standing gall stones increase the risk for gallbladder carcinoma.

o Acalculous cholecystitis – Seen in patients with severe illnesses, on mechanical ventilators and on prolonged total parenteral nutrition. It occurs due to bile stasis and increased lithogenicity of bile.

e.g.,

5. Gallbladder polyp. 6. Porcelain GB.

o Acute emphysematous cholecystitis – Cause by gas forming organisms like Clostridium. It is a highly fulminant condition and urgent cholecystectomy should be done.

7. These days early laparoscopic cholecystectomy is preferred as opposed to conservatively managing gall stones. – Most important step in the procedure is to identify the boundaries of the Calot’s triangle and then proceed with a careful dissection. – Hospital stay is minimal (day care procedure). – Recovery is relatively faster.

•

Clinical Presentation: o Classical description includes a fat fertile female (3Fs) complaining of severe colicky right upper quadrant abdominal pain.

– Post-operative pain can be managed easily.

o The pain might radiate to the back or to the right shoulder tip.

– Complications:

o Abdominal tenderness and guarding.

1. Injury to abdominal organs while inserting the ports. 2. Pneumoperitoneum – Compression of IVC, renal vein or aorta. 3. Hypercapnia due to increased absorption of CO 2 (used to create an artificial pneumoperitoneum).

o Murphy’s sign–Palpate the edge of the patient’s liver and ask the patient to take a deep inspiration. Press inwards at the same time. This causes the patient to “wince in pain” at the peak of inspiration. o Boas’ sign–Hyperaesthesia over the 9-11th ribs posteriorly on the right side.

Liver and The Biliary System

•

Investigations:

•

Fatty food intolerance.

o Leucocytosis, elevated ESR.

•

Treated by cholecystectomy.

o Plain abdominal X-ray – For radio-opaque stones.

•

Ideally, the GB specimen should be sent for histopathology to rule out development of carcinoma.

o Ultrasound abdomen. o HIDA scan – The 99mTc labelled HIDA does not reach the GB due to oedema of the cystic duct wall. This is especially important for acalculous cholecystitis. •

Treatment: o Conservative management. – Patient is admitted and a nasogastric tube decompression of the stomach is done. – Analgesia in the form of morphine is provided. – Patient is kept nil orally and IV fluids are given to maintain hydration. – Broad spectrum antibiotics are given.

CHOLECYSTOSES 1. Cholesterosis or Strawberry Gallbladder– Accumulation of cholesterol crystals in the crypts of Luschka. Grossly, the GB appears like a strawberry, its mucosa studded with yellow crystals. 2. Gallbladder polyposis–Multiple polypoidal projections of the GB mucosa into its lumen. 3. Diverticulosis of the GB. 4. All of these cholecystoses cholecystectomy.

are

treated

by

MUCOCOELE •

It results when a stone or wall oedema blocks the opening of the cystic duct.

•

The mucous secreted by the glands in the GB neck accumulate.

•

Bile is reabsorbed.

•

Therefore, the gallbladder is palpated as a soft, fluctuant globular mass in the right upper quadrant and it is filled with mucous.

Complications:

•

Treatment is cholecystectomy.

o Chronic cholecystitis.

•

An infected mucocoele becomes a pyocoele (Empyema of the GB).

– Patient is scheduled for an cholecystectomy 6 weeks later.

elective

o Laparoscopic cholecystectomy can be done without waiting if the hospital team and surgeon are well experienced and confident. It is the treatment of choice these days. Antibiotics are usually administered at the time of inducing anaesthesia in the operation theatre. •

41

o Mucocoele. o Pyocoele. o Perforation of the GB wall. o Gangrene of the GB wall.

MIRIZZI’S SYNDROME •

This occurs when a gall stone impacts in the cystic duct or in the neck of the GB and externally compresses the adjacent CBD or common hepatic duct.

•

The compression and obstruction cause an obstructive jaundice with a distended GB.

o GB cancer. o Mirizzi’s syndrome.

CHRONIC CHOLECYSTITIS •

Cholelithiasis if left untreated can gradually result in chronic inflammation within the GB.

•

Mirizzi’s syndrome is an exception to the Courvoisier’s Law.

•

Small, contracted, fibrosed GB with grossly thickened wall.

•

•

Gall stones present.

The stone might result in necrosis of the wall of the cystic duct and bile duct resulting in a cholecystocholedochal fistula.

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Review of Surgery for Students

It is of 4 types, Type I having no fistula and Types IIIV having various degrees of fistulas.

o Coagulopathy.

Treatment includes cholecystectomy with a T-tube insertion or with a bilioenteric anastomosis.

o CT scan of abdomen.

o Ultrasound abdomen. o Barium meal – To distinguish the choledocholithiasis from periampullary carcinoma (both have obstructive jaundice). Barium meal follow through shows the ‘Inverted 3’ sign at the duodenum.

Courvoisier’s Law It states that in the presence of a palpably enlarged gall bladder accompanied with jaundice, the cause is unlikely to be gall stones.

o Endoscopy – To visualise a periampullary carcinoma. o ERCP.

Principle: Gall stones usually result over a long time and the resultant chronic inflammation cause fibrosis and contraction of the GB. Therefore, in gall stone disease the GB is expected to be small and not enlarged.

– Endoscopic retrograde cholangiopancreatography. – CBD stones appear as filling defects in the CBD or hepatic ducts. – ERCP has therapeutic role also as it can be used to perform a sphincterotomy, basket extraction, papillotomy and biliary stenting.

CHOLEDOCHOLITHIASIS •

Stone in the common bile duct.

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It occurs when a small stone slips from the GB into the CBD and impacts there, causing obstruction.

o Percutaneous transhepatic cholangiography.

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Clinical Presentation:

o MRCP–Magnetic pancreatography.

o Charcot’s Triad o Intermittent pain – Severe biliary colic due to spasm of the CBD. o Intermittent fever – Due to infection of the bile. o Intermittent jaundice – Due to obstruction. o The 3 primary features occur intermittently because the obstruction is never complete and there are periods of subsided inflammation when these symptoms abate and the recur.

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cholangio-

Treatment: o Cholecystectomy has to be done in every patient of choledocholithiasis because GB is the source of these stones. o Stone in Intraduodenal CBD: – Papillotomy – Increase the size of the Ampulla of Vater to facilitate passage of stone into the duodenum. – Sphincterotomy – If the stone does not still pass, the sphincter of Oddi can be cut.

o Pruritus is mild. o On examination, there might be a hepatomegaly with smooth rounded borders and firm in consistency. GB is not palpable as per the Courvoisier’s law.

resonance

– These procedures should be followed up with a laparoscopic cholecystectomy. o Stone is supraduodenal CBD:

Investigations: o Abnormal LFTs –Raise alkaline phosphatase.

Flowchart 4.6

– Cholecystectomy + Choledocholithotomy. (See Flowchart 4.6).

Liver and The Biliary System

Flow chart

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o If the patency of the distal part of the CBD is questionable and the CBD is dilated >1.5 cm, then a choledochoduodenostomy can be performed in addition to cholecystectomy and choledocholithotomy.

Clinical Presentation: o Bile duct injuries can be identified at the time of the surgery by leakage of bile. o Otherwise, biliary strictures result in slow, painless obstructive jaundice.

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o Burhenne’s technique – Basket removal of stone through a T-tube inserted percutaneously.

Investigations: o Ultrasound. o MRCP.

BILIARY STRICTURES (Fig. 4.4)

o ERCP.

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o PTC.

Injuries to the bile ducts during surgery can result in a stricture.

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Classification:

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Upto 80% of biliary strictures are iatrogenic.

Table 4.4: Bismuth’s classification of biliary strictures

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Causes:

Class

Description

o Bile duct injury.

Type I

Stricture in lower part of CBD, residual stump >2 cm

Type II

Stricture in common hepatic duct, residual stump