Illustrated surgery : a road map [1 ed.] 9789385891205, 9385891200

Table of contents :
Prelims
Chapter-01_Wound Healing
Chapter-02_Fluid, Electrolyte and Acid-base Balance
Chapter-03_Hemostasis-Coagulation-Hemorrhage
Chapter-04_Gallbladder and Extrahepatic Biliary System
Chapter-05_Liver
Chapter-06_Pancreas
Chapter-07_Spleen
Chapter-08_Abdominal Wall, Peritoneum, Mesentery, Retroperitoneum
Chapter-09_Stomach
Chapter-10_Intestine
Chapter-11_Appendix
Chapter-12_Rectum and Anal Canal
Chapter-13_Breast
Chapter-14_Thyroid
Chapter-15_Parathyroid, Adrenal, Endocrine Pancreas and MEN
Chapter-16_Trauma
Chapter-17_Burn
Chapter-18_Arterial Diseases, Venous Diseases and Diseases of Lymphatics
Chapter-19_Hernia
Chapter-20_Diseases of the Testes, Scrotum and Penis
Chapter-21_Diseases of the Esophagus
Chapter-22_Diseases of the Salivary Gland
Chapter-23_Skin and Adnexal Lesion
Chapter-24_Ulcer, Sinus and Fistula
Chapter-25_Urology
Chapter-26_Minimally Invasive Surgery, Robotic Surgery
Chapter-27_Nerve Injury
Chapter-28_Surgery of Hand
Chapter-29_Neck Swelling
Chapter-30_Cleft Lip and Palate
Chapter-31_Anesthesia
Chapter-32_Instrument
Index

Citation preview

Illustrated Surgery

A Road Map

Illustrated Surgery

A Road Map

Nilay Mandal MS (General Surgery) Associate Professor Department of Surgery

Bankura Sammilani Medical College Bankura, West Bengal, India



The Health Sciences Publisher New Delhi | London | Philadelphia | Panama

Jaypee Brothers Medical Publishers (P) Ltd Headquarters Jaypee Brothers Medical Publishers (P) Ltd 4838/24, Ansari Road, Daryaganj New Delhi 110 002, India Phone: +91-11-43574357 Fax: +91-11-43574314 E.mail: [email protected] Overseas Offices J.P. Medical Ltd 83 Victoria Street, London SW1H 0HW (UK) Phone: +44-2031708910 Fax: +44 (0)20 3008 6180 E.mail: [email protected]

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Jaypee Brothers Medical Publishers (P) Ltd Bhotahity, Kathmandu, Nepal Phone: +977-9741283608 E.mail: [email protected] Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © 2016, Jaypee Brothers Medical Publishers The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and do not necessarily represent those of editor(s) of the book. All rights reserved. No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. Medical knowledge and practice change constantly. This book is designed to provide accurate, authoritative information about the subject matter in question. However, readers are advised to check the most current information available on procedures included and check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and duration of administration, adverse effects and contraindications. It is the responsibility of the practitioner to take all appropriate safety precautions. Neither the publisher nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property arising from or related to use of material in this book. This book is sold on the understanding that the publisher is not engaged in providing professional medical services. If such advice or services are required, the services of a competent medical professional should be sought. Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any have been inadvertently overlooked, the publisher will be pleased to make the necessary arrangements at the first opportunity. Inquiries for bulk sales may be solicited at: [email protected] Illustrated Surgery—A Road Map First Edition: 2016 ISBN 978-93-85891-20-5 Printed at

Dedicated to My teachers, my parents, spouse Tapati and daughter Tannistha, for their love and support

Preface

Contents 

‘Books are the compass and telescopes and sextants and charts which other men have prepared to help us navigate the dangerous seas of human life.’ I strongly believe that in the seas of life we all need some help in any moment from others. I also believe that in midst of seas of medical science, all medical personnels particularly the medical students need a GPS and a philosopher. That GPS can come in his or her life in the form of a teacher or a good book or both. In my short period of teaching, I have experienced that most of the students can remember the diseases and their management as a whole but without understanding the disease process, it’s pathophysiology or the principles of treatment. From my understanding, the reason is so many subjects in a too short period. In this book I have attempted to describe the diseases in such a illustrative manner so that the students can understand as well as recover his or her memories from the illustrations. Better understanding , not a better memory make a average medical student to a good doctor. As the book is based on illustrations, most of the diseases are described in a illustrative manner, less text more illustrations. I hope that the book will be more of a guide book for travelling in seas and mountains of medical science than a reference book. Your safe journey can only make me happy. Wish you a happy journey.

Nilay Mandal

7

Acknowledgments

Contents 

‘Writing a book is a horrible, exhausting struggle,like a long bout with some painful illness. One would never undertake such a thing if one were not driven on by some demon whom one can neither resist nor understand.’ I am grateful to my teachers, my students and friends whose encouragement and emotional support make me courageous to do this task. I am also grateful to Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Managing Director) and Mr Tarun Duneja (Director-Publishing) of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India, for publishing this book. I would also like to thank all staff members of Kolkata production unit of Jaypee Brothers Medical Publishers (P) Ltd for their constant support and cooperation to complete this book.

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Contents 0Chapter 1   Wound Healing Introduction 3

Wound healing involves any of the two processes 3 Classification of wound 4 Types of wound healing 4 Three phases of wound healing 5 Role of growth factors in healing 8 Factors affecting wound healing 8 Complications of abnormal wound healing 9 Wound closure techniques 11 Treatment of wound 12

0Chapter 2   Fluid, Electrolyte and Acid-base Balance Fluid, Electrolyte and Acid-base Balance 15





1–12

13–27

Body fluids 15 Fluid input-output 16 Disturbances in fluid balance 16 Electrolyte imbalance 18 Acidosis and alkalosis 25

Chapter 3   Hemostasis-Coagulation-Hemorrhage

28–35

Hemostasis-Coagulation 30 Evaluation to assess risk of bleeding during surgery 30 Congenital hemorrhagic disorders 31 Acquired hemorrhagic disorders 31 Hemorrhage 32 Transfusion of blood and its components 33

Chapter 4   Gallbladder and Extrahepatic Biliary System



Anatomy of the Gallbladder and Extrahepatic Biliary System 38 Things to Remember 38



Pathologies of Gallbladder and Biliary System 40



Benign pathology 40



Malignant pathology 40



Gallstone 41



Risk factors 41



Varieties 41

36–119

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Road Map



Pathogenesis of Gallstone 42



Pathogenesis of cholesterol stone 42



Pathogenesis of black pigment stones 42



Pathogenesis of brown pigment stones 43



Things to Remember 43



Spectrum of gallstone disease 44



Spectrum of symptomatic gallstone disease 44



Complicated case scenario 48



Prepare for emergency cholecystectomy 48



Be prepared for partial cholecystectomy 48



More careful during cholecystectomy 48



Acute acalculous cholecystitis 58



Biliary dyskinesia 59



Choledocholithiasis 60



Acute cholangitis 67



Choledochal cyst 69



Recurrent pyogenic cholangitis (cholangiohepatitis) 76



Primary sclerosing cholangitis 77



Gallbladder carcinoma 78



Cholangiocarcinoma 86



Anomalous Anatomy 96



Anomalous gallbladder anatomy 96



Variations of cystic duct insertion with common hepatic duct 97



Variations in arterial supply of gallbladder 97



Endoscopic Therapeutic Approaches to Biliary System 98



Percutaneous transhepatic approach 98



Removal of retained cbd stone through T-tube tract 99



Removal of cbd stones by endoscopic sphincterotomy 99



Surgical Approaches to Gallbladder and Biliary System 101



Cholecystectomy 101



Open cholecystectomy 105



Why bile duct injury? 107



Bile duct injury recognized at operation 108



Injuries recognized in immediate postoperative period 110



Injuries presenting at an interval after initial operation 111

Laparoscopic management of cbd stones 112 Management of cbd stone (open approach) 115 Choledochoduodenostomy 117 Roux-en-y hepaticojejunostomy 118

Contents 



Chapter 5   Liver



Diseases of the Liver 122 Couinaud system of segmental nomenclature 122 Segmental anatomy of the liver by ct scan 123 Benign pathology 124 Malignant pathology 124 Pyogenic abscess of liver 125 Amebic liver abscess 131 Hydatid cyst 136 Congenital liver cyst 148 Polycystic liver disease associated with polycystic kidney disease 150 Cystadenoma 151 Solid benign neoplasm 152 Hepatocellular carcinoma 153 Liver metastases 161



Portal hypertension 162





Chapter 6   Pancreas

120–172

173–206

Diseases of the Pancreas 175 Anatomy 175 Acute pancreatitis 175 Chronic pancreatitis 187 Cystic neoplasms of pancreas 195 Pancreatic carcinoma 199

Chapter 7   Spleen



Splenic Pathologies 209 Anatomy 209 Functions of spleen 211 What is accessory spleen? 212 What is ectopic spleen (wandering spleen)? 212 What is splenosis? 212 When to do splenectomy? 213 Cyst and tumors of spleen 214 Iatrogenic splenectomy 215



Incidental splenectomy 215



Postsplenectomy blood picture 217



xiii

Chapter 8   Abdominal Wall, Peritoneum, Mesentery, Retroperitoneum Abdominal Wall 220



Congenital defect 220



Acquired abnormalities of the abdominal wall 227



Peritoneum and Peritoneal Cavity 229



Abdominal abscess 230

207–217

218–240

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Malignant peritoneal mesothelioma 233



Pseudomyxoma peritonei 233



Mesentery 234



Mesenteric cyst 234



Acute mesenteric lymphadenitis 234



Mesenteric panniculitis 235



Malignancies of the mesentery 235



Omentum 235



Omental infarction 235



Omental cyst 235



Omental graft and transpositions 236



Retroperitoneum 236



Retroperitoneal abscess 236



Retroperitoneal hematoma 236



Retroperitoneal fibrosis 237



Retroperitoneal neoplasm 239

0Chapter 9   Stomach Diseases of the Stomach

243

Anatomy 243 Peptic ulcer disease 243 Pathophysiology 246 Clinical presentations of gastric ulcer 247 Investigations 248 Treatment 251 Perforation 258 Bleeding peptic ulcer 262 Gastric outlet obstruction 263 Gastritis 266 Malignant neoplasms of stomach 267 Gastrointestinal stromal tumor (gist) 280 Gastric lymphoma 283 Other gastric lesions 284 Postvagotomy syndromes 287

Chapter 10   Intestine Diseases of the Intestine

241–291

292–375 294

Intestinal obstruction 294 Small intestinal obstruction 294 Clinical features of intestinal obstruction 297 Diagnostic evaluation 299 Treatment 300 Principles of surgery in intestinal obstruction 301

Contents 

Treatment 304 Intussusception 306 Crohn’s disease 309 Typhoid enteritis 320 Intestinal tuberculosis 321 Jejunal and ileal diverticula 324 Duodenal diverticula 325 Meckel’s diverticulum 326 Neoplasm of small intestine 330 Short bowel syndrome 331 Diverticular disease of colon 333 Volvulus of the colon 339 Ileosigmoid knotting 344 Large bowel obstruction 344 Ulcerative colitis 345 Colorectal polyp 353 Familial adenomatous polyposis (fap) 359 Cancer of colon 361

Chapter 11   Appendix Acute Appendicitis

378 How it develops? 378 How appendix looks in acute appendicitis 380 Clinical presentation 380 Risk factors for perforation 381 Investigations to confirm diagnosis 381 How diagnostic laparoscopy helpful 382 Think other possibilities also 382 Special consideration in 383 What is alvarado scoring? 384 Treatment 385



Appendiceal Mass (Appendicular Lump) 390 During appendectomy if these things happen 391



Neoplasm of the Appendix 392 Carcinoid tumor (argentaffinoma) 392

Chapter 12   Rectum and Anal Canal Prolapse of the Rectum 395

xv

How it develops? 395 Associated with some anatomical changes 396 How will you differentiate complete rectal prolapse from mucosal prolapse? 397 Clinical presentation 397 Investigation 398 Treatment 398

376–392

393–431

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Solitary Rectal Ulcer Syndrome 399



Fissure-in-ano 400 Location of fissure 400 How fissure develops? 401 Clinical presentation 401 Treatment 402



Anorectal Abscess 404 Sites of anorectal abscess 404 Clinical presentation 404 Investigations 404 Treatment 405



Fistula-in-ano 406 Classification of fistula 406 Clinical presentation 407 How to examine a fistula? 408 Investigation 409 What is Goodsall’s rule? 410 Treatment 410



Hemorrhoids or Piles 413 What is hemorrhoids? 413 What is anal cushion? 413 Types 414 Clinical presentation 415 How to examine a patient with hemorrhoids? 415 Treatment 416 Principles of hemorrhoidectomy 419 Postoperative complications 420 Pilonidal Sinus 420 How it develops? 420 Clinical presentation 421 Treatment 421



Rectal Cancer 423 Spread of rectal carcinoma 423 Clinical presentation 424 Assessment of tumor 424 Preoperative staging 425 Treatment 425



Cancer of the Anus 429 Risk factors 429 Pathology 430 Clinical presentation 430 Assessment of the tumor and investigations to confirm diagnosis 430 Treatment 431

Contents 

Chapter 13   Breast Diseases of the Breast

432–472

434 Inflammations and infections of breast 434 Other uncommon infections of the breast 441 Breast lump 441

Chapter 14   Thyroid Diseases of the Thyroid Gland

xvii

473–513

475 Different thyroid pathologies 475 Thyroiditis 491 Neoplasm of thyroid 496 Surgical approaches to thyroid 509

Chapter 15   Parathyroid, Adrenal, Endocrine Pancreas and MEN Parathyroid 516

514–562

Sites of ectopic parathyroid 516 Under microscope 517 How ca2+ level maintains? 517 Diseases of parathyroid 518

Diseases of Adrenal Gland 531 Anatomy and anatomical variations 531 Variant drainage of right adrenal vein 532 Microscopic features of adrenal gland 533 Hyperaldosteronism 534 Hypercortisolism [Cushing syndrome] 537 Adrenogenital syndrome 543 Adrenal insufficiency 544 Adrenal crisis 545 Diseases of adrenal medulla 546 Principles of adrenal surgery 552



Endocrine Pancreas 553 Pancreatic endocrine neoplasms 554



Multiple Endocrine Neoplasia (MEN) Syndromes 560 Multiple endocrine neoplasia type I 561 Multiple endocrine neoplasia type II 562

Chapter 16   Trauma Introduction

565 Types of injury 565 Head injury 582 Assessment of severity of brain injury 595 Maxillofacial injuries 597 Neck injury 602 Thoracic trauma 612

563–673

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Abdominal injuries 624 Damage control surgery 670 Abdominal compartment syndrome 673

Chapter 17   Burn Introduction

676 Different mechanisms of burn injury 676 When you refer a burn patient to a dedicated burn center? 677 Management of burn injury 677 Prognosis 680 Management 681 Systemic changes in burn 688 Electric burn 689 Chemical burn 692 Late complications of burn 692

Chapter 18   Arterial Diseases, Venous Diseases and Diseases of Lymphatics Diseases of the Arteries 696

Arterial occlusive diseases 696 Acute arterial occlusion of the extremity 701 Chronic occlusive disease of the extremity 709 Arterial occlusive disease of the upper extremity 712 In aortoiliac occlusive disease 716 In femoral, popliteal and tibial occlusive disease 716 Upper extremity occlusive diseases 716 Thromboangiitis obliterans 717 Chronic visceral ischemia 718 Aneurysmal vascular disease 724 Diseases of thoracic aorta 738 Vascular trauma 746



Venous Diseases 749 Different types 749 Deep vein thrombosis (dvt) 750 Venous insufficiency 754 Venous ulcer 765



Disorders of Lymphatic System 765 Acute lymphangitis 766 Lymphedema 766

Chapter 19   Hernia Introduction

674–693

776 Different types of hernia 778 Nyhus classification of groin hernia 783

694–773

774–812

Contents 

Anatomy of the groin 783 Inguinal hernia 785 Special types of inguinal hernia 795 Some unusual types of hernia 796 Fermoral hernia 797 Umbilical hernia 799 Epigastric hernia 801 Incisional hernia 802 Unusual hernia 808

Chapter 20   Diseases of the Testes, Scrotum and Penis Diseases of the Testes 815

832–863

Gastroesophageal reflux disease (gerd) 837 Esophageal motility disorder 841 Esophageal diverticula 846 Esophageal perforation 849 Cancer of esophagus 857

Chapter 22   Diseases of the Salivary Gland Salivary Gland Pathologies 866

864–878

Inflammatory pathologies 866 Obstructive pathology 868 Salivary gland tumors 871 Surgical procedures for salivary gland pathology 875

Chapter 23   Skin and Adnexal Lesion Diseases of the Skin and its Adnexa

813–831

Undescended testis 815 Torsion of the testis (syn. Torsion of the spermatic cord) 822 Varicocele 823 Hydrocele 825 Hematocele 828 Pyocele 828 Chylocele 828 Other scrotal swellings 828 Other scrotal diseases 829 Phimosis 830 Paraphimosis 831

Chapter 21   Diseases of the Esophagus Hiatus hernia 834

xix

Cystic lesions of the skin 881 Ganglion 883 Vascular lesions of the skin 884

879–911 881

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Benign tumors 890 Skin infection 895 Benign pigmented lesions 898 Premalignant lesions 900 Malignant lesions 901 Other malignancies of the skin 910

Chapter 24   Ulcer, Sinus and Fistula Ulcer 914

912–928

Basic priniciples of ulcer dressing 926 Sinuses and Fistula 927 Sinus 927 Fistula 927

Chapter 25   Urology Diseases of the Kidney

929–1036 931



Urinary symptoms 931 Diseases of Kidney and Uretzer 936 Congenital malformations 936 Cystic disease of kidney 943 Other malformations 946 Hydronephrosis 948 Renal stone 950 Percutaneous nephrolithotomy 959 Open surgery for renal stone 961 Infections of kidney 963 Tuberculosis of kidney 972 Kidney tumors 975



Diseases of Ureter 984 Ureteral calculi 984 Urothelial tumors of renal pelvis and ureter 985



Urinary Bladder 988 Congenital anomalies 988 Bladder calculi 990 Schistosomiasis of the urinary bladder 994 Bladder tumor 996



Diseases of Prostate 1000 Benign prostatic hyperplasia 1000



Prostate 1010 Prostatitis 1010 Carcinoma of prostate 1011



Urethra 1016 Urethral stricture 1016 Hypospadias 1019

Contents 

Priapism 1022 Peyronie's disease 1024 Carcinoma of penis 1025 Neoplasms of Testis 1031

Chapter 26   Minimally Invasive Surgery, Robotic Surgery Minimally Invasive Surgery 1039

1072–1082

Anatomy of neck 1074 Neck swellings 1075

Chapter 30   Cleft Lip and Palate Cleft lip 1085

1063–1071

Infections in hand 1067 Injuries in hand 1069

Chapter 29   Neck Swelling Neck 1074

1054–1062

Classification of nerve injuries 1056 Sunderland's classification 1058 Clinical features 1058 Management of nerve injury in closed injury 1059 Management of nerve injury in open injury 1059 Principles of nerve repair 1059

Chapter 28   Surgery of Hand Introduction 1065

1037–1053

Different minimal access techniques 1039 Physiology of pneumoperitoneum 1041 Access 1042 Port placement 1045 Instrumentation 1045 Advantages and disadvantages 1049 Examples of laparoscopic procedures 1049 Contraindications 1050 Complications 1050 New techniques of minimally invasive surgery 1050 Robotic surgery 1051

Chapter 27   Nerve Injury Introduction 1056

xxi

Cleft palate 1088

1083–1089

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Chapter 31   Anesthesia

Introduction 1092 Types of anesthesia 1092 Preoperative evaluation 1101 Intraoperative management 1102 Complications of general anesthesia 1103

Chapter 32   Instrument Surgical Instruments

Index

1090–1103

1104–1131

1106 Parts of an instrument 1106 Instruments used for antiseptic dressing and draping 1106 Instruments used for fixation 1107 Instruments used for giving incision over the skin 1107 Instruments used for hemostasis 1108 Instruments used for holding tissues 1112 Instruments used for suturing 1115 Other methods of skin closure 1119

1133–1140

Chapter 1

Wound Healing

Important Topics

zzProcess

of Wound Healing

zzClassification

of Wound

zzPhases

of Wound Healing

zzGrowth

Factors in Wound Healing

zzFactors

Affecting Wound Healing

zzComplications zzTreatment

of Wound Healing

of Wound

‘It is a most gratifying sign of the rapid progress of our time that our best textbooks become antiquated so quickly.’ Christian Albert Theodor Billroth (1829 –1894) Austrian Surgeon

Wound Healing 

Introduction

SS Wound

healing is the normal body response to injury (surgical/traumatic) to restore the normal structure and function.

Wound Healing Involves Any of the Two Processes

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Classification of Wound

Types of Wound Healing

Wound Healing 

Three Phases of Wound Healing Inflammatory (reactive) phase Proliferative (reparative) phase zz Maturational (remodeling) phase zz zz

[The 3 phases often overlap]

Inflammatory (Reactive) Phase Day 1 SS Immediately

after injury, blood vessels are disrupted, resulting in exposure of subendothelial collagen to platelets, leads to platelet aggregation and activation of coagulation pathway. SS The end product of coagulation cascade is fibrin, which plays an important role in clot formation and wound healing. This fibrin acts as scaffold for migration of PMN and monocytes into the wound. It also serves as a reservoir for cytokines. SS Platetet and granulocytes release a number of substances, such as platelet derived growth factor (PDGF), transforming growth factor-β (TGF-β), fibronectin, serotonin and histamine.

Day 1–4 SS Leukocytes

begin to migrate out from the vessels to the wound. The release of histamine and serotonin causes increased vascular permeability and various chemotactic factors facilitate migration. SS PMNs are the first inflammatory cells to enter the wound. Increased vascular permeability and presence of chemotactic substancs (e.g. IL-1, TNF-α, TGF-β, PDGF) facilitate migration of PMNs. In the first 24–48 hours, neutrophils make about 50% of all cells in the wound. These PMNs phagocytize bacteria, foreign material and devitalized tissue. They also release TNF-α2 (an important cytokine for angiogenesis and collagen synthesis) and collagenases. Over time, neutrophils are removed by apoptosis or macrophage phagocytosis. SS Macrophages start to migrate in the wound after about 48 hours of injury, and present till healing proces is completed. Macrophages also participate in phagocytosis. They synthesize oxygen radical and nitric oxide, release cytokines and growth factors such as TGF-β, VEGF, Insulin-like growth factor (IGF), epithelial growth factor (EGF) and thereby regulate cell proliferation, matrix synthesis, remodelling and angiogenesis. SS T lymphocyles also migrate to the wound usually about 5–7 days after injury. They take part in wound healing by producing stimulatory cytokines (e.g. IL–2) and inhibitory cytokines (e.g. TGF-β, TNF-a).

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SS Mast cells are also recruited in this phase. Degranulation of mast cells release histamine, TNF-α , prostaglandins and

protease resulting in increased vascular permeability, cellular activation.

Proliferative (Reparative) Phase SS It

is the second phase of healing. phase involves angiogenesis, fibroplasia and epithelialization, and spans from day 4 to day 12. SS Angiogenesis—Endothelial cell migration, its replication and new capillary tube formation result from complex interaction of extracellular matrix material (e.g. fibronectin, hyaluronic acid) and cytokines (e.g. TGF-β, IL-8, VEGF). The angiogenesis is regulated by TNF-α, TGF-b, VEGF, PDGF those are derived from platelets, macrophages, damaged epithelial cells. Metabolic environment of the wound also influences angiogenesis. Increased lactate, decrease pH and oxygen tension result in reduction of NAD+ (inhibitor or angiogenesis). SS Fibroplasia— The quiscent fibroblasts are chemoattracted to the injury site, where it replicates and proliferates, being stimulated by macrophage and platelet derived cytokines (e.g. TGF-β, EGF, IGF–1). PDGF is the most potent chemotactic and mitogenic factor for fibroblasts. The activated fibroblasts now synthesize collagen and other components of extracellular matrix (ECM). ECM consists of fibroblast-derived collagen monomer, proteoglycans and fibronectin. Two types of collagen are important for wound repair, Type I and Type III. Among them, Type III collagen plays significant role. Collagen synthesis significantly begins about 1 week postinjury. Oxygen, vitamin C, iron are cofactors for cross-linkge of collagen fibers. Fibroblasts also produce matrix metalloproteinases (MMP) which helps to degrade matrix substances resulting in smooth migration of fibroblasts. SS Epithelialization—Epithelialization of wound develops due to migration of epithelial cells from the edges of wound, mediated by EGF, TGF-β, PDGF, IGF-1. Migration of epithelial cells occur at the rate of 1 mm/day and it begins within hours after injury. The attachments between hemidesmosomes of the basal cells and the laminin of the basal lamina are broken down, leading to migration of epithelial cells. Reepithelialization is completed within 48 hours in approximated incised wound. [If epithelium and superficial dermis is only damaged, then the repair process involves reepithelialization without any fibroplasia (no scar formation at all).] SS This

Wound Healing 

Maturational (Remodeling) Phase SS Wound

contraction: zz This process involves movement of the wound edge toward the center of the wound by the action of myofibroblasts. zz The process starts 4–5 days after injury and continues for 12–15 days. zz Matrix metalloproteinases (MMPs) are important factors for wound contraction. SS Remodeling: zz The process begins about 21 days after injury. zz Collagen synthesis is downregulated, collagen (type III) is broken down by MMPs and replaced by denser collagen (collagen I) that is organized along the lines of stress. An early wound consists of about 30% type III collagen (uninjured connective tissue composed of 80–90% type I collagen and 10–20% type III collagen). Higher concentration of type III collagen in matrix, more weaker the wound. With time, the ratio of type I and III collagen changed to the ratio of intact connective tissue. zz Cellularity of the wound decreases. zz As a result, a mature, avascular, acellular collagen rich scar develops. zz This process reaches a steady state after 12–18 months. By about 6 months, the wound regains 80% of the strength of an unwounded tissue.

[A well-healed wound never achieves the strength of an unwounded tissue. By 3 weeks, the tissue strength reaches 30% of original strength. After 3 months, the strength reaches the maximum, about 80% of its original strength.]

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SS Healing

by secondary intention: zz The pathological process and phases are almost same, the differences are quantitative.

Role of Growth Factors in Healing SS Different

growth factors are: Platelet-derived growth factor (PDGF) zz Transforming growth factor α and β (TGF-α, TGF-β) zz Fibroblast growth factor (FGF) zz Vascular endothelial growth factor (VEGF) zz Granulocyte-macrophage colony-stimulating factor (GM-CSF) zz Insulin-like growth factor (IGF-1, IGF-2). SS Growth factors act on cells by surface receptor binding. SS Growth factors have different actions on different cells: zz Chemotaxis of PMNs, macrophages, fibroblasts zz Stimulation of angiogenesis zz Stimulation of fibroblasts leads to replication and proliferation zz Stimulation of collagen synthesis zz Regulation of ECM synthesis. zz

Factors Affecting Wound Healing Factors affecting wound healing

Systemic factors

Local factors

Systemic Factors SS Malnutrition—Normal

healing process is delayed and impaired, leads to weak scar formation. wound environment—Optimal collagen synthesis for wound healing requires oxygen as a cofactor. Factors causing hypoxia in wound (e.g. cardiac failure, arterial insufficiency, excessive tension on tissue) affect proper wound healing. SS Diabetes mellitus—The lack of insulin (insulin restores collagen synthesis and granulation tissue formation) and hyperglycemia (by affecting the migration and phagocytic function of inflammatory cells and proliferation of fibroblasts and endothelial cells) leads to impaired wound healing. SS Hypoxic

Wound Healing 

The micro and macroangiopathy, associated nephropathy—All adversely affect wound healing. Diabetic wound also lacks adequate growth factors. SS Chronic renal and hepatic disease—Decreased collagen synthesis leads to weak scar formation. SS Collagen vascular disease—The disease itself as well as medications are responsible for impaired inflammatory cell migration and collagen deposition. SS Smoking—Impairs wound healing by causing cutaneous vasoconstriction, nicotine impairs collagen synthesis. SS Steroid and antineoplastic drugs—Steroids inhibit the inflammatory phase of wound healing. It impairs collagen synthesis, inhibit epithelialization and wound contraction. Antineoplastic drugs impair proliferation of fibroblasts as well as inhibit the inflammatory phase of wound healing. SS Vitamin and mineral deficiency— Vitamin C deficiency leads to failure in collagen synthesis as well as cross-linking. Vitamin A increases the inflammatory responses after injury increases the migration of macrophages, helps its activation. It also increase collagen synthesis. Vitamin A can restore wound healing that are impaired by diabetes, radiation, cyclophosphamide. Zinc deficiency leads to decreased fibroblast proliferation, delayed epithelialization, decreased collagen synthesis.

Local Factors SS Infection:

Presence of infection delays wound healing. Infection alters the effects of cytokines, leads to delayed healing. SS Wound hypoxia: Local damage to the vessels following trauma, edema around the wound, excessive tension due to suturing lead to wound hypoxia. Hypoxia leads to impaired fibroblast proliferation and collagen synthesis. SS Edema: Leads to increased tendency to skin breach and development of infection. SS Ionizing radiation: Leads to abnormal wound healing. SS Chemical agents: Chlorhexidine or povidone-iodine impairs inflammatory cell migration, leads to delayed wound healing.

Complications of Abnormal Wound Healing SS Poor

alignment: When a wound crossed the definite anatomical structure such as vermilion border of lip, without proper alignment during repair, defect in alignment develops.

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SS Contracture:



If a linear wound crosses flexor creases vertically, there is development of scar contracture. Deep and extensive burn scar also causes scar contracture.

SS Altered

pigmentation: Most of the scars are hypopigmented, hyperpigmentation may also occur. Dirt or soot particles may become implanted in untidy wounds and results in tattooing of scar. SS Hypertrophic scar: Raised scar that confines of the original wound. zz Both increased collagen production and collagen breakdown, but the final result is excess collagen in tissue. zz Stretched collagen bundles are aligned in same plane of epidermis, whereas the collagen bundles are randomly arranged and relaxed in normal scar. zz More cellular and vascular than normal scar, also contains aggregates of abundant fibroblasts, vessels and collagen fibers. zz A hypertrophic scar can develop anywhere in the body and frequently regress spontaneously. zz The development of hypertrophic scar can be minimized by choosing appropriate direction of incisions (hypertrophic scar usually occur at areas of tension and flexor surface). zz Custom made pressure garments aids collagen maturation, increases collagenase activity and makes the scar less cellular. SS Keloid: Keloids are proliferative scar that grows beyond the limits of the wound. zz Thicker, more abundant stretched collagen bundles aligned in the same place of the epidermis, as well as acellular. zz Rarely regress spontaneously. zz Genetic predisposition is present. zz More common in darker-pigmented peoples—African and Asian population. zz May develop after surgery, burn, tattoos, ear piercing. zz Certatin body parts have increased tendency of keloid formation—Presternal, deltoid, earlobe, upper back. zz Treatment: Intralesional corticosteroids (e.g. triamcinolone acetate) is the first line of treatment. zz Surgery and postoperative interstitial radiotherapy is the another option. SS Chronic nonhealing wound—e.g. diabetic ulcer, pressure sore. SS Tattooing:

Wound Healing 

Keloid

Hypertrophic scar

Intrakeloidal triamcinolone injection

Wound Closure Techniques SS Suturing—

e.g. skin suturing with nonabsorbable, monofilament suture SS Stapling—Allows quick closure SS Steri-strips— zz Least invasive way of skin closure zz Particularly used after suture or staple removal. SS Skin adhesive (octyl-cyanoacrylate)— zz Provide a waterproof, antimicrobial barrier zz No need of removal of suture or staples.

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Treatment of Wound SS History

taking SS Examination of wound— zz To assess depth zz To identify foreign bodies, dirt zz Presence of nonviable tissue. SS Tetanus prophylaxis SS Local care of the wound— zz Irrigation of the wound with normal saline zz Removal of foreign body

Debridement of nonviable tissues All hematomas are evacuated and bleeding points are secured zz Wound edges must be debrided to get a fresh edge for suturing zz In case of tissue loss, skin graft or flap may be required. SS Antibiotics—Choice of antibiotic depends on organisms most likely to be found in the wound and patient's immune status. SS Dressing— zz The goal of dressing is to provide an ideal environment for wound healing zz Characteristics of ideal dressing— „„ Cost effective „„ Permeable to gases and water vapor „„ Impermeable to microorganisms „„ Comfortable „„ Nonirritant „„ Minimal pain during change of dressing. zz Different types of dressing— „„ Occlusive and semiocclusive dressing „„ Hydrophilic and hydrophobic dressing „„ Medical dressing „„ Alginates „„ Absorbent dressing. zz zz

Chapter 2

Fluid, Electrolyte and Acid-base Balance

Important Topics

zzHypovolemia zzVolume

Overload

zzElectrolyte

Imbalance

zzMetabolic

Acidosis

zzMetabolic

Alkalosis

zzRespiratory

Acidosis

zzRespiratory

Alkalosis

‘There is a strange disparity between the sciences of inert matter and those of life. Astronomy, mechanics, and physics are based on concepts which can be expressed, tersely and elegantly, in mathematical language. ………….Those who investigate the phenomena of life are as if lost in an inextricable jungle, in the midst of a magic forest, ………… but are incapable of defining in algebraic equations.' Alexis Carrel (1873 – 1944) French-born American Surgeon

Fluid, Electrolyte and Acid-base Balance 

Disorders of Fluid, Electrolyte and Acid-base Balance

Body Fluids SS Total

body water (TBW)— 50–60% of total body weight. zz Muscles and solid organs have higher water content than fat and bones. zz In males: TBW is 60% of total body weight. zz In females: TBW is about 50% of total body weight (higher adipose tissue and less muscle mass). zz In newborn: TBW is about 80% of total body weight. zz

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SS Composition

Road Map

of fluid compartments—

Water is freely diffusible, where as movements of ions and protein are restricted through the fluid compartments.

Fluid Input-output

Disturbances in Fluid Balance SS Volume

overload (generally means both water and salt loss).

SS Hypovolemia

Fluid, Electrolyte and Acid-base Balance 

Hypovolemia Causes

Clinical Manifestations ↓jugular venous pressure skin turgor SS Thirst—Dry mouth, sunken eyes SS Oliguria SS Tachycardia SS Hypotension SS Mental obtundation. SS Fatigue—

SS Weakness—Diminished

Blood Parameters SS ↑blood

urea nitrogen (BUN)

SS ↑creatinine SS Acid-base

imbalance SS ↑urine osmolality.

Treatment SS Replacement

of fluid with isotonic, 'normal' saline (0.9% NaCl) solution SS Amount of fluid needed is guided by clinical signs and urinary output.

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Volume Overload Causes SS Excess

fluid infusion dysfunction SS Congestive heart failure. SS Renal

Clinical manifestations SS Peripheral

edema SS Distended neck vein SS ↑CVP SS Pulmonery edema SS Cardiac failure.

Treatment SS Restriction

of fluid intake SS Diurectic (e.g. furosemide) may be required.

Electrolyte Imbalance Sodium SS Sodium

is the principal cation of ECF SS Bone is a big source of sodium. When abnormal loss of sodium develops, storage in bone compensates it SS Charges in TBW is inversely proportional to serum sodium.

Hyponatremia Plasma Na+ concentration < 135 mEq/l.

Causes

Fluid, Electrolyte and Acid-base Balance 

19

Clinical features confusion, seizures, ↑ intracranial pressure SS Weakness, fatigue, muscle cramp SS Lacrimation, salivation. SS Headache,

Treatment SS In

most cases, calculated sodium is administered in isotonic solution severe hyponatremia ( 34 mmHg. Class II stockings is used for uncomplicated varicose vein. Class III stockings is used for complicated varicose vein. [Contraindicated in peripheral arterial disease and cardiac failure.] z z

3. Pharmacological—Indicated in early stage of varicose veins, in association with compression therapy S Commonly

used phlebotropic drugs: z Micronized purified flavonoid fraction—Acts by— z Improving RBC rheology z Antiinflammatory property z Protective effect on venous valve z Protective effect on venous wall. Calcium dobesilate—Acts by— S Increasing venous tone S Antiedema and capillary protection effects. Diosmin—Acts by— S Profibrinolytic action S Anti inflammatory property. Rutin and troxerutin—Acts by— S Improving RBC rheology S Protective effect on venous wall.

4. Surgery—Indicated in S Varicosities

> 4 mm in diameter S Varicosity with complication S Refractory to medical therapy or compression therapy.

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Trendelenburg’s surgery

Contd...

Arterial Diseases, Venous Diseases and Diseases of Lymphatics Contd...

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S What

is SEPS [subfascial endoscopic perforator surgery? z Endoscopic method of interrupting incompetent medial calf perforators. [In presence of lipodermatosclerosis, lack of space in subfascial area leads to difficulty in introduction of endoscope and visualisation of perforators.]

5. Minimally invasive methods— S Sclerotherapy—

Indicated in telangiectasias, reticular varicosities and small varicose veins Sclerosing agents— „ 0.2% sodium tetradecyl sulfate „ Polidocanol „ Hypertonic saline. 25–30 gauge needle is used No single injection dose exceeds 0.1 ml Multiple injections may required Pressure dressings must be kept for 72 hrs after sclerosant injecton. z z

S Endovenous laser—

Using doppler USG, saphenous vein is mapped and marked The affected vein is cannulated under USG guidance and then laser fibre is introduced into the vein z Then, the laser energy is fired. z z

S Radiofrequency ablation—

Using doppler USG, saphenous vein is mapped and marked Under USG, guidance, special heater probe is inserted into the vein z Collagen tissue of vein is denatured by heat. z z

S Foam sclerotherapy— z

Not more than 20 ml foam should be injected at one sitting. Multiple sitting may be required for maximum success.

S Other methods—

Catheter directed sclerotherapy z Obliteration of varicose vein by hyperheated steam. z

Arterial Diseases, Venous Diseases and Diseases of Lymphatics

765

Venous Ulcer S One

of the common causes of leg ulceration is venous disease of the lower limb. S Ulcer lying just proximal to the medial malleolus, associated with skin changes (lipodermatosclerosis)—Think of venous ulcer. S Examine the peripheral pulses—To rule out PAD. S Examine the sensation, loss of sensation in foot with ulcer—Think of diabetic ulcer. S Duplex USG of venous system and measurement of Doppler ankle blood pressure—Most appropriate investigation. S Management— z Venous ulceration due to—Superficial venous incompetence alone „ Patient fit for surgery „ Patient willing to undergo surgery

z

Varicose vein surgery Venous ulceration due to–Deep venous insufficency „ Patient unfit for surgery „ Patient unwilling to undergo surgery

Local ulcer management + Debridement of ulcer + Irrigation with NS + Topical steroids (if eczematous reaction around the ulcer) [Topical antibiotics should be avoided.]

Compression therapy (by class III graduated compression stockings)

Disorders of Lymphatic System

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Acute Lymphangitis S Acute

inflammation of the lymphatics when an area infected by pyogenic bacteria (specially, streptococci and Staph.aureus), drained by the lymphatic system. S Affected lymphatics are dilated and filled with exudate of neutrophils and monocytes.

S Clinically,

lymphangitis is manifestated by red painful subcutaneous streaks (inflammed lymphatics) with tender, enlarged draining lymph nodes (acute lymphadenitis).

S Treatment—

Rest of the affected part (to reduce lymphatic drainage) Elevation (to reduce swelling) z Intravenous antibiotic (to treat the primary infection). z z

Lymphedema Pathophysiology S Lymphedema

is the end result of improper lymphatic outflow due to aplasia, hypoplasia, hyperplasia, primary decreased lymphatic contractility or inflammatory obliteration.

1.

Arterial Diseases, Venous Diseases and Diseases of Lymphatics

2.

3.

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Illustrated Surgery—A

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S Secondary

lymphedema is for more common than primary lymphedema S Most common form of primary lymphedema is lymphedema praecox S Most common form of secondary lymphedema worldwide is filarial lymphedema S In developed countries, common causes of secondary lymphedema are— z Tumor invasion z Resection or ablation of regional lymph nodes by surgery, radiation therapy.

Clinical Presentation S Lymphedema

characteristically involves the foot. of the ankle is lost due to filling of submalleolar depression. S ‘buffalo hump’ forms on the dorsum of the foot. S Toes appear ‘square’. S Skin over the edema cannot be pinched due to subcutaneous fibrosis (Stemmer’s sign). S In early cases, pitting edema. In advanced stage, nonpitting edema due to fibrosis and dermal thickening. S In advanced stage, chronic eczema, fungal infection of skin (dermatophytosis) and nail (onychomycosis), fissuring, verrucae, papillae are seen. S Ulcer may develop after a minor trauma. S Chylous ascites, chylothorax, chyluria, chylorrhea (discharge of lymph from skin vesicles) suggest lymphangectasia and chylous reflux. S Ulceration, nonhealing bruise, purple-red nodules, if present—Think of lymphangiosarcoma. S Contour

HEJE?=H H=OOEł?=PEKJKB)UILDA@AI= S Subclinical—

Histological abnormalities in lymphatics and lymph nodes No clinically apparent lymphedema. S Grade I— z Edema pits on pressure z Swelling mostly or completely disappears on elevation and bed rest. S Grade II— z Edema does not pit z Swelling does not significantly reduce on elevation. S Grade III— z Edema is associated with irreversible skin changes—Fibrosis, papillae, fissuring, verrucae. z z

Lymphedema congenita (10%) S Onset before 1st year of life S More common in males S More commonly bilateral and involving the whole leg S The familial version is called the ‘Milroy’s disease’ S May be associated with disorders like yellow nail syndrome and Pierre-Robin syndrome.

Arterial Diseases, Venous Diseases and Diseases of Lymphatics

Lymphedema praceox (80%) S Onset from 1–35 years of age S More common in females, peak incidence shortly after menarche S More commonly unilateral S Only extends upto the knee S Familial version is called “Meige’s disease”.

Lymphedema tarda (10%) S Onset after 35 years of age S Patient must be investigated for malignancy of the pelvic organs, prostate and external genitalia.

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KJłNI=PEKJKB!E=CJKOEO S It

is rather easy to clinically diagnose a case of lymphedema in second or third stage is difficult when the disease in a first stage

S Diagnosis

t


Primary? Lymphoscintigraphy —Diagnostic test of choice – Almost 100% specific to differentiate lymphedema from other causes of limb swelling

t
t


Secondary? CT and MRI—Can exclude any mass obstructing the lymphatic channels MRI can differentiate lymphedema from chronic venous edema and lipedema (excessive subcutaneous fat and fluid)

– Cannot differentiate between primary and secondary type

Lymphoscintigraphy

Lymphangiography S Invasive

study.

S This investigation is reserved for preoperative evaluation of a patient who is waiting for operations of the lymphatic

channels.

Arterial Diseases, Venous Diseases and Diseases of Lymphatics

771

Management Management

Conservative

2SHUDWLYH

Conservative measures S Objectives

are— Edema control z Meticulous skin care z Avoid injuries z Avoid cellulitis and lymphangitis. z

Different measures S General

measures— z Patients must be educated about skin care and avoidance of injures z Patients must be instructed to attend his/her physician whenever there is early signs of infection z Infections must be aggressively treated with appropriate antibiotics z Eczema requires treatment with steroid. S Leg elevation— z Avoid prolonged standing , foot end of the bed must be elevated. S Compression garment— z Graded compression stockings should be worn all time except at night z Degree of compression required 20–60 mmHg z Offer a protection against external trauma. S Complex decongestive physical therapy (CDP)— z Specialized technique to stimulate the remaining functional lymph vessels, evacuate stagnant protein rich fluid and redirect lymph fluid to areas where lymph flow is normal. S Compression pump therapy— z Pneumatic compression pump therapy is a method—Similar principle to CDP. S Pharmacotherapy— z Benzopyrones, by stimulating proteolysis by tissue macrophages and also by stimulating the peristalsis and pumping action of the collecting lymphatics may reduce lymphedema. z Role is still doubtful.

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Operative S Only

about 10% of the patients need surgical intervention.

S May be considered in patients with stage II and stage III lymphedema with severe functional impairment or recurrent

episodes of lymphangitis. S 2 types of interventions

t
t


Reconstructive Indicated where lymphatic circulation is proximally obstructed with normal distal lymphatic channels Different methods— (a) Omental pedicle (b) Anastomosis of lymph nodes to veins (c) Ileal mucosal patch (d) Anastomosis of residual dilated lymphatics to nearby veins

Excisional (a) Sistrunk operation

(b) Homan’s operation (c) Charles operation

Chylothorax— S Chylous pleural effusion. S Due to thoracic duct trauma or advanced malignancy with lymphatic metastasis. S Presence of chylomicron in pleural fluid and triglyceride > 110 mg/dl in pleural fluid—Diagnostic. S Tube thoracostomy and medium-chain-triglyceride rich diet are the initial treatment. S In patient with thoracic duct injury, if effusion persists for more than 1 week, ligation of the thoracic duct should be done using video-assisted thoracoscopy. S Pleurodesis is the last option.

Chylous ascites— S Causes are— z Congenital lymphatic abnormality z Malignancy involving abdominal lymph nodes S Presence of chylomicron and triglyceride level > 110 mg/dl in ascitic fluid is diagnostic S Treatment is abdominal poracentesis and medium-chain triglyceride rich diet S In duct injury, if chylous ascites not responds after 2 weeks duct must be ligated.

Arterial Diseases, Venous Diseases and Diseases of Lymphatics

Chyluria— S Filaria is the most common cause. Other causes are— z Ascariasis z Tumor z Tuberculosis. S Presents as painless passage of milky white urine, particularly after a fatty meal S IVU/Lymphangiography demonstrate the presence of lymphourinary fistula S Treatment is low fat diet, plenty of fluid to prevent clot, ligation of involved lymphatic channel.

Tumors of the lymphatics

Lymphangioma ‡ %HQLJQ YDVFXODU OHVLRQ ZLWK O\Pphatic differentiation ‡ 7ZRW\SHV² – Capillary lymphangioma – Cavernous lymphangioma or cystic hygroma ‡ 0RVWRIWKHO\PSKRQJLRPDVF\VWLF K\JURPD SUHVHQWDWELUWK ‡ &\VWLF K\JURPD PRVW FRPPRQO\ SUHVHQW LQ WKH QHFN D[LOOD LQ WKRUDFLFDQGDEGRPLQDORUJDQV ‡ 7UHDWPHQWLVVXUJLFDOH[FLVLRQ

Lymphangiosarcoma ‡ 'HYHORSV DV D FRPSOLFDWLRQ RI long-standing lymphedema ‡ 2ULJLQDOO\ GHVFULEHG LQ SRVWPDVtectomy lymphedema (StewartTreves syndrome) ‡ &OLQLFDOO\ SUHVHQWV DV JUDGXDOO\ LQFUHDVLQJHGHPDDSSHDUDQFHRI VXEFXWDQHRXVQRGXOHV ‡ 7UHDWPHQW LV SUHRSHUDWLYH FKHPR WKHUDS\UDGLRWKHUDS\IROORZHGE\ H[FLVLRQ ‡ 3URJQRVLVLVSRRU

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Chapter 19

Hernia

Important Topics

zzDifferent zzNyhus

Types of Hernia

Classification of Groin Hernia

zzAnatomy

of the Groin

zzInguinal

Hernia

zzFemoral

Hernia

zzUmbilical

Hernia

zzEpigastric

Hernia

zzIncisional

Hernia

zzUnusual



Hernia

‘The history of science, like the history of all human ideas, is a history of irresponsible dreams, of obstinacy and of error. But science is one of the very few human activities—perhaps the only one— in which errors are systemically criticized and fairly often, in time, corrected. This is why we can say that, in science, we often learn from our mistakes, ………..’ Karl Raimund Popper (1902–1994) Austrian born British Philosopher of Science

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Introduction

SS The

word ‘hernia’ derived from latin word meaning ‘a rupture’ is an abnormal protrusion of an organ or tissue through a defect in its surrounding wall SS Hernia can occur in various sites, but it develops most commonly through the abdominal wall. SS Hernia

Other sites of hernia—

Hernia  There must be a weakness Normal weakness

Abnormal weakness

Present in all persons, due to anatomical configurations Due to congenital weakness In connective tissue disorders, e.g. – Osteogenesis imperfecta – Ehler-Danlos syndrome – Marfan syndrome

•

Composition of hernia

Acquired

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Different Types of Hernia According to Presentation zz

External hernia—Protrusion through all layers of the abdominal wall

zz

Internal hernia—Herniation of intestine or other abdominal viscera through a defect in peritoneal cavity.

According to Complication SS Irreducible

hernia—

Hernia 

SS Obstructed

hernia—

SS Strangulated

hernia—

Femoral hernia is more likely to strangulate because of— SS Narrow neck SS Rigidity of surrounding structures.

According to Site SS Inguinal

hernia—

Neck of inguinal hernia is above and medial to pubic tubercle.

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SS Femoral

hernia—

SS Umbilical

hernia—

SS Epigastric

hernia—

Road Map

Hernia 

SS Incisional

hernia—

SS Obturator

SS Spigelian

hernia—

hernia—

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SS Lumbar

SS Sciatic

hernia—

hernia—

SS Perineal

hernia—

Road Map

Hernia 

783

Nyhus Classification of Groin Hernia SS Type

I—Indirect inguinal hernia zz Internal inguinal ring normal. SS Type II—Indirect inguinal hernia zz Internal inguinal ring dilated zz Posterior wall intact. SS Type III—Posterior wall defect A. Direct inguinal hernia B. Indirect inguinal hernia—Internal ring dilated and medially encroaching the transversalis fascia C. Femoral hernia. SS Type IV—Recurrent hernia A. Direct B. Indirect C. Femoral D. Combined.

Anatomy of the Groin SS Anatomy

is to be understood according to the surgeon’s approach to hernia repair. SS When one is operating through a open approach, anatomy is to be considered from skin to the peritoneal cavity. When one is operating through a laparoscopic approach, one should consider anatomy from abdominal cavity to the skin. SS Surgeon must know the anatomy to select the most suitable approach for repair, to lower the recurrence rate and to avoid the complications.

What is Myopectineal Orifice of Fruchaud SS According to Fruchaud, all groin hernias (indirect, direct and femoral) arise due to a common anatomic defect rather

than a isolated cause for each one. concept is that, all groin hernias are due to failure of the transversalis fascia over myopectineal orifice to retain the peritoneum. SS The myopectineal orifice is surrounded— zz Superiorly, by internal oblique and transversus abdominis zz Inferiorly, by Cooper’s ligament zz Medially, by lateral border of rectus muscle and sheath zz Laterally, by Iliopsoas muscle. SS The inguinal ligament and iliopubic tract divide the myopectineal orifice of Fruchaud into superior and inferior compartment. SS His

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The procedure ‘giant prosthetic reinforcement of visceral sac’ (GPRVS), developed by Stoppa, is basically reinforcing the transversalis fascia over Fruchaud’s myopectineal orifice with the help of a prosthesis.

Basics of Anatomy of Groin

Hernia 

Inguinal Hernia SS About

75% of all hernias are inguinal hernias SS In both male and female, inguinal hernias are the most common type of hernia SS Men are 25 times more likely to develop groin hernia SS Among inguinal hernias, about 75% are indirect and rest are direct hernias SS Bilateral hernias are commonly direct hernias than indirect SS Both indirect and femoral hernias commonly occur in right side zz Due to delayed obliteration of processus vaginalis zz Due to tamponading effect of sigmoid colon on the left femoral canal. SS The prevalence of hernias as well as likelihood of strangulation increases with age SS Among all strangulated hernias, most are indirect inguinal hernias.

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Clinical Presentation

from the parents is more important than the physical examination—In the case of pediatric hernias SS All patients with small-bowel obstruction must be searched for presence of obstructed hernia. SS History

On Examination SS Patient

must be examined both in lying and standing position. appears in the groin on standing and after coughing, peristaltic sound in the swelling, swelling is nontransilluminant— Most likely inguinal hernia.

SS Swelling

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787

hernia that descends into the scrotum—Certainly an indirect inguinal hernia. moving lateral to medial in the inguinal region after coughing—Most likely indirect inguinal hernia. SS On straining, swelling (symmetric, circular) near the external ring appears from deep to superficial—Most likely direct inguinal hernia. SS When reducing the hernia, a gurgling sound is audible—Most likely an enterocele. SS A patient who is used to reduce the swelling manually now cannot do it and surgeon cannot reduce the hernia by ‘Taxis’—It is an irreducible hernia. [The distinction between indirect and direct inguinal hernia cannot be done accurately by clinical methods always and it is not essential to differentiate because repair is approached in a same way regardless of type of hernia.] SS A

SS Bulge

Diagnosis SS Appearance

of swelling in groin after standing or coughing, presence of cough impulse, gurgling sound during reduction—These clinical findings are highly suggestive of inguinal hernia, in most cases. No need of further investigation for confirmation. SS According to patient, swelling appears in the groin after straining, but not present on clinical examination—Makes a dilemma both in pediatric and adult patients. zz Standing or ambulatory for a period sometimes makes the undiagnosed hernia to become visible zz Repeat examination at another time is also helpful. SS USG has high degree of sensitivity and specificity in delection of occult direct and indirect hernias. SS CT is also very much sensitive in doubtful situations. SS Laparoscopy is the final approach to detect the exact nature of groin pathology.

Treatment SS Temporary

management is manual reduction. Be aware of the possibility of reduction en masse.

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SS Inguinal

hernias should be electively repaired unless specific contraindications present. SS Elderly patient can also well tolerated elective repair if associated medical problems can be controlled and local anesthesia is perferred. SS Patient with chronic bronchitis should not be denied repair, for these are the people having increased chance of developing strangulated hernia. SS Postoperative morbidity and mortality after a laparotomy for strangulated hernia are much more than elective repair. SS If patient has associated significant prostatic hyperplasia, chronic constipation, chronic cough—It should be treated first. SS Choice of anesthetic—LA, regional (spinal /epidural), GA. zz In laparoscopic repair, GA is preferred to achieve complete muscle relaxation for insufflation. SS Goals of hernia rapair

Elimination of peritoneal sac (herniotomy)

Repair of fascial defect in inguinal floor (herniorrhaphy/hernioplasty)

Only herniotomy is indicated in pediatric hernia and hernia in young adults.

Hernia  SS Surgical

management includes— zz Treatment of hernial sac zz Reconstruction of inguinal floor.

Treatment of hernial sac SS In

indirect herina, the sac (pearly white structure lying on outer side of cord) is dissected from the card structures (pampiniform plexus, vas deferens) and cremasteric muscle. SS During posterior dissection of sac, care must be taken to avoid injury to vas and spermatic artery. SS Large indirect sac extending upto the scrotum should not be dissected beyond the pubic tubercle due to increased risk of ischemic orchitis.

Sac is identified by its pearly white color

SS Sac

is opened, taking care not to injure any hernial contents (intestine or omentum).

Sac is opened to look for any contents (intestine or omentum)

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SS Contents

are reduced, sac is dissected upto the neck (extraperitoneal fat is seen and inferior epigastric vessels on the medial side). Sac is ligated at the neck with absorbable suture.

Sac is ligated at the neck

SS Direct

sacs should not be opened or ligated, but must be freed from transversalis fibers. SS In preperitoneal approach, sac is reduced but not ligated. SS In sliding hernia, sac is opened but no attempt should be made to dissect the contents from the sac, then the sac is inverted. SS Mobilizing the testis into the inguinal canal should be avoided to minimize the risk of testicular ischemic injury.

Reconstruction of inguinal floor Primary tissue repair SS Mostly

abandoned due to high recurrence rates. indicated in strangulated inguinal hernia where mesh repair is contraindicated. SS Different approaches— SS Particularly

1. Bassini repair SS Conjoint

tendon is approximated to the inguinal ligament with the help of nonabsorbable suture (polypropylene)

Hernia 

791

2. Shouldice repair SS A

multilayer repair of the posterior wall of the inguinal canal by continuous running suture technique.

SS The

3rd layer brings together the conjoint tendon medially with the inguinal ligament laterally. SS The 4th layer brings together the anterior rectus sheath medially with the posterior aspect of the external oblique aponeurosis laterally.

3. McVay (Cooper’s ligament) repair SS Is

the only technique that repairs both inguinal and femoral hernia SS Edge of transversus abdominis is approximated to Cooper's ligament with nonabsorbable sutures.

4. Iliopubic tract repair SS Transversus

abdominis aponeurotic arch is approximated to the iliopubic tract with nonabsorbable interrupted sutures.

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Tension-free repair SS Placement

of a synthetic mesh prosthesis avoids any tension during repair—Therefore very few chances of recurrence. SS Different types of tension free repair—

1. Lichtenstein repair A piece of polypropylene mesh is placed over the floor of inguinal canal. SS Mesh is sutured to the zz Fascia overlying the pubic tubercle, inferiorly. zz Conjoint tendon, medially. zz Inguinal ligament, laterally. SS Mesh is slit at the level of internal ring, the two limbs are crossed around the spermatic cord, thus creating a new internal ring.

Polypropylene mesh (6"×3")

Lichtenstein tension free repair (prolene mesh is placed over the fascia transversalis)

Hernia 

793

2. Plug-and-patch technique SS First

described by Gilbert. SS Original Gilbert method—A mesh plug in the form of ‘upside down umbrella’ or ‘cone’ is snugly placed in the internal ring.

SS Modified

Gilbert method is—Original Gilbert method + Lichtenstein repair, also called ‘plugtenstein’.

3. Sandwich technique SS Onlay

patch is placed in the inguinal floor, underlay patch is placed in the preperitoneal space. The two patches are connected by a connector.

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Open preperitoneal approach SS Preperitoneal

space is the space between the fascia transversalis and the peritoneum. SS This approach is based on the principle that the repair fixes the hernia defect in the space between hernial contents and hernia defect. SS Indicated in recurrent inguinal hernia, sliding hernia, bilateral hernia. SS Large mesh is placed in the preperitoneal space to cover the inguinal floor and myopectineal orifice.

Laparoscopic approach SS This

approach is based on the principle of preperitoneal approach. SS Particularly indicated in bilateral and recurrent inguinal hernias. SS 2 techniques : zz TAPP Final target is same (preperitoneal space), but initial access is different zz TEP

}

In TAPP repair, the preperitoneal space is accessed after entering into the peritoneal caity

In TEP repair, the preperitoneal space is created using a balloon dissector.

Hernia 

Special Types of Inguinal Hernia Sliding Inguinal Hernia (Hernia-en-glissade) SS A

type of indirect inguinal hernia where the posterior wall of the sac is formed by the sliding visceras. SS On the right side, the cecum is most commonly involved; on the left side, the sigmoid colon; and on either side, part of urinary bladder. SS Exclusively found in males, most of them are present in the left side. [It should be suspected in any large hernia that cannot be completely reduced.] [It is essential to identify the condition early in the operation otherwise inadvertent entry into the bowel or bladder may occur.] SS After dissecting the sac from the cord, the sliding hernial sac can be reduced by series of inverting sutures (Bevan technique) and then reconstruction of the posterior wall of the inguinal canal.   Very large sliding hernia can be treated by entering the peritoneum through a separate incision, pulling the bowel back into the abdomen, fixing it to the posterior abdominal wall and then reconstruction of floor of the canal. [No attempt should be made to dissect the sliding viscera free from pertoneum, it may cause fistula or peritonitis due to devascularization.] SS High recurrence rate in compare to simple hernia.

Strangulated Inguinal Hernia SS Indirect

inguinal hernias are more commonly strangulated than direct hernias. SS The risk of strangulation is highest in the first months to years after the initial presentation. SS Usually, the small intestine is involved in strangulation. Large intestine rarely become involved. SS Treatment is resuscitation (with IV fluids, Nasosgastric suction, IV antibiotics) + surgical intervention (resection of gangrenous gut and primary tissue repair). [Mesh repair of hernia should be avoided due to increased risk of bacterial translocation and wound infection.]

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Some Unusual Types of Hernia 1. Richter’s hernia

3. Littre’s hernia

Strangulation without obstruction.

2. Maydl’s hernia

4. Pantaloon hernia

A cause of recurrence, if one of the sacs may be overlooked.

Hernia 

797

Fermoral Hernia SS Protrusion

of extraperitoneal fat or abdominal contents through the femoral canal. SS Femoral canal is surrounded by bone and ligaments on three sides. The narrowness of the sac and the rigidity of femoral ring makes it most likely to be strangulated.

SS Most

of the patients are 60–80 years old female patients. SS More common in women than men. SS May present with intermittent groin bulge or tender groin lump. [An elderly female patient presenting with small bowel obstruction, but no history of abdominal surgery—Think of occult femoral hernia.] SS On clinical examination, rounded bulge appears in the upper thigh just below the inguinal ligament, below and lateral to the pubic tubercle.

Tender femoral hernia without features of intestinal obstruction—Think of Richter’s hernia.

SS Surgery

is warranted once the diagnosis is made, because chance of strangulation is high. approaches to the hernia, but all approaches follow the same principles— zz Complete excision of hernial sac zz Inspection of the contents zz Closure of the defect in femoral canal.

SS Several

798 

Illustrated Surgery—A

Road Map

SS Incision

similar to inguinal hernia, but closer to the inguinal ligament. SS Fascia transversalis is incised along the line of incision. SS Sac is identified and after opening it, is excised. SS Femoral ring is obliterated by suturing the inguinal ligament to the Cooper’s ligament. SS Posterior wall of the inguinal canal must be reconstructed as it has been weakened by exposure.

1. Inguinal (Lotheissen)

2. Low operation (Lockwood)

Different Approaches SS Incision is 1 cm below and parallel to the inguinal ligament.

3. McEvedy

SS Vertical

incision over the swelling and extended above the inguinal ligament.

Hernia  SS Femoral

mesh.

799

ring is obliterated either by suturing the inguinal ligament to the Cooper’s ligament or by placement of

SS During

repair, laterally femoral vein and medially bladder must be protected. [Be aware about the presence of aberrant obturator artery (originates from inferior epigastric artery) during placement of medial suture, aberrant obturator artery, if present, may be injured.]

Umbilical Hernia

Different types

1. Congenital umbilical hernia

SS Congenital

2. Acquired umbilical hernia

3. Paraumbilical hernia

umbilical hernia develops when umbilical scar fail to develop or weak.

800 

Illustrated Surgery—A

SS Acquired

umbilical hernia develops when umbilical scar is stretched by raised intraabdominal pressure.

SS Paraumbilical

SS Umbilical

Road Map

hernia develops just above or just below the umbilicus.

hernia in infants and children are congenital umbilical hernia.

SS Usually, spontaneous closure of congenital umbilical hernia occurs by the age of 2 years. If defect persists even after

5 years, surgery is to be considered. SS In

adults, umbilical hernias are acquired.

SS Acquired

umbilical hernias are more common in women, usually associated with pregnancy, obesity, ascites.

SS Strangulation

is uncommon.

SS Small

asymptomatic acquired hernia need no active intervention.

SS Large

hernia, incarcerated hernia, thining of overlying skin, hernia due to uncontrolled ascites warrant repair.

SS Traditional

‘vest-over-pants’ technique by Mayo is not used nowadays due to increased recurrence rates.

SS Small

defects (≤ 3 cm) can be repaired primarily with nonabsorbable sutures after dissecting the sac from the umbilicus.

SS Larger

defect > 3 cm need repair with prosthetic mesh.

Hernia 

801

Epigastric Hernia Also called 'fatty hernia of the linea alba'.

SS This

hernia occurs through a defect in the linea alba anywhere between the xiphoid process and the umbilicus. defect develops due to weakened decussating fibers of linea alba associated with increased intraabdominal pressure or chronic strain in abdominal wall.

SS This

802 

Illustrated Surgery—A

Road Map

SS In

most cases, the hernia contains preperitoneal fat only and no sac. If sac presents, it usually contains omentum and rarely intestine. SS Middle aged male persons are mostly affected. SS Multiple epigastric hernia is not so common, but not a rare finding. [Failure to recognize the other hernial defects is the cause of ‘recurrence’.] SS In most cases, epigastric hernias are asymptomatic. It is better felt than it can be seen. In symptomatic cases, it is felt as a small, soft, reducible, mildly tender mass in the midline anywhere between xiphoid and umbilicus. This mass becomes more prominent with standing and Valsalva maneuver. SS Rarely, imaging is needed for diagnosis. If needed, then CT scan is the preferred imaging method. SS All symptomatic hernias must be repaired. SS Small defects can be repaired by primary closure using nonabsorbable suture. In larger defects (> 4 cm), the repair should be reinforced with prolene mesh.

Incisional Hernia SS Develops

at previous incision as a result of improper healing of fascial tissues. occur at any type of abdominal wall incision, increased incidence in midline, standard paramedian, transverse incisions, low incidence in appendicectomy and Pfannenstiel incisions. May also develop in tocar sites (10 mm).

SS Can

Hernia 

Factors responsible

Patient related factors • • • • • • • • • • • • • •

Operative factors

Advanced age Ascites Anemia Corticosteroid use Cancer (malignancy) Cytotoxic drugs C vitamin deficiency Cigaret smoking Debilitated state (malnutrition) Diabetes mellitus Jaundice Uremia Obesity Surgical site infection

1. Types of surgery

Elective

2. Types of incision

Emergency ↑ risk of hernia

803

804 

Illustrated Surgery—A

Road Map 3. Technique of closure

Mass closure/layered closure



Inadequate fascial bites Tension of fascial edges Excessive tight closure

}

↑↑ risk

Placement of drain or stoma in the primary operative wound— ↑ risk

4. Suture material

Absorbable/nonabsorbable

Length of suture material in respect to incision length

Hernia 

Clinical Presentation SS Appearance

of bulge over the operative scar on straining. SS In large hernias, skin may become pressure necrosed leading to ulceration. SS Sometimes present with intestinal obstruction or strangulation. SS On examination, the entire length of incision must be inspected and palpated carefully, as multiple defects may be present.

SS In

obese patients with suspected hernia, CT abdomen is helpful to make the diagnosis.

Treatment Surgical repair of hernia.

SS Three

different types of repair— Repair

1. Primary suture repair

2. Open mesh repair

Primary suture repair SS If

hernia defect 3 cm) must be repaired with mesh.

Various techniques of placing mesh

Onlay technique • Primary closure of the fascial defect ⇓ • Placing of polypropylene mesh over the fascia • Disadvantages— – Increased chance of infection – Increased chance of seroma formation – More chance of recurrence

Underlay technique

Placement of mesh in retrorectus space

Placement of mesh in preperitoneal space

Hernia 

807

SS Advantages

of underlay technique— zz Less chance of infection zz Less chance of recurrence.

Mesh should be extended 5–6 cm beyond the superior and inferior borders of the defect.

Mesh is placed in the retrorectal space

Laproscopic mesh repair SS Intraperitoneal

or preperitoneal mesh application is done in laparoscopic repair.

Polypropylene mesh in intraperitoneal position should be avoided to prevent enterocutaneous fistula formation [Preperitoneal mesh repair is the commonly used method for laparoscopic repair of incisional hernia.]

Components separation technique Particularly useful in patients with large strangulated ventral hernia where mesh application is contraindicated.

808 

Illustrated Surgery—A

Road Map

Unusual Hernia Obturator Hernia SS One

of the rarest hernias. male 6:1 — due to • broader pelvis • wide obturator canal SS Most of the hernias present in the 7th and 8th decades. SS Weakening of the obturator membrane results in enlargement of the canal and development of hernial sac. SS Female:

4 cardinal findings

1. Acute intestinal obstruction • Most common presentation • Small bowel is most frequently obstructed

2. Howship-Romberg sign

3. Recurrent episodes of intestinal obstruction

• Second most common presentation • Pain along the medial thigh due to cornpression of the obturator nerve between the canal and the sac

4. Palpable mass in medial aspect of thigh • Uncommon presentation

Another finding may be present — Hannington-kiff sign ↓ Loss of adductor reflex

An elderly female patient presents with small bowel obstruction —Think of obturator hernia. Elderly female patient with history of pain in medial thigh or history of recurrent episodes of intestinal obstruction— Think of obturator hernia. SS Usually, patient with obturator hernia presents as acute small bowel obstruction. So, most of the time this hernia is approached through a midline laparotomy approach (lower midline). SS Three operative approaches 1. Lower midline transperitoneal 2. Lower midline extraperitoneal 3. Anterior thigh exposure

Hernia 

Perineal Hernia Also termed pelvic hernia, ischiorectal hernia SS Heriniation through weakened pelvic floor.

SS Different

types of perineal hernia—

Perineal hernia

According to etiology

According to location of hernial defect Primary • Atleast 5 times more common in women due to – Broader pelvic floor – Long-term effects of pregnancy and child birth – Elongated pouch of Douglas

Secondary • More common than primary ones and develops after APR, perineal prostatectomy or pelvic exenteration

Anterior

Posterior

809

810 

Illustrated Surgery—A

Road Map

SS Anterior

perineal hernia emerges anterior to the transverse perinei muscle and presents as a swelling in posterior part of labia majora. Posterior perineal hernia presents as a bulge in perineum in men, and in women, as a bulge in the posterior vagina. [Perineal hernias must be differentiated from more common cystocele or rectocele.] SS Three approaches of repair 1. Transperitoneal—preferred method 2. Perineal 3. Combined

Spigelian Hernia SS Spigelian

hernia develops through the spigelian fascia along the semilunar line. [Semilunar line traverses along the lateral rectus border from the ninth costal cartilage to pubic tubercle.] [Spigelian fascia is an aponeurotic structure between the transversus abdominis laterally and posterior rectus sheath medially.]

SS These

hernias are often interparietal, most common type passed through the transversus abdominis and the internal oblique aponeuroses. SS Patients present with swelling in the lower abdomen just lateral to the rectus muscle. SS USG is sometimes necessary when diagnosis is in doubt. SS Treatment is repair of the defect. Primary suture repair by apposing medial and lateral edges of the internal oblique and transversus abdominis aponeuroses. Large defects need mesh repair.

Hernia 

811

Lumbar Hernia Different types

Congenital

Acquired

SS Most

Hernia through superior lumbar triangle (Grynfeltt triangle

Hernia through inferior lumbar triangle (Petit's triangle)

commonly found in older males. lumbar hernias are usually associated with—Back trauma, surgery in lumbar region, use of iliac crest as donor site. [Strangulation is rare, because three boundaries of the defect are soft and muscular.] SS Patients usually present with a soft reducible swelling in the lumbar region, size increases after straining or valsalva maneuver. SS USG or CT is usually needed to confirm the diagnosis. SS The defect is repaired by mesh repair. SS Acquired

Sciatic Hernia Herniation through greater or lesser sciatic foramen.

812 

Illustrated Surgery—A

Road Map

SS Patient

usually presents with pain in the buttock that radiates down the leg in sciatic nerve distribution or tender lump in the buttock or infragluteal region. SS Treatment is surgical (transperitoneal or transgluteal approach).

Interparietal Hernia SS Hernia

sac lies between the layers of the abdominal wall hernias are almost always interparietal SS Clinically, it is difficult to diagnose. CT is useful to make correct diagnosis SS Mesh repair or components separation technique is the surgical approach for repair. SS Spigelian

Chapter 20

Diseases of the Testes, Scrotum and Penis

Important Topics

zzUndescended Testis zzVaricocele zzHydrocele zzHematocele zzPyocele zzChylocele zzOther Scrotal Swellings zzFournier's Gangrene zzPhimosis zzParaphimosis



‘Science can never be a closed book. It is like a tree, ever growing , ever reaching new heights. Occasionally the lower branches, no longer giving nourishment to the tree, slough off. We should not be ashamed to change our methods; rather we should be ashamed to do so.’ Charles Value Chapin (1856–1941) American Physician and Public Health Officer

Diseases of the Testes, Scrotum and Penis 

815

Diseases of the Testes

Undescended Testis SS Present

any where between the abdominal cavity and just outside the anatomic scrotum of incomplete descent

SS Variations





Right sided undescended testis

Imperfect descent



Ectopic testis

Descent is arrested anywhere in the path of its Descent along the normal pathway upto external ring descent ⇓ Then, it rests on an ectopic location (superficial inguinal pouch, medial thigh, root of the penis, perineum) Ectopic testis is fully developed.

SS Is

it so common? zz Found in 3% of full-term male newborns and 30% of preterm newborns zz More prevalent in preterm, small for gestational age, low birth weight and twin neonates. SS Don't become worry, wait for atleast 3 months— zz About 70–77% of undescended testes will spontaneously descend, by 3 months of age zz By the age of 1 year, incidence of spontaneous descent become 1%. SS Brother is affected, chance is more— zz Risk is 6.9 fold if brothers is affected, risk is 4.6 fold if father is affected.

816 

Illustrated Surgery—A

Road Map

SS When

testis becomes nonpalpable? zz Testis is intraabdominal zz Absent (vanishing) testis zz Atrophic testis zz Missed on clinical examination.

Is 'Retractile Testis' Needs Attention?

Testis is retracted out of the scrotun toward the inguinal canal due to overactive cremasteric reflex.

Retracted testis can be brought down into a dependant position of the scrotum and remains there after traction is released.

Diseases of the Testes, Scrotum and Penis 

817

SS It

is not a true cryptorchid testis, not a perfectly descended testis SS Patient with retractile testis should be monitored yearly, upto puberty or till the testis no longer retractible.

How Testis Descends and Why It Maldescends? SS Testicular

descent is divided into 3 phases:

SS After



23rd weeks of gestation: Testis descends to just inside the internal ring

SS After

28th weeks of gestation: Testis travels through the inguinal canal alongside and posterior to processus vaginalis.

SS After



Factors Responsible for Testicular Descent

28th weeks of gestation: From external ring to the scrotum.

818 

Illustrated Surgery—A

SS Decreased

Road Map

cells, degenerated cells in cryptorchid testis—

zz

Changes started in between 1–2 years of age.

zz

Changes— „„

Decreased no. of Leydig cells

„„

Degenerated Sertoli cells

„„

Delayed disappearance of gonocytes

„„

Delayed appearance of adult dark (Ad) spermatogonia

„„

Developmental failure of primary spermatocytes

„„

Decreased number of total germ cell counts.

[Hypoplasia of the Leydig cells–earliest postnatal histological abnomality.]

Complications of Cryptorchidism SS Infertility—Paternity

is almost 90% in unilateral cryptorchidism, 35–65% in bilateral cryptorchidism.

SS Neoplasia—Men

with persisting or treated cryptorchidism have a relative risk of 3.6 for developing testicular cancer (seminoma); no increase in risk in men with history of spontaneous descent.

[Most common tumor in cryptorchid testis is seminoma.] SS Hernia—Patent SS Torsion

processus vaginalis is found in more than 90% of patients.

of testis— Increased susceptibility is due to developmental anatomic abnormality between the testis and its mesentery.

Diseases of the Testes, Scrotum and Penis 

819

Where is the Cryptorchid Testis?

SS Patient

must be examined in supine, sitting and also in squatting position SS Examiner's palpating fingers are to be swept down from just above the internal ring along the inguinal canal into the scrotum SS Examiner may feel the testis moving back under the fingertips or a 'pop' as the testis retracts back into its cryptorchid position SS Ectopic areas of descent must be examined

SS Less

SS Accuracy

SS Options

accurate (44%) USG MRI

SS With

Check that the following queries have answered: SS Unilateral or bilateral? SS Imperfect descended testis or ectopic testis? SS Testis palpable or not? SS Are other abnormalities present or not? SS Are associated penile malformations present?

>95% the existing ports, the procedure can be converted to a therapeutic procedure

820 

Illustrated Surgery—A

Road Map

When to Treat, How to Treat and Why SS Definitive

treatment should be started between 6 and 12 months of age, particularly in bilateral or unilateral intraabdominal testis (to preserve most of the testicular tissues).

SS Child

presenting after this time period also must be treated by orchiopexy to prevent further testicular impairment (spermatogenic as well as endocrinal) and to attain the scrotal position for easy palpation (early detection is possible if any malignant transformation). Orchiopexy does not reduce the risk of development of cancer.

SS Orchiectomy

is indicated only for postpubescent patients with contratateral normally descended testis.

Diseases of the Testes, Scrotum and Penis 

821

Standard Orchiopexy (Open Approach)

Operative picture showing complete mobilization of spermatic cord and testis

Placement of testis in dartos pouch

Fowler–Stephens Orchiopexy (One Stage/Two Stage Procedure) SS Indicated

in high inguinal or intraabdominal testis. SS In one stage procedure, ligation of the testicular vessels is done with a wide pedicle of peritoneum to preserve the collateral circulation (deferential artery, a branch of inferior vesical artery; cremasteric artery, a branch of inferior epigastric artery). SS In two stage procedure, ligation of spermatic vessels is done as close to origin as possible. After 6 months or more (allow to grow collaterals), the testis is mobilized and placed in the dartos pouch.

822 

Illustrated Surgery—A

Road Map

Torsion of the Testis (Syn. Torsion of the Spermatic Cord) SS Torsion

of the testis is a true surgical emergency. Irreversible ischemic injury to the testis may develop as early as after 4 hours of torsion. SS Predisposing factors: 1. High investment of tunica vaginalis—

2. Epididymis with a pedicle—



SS How

Torsion is confined to pedicle that connects the testis with epididymis No torsion of the cord

torsion develops? zz When there is sudden contraction of cremasteric muscle (following trauma, athletic activity, lifting a heavy weight, sexual intercourse) ⇓ Spiral attachment of cremaster onto the cord favors rotation around a vertical axis (as much as 360°)

Diseases of the Testes, Scrotum and Penis 

zz

823

Also develop spontaneously (in sleep). In many cases, adolescent boys are awakened from sleep after developing torsion.

SS Patient

presents with—Acute onset scrotal pain associated with nausea and vomiting. Many patients had history of previous episodes of selflimited acute scrotal pain. SS On examination, high lie of the testis and thickened, tender, twisted cord that can be palpated above the testis. Absence of cremasteric reflex is a good clinical sign. Torsion and acute epididymo-orchitis present almost similarly. So torsion must be differentiated as it is a true surgical emergency. Elevation of testis reduces pain in epididymo-orchitis but it is not a reliable clinical finding. SS When torsion is suspected, Color Doppler study is to be done as early as possible (specificity 98.8%). If there is any doubt about diagnosis, the scrotum should be explored urgently. SS On exploration, testis with good or marginal viability must be preserved and after detorsion, it must be placed in dartos pouch and fixed with fine, nonreactive, nonabsorbable suture. If necrotic testis is found, orchidectomy should be done. Contralateral hemiscrotum must be explored and the testis must be fixed to prevent subsequent torsion.

Varicocele SS When SS How

SS Left

veins of the pampiniform plexus becomes ectatic and tortuous, it is called varicocele. varicosity develops—

side is affected in 95% of cases. SS Tall, thin men with pendulous scrotum are more frequently develop varicocele. SS Most of the varicoceles are asymptomatic. Most of them discovered during routine physical examination for preemployment check up. SS Patient must be examined in both supine and standing position, with and without a valsalva maneuver. SS On clinical examination, it is manifested as painless compressible mass (consistency of a "bag of worms") above or surounding the testis, that decompresses when patient is in supine position.

824 

Illustrated Surgery—A

Road Map

SS Grading—

I. Small, palpable only after valsalva maneuver II. Moderately sized, easily palpable without a valsalva maneuver III. Large, visible through the scrotal skin. SS Assessment of testicular consistency and volume is very much crucial

Subjective

Can be assessed by Prader or disk orchidometer

SS Testis

volume measurement is the mainstay of assessment of whether surgical intervention is needed or not. SS If ipsilateral testis volume loss > 2 ml — Adolescent varicocele ablation is needed. SS Treatment options —Different options, but same outcome.

Varicocele is approached through inguinal approach

Diseases of the Testes, Scrotum and Penis 

825

Hydrocele SS Abnormal SS Different

SS Due

collection of fluid in tunica or processus varginalis. types:

to delayed closure of processus vaginalis ⇓ Fluid trapped within the tunica vaginalis SS Commonly seen at birth. SS Tense, nontender swelling. SS Transillumination positive. SS Most of them resolve mithin 2 years of life. SS If surgical intervention is indicated it must be intervened through inguinal approach.

SS Persistence

of processus vaginalis allows peritoneal fluid to communicate with the tunica vaginalis. SS Classic description is that, the swelling is smaller in the morning and becomes more prominent as day progresses. SS Communication is too small to allow herniation of intraabdominal contents. SS Most communicating hydroceles close spontaneously by 1 year of age. SS All persistent communicating hydroceles must be explored through inguinal incision.

SS Due

to segmental closure of processus vaginalis. SS Manifested as painless groin swelling contiguous with the cord structures. SS Can be palpated at any position just above the testis to superficial inguinal ring. SS Swelling moves downwards and becomes less mobile when testis is pulled downwards. SS Exploration must be done through inguinal approach. Ligation of the processus vaginalis at internal ring and excision or unroofing of the cyst is the treatment. [Hydrocele of the canal of Nuck is the counterpart in females.]

826 

Illustrated Surgery—A

Road Map

Primary Vaginal Hydrocele SS Most

common in middle and later life. SS Develops due to defective absorption of fluid in tunica vaginalis. (imbalance between secretion and absorption)

SS Nontender

scrotal swelling, 'get above the swelling' present, transillumination positive.

Typical color of fluid in primary vaginal hydrocele

Diseases of the Testes, Scrotum and Penis 

827

Operatic picture of Jaboulay's procedure

828 

Illustrated Surgery—A

Road Map

Secondary Hydrocele SS It

is due to Epididymorchitis Testicular tumor Filaria SS Clinically, lax hydrocele and underlying testis is palpable SS Best treated by treating the cause of the hydrocele. [A young patient with lax hydrocele—Always exclude testicular tumor before any surgical interventions.]

Hematocele SS Bloody

fluid in tunica vaginalis SS Usually develops following trauma SS Drainage is the treatment of choice.

Pyocele SS Pus

in tunica vaginalis SS Drainage of pus after opening the tunica vaginalis is the treatment. SS Sometimes, orchidectomy is needed.

Chylocele SS Develops

following rupture of lymphatic varix resulting in discharge of chyle into tunica vaginalis SS Fluid is rich in cholesterol SS Treatment is rest and aspiration.

Other Scrotal Swellings SS Epididymal

cyst Cystic degeneration of epididymis zz Usually both epididymis are involved zz Contains crystal-clear fluid, therefore briliantly transilluminant zz If cyst causing symptoms, then only it should be excised. zz

Diseases of the Testes, Scrotum and Penis  SS Cyst

of a testicular appendage zz Usually unilateral zz Globular swelling at the superior pole. zz Liable to torsion, so early intervention is indicated.

SS Spermatocele

Unilocular retention cyst contains spermatozoa Always present in the head of epididymis zz Clinically palpable as a soft, cystic lesion, above and behind the upper pole of testis zz If it becomes larger, patient may feel it as a 'third testis' zz Smaller ones need observation. Larger ones need to be aspirated or excised. zz zz

Other Scrotal Diseases Idiopathic scrotal gangrene (Fournier's gangrene) SS Sudden onset gangrene, resulting in sloughing out of scrotal skin. SS It is basically a variety of necrotizing fascitis involving male genitalia and perineum. Testis is not involved. SS Cause is unknown in most of the cases. SS Precipitating factors— zz Procedures in the perineal or periurethral area (e.g. urethral dilatation, sclerotherapy of hemorrhoids) zz Diabetes mellitus zz Immunocompromised state. SS Organisms most commonly found— Staphylococcus, hemolytic streptococcus, E. coli, C. welchil. SS Parenteral broad-spectrum antibiotics and debridement are the treatment. Reconstruction is indicated if extensive tissue loss develops. Sebaceous cyst in scrotum SS Scrotum is a common site for sebaceous cyst SS Single cyst is excised SS If small, multiple cysts involve a part of scrotal skin, that part of skin is excised along with cysts. Multiple sebaceous cyst in scrotum

829

830 

Illustrated Surgery—A

Road Map

Carcinoma of Scrotum SS Also called 'chimney sweeper's cancer' or 'mule-spinner's cancer'. SS Workers using tar and shale oil are at more risk. SS Carcinoma starts as a wart or ulcer. SS Treatment is wide excision ± bilateral inguinal block dissection upto external iliac group of lymph nodes.

Phimosis SS Inability

to retract the foreskin over the glans penis.

SS Upto 3–4 years, a physiological phimosis present because of natural adhesion between prepuce and gland (preputial

glanular adhesion). SS Accumulation of epithelial debris and intermittent penile erection gradually make the foreskin more retractable. SS By the age of 3 years, 90% of the foreskin are retractable. SS Phimosis after 4–5 years, phimosis with balanoposthitis, topical corticosteroids to the foreskin 3–4 times daily for 6 weeks loosens the phimotic ring in about 80% of cases. SS Phimosis after age 7 years resistant to topical corticosteroid, phimosis with ballooning of foreskin or recurrent balanitis— Circumcision is strongly indicated. Circumcision should not be performed— zz In neonates with hypospadias zz Chordee without hypospadias zz Dorsal hood deformity zz Webbed penis zz Micropenis zz Neonate with large hydrocele or hernia. SS Other indications of circumcision— zz Religious reason—In muslims and jews zz Prior to radiotherapy for carcinoma penis—To expose the glans zz In suspected penile growth— To perform incisional biopsy from the lesion.

After circumcision

Diseases of the Testes, Scrotum and Penis 

831

Paraphimosis SS Develops

SS Arterial SS Manual

when a tight prepuce is retracted beyond the corona that cannot be reduced to its normal position.

supply to glans may be compromised, so emergency reduction must be done. compression of edematous foreskin followed by forceful reduction of foreskin is sucessful in most of the

cases. SS If reduction fails, then the constriction ring is incised or circumcision have to be done. SS If manual reduction is successful, patient must be informed about the necessity of circumcision, but that procedure is better to be deferred till swelling subsides.

Chapter 21

Diseases of the Esophagus

Important Topics

zzHiatus Hernia zzGastroesophageal Reflux Disease zzEsophageal Motility Disorder zzEsophageal Diverticula zzEsophageal Perforation zzCancer of esophagus

‘Everything should be made as simple as possible, but not simpler.’

834 

Illustrated Surgery—A

Road Map

Hiatus Hernia SS Hiatus hernia develops when a lax or defective phrenoesophageal membrane allows herniation of stomach through

the esophageal hiatus of the diaphragm. commonly develop in women of 5th and 6th decades.

SS Most

Different Types

Type II

Type I SS Focal

defect in phrenoesophageal ligament (defect in anterior and lateral to esophagus). SS Gastroesophageal junction is anchored within the abdomen.

SS Phrenoesophageal

ligament is intact but lax. SS Gastroesophageal junction is above the diaphragm. Most common type of hiatal hernia. Type III SS More

common than type II.

Diseases of the Esophagus 

835

Clinical Presentation SS Patient

with sliding hiatal hernia presents with symptoms related to gastroesophageal reflux (heartburn, regurgitation, dysphagia). SS Type I and III hernias present with postprandial pain or bloating, early satiety, difficulty in breathing during food intake, dysphagia. SS Herniated gastric part is susceptible to volvulus (organoaxial), obstruction, infarction. SS About one third of patients with paraesophageal hernia become anemic, due to recurrent bleeding from ischemic longitudinal ulcers in the mucosa of herniated stomach (Cameron ulcer).

Detect the Hernia— Presence and Type 1. Presence of air-fluid level in the posterior mediastinum in lateral view of chest X-ray— Think of hiatal hernia. 2. Contrast esophagogram— gives information about the extent of hernia, location of gastroesophageal junction and type of hernia. It also gives functional information by assessing gastric emptying and evidence of gastroesophageal reflux. [Contrast study is more accurate in detecting paraesophageal hernia because it is a permanent herniation of stomach into thoracic cavity.] 3. Endoscopy— Fiberoptic esophagoscopy is very much useful for diagnosis and classification of hiatal hernia.

Identification of pouch lined with gastric rugal folds at least 2 cm proximal to the crura—Sliding hiatal hernia. Type I hiatal hernia.

On retroversion of the scope, a separate orifice adjacent to gastroesophageal junction identified and where gastric rugal folds ascend— Type II hiatal hernia.

The scope is entering the pouch through a separate orifice proximal to the crura— Type III hiatal hernia.

836 

Illustrated Surgery—A

Road Map

4. Manometry is not mandatory for evaluation of paraesophageal hernia.

Management 1. Asymptomatic sliding hernia—No treatment required 2. Symptomatic sliding hernia warrants hiatal hernia repair 3. All patients of type II, III, IV require surgical intervention.

Approach

Abdominal

Open

Thoracic

Laparoscopy

Operative principles SS As

much as hernial sac is removed without injuring pleura, esophagus and inferior pulmonary veins. SS Crura is reapproximated with nonabsorbable interrupted suture or defect is closed with prosthetic material. SS As more than half of the patients of paraesophageal hernias have associated GERD and hypotensive LES, most of the Surgeon perfer associated antireflux procedure.

Diseases of the Esophagus 

837

Gastroesophageal Reflux Disease (GERD) SS GERD

is one of the common upper gastrointestinal disorders worldwide.

How it Develops?

Clinical Presentation SS Typical

symptoms: Heartburn, regurgitation, dysphagia. Substernal or epigastric burning pain that is aggravated in lying down position and promptly relieved after taking antacids— Is the classic symptom. SS Atypical symptoms: Cough, wheezing, chest pain, hoarseness. SS On clinical examination, no specific findings found.

838 

Illustrated Surgery—A

Road Map

Investigations to Confirm Diagnosis 1. GERD can be reliably diagnosed if— Patient having typical symptoms + Alleast one objective evidence of reflux (abnormal esophageal acid exposure on 24 hour pH monitoring/visible esophagitis on endoscopy). Or, patient having atypical symptoms + two objective evidence of reflux. 2. Upper gastrointestinal endoscopy—To evaluate for esophagitis and presence of Barrett's esophagus. New Savary–Miller classification of reflux esophagitis Grade 1— Single or multiple erosions on a single fold Grade 2— Multiple erosions affecting multiple folds Grade 3— Multiple circumferential erosions. Grade 4— Ulcer, stenosis or shortening of esophagus Grade 5— Barrett's epithelium. 3. Esophageal pH testing— zz Gold standard for diagnosing GERD. zz Electrodes are placed in the esophagus and they are capable of sensing pH fluctuations. zz Several informations are collected (e.g. total no. of reflux episodes, largest episode of reflux, extent of reflux in upright and supine position). zz With the help of Demeester scoring, GERD is diagnosed or excluded. 4. Esophageal manometry— zz Is indicated when surgery is planned. zz Can define the location and function of LES and helps to exclude other esophageal motility disorders. zz Can also assess the status of esophageal contractility and peristatic wave progression, so that Surgeon can choose the best antireflux procedure. 5. Contrast study— zz Can detect the presence of haital hernia as well as any evidence of strictures and ulcers. 6. Esophageal impedance measurement— zz Multiple intraluminal impedance (MII) is a technique to detect the flow of gas and liquid through a lumen zz MII combined with pH monitoring is the most sensitive method for diagnosis of GERD.

Diseases of the Esophagus 

Treatment

SS Avoid lying down after taking

meals. SS Avoid postural maneuvers (bending, straining) that aggravate reflux. SS Head of the bed to be elevated to 6–8 inches. SS Obese patients are advised to lose weight.

SS Avoid

fatty foods, alcohol, caffeine, chocolate. SS Avoid smoking. SS Eat smaller amount more frequent meals.

Surgical management SS Is

indicated if— Manometric evidence of defective LES zz No relief after maximal medical management zz Respiratory complications zz Presence of Barrett's esophagus. zz

SS H

receptor antagonists pump inhibitors SS Prokinetic agents. 2

SS Proton

839

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Road Map

Diseases of the Esophagus 

841

Esophageal Motility Disorder

1. Achalasia 2. Vigorous achalasia 3. Diffuse and segmental esophageal spasm 4. Hypertensive lower esophageal sphincter.

1. Secondary to collagen vascular diseases 2. Secondary to neuromuscular diseases.

Achalasia (Faliure to Relax) SS Most

common primary esophageal motility disorder. SS Best understood and best known primary motility disorder of esophagus. SS Etiology is unknown. SS Characterized by loss of effective esophageal peristalsis and failure of LES to relax, resulting in impaired esophageal emptying and gradual esophageal dilation.

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Road Map

[In Hirschsprung's disease, dilated colon contains normal ganglion cells, constricted part is aganglionic.] SS Characteristic pathology is loss of ganglion cells in Aurbach plexus. SS Increased risk of malignant transformation, particularly squamous cell carcinoma. SS Patients usually present with classic triad of symptoms— 1. Dysphagia—Initially with liquids and then progress to solids. Stress and cold liquid exacerbate dysphagia. 2. Regurgitation—Regurgitation of undigested foods with foul odor tends to regurgitate after meals and in supine position. 3. Weight loss Other symptoms—Pneumonia, lung abscess, bronchiectasis may develop in longstanding achalasia due to recurrent aspiration. [Rapid onset of symptoms with significant weight loss—Suspect pseudoachalasia (secondary to malignancy or extraluminal obstruction)] SS Investigations to confirm diagnosis— zz Esophagogram— „„ Dilated esophagus with a distal narrowing 'bird's beak' appearance. „„ Lack of peristaltic waves in the body and failure of relaxation of LES. „„ Lack of gastric air bubble. „„ In advanced stage, massive esophageal dilation, sigmoidal esophagus (megaesophagus) is seen. ['Birds beak' appearance is not specific for achalasia, but seen in other pathologies also (e.g. benign stricture, carcinoma).] zz Esophageal manometry— „„ Gold standard investigation. „„ Characteristic findings— –– Elevated LES pressure –– Incomplete relaxation of LES in response to swallowing –– Absence of peristalsis in body of esophogus –– Elevated intraesophageal pressure. zz Endoscopy— „„ Must be performed to rule out strictures or malignancy. „„ Characteristic findings Atonic, dilated esophagus with a tightly closed LES that fails to open with insufflation. With gentle pressure, the scope can be admitted.

Diseases of the Esophagus 

843

Treatment SS Treatment SS Goal

is directed to relieve the symptoms, not to correct the pathology. of all treatments is to relieve the functional obstruction of distal esophagus.

Different treatment options

1. Medical • Nitrates and Ca2+ channel blockers • Botulinum injection.

2. Endoscopic • Pneumatic graded balloon dilation.

3. Surgical • Heller myotomy • Modified Heller myotomy.

SS Medical—

Nitrates and calcium channel blockers „„ Relax smooth muscle and thus decrease lower esophogeal sphincter pressure transiently. zz Botulinum toxin type A injection into LES „„ Botulinum blocks acetylcholine release from nerve terminals. [Medical therapy can be used for extended periods if patient is not suitable for definite treatment.] SS Endoscopic— zz Under fluoroscopic guidance, pneumatic polyethylene balloon (30 mm) are passed through LES and then inflated, causing disruption of fibers of LES. „„ Single dilatation for each session. Multiple sessions of dilatation are required. zz

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SS Surgical— zz

Heller myotomy (originally described by Ernest Heller) Two myotomies along the GE junction (anterior and posterior)

„„

zz

Modified heller myotomy (only anterior myotomy).

SS Approaches—

Transthoracic Transabdominal zz zz



Open

Laparoscopic [preferred approach due to excellent visualization of distal esophagus and stomach]

SS Associated

antireflux procedure is necessary or not? zz Most surgeons prefer an associated antireflux procedure zz Total (Nissen) or partial (Dor or Toupet) fundoplication?

Diseases of the Esophagus 

845

SS A

partial one, particularly Toupet (posterior) fundoplication is preferred by most surgeons.

Vigorous Achalasia SS A

varlant of achalasia SS Patients present with clinical and manometric features of classic achalasia and diffuse esophageal spasm SS Patients also may present with spastic pain and more severe dysphagia SS Treatment is a longer esophagomyotomy (proximal extension upto the aortic arch).

Diffuse Esophageal Spasm SS Loss

of normal peristaltic coordination resulting in simultaneous contraction of segments of the esophageal body.

SS Patients

present with severe spastic pain, dysphagia, regurgitation and weight loss. SS Diagnosis is confirmed by esophageal manometry zz Characteristic finding – Spontaneous, repetitive, prolonged, high amplitude contractions. SS Barium esophagogram may reveal classic ‘corkscrew’ esophagus. SS Mainstay of treatment is nonsurgical: zz Pharmacologic/endoscopic + treatment of associated psychiatric disorders (depression, anxiety, etc.) nitrates, calcium channel blockers, anticholinergics are used as pharmacologic therapy. SS Surgery is only indicated when patients not responding to medical treatment. Long esophagomyotomy [proximal extension upto the aortic arch] along with Dor (anterior, partial) fundoplication is the surgery of choice.

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Nutcracker Esophagus SS Hypermotility

disorder characterised by high amplitude (> 180 mmHg), prolonged (>6s) peristaltic contractions present with chest pain and dysphagia SS Peristaltic contractions 2 standard deviations above the normal values in manometric study is diagnostic 2+ SS Treatment is medical (Ca channel blocker, nitrates, antispasmodics) [Caffeine, hot foods, cold should be avoided as these factors trigger abnormal peristaltic contractions.] SS Patients

Esophageal Diverticula SS Diverticula

are focal pouches of esophageal wall consisting of mucosa, submucosa and sometimes muscular coat types— zz According to location „„ Pharyngoesophageal diverticulum [Zenker’s] „„ Parabronchial [midesophageal] „„ Epiphrenic [supradiaphragmatic] zz According to pathophysiology „„ Traction diverticula [resulting from an extrinsic process]— They are true diverticula (consists of mucosa, submucosa and musculoris). „„ Pulsion diverticula [resulting from elevated intraluminal pressure]— They are false diverticula (consists of mucosa and submucosa only)

SS Different

Pharyngoesophageal (Zenker’s) Diverticulum SS It

is a pulsion diverticulum. common esophageal diverticulum. SS This diverticulum herniates through the killian’s triangle—triangle formed by oblique fibers of the thyropharyngeus muscle and horizontal fibers of cricopharyngeus muscle. SS Most

Diseases of the Esophagus  SS Diverticulum

847

develops due to loss of coordination during the second stage of swallowing. Loss of coordination during 2nd stage of swallowing

Loss of tissue elasticity (in old age)

Killian triangle is exposed to high pressure

Diverticula formation—Diverticula emerges through the left side of the esophagus into the superior mediastinum

SS Patients

present with progressive cervical dysphagia, cough on recumbent position, spontaneous regurgitation of undigested food. SS Barium esophagogram is useful modality for diagnosis. SS Esophagoscopy is indicated only when malignancy is suspected. SS Surgical or endoscopic repair is the treatment, regardless of size. [Dohlman procedure] SS If diverticulum is small (< 2 cm), myotomy alone is sufficient.

SS If

diverticulum is large, myotomy and diverticulectomy or diverticulopexy is indicated.

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Midesophageal (Parabronchial) Diverticula SS It

is a traction diverticula. in conjunction with mediastinal granulomatous diseases (eg. tuberculosis, histoplasmosis).

SS Develops

SS Most

of the patients are asymptomatic. SS Lateral view of barium esophagogram is needed to assess the size and location of diverticula. SS CT is helpful to identify mediastinal structures as well as diverticula. Manometric study is required in all patients to rule out primary motor disorder. SS Diverticulum < 2 cm — Can be observed. SS Diverticulum > 2 cm — Diverticulopexy is indicated.

Epiphrenic Diverticulum SS It

is a pulsion diverticulum SS Typically present within the distal 10 cm of thoracic esophagus. SS Develops due to high intraluminal pressure secondary to a relatively distal obstructon. SS Most patients are asymptomatic. The diverticulum is often diagnosed as incidental finding during workup of a motility disorder. SS Contrast esophagogram is essential for diagnosis, but manometric study and endoscopic examination are also indicated to assess the underlying physiology. SS Asymptomatic, small (< 2 cm) diverticula do not need any surgical intervention.

Diseases of the Esophagus  SS Patients

with symptoms, documented motor abnormality warrants surgical intervention.

Esophageal Perforation It is a surgical emergency. SS Etiologies:

Intraluminal causes— SS Instrumentation (75%) zz Endoscopy zz Dilatation for stricture zz Sclerotherapy for varices zz Stent insertion. SS Ingested caustic substances (Alkali) zz Causes liquefaction necrosis. SS Foreign bodies—From sharp objects (e.g. fish bone) zz Erosion due to impacted bolus. SS Barotrauma —Induced by Heimlich maneuver, forceful vomiting, during childbirth SS Cancer of esophagus SS Medications — NSAIDS, etidronate, potassium chloride. Extraluminal causes— SS Penetrating injuries, most commonly gunshot wounds SS Blunt trauma — Due to compression between sternum and spine SS Iatrogenic — During thyroidectomy, vagotomy, fundoplication. [Absence of true serosa makes the esophagus more susceptible to perforation.]

849

850  SS Site

Illustrated Surgery—A

Road Map

of perforation—

SS Clinical

presentation depends on the location of injury and time interval since occurence of injury zz Injuries in cervical esophagus usually present with subcutaneous emphysema in neck, dysphagia or odynophagia, pain in neck and stiffness. zz Thoracic perforations present with shortness of breath and retrosternal chest pain. zz Abdominal perforations usually present with symptoms and signs of acute abdomen. zz History of recent esophageal instrumentation along with these symptoms and signs — Suspect esophageal injury. SS Make early diagnosis— zz Early diagnosis can reduce the morbidity and mortality. zz Plain X-ray of neck, chest may reveal subcutaneous emphysema in neck and mediastinum, free gas under diaphragm, pleural effusion. zz Contrast esophagogram (in upright and lateral decubitus position). [Barium is used for suspected thoracic perforation and gastrograffin for abdominal perforation.] [Barium is inert in chest but may cause peritonitis, gastrograffin can cause pneumonitis.] zz High index of clinical suspicion but esophagogram is equivocal ⇒ CT chest is indicated. zz Endoscopy is planned when esophagogram is inconclusive and surgical intervention is planned.

SS Management:

1. Conservative 2. Surgical zz Conservative management— [All patients with suspected perforations need initial conservative measures] „„ IV fluids „„ Broad-spectrum antibiotics „„ Catheterization „„ Nil per mouth „„ Access for TPN „„ Nasogastric decompression.

Diseases of the Esophagus 

SS Then

851

think —Conservative measures to be continued? Or proceed to surgical intervention? SS Consider following points to take decision— zz Patient stable or not? zz Location of perforation zz Leakage is contained or not? zz Underlying esophageal disease (e.g. distal obstruction, malignancy) present or not? SS Stable patient with minimal symptoms and contained perforation may be treated with conservative measures SS If surgery is planned, consider which one is appropriate— Primary repair SS The first 24 hours is the golden period for primary closure SS At any time, during surgical exploration, healthy tissue bed is found—Primary closure may be considered. Muscle flap SS If tissue bed is friable, severe mediastinitis—Muscle flap to be considered. Exclusion? resection? SS If primary repair not feasible or muscle flap fails —Cervical esophagostomy + gastrostomy/feeding jejunostomy ⇒ Delayed reconstruction.

Management of Cervical Perforation SS Approach—Incision

parallel to the anterior border of left sternocleidomastoid.

SS Basic

steps of repair — Thyroid, trachea and larynx are retracted medially and carotid sheath laterally zz Primary repair + drainage (closed suction drain) zz If no perforation is identified, only drainage.

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Management of Thoracic Perforation SS Approach—

Through right chest for upper two-thirds of esophagus. zz Through left chest for lower third of esophagus. SS Different methods— zz Primary closure with muscle patch zz T-tube enterocutaneous fistula formation zz Exclusion and diversion zz Resection. zz

Primary closure with muscle flap

T-tube enterocutaneous fistula formation

SS In

extensive injuries, perforation associated with malignancy—Resection may be considered if patient is stable. SS In unstable patient with severe contamination and delayed presentation—Cervical esophagostomy + drainage of mediastinum + gastrostomy + feeding jejunostomy.

Diseases of the Esophagus 

853

Management of Abdominal Perforation SS Approach SS Basic

through chest or abdomen principles are same.

What is Boerhaave’s Syndrome? SS Professor

Hermann Boerhaave first described this syndrome. SS Postemetic rupture of esophagus is classically described as Boerhaave’s syndrome. Similar events occur after blunt thoracic injury, seizure, childbirth. SS Increased intrathoracic esophageal pressure causes perforation.

What is Mallory-Weiss Tear? SS Tear

in esophageal mucosa following persistent retching, paroxysmal coughing. and Weiss first described this syndrome. SS This tear is characterized by arterial bleeding, so bleeding may be severe. SS Upper GI endoscopy confirms the diagnosis (one or more longitudinal fissures in the mucosa which are the source of bleeding.) SS In most of the cases, bleeding stop spontaneously. SS Endoscopic epinephrine injection in the tear site is helpful. In some cases, surgical intervention (oversewing the tear) is indicated. SS Mallory

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Stricture of esophagus

Benign

Malignant

Congential • Due to presence of congenital web (as a result of inappropriate canalization of esophagus during development)

Acquired 1. GERD 2. Corrosive ingestion 3. Iatrogenic (after esophagectomy, sclerotherapy for varices, after radiation therapy) 4. Schatzki’s ring 5. Medications (potassium chloride, quinidine, ferrous sulfate, NSAIDs) 6. Sarcoidosis 7. Infection (Candida albicans)

Schatzki’s ring—A concentric ring at the squamocolumnar junction, consists of inflammatory cells and fibrous tissue in mucosa and submucosa. Commonly found in association with hiatus hernia. Usually detected in barium swallow study and in esophagoscopy]

SS Clinical

presentation Dysphagia to solid food is the typical presenting feature zz In advanced stage, dysphagia to liquid develops. SS Diagnosis zz Barium swallow should be the initial investigation —Can evaluate the location, number and length of strictures zz Esophagoscopy is also essential to assess the location, length, distensibility and to obtain biopsy or brushings. zz

Diseases of the Esophagus 

855

Treatment

Surgery

Dilatation • Most of the strictures are amenable to dilatation • 2 types of dilators (dilators fracture the fibrous tissue of stricture)

Bougies

• Indicated for recurrent or persistent strictures • The preferred technique is esophagectomy followed by colon interposition between cervical esophagus and stomach Balloon dilators

What is Barrett Esophagus? SS Replacement

of distal esophageal stratified squamous epithelium by metaplastic columnar epithelium containing goblet cells. SS It is a complication of long standing GERD.

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SS Many

Road Map

patients are asymptomatic and undiagnosed males are commonly affected. SS Complications— 1. Barrett ulcer „„ Penetrating ulcer in metaplastic columnar epithelium „„ Can cause bleeding, perforation. 2. Stricture „„ Located in squamocolumnar junction. 3. Dysplasia „„ Dysplasia may be low or high grade. 4. Carcinoma „„ Risk of developing adenocarcinoma is 50–100 times that of general population. SS Diagnosis—By endoscopy and biopsy. Repeat endoscopy and biopsy often required as Barrett mucosa is quite focal and variable. Identification of dysplastic changes in Barrett mucosa is very much crucial for early detection of malignant change. Digital chromoendoscopy (narrowband imaging type) paired with manification endoscopy has high diagnostic precision for the diagnosis of high grade dysplasia in Barrett’s esophagus. SS Treatment— 1. Asymptomatic patient, no complication „„ No specific therapy „„ Annual endoscopic surveillance and biopsy. 2. Symptomatic patient, no complication „„ Antireflux surgery + annual endoscopic surveillance and biopsy. 3. Barrett ulcer „„ Proton pump inhibitors „„ Nonhealing ulcer warrants rebiopsy from ulcer + antireflux surgery. 4. Stricture „„ Esophageal dilation + medical therapy „„ Recurrent stricture needs antireflux surgery and repeated dilation. 5. Dysphagia „„ Low grade dysplasia needs 3 monthly surveillance endoscopy and biopsy + medical therapy for GERD „„ High grade dysplasia needs definite intervention (surgery/photodynamic therapy). 6. Carcinoma „„ Esophagectomy. SS White

Diseases of the Esophagus 

857

Cancer of Esophagus SS Esophagus

is a unique organ because it covers three anatomic compartments: Neck, thorax and abdomen.

SS Esophageal cancer is unique among GI malignancies because it may present two distinct histopathologic varieties—

Squamous cell carcinoma and adenocarcinoma.

Risk Factors Tobacco and alcohol use SS Independent risk factor for squamous cell carcinoma SS Risk factor for adenocarcinoma SS Quiting smoking decrease the risk of squamous cell carcinoma, but not the risk of adenocarcinoma. [Tobacco + alcohol – highest risk of squamous cell carcinoma] SS Alcohol is an independent risk factor for squamous cell carcinoma SS Amount of alcohol, type of beverage have relationship with risk SS No risk of adenocarcinoma in use of alcohol. Dietary factors SS Deficiency of vitamins (A, C, E) SS Deficiency of trace metals (zinc, molybdenum, selenium) SS Fungal contamination of foods SS Presence of nitrosamines and their precursors (nitrate, nitrite). Esophageal disorders SS GERD—One of the strongest risk factors of adenocarcinoma SS H. pylori infection—H. pylori (particularly cag A + strain) is related to adenocarcinoma SS Barrett esophagus—Single most important risk factor for adenocarcinoma SS Tylosis—An autosomal dominant disorder characterized by hyperkeratosis of palm, sole and esophageal papilloma. SS Plummer-Vinson syndrome—Characterized by iron-deficiency anemia, glossitis, cheilitis, splenomegaly and esophageal webs. [About 10% of patient develop esophageal epidermoid carcinoma.] SS Corrosive stricture—Squamous cell carcinoma may develop after lye stricture, usually 40–50 years after injury SS Achalasia—16–30 fold ↑ risk of developing squamous cell carcinoma. Human papillomavirus infection SS Responsible for squamous cell carcinoma in high-incidence regions. Other aerodigestive malignancies SS Patient with other aerodigestive malignancies are at a risk of developing squamous cell carcinoma, most likely due to exposure to similar environment carcinogens and field cancerization.

Pathology SS Squamous

cell carcinoma and adenocarcinoma are the commonest types. cell carcinoma usually affects the upper two-thirds (cervical, upper and middle third of thoracic esophagus). Adenocarcinoma affects the lower one-third. SS Incidence of adenocarcinoma is in a increasing trend.  SS Squamous

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Classification of Esophageal Tumors

Clinical Presentation SS Most commonly present with progressive dysphagia—Initially difficulty in swallowing solids, then liquids and lastly

saliva. SS Weight loss. SS Symptoms of local invasion and distant metastases— zz Odynophagia, dull retrosternal pain, cough, hoarseness of voice. SS Unusual presentation— zz Pneumonia (due to tracheoesophageal fistula) zz Exsanguinating hemorrhage (due to aortic invasion). [Dysphagia usually develops late in the disease process, because lack of serosal layer allows smooth muscle to dilate more.]

Investigations to Confirm Diagnosis SS Esophagogram—

Barium esophagogram must be the initial study in any patient with dysphagia Helpful to differentiate whether the lesion is intraluminal or extraluminal zz The classic ‘apple-core lesion’ is highly suggestive. SS Endoscopy and Endoscopy guided biopsy— zz Location or site of the lesion zz Nature of the lesion can be assessed zz Relationship of lesion to the cricopharyngeus, GE junction and cardia. SS Biopsy along with cytologic brushings—Can be performed. zz zz

Diseases of the Esophagus 

859

Pretreatment Staging SS Staging

is for determination of zz Extent of disease zz Depth of esophageal wall involved zz Regional lymph node status zz Presence or absence of distant metastases. SS For staging, following investigations are helpful: 1. CT scan of chest, abdomen and pelvis „„ Can detect liver and lung metastases „„ Can detect peritoneal carcinomatosis „„ Highly accurate for detection of aortic and tracheobronchial involvement. 2. Endoscopic ultrasonography „„ EUS is highly accurate in both T and N staging and is superior to CT. „„ Biopsy can be taken from the tumor mass as well as from the lymph node. 3. FDG–PET „„ The accuracy in assessing regional lymph nodal status is superior than CT, but not so accurate like EUS „„ Superior to CT in detecting distant metastases „„ Useful modality for evaluating response to chemo and radiotherapy. 4. Bronchoscopy „„ Indicated for tumors in upper and middle esophagus to rule out involvement of membranous trachea and tracheoesophageal fistula.

Treatment 1. Treatment of high grade dysplasia and T1 disease— zz Different options: a. Intensive surveillance b. Mucosal ablation c. Endoscopic mucosal resection (EMR) d. Minimally invasive esophagectomy. a. Intensive surveillance „„ Serial endoscopy at 3 – 6 monthly interval + multiple four-quadrant biopsies. [Serial endoscopy can detect the cancer at an earlier stage.] b. Mucosal ablation „„ This method eliminates the premalignant mucosa and allows to regenerate squamous epithelium. „„ Different techniques of ablation: −− Photodynamic therapy −− Multipolar electrocoagulation −− Laser (Nd : YAG) −− Argon beam.

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c. Endoscopic mucosal resection (EMR) „„ By separating the lesion from underlying muscular layer using submucosal injection of fluid Or, by using suction to trap the mucosal lesion. d. Minimally invasive esophagectomy „„ Most definite intervention „„ Different approaches: −− Laparoscopic −− Thoracoscopic −− Combined laparoscopic and thoracoscopic. [No significant role of radiation therapy and chemotherapy in T1 disease] 2. Treatment of localized resectable disease (T1–2, N0)— zz Localized, resectable cancer in cervical esophagus is rarely found at the time of management because of early invasion of larynx, trachea and great vessels. zz T1–2 and without lymph node involvement in middle third of esophagus—Resection is the treatment (transhiatal esophagectomy or transthoracic esophagectomy video assisted thoracic surgery). zz T1–T2 in lower esophagus and cardia – Resection includes cervical division of esophagus and proximal gastrectomy. [GI tumors have increased propensity to submucosal spread] 3. Treatment of locally advanced disease– (T1–3, N1) between 6–8 weeks Resection zz Preoperative chemotherapy (cisplatin + 5-FU) + radiation, [Before 6 weeks, due to inflammation, resection because hazordous. After 8 weeks, scarring in the perioesophageal tissue makes dissection difficult]. 4. Treatment of disseminated disease (any T, any N, M1) zz Grade I – III dysphagia—Chemoradiation zz Grade IV and more—Indwelling esophageal stents zz Dysphagia due to cancer at GE junction—Stent must be avoided to prevent severe gastroesophageal reflux. Radiation therapy alone is sufficient. zz For feeding access—Laparoscopic jejunostomy.

Minimally invasive transhiatal esophagectomy SS Five

or six small incisions in upper abdomen for port introduction and one transverse cervical incision for removal of specimen and for cervical esophagogastrostomy. SS Laparoscopic creation of 4 cm neoesophagus (gastric conduit). SS A vein stripper is passed from the neck down into the abdomen followed by inversion of the esophagus in the posterior mediastinum and removal through the neck. SS Gastric conduit is delivered to the neck with a chest tube and anastomosed to the cervical esophagus in a end-to-side fashion.

Diseases of the Esophagus 

861

Minimally invasive two and three field esophagectomy SS In

three field esophagectomy, the esophagus is dissected along its length with dissection of lymph nodes in upper, middle and lower posterior mediastinum, with division of azygos vein— zz Thoracic dissection—Is done through a mini thoracotomy at sixth intercostal space (right) with the help of conventional surgical instruments. Videoscope is accessed through the ninth intercostal space (right). zz Abdominal—Abdominal part of the operation is similar to minimally invasive transhiatal esophagectomy. zz Cervical gastric conduit is delivered to the neck and anastomosed to the cervical esophagus. SS In two-field esophagectomy— zz Abdominal—Creation of gastric conduit. zz Thoracic—Through right thoracotomy, the esophagus is dissected and then anastomosis (stapled) is done in high thorax.

Open transhiatal esophagectomy SS Division

of the diaphragmatic crus allows enlargement of the hiatus. This is essential because, the esophageal dissection is performed with the finger tips rather than surgical instruments. SS Lower mediastinal and upper abdominal lymph node basins can be resected. The mediastinal lymph nodes above the inferior pulmonary vein can not be resected. SS Creation of gastric conduit and techniques of anastomosis are same as minimally invasive transhiatal esophagectomy.

Ivor Lewis (en bloc) esophagectomy SS Midline

laparotomy Lymphnode dissection around celiac trunk and its branches, around porta hepatis and along the splenic artery, along lesser curvature of stomach ⇓ zz Greater curvature gastric conduit is constructed SS Anterolateral thoracotomy [through right 6th intercostal space] SS Azygos vein is divided ⇒ Resection of thoracic duct; periaortic tissues; peribronchial, hilar and tracheal lymph nodal basins ⇒ Gastric conduit is pulled up into the thorax and anastomosis is done between upper thoracic esophogus and gastric conduit. zz

Three field open esophagectomy SS Similar

to minimally invasive three field esophagectomy except that all accesses are through open incisions. [The advantage of placing a anastomosis in neck—Leakage of anastomosis is unlikely to create a severe systemic effect.] SS Anastomosis in high chest minimized the risk of injury to vital structures of neck particularly RLN.

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MIS 3 field esophagectomy

Road Map

MIS 2 field esophagectomy

Open transhiatal esophagectomy [orringer’s]

Ivor Lewis (en bloc) esophagectomy

Diseases of the Esophagus 

Three field open (Mckeown’s) esophagectomy

Creation of gastric conduit

863

Chapter 22

Diseases of the Salivary Gland

Important Topics

zzInflammatory Pathologies zzObstructive Pathologies zzSalivary Gland Tumors zzSurgical Procedures

‘Education is what remains after one has forgotten everything he learned in school.’

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Salivary Gland Pathologies

SS Salivary

glands consist of— zz Paired parotid, submandibular, sublingual glands. zz Tiny accessory glands all over the oral mucosa. SS Diseases of salivary glands are due to— zz Inflammation zz Obstruction and trauma zz Neoplasm.

Inflammatory Pathologies SS Inflammatory

pathology of salivary gland are due to— zz Viral infection zz Bacterial infection zz Autoimmune causes.

Viral Sialadenitis SS Most

commonly caused by mumps virus (a paramyxo virus) affect all salivary glands but predominantly affects both parotid glands SS Childhood mumps is a self-limited disease. In adults, it may cause bilateral orchitis. SS May

Acute Ascending Bacterial Sialadenitis SS Mostly

affects the parotid glands. salivary flow and oral sepsis resulting in bacterial colonisation in parotid duct, gradually parotid parenchyma is affected (pathophysiology of acute sialoadenitis in postoperative patients).

SS Reduced

Diseases of the Salivary Gland 

867

SS Nowadays,

poorly fitting dentures is one of the causes of acute sialoadenitis organism is Staphylococcus aureus or Streptococcus viridans SS Patients present with tender, red parotid swelling associated with fever and regional lymphadenopathy. SS Infecting

SS USG

shows characteristic dilation of the acini [Sialography should not be done during acute phase of infection.] SS If patient presents before abscess formation, antibiotics are useful SS If abscess develops, the pus must be drained

SS Small

transverse incision to avoid injury to facial nerve. [As abscess develops in the superficial part of the gland, during drainage, chance of facial nerve injury is low.]

Chronic Bacterial Sialadenitis SS More

common in the submandibular salivary gland and usually secondary to chronic obstruction SS Submandibular gland has increased tendency to chronicity following infection.

Autoimmune Sialadenitis SS Seen

in Sjögren syndrome syndrome is characterized by— zz Keratoconjunctivitis sicca zz Xerostomia zz Bilateral parotid swelling zz Rheumatoid arthritis.

SS Sjögren

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Road Map

Rare Causes of Sialadenitis SS Infective

causes Mycobacteria zz Cat-scratch disease (caused by Bartonella henselae) zz Syphilis zz Toxoplasmosis (caused by T. gondii) zz Deep mycoses zz Sarcoidosis. SS Radiation sialoadenitis SS HIV-associated sialoadenitis. zz

Obstructive Pathology SS Sialolithiasis SS Mucoceles.

Sialolithiasis SS About

80% of sialolithiasis occur in the submandibular gland, 10% in the parotid gland, rest in the minor salivary gland. SS Most of the sialolithiasis occur in the submandibular gland, because— zz Secretions contain mucus and more viscous zz Gland lies below the opening of its duct.

[Calculus composed of: Mucus, bacteria, calcium and magnesium phosphates, cellular debris.]

SS Classic presentation is acute pain and appearance of swelling beneath the

jaw within a minute of starting the meal; both pain and swelling resolves after the meal but the pain resolves earlier. SS This classic presentation is seen only when there is complete obstruction.

Diseases of the Salivary Gland 

869

SS On

examination, in early periods of obstruction, the gland is not palpable in between meals SS Later, a chronically infected gland becomes palpable with rubbery hard consistency.

Bimanual palpation SS To know the relations of the lump to the floor of the mouth and tongue SS To feel the course of the duct in the floor of the mouth to note any discharge from the orifice of the duct. SS Plain

X-ray of jaw is all that is required, because most of the submandibular calculi (about 80%) are radioopaque. No further investigation is necessary. SS Majority of parotid stones are radiolucent. SS In equivocal cases, sialography is indicated.

Treatment

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Mucoceles SS Mucus

retention or extravasation cysts arise as a result of damage of minor salivary gland or its ducts. SS Most commonly present on the mucosal aspect of lower lip and in the posterior buccal mucosa. SS Treatment is excision of the cyst along with underlying minor glands.

SS Ranula

is a large mucocele arising as a result of ruptured sublingual gland. SS Classically, ranula presents as large, tense, bluish, translucent, spherical swelling in the floor of the mouth. SS Occasionally, ranula extends through the myelohyoid muscle and enter the submental space, presenting as a swelling in upper neck. This type of ranula is called ‘plunging ranula’.       SS Treatment is excision of ranula along with sublingual gland.

Diseases of the Salivary Gland 

871

Salvary Gland Treatment Salivary GlandTumors Tumors SS Tumors arise from both major salivary gland (parotid, submandibular

and sublingual) as well as from minor salivary glands. SS Majority of salivary gland tumors arise from parotid gland. zz Majority of parotid gland tumors are benign (about 70–80%), about 50% tumors of submandibular and sublingual glands are benign, whereas only 25% tumors arising from minor salivary glands are benign. [Smaller the salivary gland, more likely the tumor to be malignant.] SS Most of the salivary gland tumors arise from ductal lining epithelium and underlying myoepithelial cells.

Classification of salivary gland tumors

Benign

Epithelial tumors • Pleomorphic adenoma • Warthin’s tumor • Oncocytoma • Basal cell adenoma • Clear cell adenoma

Malignant

Nonepithelial tumors • Neural sheath tumor • Hemangioma • Lipoma • Lymphangioma

Low grade • Mucoepidermoid carcinoma • Acinic cell carcinoma

High grade • Adenoid cystic carcinoma • Adenocarcinoma • Squamous cell carcinoma • Undifferentiated carcinoma

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Clinical Presentation SS Parotid

tumor usually present with slow growing, well-circumscribed painless swelling in the parotid region with rubbery hard consistency. SS Facial nerve palsy, skin invasion are suggestive of malignancy. Lymph node metastasis is uncommon in low grade salivary malignant tumor (intra and periglandular, level II). SS Submandibular and sublingual gland tumors present with slow-growing, well circumscribed, painless swelling in the neck or floor of the mouth. zz Bimanual palpation is essential to evaluate the relationship of the tumor with floor of mouth, tongue and mandible. zz Numbness in anterior two-thirds of the tongue suggests infiltration of the lingual nerve by malignant submandibular tumor. Level Ia, Ib, II, III groups of lymph nodes may be involved. „„ Minor salivary gland tumors present as painless mass in the oral cavity, mostly at the junction of hard and soft palate.

Investigation SS CT and MRI, both are useful maging methods. They can define the extent of tumor, relationship of tumor to adjacent

structures, status of cervical lymph nodes. MRI is more sensitive than CT. zz FNAC is useful to rule out malignancy. As facial nerve sacrifice may be necessary in malignant parotid tumors, preoperative councelling is Indicated when a surgeon is planning for resection of malignant tumor. SS Open surgical biopsy is contraindicated to avoid microscopic spillage of tumor cells in surrounding tissues.

Diseases of the Salivary Gland 

873

Pleomorphic Adenoma SS It

is a true adenoma of the parotid gland. SS It consists of epithelial cells mixed with myxoid, mucoid and chordroid elements (that is why termed as pleomorphic’ or mixed). SS It is a well demarcated encapsulated lesion wtih incomplete capsule. The tumor has projections that protrude beyond the capsule through the defects. [This feature limits the scope of enucleation of the tumor and warrants excision of the involved lobe of the gland.]

SS This

tumor develops at any age with equal male: female ratio. two-third of parotid tumors and half of submandibular tumors are pleomorphic adenoma. SS A slow growing, painless smooth mass rubbery hard consistency, present in the typical site-between angle of mandible and mastoid process. SS Rarely, this tumor may undergo malignant change. SS This tumor is susceptible to recurrence. SS About

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Warthin’s Tumor (Adenolymphoma) SS It

is benign tumor of the parotid gland. develops only in the parotid gland. SS A tumor of elderly population with a male: female ratio 4:1. SS This tumor contains 2 components: 1. Epithelial element (originated from embryonic parotid ducts which have separated from main ductal system). 2. Lymphoid element (originated from normal lymph tissues). SS Usually develops in the lower part of the parotid gland, level with the lower border of the mandible, soft in consistency. SS Malignant transformation is rare. SS It

Oncocytoma SS A

benign slow growing tumor of the major salivary gland SS The tumor consists of acini or tubules of large cells with glandular eosinophilic cytoplasm (termed as ‘oncocyte’).

Carcinoma of Salivary Glands SS Can

be classified as low grade and agressive carcinoma. SS Low grade malignancies are mucoepidermoid carcinoma and acinic cell carcinoma. SS Aggressive malignancies are adenoid cystic carcinoma, adenocarcinoma, squamous cell carcinoma and undifferentiated carcinoma. SS These aggressive malignancies have a poor prognosis regardless of treatment. SS Mucoepidermoid carcinoma zz It is the most common malignant salivary gland tumor. zz Adults (age 30–60 years) are more commonly affected, but it is also the most common malignant salivary tumor in pediatric population. zz Based on aggressiveness, this tumor exists in any form: Low grade and high grade. Low grade mucoepidermoid carcinoma is composed of predominantly mucin secreting cells, whereas in high grade tumors, epidermoid cells are more abundant. SS Adenoid cystic carcinoma zz Second most common malignant salivary gland tumor zz This tumor has typical propensity for neural invasion zz Distant metastasis is more common than other maligant salivary tumors. SS Carcinoma ex pleomorphic adenoma zz An aggressive malignant tumor arises from a benign mixed tumor. zz Malignant transformation develops in later age (6th decade) zz It more often develops in recurrent tumors.

Diseases of the Salivary Gland 

Nonepithelial Tumors SS In

chilhood, hemangioma and lymphangioma may develop in the salivary gland SS Hemangioma usually regresses by the age of 2 years, but lymphangioma needs excision SS Neurofibroma and neurilemmomas may develop in the adults. Malignant lymphoma SS Most of the salivary gland lymphomas develop in the parotids SS Treatment is total parotidectomy and adjuvant radiotherapy.

Surgical Procedures for Salivary Gland Pathology Excision of Sublingual Gland SS A

linear incision is made in the floor of the mouth just lateral and parallel to the submandibular duct. The incision should not be extended beyond the 1st molar tooth to avoid injury to the lingual nerve.

875

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SS The

submandibular duct, sublingual gland and lingual nerve is identified SS The sublingual gland is mobilised from the inner cortex of the mandible.

[Avoid injury to the submandibular duct and lingual nerve.]

Excision of Submandibular Gland SS A

horizontal skin crease incision atleast 3 cm below the ramus of the maindible to avoid injury to the mandibular branch of facial nerve.

[Avoid injury to marginal mandibular branch of facial nerve]

SS Facial

vein lies superficial to the gland and it is ligated and divided.

SS Facial

artery is dissected from the deeper surface of the gland and is ligated above and below. SS The superficial part of the gland is dissected off mylohyoid. SS Mylohyoid is retracted anteriorly to expose the deeper part of the gland and its duct. Lingual nerve is now becomes visible.

[Avoid injury to lingual nerve]

SS Hypoglossal

nerve is also visible at the lower part of the operative field, but in a deeper plane.

Diseases of the Salivary Gland 

[Avoid injury to the hypoglossal nerve.]

Submandibular duct is ligated as anterior as possible. zz The only attachment of the gland, part of facial artery is again ligated at the lower border of the posterior pole of the gland, and is removed along with the gland. zz

Superficial Parotidectomy SS Preauricular

SS Anteriorly,

incision extending downwards in the neck (lazy ‘S’ incision)

skin and platysma flap is elevated to expose the parotid gland along with parotid fascia.

[Avoid injury to the branches of facial nerve emerging from the anterior border of the gland.]

The principle of superficial parotidectomy is to— 1. Identification of facial nerve before it enters the gland 2. Following the nerve and it’s branches, the gland is dissected superficial to the fasciovenous plane.

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Identification of facial nerve SS Method No. 1 A plane is made anterior to the external auditory meatus and dissection is done just superficial to styloid process and stylomastoid formen. This plane is then opened in inferior direction by blunt dissection till facial nerve is visible. SS Method No. 2 This method is particularly suitable when the tumor is large with posterior extension. Inferior pole of parotid is lifted off from sternocleidomastoid muscle through the cervical extension of the incision. Great auricular nerve is visible in this stage and needs sacrifice. Anterior border of sternocleidomastoid is retracted inferiorly, then posterior belly of digastric is identified.

SS Digastric

muscle is traced upwards to backwards upto its insertion to mastoid which lies immediately below the stylomastoid foramen. zz The nerve can also be located 1 cm medial and inferior to the ‘pointer’ of tragal cartilage. SS After leaving the stylomastoid foramen, the nerve becomes more superficial and divides into zygomaticofacial trunk and cervicofacial trank.

Dissection of parotid SS The five branches of facial nerve are followed peripherally throughout the parotid. SS Between each branch of the nerve, the parotid tissue bridging between superficial and deep lobe must be divided carefully. SS Use of unipolar diathermy is contraindicated during dissection. Ligature or bipolar diathermy must be used for hemostasis. SS Following removal of superficial lobe, the nerve trunk and its branches can be seen.

SS If

deep lobe is involved, total parotidectomy to be done by retracting the nerve with slings. SS If nerve is injured or partially excised, primary suturing or nerve grafting (using great auricular nerve or sural nerve) using operating microscope. SS During total parotidectomy for malignant tumor, only branches that directly invaded must be sacrificed without disturbing others.

Chapter 23

Skin and Adnexal Lesion

Important Topics

zzCystic

Lesions of the Skin

zzGanglion zzVascular zzBenign zzSkin

Lesions of the Skin

Tumors

Infection

zzBenign

Pigmented Lesions

zzPremalignant zzMalignant

Lesions

Lesions

‘If you cannot explain it to a six year old, you don’t understand it yourself.’

Skin and Adnexal Lesion 

881

Diseases of the Skin and its Adnexa

Cystic Lesions of the Skin Sebaceous cyst (epidermal inclusion cyst) SS A retention cyst formed as a result of obstruction of the pilosebaceous follicles → gland becomes distended by its own secretion. SS Develop in all ages. SS Can develop wherever there are sebaceous gland, but commonly occur in face, scalp, neck, scrotum. [Palm of hands and sole of the feet devoid of sebaceous glands.] SS On clinical examination, the cyst is smooth, soft or firm and sometimes a pathognomonic punctum (attached to skin).

Sebaceous cyst with punctum SS Complications

are infection, Cock’s peculiar tumor and sebaceous horn. is excision of the cyst with complete cyst wall removal. [retained cyst wall may cause cyst recurrence.] SS Infected cyst (commonly found organisms are Staphylococcus, group A streptococcus, E. Coli, peptostreptococcus, bacteroides) can be safely excised with antibiotic coverage and proper wound care. SS Treatment

[A length to width ratio of 3:1 is necessary to make the ellipse]

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What is sebaceous horn? SS Content of the cyst exudes slowly from a large punctum ⇓ become dry and harden to take a shape of conical spike

What is Cock’s peculiar tumor? SS An infected, open, granulating sebaceous cyst. SS Granulation tissue arising from the lining of the cyst bursts through ruptured cyst and makes the lesion an angry looking lesion with an everted edge. SS It looks like a squamous cell carcinoma. [Epidermal inclusion cyst may be associated with Gardner syndrome, so individuals with extensive cysts warrant GI neoplasm work up.]

Dermoid Cyst Congenital dermoid cyst SS Congenital

dermoid cyst arise from separated epidermal cells during fusion of the embryonic clefts and therefore found at the lines of fusion. SS External angular and at the root of the nose are two most common sites of this cyst. SS Cyst contain thick opaque mixture of sebum, sweat and desquamated epithelial cells. SS Soft, nontender, cystic swelling, not fixed to the skin but fixed to the underlying bone. SS Rarely, the cyst has a intracranial communication. So a skull X-ray or CT is essential to exclude this. SS Excision of the cyst is the treatment of choice.

Dermoid cyst in external angular region

Skull CT is indicated to exclude extracranial communication

Skin and Adnexal Lesion 

Implantation dermoid cyst SS It

is an acquired dermoid cyst, develops following an injury. SS Injury results in implantation of epithelial cells into the subcutaneous tissue. SS The cysts are often found in tailors, gardeners. SS In most of the cases, patient can’t remember the event of injury. SS Overlying skin is often scarred. SS Excision is the treatmentof choice.

Ganglion SS A

unilocular, nonneoplastic, pseudocystic swelling as a result of cystic, myxomatous degeneration of synovial tissue in relation to joints or tendons. SS Most commonly located in dorsum of the wrist, followed by volar wrist, flexor tendon sheath. SS Clinically, it is a nontender, smooth, firm swelling not fixed to the overlying skin. SS On compression, a ganglion may slip away between deeper structures, giving the false impression that the contents have reduced into the joint. [A true ganglion is not connected with the joint.]

Ganglion in dorsum of wrist

883

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SS Mobility

of ganglion is restricted when the underlying structures (joint capsule, tendon sheath) becomes tense. SS Treatment is excision or threading or intralesional sclerosant injection. SS Definite therapy is excision of the stalk of the ganglion and debridement of the synovial origin. SS In Dorsal wrist ganglion—Excision of the stalk followed by debridement of dorsal wrist capsule over the scapholunate ligament. SS In volar wrist ganglion—Excision of the stalk followed by debridement of volar wrist capsule over the radioscaphocapitate ligament. [Protection of radial artery and superficial radial nerve is crucial during excision.]

After excision of ganglion

Vascular Lesions of the Skin SS Hemangiomas SS Vascular

malformations

SS Ectasia SS Other

lesions.

Hemangiomas SS They

basically arises due to endothelial hyperplasia SS They are benign vascular neoplasm.

Skin and Adnexal Lesion 

885

Strawberry nevus (Capillarycavernous angioma) SS Small red mark is noted usually 1–3 weeks after birth, that rapidly increasing in size over a few weeks to take the shape of a strawberry.

Strawberry nevus is intradermal collection of dilated vessels

SS Raised,

compressible, nonpulsatile lesion covered with smooth, pitted epithelium, commonly found in face, scalp and neck region. SS About 90% of the lesions regress spontaneously over time (within 5–9 years) with accepted cosmetic outcome. SS Treatment is conservative except in lesions causing difficulty in vision, feeding. Those lesions warrant early surgical intervention.

Strawberry nevus

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Vascular Malformations

Vascular malformations SS Structural

abnormalities due to aberrant morphogenesis in embryological period. SS Lesions present at birth, grow in proportion to the body and do not regress. SS Different types according to hemodynamic characteristics— zz High-flow lesion [Arteriovenous malformation, arteriovenous fistula.] zz Low-flow lesion [Capillary malformation, venous malformation, lymphatic malformation] „„ Port-wine stain –– These are intradermal capillary malformation. –– Histologically, they are collections of ectatic capillaries lined by mature endothelium. –– Commonly present in face, shoulder, neck. Sometimes, they are confined to a single dermatome (along a trigeminal distribution in face). –– Occasionally, they present as a part of syndromes— `` Sturge-Weber syndrome (leptomeningeal angiomatosis, epilepsy, glaucoma). `` Klippel-Trenaunay syndrome (varicose vein, limb hypertrophy, port-wine stain). Port-wine stain is intradermal collection of ectatic capillaries –– Treatment is pulsed dye laser therapy.

Skin and Adnexal Lesion 

887

Ectasia –– Dilated vessels but normal endothelial turnover. Spider nevus SS They are solitary dilated skin arteriole feeding a number of small branches. „„

SS This

lesion typically found in preschool and school-aged children. SS They are present in the drainage area of SVC (upper half of trunk, face, arm). SS After release of compression, it fills from the center outwards. [Systemic examination should be done becaue it is associated with liver diseases (cirrhosis, hepatic tumors). SS Spontaneous resolution may happen; if treatment is indicated, pulsed dye laser is the treatment.

zz

Venous malformations Most common type of vascular anomalies. „„ Venous malformations usually present as blue, soft, compressible lesion. „„ Histologically, venous malformations are composed of thin-walled, dilated, sponge-like alonormal channels with surrounding smooth muscle. „„ MRI is the most useful imaging modality. „„ Treatment is sclerotherapy and surgery. „„

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Lymphangioma SS Cluster of dilated lymph sacs in the skin and subcutaneous tissues, not connected with the main lymphatic system. SS Large, translucent lymph cysts mostly found in the neck—Known as ‘Cystic hygroma’. SS Lymphangioma is classified according to size— 1. Microcystic (1 cm) 3. Combined. SS Lymphangiomas are commonly located in cervicofacial region (70%–80%), axilla, chest, mediastinum, buttock. SS Prenatal USG can detect macrocystic lymphangiomas at second or third trimester. USG can detect presence of macrocystic lymphangiomas, but MRI is the most useful imaging modality. SS Treatment—(1) Sclerotherapy (2) Surgery zz Sclerotherapy—Sclerotherapy acts by obliterating lymphatic lumen by endothelial destruction followed by fibrosis. „„ Commonly used sclerosants are—sodium tetradecylsulfate, ethanol, bleomycin. „„ Sclerotherapy is more effective in macrocystic lymphangiomas. Repeated sessions of sclerotherapy are required to achieve satisfying result. zz Surgery—Staged excision is often necessary. During surgery, surgeon must keep in mind few principles— Attempts to minimize blood loss, focus on a defined anatomic region, thorough dissection as possible.

Other Vascular Lesions a. Campbell de Morgan spots zz Bright red, small spots in upper half of the trunk, in middle aged and elderly persons zz No clinical significance. b. Salmon patch zz Present at birth and regresses completely at the age of 1 year zz Found in forehead and occipital region.

c. Pyogenic granuloma Acquired lesion of skin and mucous membrane develops after a minor trauma. At the phase of healing of ulcer or wound, sometimes capillary loops grow rapidly, thereby forming a protruding lesion consists of capillaries covered by epithelium. This mass becomes infected and forms a pyogenic granuloma. zz Typical natural history is usually present— „„ History of minor injury → appearance of nontender lump that rapidly grows → bleeds on minor touch. zz zz

zz

Treatment is excision.

Pyogenic granuloma

Skin and Adnexal Lesion 

889

d. Glomus tumor zz A tumor arises from glomus body [glomus body, an arteriovenous shunt in the skin that have a role in temperature regulation, are present throughout the skin with special preference in fingers and toes] zz Small, firm, bluish-gray, extremely tender nodules mostly found in subungual region. The clinical triad of— (1) Hypersensitivity to cold (2) Paroxysmal pain and (3) Pin point pain suggestive of glomus tumor. zz Three clinical tests can be performed for diagnosis— 1. Love's test— Pressure is applied over the tumor by pin/paper clip ⇒ severe pain (positive result). 2. Hildreth's test—Touruiquet is applied proximal to the tumor site ⇒ Love's test is performed ⇒ No pain (positive result). 3. Cold sensitivity test—Increased pain with exposure to cold. zz As they are extremely tender, these malformations must be excised.

Arteriovenous malformations AVMs are high-flow vascular malformations consist of disorganized arteries and veins that communicate. „„ AVMs are manifested as warm, pink patch in the skin with underlying thrill or bruit. „„ A clinical staging system exists: Schobinger clinical staging system for AVMs Stage I (quiescence) Pink-bluish stain, warmth, and arteriovascular shunting by continuous Doppler scanning or 20 MHZ color Doppler scanning. zz

„„

Stage II (expansion)

Same as stage I plus enlargement, pulsations, thrill, bruit and tortuous/tense veins.

Stage III (destruction)

Same as stage II plus either dystrophic skin changes, ulceration, bleeding, persistent pain, or tissue necrosis.



Stage IV (decompensation) Same as stage III plus cardiac failure. SS Doppler USG can detect the fast flow of AVM. CT, MR angiograply can also detect the presence of AVMs. SS Treatment is angiographic embolization alone or in combination with surgical excision. zz Treatment is indicated if symptoms (e.g. ischemic changes, pain, intermittent bleeding, ulceration) are present or endangering signs (e.g. recurrent ulceration, increased cardiac output, Schobinger stage III and IV) are present.

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Benign Tumors Papilloma SS Overgrowth

of all layers of skin with a central core of cannective tissue, blood vessels and lymphatics. epithelial proliferation, it is thrown into folds and takes the shape of a papilloma. Along with epithelial proliferation, the connective tissue and blood vessels grow.

SS With

Papilloma SS It

may present as sessile or pedunculated polypoidal lesion.         

SS Surgery

is indicated if the lesion is cosmetically unacceptable or vulnerable to injury.

Skin and Adnexal Lesion 

Lipoma SS It

is composed of adult type fat cells. SS Lipoma may present any where in the body, that is why it is also called 'universal tumor'.

SS Different

types— 1. According to presence of edge „„ Encapsulated lipoma [has a definite edge] „„ Diffuse lipoma [no definite edge]. 2. According to number „„ Solitary. „„ Multiple lipomatosis [multiple lipomas of different sizes are present particularly in the trunk]. 3. According to presence of other tissues „„ Angiolipoma „„ Plemorphic lipoma „„ Fibrolipoma „„ Neurolipoma „„ Nevolipoma „„ Myelolipoma. 4. According to location „„ Subcutaneous lipoma – Commonest type – Commonly found in the shoulder, back. „„ Subfascial lipoma – Present deep to palmar and plantar fascia. „„ Subsynovial lipoma—in the knee. „„ Intraarticular lipoma. „„ Intermuscular lipoma—In thigh or shoulder. „„ Retroperitoneal lipoma. „„ Submucous lipoma—Deep to mucous membrane of alimentary tract or respiratory tract.

Lipoma

Lipoma after excision–lobulated pattern is obvious

891

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SS Complications—

Myxomatous degeneration Saponification zz Calcification zz Sarcomatous change (rare). SS On clinical examination, lipomas are usually spherical shaped, lobulated, slips away from examining finger (slip sign). SS Investigation— zz Typical subcutaneous lipoma does not need preoperative imaging. Imaging (USG/CT/MRI) is indicated if lipoma > 5 cm, irregular in shape or myofascial involvement. MRI is the most sensitive imaging modality. SS Surgery is mostly indicated for cosmetic reason. Other indications of surgery are—Nerve impingement, pain, functional limitation, increase in size, case needle biopsy showing atypical histology, involvement of deep fascia. SS Uncommon varieties of lipoma— zz Adiposis dolorosa (Dercum’s disease)—It is characterized by tender multiple lipomas in the trunk. zz ‘Lipoma aborescens’—Pedunculated subcutaneous lipoma. SS Uncommon varieties of adipose tissue tumors— zz Hibernoma—Benign tumor composed of brown fat zz Lipoblastoma—Benign tumor composed of immature adipocytes. SS Syndromes associated with lipoma— 1. Adiposis dolorosa 2. Gardner syndrome 3. Madelung disease 4. Bannayan-Riley-Ruvalcaba syndrome (BRRS). zz zz

Skin and Adnexal Lesion 

Neurofibroma SS Solitary

benign tumor arising from connective tissue of a nerve sheath (epineurium) 

      SS Contains both neural (ectodermal) and fibrous (mesodermal) elements SS Present as tender, subcutaneous, nodular swelling, most freely moves in right angle to the course of the nerve Patient may present with tingling sensation in the distribution of the nerve from which it arises.

SS Treatment

is excision of the tumor Increased tendency for local recurrence zz Sarcomatous changes rerely develop in neurofibroma, particularly in multiple neurofibromatosis. zz

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Multiple Neurofibromatosis This multiple, congenital, familial (autosomal dominant inheritance) neurofibromatosis is also called von Recklinghausen’s disease. SS This is type 1 neurofibromatosis with mutation in chromosome 17. SS

SS It

arises from endoneurium.

Multiple neurofibromatosis–some nodules having malignant transformation SS Characterized

by zz Multiple cutaneous neurofibromas zz Cutaneous hyperpigmented macules ('cafe' au 'lait spot) zz Pigmented nodules of the iris (lisch nodule) zz Gliomas of the optic nerve. SS Patients present with nodules of varying sizes from a milimeter sized to large varieties. Some of them in the skin, some are subcutaneous and few of them become pedunculated. SS Examination of the spinal nerve and hearing tests are essential to exclude major nerve involvement. SS Patient with NF 1 gene have a greater chance of malignant transformation of the tumors. SS Tumor with ulceration, large pedunculated and tumor with sarcomatous changes need excision.

Plexiform Neurofibromatosis SS Excessive

overgrowth of neural tissue in subcutaneous fat commonly seen in relation to distribution of trigeminal nerve, sometimes seen in extremities SS Presents as a folded, irregular mass hanging from the face with hyperpigmentation SS The nerves are heavily thickened due to myxomatous degeneration of endoneurium SS Very rarely, sarcomatous changes may develop. SS More

Skin and Adnexal Lesion 

Elephantiasis Neurofibromatosis SS Rare,

congenital variety of plexiform neurofibromatosis SS Skin becomes coarse, dry and thickened and resembles an elephant’s skin.

Skin Infection

Furuncle (boil) SS Staphylococcal

infection of pilosebaceous unit with perifolliculitis. proceeds to suppuration and then central necrosis. SS Commonly present in back and neck. SS Usually presents as tender, indurated swelling around a hair follicle with surrounding edema. Within a few days, the center softens, after that it bursts spontaneously. SS Commonly associated with generalised debility and diabetes mellitus. SS Incision is usually not necessary for drainage of pus. Local application of iodine aggravates spontaneous rupture. SS Removal of affected hair follicle also helps in drainage. SS Antibiotics coverage against staphylococcus is indicated in blind boil (boil without suppuration). SS Infection

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Impetigo SS Intradermal

bacterial infection caused by staphylococcus and streptococci. SS Commonly involves the hand and face. SS Presents as vesiculopustular lesion and then ruptures and then formation of characteristic yellowish crust. SS Treatment is washing the lesion and removal of crust with chlorhexidine lotion.

Carbuncle SS Infective

gangrene of the subcutaneous tissue with multiple openings in the skin. SS Usually caused by Staphylococcus aureus, sometimes streptococci and gram-negative bacilli are responsible. SS Commonly found in back, nape of the neck (vitality of the tissues are less in these region).

SS Older

diabetic patients are commonly affected. and local application of magnesium sulfate (helps to decrease the edema and softening the center of carbuncle) is necessary in initial stage. SS Surgical intervention is needed if the infection not responds to conservative management. SS Antibiotics

Carbuncle

Skin and Adnexal Lesion 

897

Hidradenitis Suppurativa SS Chronic

infection of the apocrine sweat glands due to blockage of the ducts of apocrine glands (compound sweat glands). SS More common in women in tropical countries. Perianal hidradenitis suppurativa is more common in men. SS Most commonly found in axilla, but may also develop in groins, perianal regions (all apocrine gland bearing regions). SS Patients present with multiple swellings in the axilla, which eventually discharges pus and then subsides spontaneously or after treatment. The swellings again appear after a few months. SS Maintaining local hygiene and avoiding of deodorant, depilation, shaving is important for preventing recurrence. Erythromycin along with metronidazole are useful for controlling infection. SS If conservative treatment fails and there is frequent episodes of infection, excision of the affected skin followed by split thickness skin grafting is indicated.

Necrotizing Fasciitis (Fournier’s Gangrene) SS Invasive

infection of skin, subcutaneous tissue and deep fascia but sparing of muscle by beta hemolytic streptococci, coliforms and anaerobes. SS Common sites are Genitalia, groin and lower abdomen. SS Predisposing factors are – Diabetes mellitus – Corticosteroid use – Malnutrition – Immunodeficiency disorders. SS Treatment is wide excision of all infected tissues along with parenteral antibiotics. [Mortality is significantly high.] SS Caused

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Benign Pigmented Lesions SS Naevi

are benign pigmented lesions of the skin due to increased number of melanocytes. SS Normally, melanocytes are present in the basal layer of the epidermis. SS Different types (according to microscopic appearance)— a. Lentigo: Increased number of melanocytes within the basal layer of epidermis. SS Usually found in face and hand of elderly person.

b. Junctional nevus: Develops due to increased number of melanocytes at dermo-epidermal junction. SS Usually found during or before puberty, as a smooth, flat pigmented lesion. [Majority of malignant melanoma arise from junctional nevus.]

c. Dermal nevus: Excess number of melanocytes cluster within the dermis. SS Presents as pigmented, elevated fleshy lesion in adults.

d. Compound nevus: Excess melanocytes both at the dermo-epidermal junction and within the dermis. SS Presents as dermal nevus or junctional nevus.

e. Blue nevus: Excess melanocytes in the deeper layer of dermis. SS Most commonly found in face, dorsum of hand and feet. SS As the clusters of melanocytes present deep in the dermis, the lesion appears bluish rather than brown.

Skin and Adnexal Lesion 

899

SS Different

types (according to clinical presentation): a. Hairy mole SS Flat, slightly raised lesion with warty epidermal covering SS Hairs grow from its surface SS Microscopically, intradermal nevi.

b. Nonhairy mole SS Epithelium is smooth and not elevated SS Microscopically, junctional or compound nevi.

c. Blue nevus SS Overlying skin is smooth and shiny. SS More often seen in children. SS Commonly found in face, dorsum of hands and feet, over the sacrum (mongolian blue spot).

d. Hutchinson’s lentigo SS Large area of hyperpigmentation. SS Seen in face and neck of older people. SS Surface is smooth, but may be raised (areas of junctional activity) as well as pale areas (areas of regression). [Increased chance of malignant transformation.]

Treatment SS Most

of the nevus are benign and do not require treatment where excision is indicated: zz Patient wants for aesthetic reasons. zz Recently discovered lesion in an adult. zz Lesions undergone change in color (more darker), change in surface (loss of skin crease), increase in size, shape and thickness. zz Lesion starts itching (early symptom). zz Lesion starts bleeding (a late symptom). zz Lesion in sole of foot or palm of the hand.

SS Conditions

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Road Map

Premalignant Lesions Solar Keratosis (Actinic Keratosis, Senile Keratosis) SS Areas

of epidermal dysplasia and hyperkeratosis in sunexposed areas of skin in elderly fair skinned males B-induced P53 mutation have been observed in these lesions SS Commonly seen in back of fingers and hands, face, rim of ears SS Presents as raised erythematous plaque of skin with rough surface SS Three possible behavior patterns Spontaneous regression SS Ultraviolet

Persistence Progression to carcinoma SS These lesions are potentially malignant (squamous/basal cell carcinoma) SS Prevention— zz Use of hat zz Use of sunprotective clothings, sunscreen. SS Treatment— zz Cryotherapy with CO or liquid nitrogen (in solitary lesion) 2 zz Topical 5–FU cream application (in multiple lesion) zz Thermocautery + curettage zz Topical imiquimod zz Photodynamic therapy. Solar keratosis not responding to treatment or presents with bleeding, rapid growth or pain—Think of SCC and should be confirmed by biopsy.

Bowen’s Disease SS It

is an intraepidermal squamous cell carcinoma in situ presents as flat, pink papular patches with well-defined margins, covered with crusts SS Exposure to arsenic is sometimes associated as an etiological factor SS Local cytotoxic therapy e.g. 5-FU, cryotherapy, cauterisation is useful but increased chance of recurrence SS Surgical excision is the best treatment option. SS Clinically

Erythroplasia of Queyrat SS It

is the Bowen’s disease of glans penis SS Most commonly found in uncircumcised males.

Skin and Adnexal Lesion 

901

Xeroderma Pigmentosum SS Autosomal

recessive disorder where sunexposed skin is mostly affected

SS Patients are in increased risk of developing squamous cell carcinoma, basal cell carcinoma and malignant melanoma.

Malignant Lesions Basal Cell Carcinoma (Rodent Ulcer) SS Commonest

of all skin cancers. SS Locally invasive malignancy of skin arising from basal layer of the epidermis. SS Most commonly seen in middle aged fair-skinned male person who have prolonged exposure to bright sunlight (U–V irradiation). Arsenic exposure is sometimes a risk factor. Other risk factor—Psoralen-plus UVA therapy. SS Most common location is face, specially a zone above a line from lobe of the ear to corner of mouth. Skin of all regions are susceptible. SS Pathology— zz Characteristic feature is proliferation of basaloid cells resembling basal layer of epidermis. zz Masses of basaloid cells with single, outer layer of cells with palisaded appearance in dermis.

Different types

According to clinical appearances 1. Nodular (most common) 2. Cystic 3. Pigmented 4. Deeply eroding ulcer 5. Geographical

According to histologic types 1. Basosquamous (rare) 2. Morpheaform 3. Adenoid 4. Infiltrative

Pigmented basal cell carcinoma should be distinguished from malignant melanoma. Basosquamous basal cell carcinoma behaves more like a squamous cell carcinoma. So this type of carcinoma should be treated aggressively.

902 

Illustrated Surgery—A

Road Map

SS Clinically

starts as nodular lesion (covered by fine vessels which give it a pink hue), that soon become ulcerated centrally. The resulting ulcer has a rolled pearly edge.

In advanced stage, the tumor erodes bone, muscle, cartilage. BCC grows slowly, BCC does not metastasize. SS Biopsy

must be obtained prior to definite treatment. SS Different methods of treatment— zz Curettage and electrodesiccation zz Cryotherapy zz Laser ablation zz Topical application of 5-FU These methods of treatment can be employed for smaller lesions, but no tissue for histology is obtained and clearance of tumor margin become uncertain. zz Radiotherapy— „„ Bcc is highly radiosensitive. „„ Indicated in patients not fit for surgery. „„ Usually 40–60 Gy radiation dose is given for a period of 2–3 weeks. zz Surgical excision— „„ Larger lesions, lesions involving adjacent structures, aggressive histologic types (basosquamous, infiltrative) need excision with 2–4 mm margin. zz Moh’s micrographic surgery— Serial horizontal excision ⇓ Each piece of tissue is undergone frozen section biopsy [entire margin of resection is examined] ⇓ Resection process to be continued until the margin is free.

This technique is particularly useful for BCC in eyelids and nose where tissue loss is undesirable, in recurrent lesions and in lesion with indistinct borders (morpheaform). Least sacrifice of uninvolved tissue. The procedure is lengthy (takes upto several days). SS No need of follow-up except in Gorlin’s syndrome (Familial BCC), nevoid BCC syndromes tumors in high risk areas.

Skin and Adnexal Lesion 

903

Squamous Cell Carcinoma SS SCC

of skin arises from the keratinocytes in epidermis found in men than women.

SS Commonly

Risk factors SS Prolonged

exposure to sunlight (SCC is less aggressive) Amount of exposure is proportional to risk. zz Persons with fair complexion, blonde hair are more susceptible than individual with dark complexion. SS Solar keratoses SS Bowen’s disease SS Xeroderma pigmentosa (1000 fold increased risk) SS Oculocutaneous albinism SS Immunosuppression (4 fold increased risk) zz Risk is related to degree of and duration of immunosuppression. zz Patient of organ transplantation (on immunosuppressive drugs, e.g. azathioprine, cyclosporine, prednisolone). zz Patient with immunosuppressive diseases (e.g. HIV and HPV infection, autoimmune diseases, lymphoma, leukemia). SS Exposure to certain chemicals (e.g. organic hydrocarbons) SS Exposure to arsenic SS Old burn scar (higher incidence of metastases) SS Long standing venous ulcer SS Chronic osteomyelitis (higher incidence of metastases) SS Tobacco use. zz

Site of tumor SS Most

commonly found in exposed areas— zz Head region (about 75%) zz Face, Pinna, back of hands zz Mucocutaneous junctions—Lip, anal canal, glans penis. SCC in external ear have increased tendency to recur and regional lymph node metastasis. Chimney-sweeper’s cancer—Cancer of scrotal skin due to repeated exposure to soot. Kangari cancer—SCC of skin of inner side of thigh and lower abdomen in natives of kashmir (Kangari is an earthenware pot containing glowing charcoal– people keep this pot close to abdomen to keep warm). Marjolin’s ulcer—SCC in old burn scar.

904 

Illustrated Surgery—A

Road Map

SS Microscopically,

well differentiated SCC have a characteristic appearance—Whorled arrangement of malignant squamous cells, in which the center of it contains laminated keratin material.

[SCC stains positive for cylokeration 1 and 10]

SS Regional

lymph nodes may become involved, either due to metastasis or from infection.

SCC in hand–ulcerated growth with everted edge are characteristic SS Clinically

presents as slightly raised hyperkeratotic macule or papule. Gradually the surface breaks down and an ulcerated growth with everted edge with indurated base develops. SS Diagnosis—Any lesion suspicious for SCC should be biopsied (shave biopsy).

Skin and Adnexal Lesion 

Treatment

905

2. Radiotherapy SS In

1. Surgery

head and neck SCC with no evidence of local invasion or metastasis. SS In elderly patients who are not fit for surgery or unwilling to surgery.

3. Electrodesiccation and curettage or Cryosurgery SSElectrodesiccation is indicated in well differenti-

ated SCC < 1 cm. SSSCC-in-situ can be treated by cryosurgery.

Traditional excision SS Tumor

size> 1 cm. in high risk areas (in old burn scar, chronic osteomyelitis, in external ear). Margin must be at least 4 mm. SS Tumor

Mohs’ micrographic surgery SS Large primary or recurrent SCC in those sites where

conservation of normal tissue is essential. SS Invasive lesion, poorly differentiated lesion, lesion in high risk anatomic sites where surgery is indicated but traditional excision can affect the function or cosmesis.

SS Treatment

of nodal metastasis— Radiotherapy, Lymph node dissection or both SS Invasive SCC need close followup zz Every 3 months during the 1st year after treatment zz Every 6 months during the 2nd year zz Then annually.

Verrucous carcinoma SS A special variety of SCC which is well-differentiated, invade locally and rarely metastasize SS Commonly found in palms and soles SS Superficial part of the tumor resembles verruca (hyperkeratosis, parakeratosis, acanthosis, papillomatosis) SS Treatment is surgical excision.

906 

Illustrated Surgery—A

Road Map

Cutaneous Melanoma SS Melanoma

is a malignant neoplasm arising from melanocytes. SS Cutaneous melanoma arises from malignant transformation of melanocytes at the dermoepidermal junction. SS More than 98% of melanomas are cutaneous melanomas. [Melanocytes also found in meninges, upper esophagus and eyes (sites where precursor melanocytes migrate from neural crest during embryonic development)].

Pathophysiology SS Progression

from normal melanocytes to metastatic melonoma is a stepwise process induced by multiple genetic mutations and involves several histologic intermediates.

Genetic mutations responsible: 1. Germline mutations in CDKN2A gene (located in 9p21) 2. Suppression of PTEN gene 3. Polymorphism in melanocortin–1 receptor (MC1R) locus. [Mutation in p53 is quite uncommon.]

Skin and Adnexal Lesion 

907

Cells in the vertical growth phase are different from cells in radial growth phase in respect of morphology, cell surface antigens, behavior in cell culture.

SS Most

of the melanomas arise de novo, few are hereditary.

Risk factors SS Exposure

to UV (UV–B) irradiation—most important risk factor of dysplastic nevus (more nevus, more risk) SS Family members with dysplastic nevi and malignant melanoma SS Xeroderma pigmentosa SS History of other skin cancers associated with UV exposure SS History of high dose irradiation in childhood SS Genetic predisposition (e.g. mutation in CDKN2A and B-RAF gene). SS Presence

SS Cutaneous

melanoma most commonly develop in back and head-neck regions in male and in lower extremities (below the knee) in female.

Malignant melanoma in face

908 

Illustrated Surgery—A

Road Map

Etiology of acral lentigenous melanoma (ALM) is most likely independent of UV exposure. ALM is more common in African, Asian and Hispanic population than in fair skinned population. Subungual lesions present as blue-black discoloration of the posterior nail fold. Additional presence of discoloration in proximal or lateral nail folds (Hutchinson’s sign) is diagnostic of subungual melanoma. Any pigmented subungual lesion should be biopsied.

Prognostic factors SS Depth

of invasion zz Best prognostic indicator of metastatic risk. zz Clark used the histologic level to measure the depth of invasion. zz Breslow used the thickness of lesion (from granular layer of the epidermis to the base of the lesion)—with the help of an ocular micrometer. zz TNM classification is the modification of these classifications.

SS Metastasis

Lymph node metastasis– Regional lymph node involvement is a poor prognostic sign. The number of positive lymph nodes is related with survival rates. zz Distant metastasis is also a grave prognostic sign. SS Ulceration—Ulceration of the lesion is a negative prognostic indicator. SS Gender—Prognosis is better in women. SS Location of tumor zz Prognosis is bettter in melanoma on extremities in comparison to melanoma in trunk, head neck zz Melanoma on acral sites have also poorer prognosis zz Significant poor prognosis in mucosal melanoma. SS Histologic growth pattern— Lentigo maligna melanoma have a better prognosis and acral lentigenous melanoma have a worse prognosis independent of Breslow thickness. SS Age of the patient—Melanoma—Associated mortality increases with age. zz

Skin and Adnexal Lesion 

909

Spread of tumor SS Lymphatic

spread—Tumor may spread to regional lymph node by embolism. zz Lymphatic permeation causes local satellite lesion. SS Hematogenous spread—Lungs, liver, brain, spinal cord, adrenals are common sites of metastasis. Unusual sites of metastasis—Small intestine, heart, breast.

Diagnosis SS Malignant

melanoma can be differentiated from benign pigmented lesions by examining the features: Asymmetry, Border irregularity, Color change, Diameter > 6 mm, Elevation (ABCDE). SS Clinical examination is to be done to assess the site of primary lesion, any satellite lesion, all major lymph nodal basins and thorough evaluation of regional lymph node basins. SS If melanoma is suspected clinically, a full thickness biopsy of skin and underlying fatty tissue along with all the visible lesion is done. If complete excision is not possible, then excision of a part of the lesion along with adjacent normal skin (full thickness) is indicated.

Treatment 1. Surgery SS Excision of primary lesion— zz Surgical excision is the treatment of choice for all type of melanomas. zz Lateral margin of 2 cm is recommended and the vertical extension of the excision must be include subcutaneous tissue. No necessity to excise the fascia or muscle beneath the lesion. zz The defect is closed by either primary closure or by skin graft or local flap. SS Lymph node dissection— zz Clinically positive lymph nodes must be removed by regional nodal dissection. Removal of lymphatics between the primary lesion and regional lymph nodes is also recommended. zz In lower extremity lesion, iliac lymph nodes have to be removed along with inguinal lymph nodes. zz In lesion on the face, anterior scalp and ear. superficial parotidectomy to remove parotid nodes and modified radical neck dissection in clinically negative lymph nodes is usually recommended in intermediate thickness lesion (1–4 mm). [lesion 4 mm are more likely to develop distant metastasis]

910 

Illustrated Surgery—A

Road Map

[Sentinel lymphadenectomy is an accepted surgical option in malignant melanoma] Metasectomy—Solitary metastatic lesion in brain, GI tract or skin should be excised if possible. 2. Immunotherapy— Interferon–α (INF–α) 26 is recommended for stage IIB and III 3. Radiotherapy SS Radiotherapy is the treatment of choice in multiple brain metastasis. SS Adjuvant Radiotherapy to the neck or axilla after radical lymph node dissection decreases regional recurrence rate. 4. Hyperthermic regional perfusion— Hyperthermic regional perfusion of the affected limb with a chemotherapeutic agent (melphalan) is indicated in local recurrence or in transit lesion that is not amenable to excision. Heated Melphalan (upto 41.5°C) is preferred for 60–90 minutes. The advantage of regional perfusion is to increase the dose of chemotherapeutic agent without increasing systemic side effects.

Other Malignancies of the Skin Kaposi’s Sarcoma SS Multicentric

angiosarcoma affecting the skin and viscera presents as rubbery bluish nodules in the extremities SS Four form of kaposi’s sarcoma— 1. Classic (European)— Locally aggressive, visceral involvement is rare 2. African (Endemic)— More aggressive than classic form, predilection to spread to lymph nodes 3. Epidemic (AIDS–associated)— Occurs exclusively in male homosexuals. Not in IV drug abusers and hemophiliacs 4. In renal transplant patients. SS Treatment is surgical excision. Other treatment options are— zz Radiotherapy zz Cryosurgery zz Laser ablation. SS Clinically

Angiosarcoma SS Highly

aggressive malignant tumor of endothelial cells SS Clinically presents as ‘bruise’ like lesion that spontaneously bleeds or enlarges, in elderly males SS Four forms of angiosarcoma— 1. As of scalp and face 2. As associated with lymphedema 3. Radiation induced AS 4. Epithelioid AS. SS Radical excision is the treatment of choice SS Prognosis is poor.

Skin and Adnexal Lesion 

911

Lymphangiosarcoma SS It may arise in areas of prior radiation therapy or in areas of lymphedema of the arm following mastectomy (Stewart–

Treves syndrome). SS Prognosis is very poor. Chemotherapy and radiotherapy are used for palliation.

Cutaneous Metastases SS Common

primary sites— Lungs Breast Color in male Colon in female Melanoma Melanoma SS Sister Mary Joseph nodule, a specific variety of cutaneous metastasis, presents as indurated umbilical nodule.

}

}

Chapter 24

Ulcer, Sinus and Fistula

Important Topics

zzDifferent zzBasic

Types of Ulcer

Principles of Ulcer Dressing

zzSinus zzFistula

‘Learn from yesterday, live for today, hope for tomorrow. The important thing is to not stop questioning.’

914 

Illustrated Surgery—A

Road Map

Ulcer

SS An

ulcer is a discontinuity of an epithelial surface. SS UIcer has some features that must be examined in clinical examination: 1. Edge— It is the junction between healthy and diseased tissue It takes characteristic form according to underlying disease: „„ Sloping edge—The edge gently slopes from normal epithelium to base of the ulcer.

All healing ulcers have sloping edge „„

Punched-out edge—The edge drops down at right angles to the skin surface.

Example – Deep trophic ulcer – Gummatous ulcer „„

Undermined edge—The disease destroys the subcutaneous tissue faster than the overlying skin.

Example–Tuberculous ulcer

Rolled edge—Lesion becomes necrotic at its center, but grows rapidly at its periphery. „„ Everted edge—When ulcer caused by fast growing disease, the edge of the ulcer heaps up due to excessive growth. „„

Typically found in basal cell carcinoma

Example – Squamous cell carcinoma – Ulcerated adenocarcinoma

Ulcer, Sinus and Fistula  2. Floor—Floor is that which is seen by a clinician Floor may be covered by— „„ Granulation tissue—In healing ulcer „„ Dead tissues (slough)—In active ulcer „„ Malignant tissue—In malignant ulcer. 3. Base—Base is that which can be palpated. „„ Marked induration of the base— In squamous cell carcinoma. „„ Base is attached to deeper structures—Varicose ulcer (attached to tibia). 4. Discharge—Serous, serosanguinous, purulent, offensive. Dicharge should be sent for culture-sensitivity.

Traumatic Ulcer SS The ulcer may present in the body but more commonly found where skin is closely

applied to the bony prominences, e.g. shin, medial and lateral malleoli, back of heel. SS They are painful, circular-shaped ulcers.

915

916 

Illustrated Surgery—A

Road Map

Arterial Ulcer (Ischemic Ulcer) SS An

ulcer that develops due to inadequate blood supply Causes Large artery occlusion • Atherosclerosis • Embolism Small artery occlusion zz Buerger’s disease zz Raynaud’s disease zz Diabetes zz Embolism zz Pressure necrosis SS Found in the tip of the toes and fingers and over the pressure areas. SS

Ulcer, Sinus and Fistula 

917

SS Floor

is often infected, the blood supply is not adequate enough to form healthy granulation tissue. SS Clinically presents as painful, deep ulcer in the distal part of the extremities associated with symptoms of PAD (intermittent claudication, rest pain, exacerbation of pain at night) and signs of peripheral ischemia (dryness of skin, hair loss, blackish discoloration, gangrene). SS Treatment— Care of the ulcer + revascularization. Unless revascularization is successful, the healing of ulcer is not satisfactory.

Venous Ulcer

Venous ulcer in typical location

SS Commonly

found around the ‘gaiter’ area of the lower leg (lower third) and on the medial side of the leg. The ulcers particularly develop at the sites of incompetent perforators—Most common over Cockett’s perforator (above the medial malleolus).

918 

Illustrated Surgery—A

Road Map

SS The

typical location of ulcer, characteristic skin changes and history of venous incompetence—Suggestive of venous ulcer. SS Treatment—Care of the ulcer + compression therapy.

Neuropathic Ulcer SS The SS

ulcer develops due to repeated injury or pressure in an area unable to appreciate pain. Causes Spinal cord lesion 

Spina bifida  Syringomyelia  Tabes dorsalis  Paraplegia

Peripheral nerve lesion zz Diabetes zz Leprosy zz Alcoholic neuropathy zz Peripheral nerve injury SS The ulcers are seen on the heel, base of 5th metatarsal, head of 1st metarsal in ambulatory patients; on the buttock and on the back of the heel in nonambulatory patients. SS Characteristic features of this ulcer— zz Painless ulcer Neuropathic ulcer at the head of 1st metatarsal zz Loss of sensation in the surrounding tissues zz Normal vascularity in the surrounding tissues. SS Clinically, neuropathic ulcers must be differentiated from ischemic ulcer by through neurological examination. SS Treatment—Care of the ulcer + use of applicances to reduce pressure + treatment of the cause.

Ulcer, Sinus and Fistula 

919

Diabetic Ulcer

SS Sensory

neuropathy causes unrecognized injury due to ill-fitting shoes, trauma and foreign bodies. Impaired proprioception causes abnormal weight-bearing during walking. Neuropathy affects pain and temperature fibers in initial phase. SS Motor neuropathy (Charcot's foot, hammer toe, claw toe deformity) causes loss of arch of foot due to dislocation of metatarsophalangeal and interphalangeal joints leads to excess pressure—Leads to ulcer formation. SS Autonomic neuropathy causes anhidrosis and decreased cutaneous blood flow in the foot—Drying of skin and fissure formation.

SS Micro

and macroangiopathy leads to impaired wound healing. SS Most commonly present in great toe and metatarsophalangeal joint areas.

920 

Illustrated Surgery—A

Road Map

Risk factors for development of ulcer SS Male

sex

SS Diabetes

mellitus > 10 years SS Poor glycemic control SS History of smoking. [About 14–24% risk of subsequent amputation following development of ulcer.]

Preventive measures SS Risk

factor modification— zz Avoidance of smoking zz Proper glycemic control zz Treatment of hypertension, dyslipidemia zz Use of orthotic shoes and devices zz Nail care SS Patient education— zz Proper selection of footwear zz Daily inspection of feet to detect any minor injury zz Keep the foot skin clean and moist zz Avoidance of bare foot walking zz Consultation with a physician if any abnormality detected. [Once ulcer develops, chance of healing is poor.]

Treatment SS Proper

control of blood sugar avoidance of weight-bearing on the ulcer—Can be done by using orthotic shoes/casts SS Debridement—Wide debridement of all necrotic and infected tissues. SS Dressing of ulcer— zz Topical antibiotics have limited role. zz Topical application of PDGF and granulocyte-macrophage colony stimulating factor has promising results. [Antiseptic agents should be avoided.] SS Antibiotics— zz Oral or IV antibiotics according to severity of infection zz Antibiotics should be used with coverage against gram (+ ve), gram (–ve) and anaerobes. SS Revascularization SS Limited amputation. SS Off-loading—Complete

Decubitus Ulcer SS Ulcer

develops when tissue necrosis develops following compression between bony prominences and external surface.

Ulcer, Sinus and Fistula 

921

[Capillary occlusive pressure–30 mmHg]

SS 4

stages of ulcer formation— zz Stage I — Nonblanchable erythema, intact skin zz Stage II — Partial thickness skin loss involving epidermis, dermis or both zz Stage III— Full thickness skin loss zz Stage IV— Full thickness skin loss with involvement of muscle and bone.

SS Usually

presents over the sacrum, over the ischial tuberosity, posterior aspect of heel, buttocks, over the shoulder, occiput. SS This ulcers have punched out edge. SS Treatment— zz Nutritional supplementation zz Debridement of ulcer zz Flap coverage or skin grafting may needed zz Care of the patient— „„ Change in position every 2 hours „„ Use of water bed/air bed „„ Maintenance of hygiene „„ Keeping the skin clean and dry.

Tuberculous Ulcer SS Usually

develops following bursting of cold abscess in neck, chest wall, groin. is often multiple, oval-shaped with irregular crescentic border and undermined edge. Tender ulcer with caseating material in the floor. Slight induration is the characteristic feature. SS Regional lymph nodes are often enlarged. SS Ulcer

922 

Illustrated Surgery—A

Road Map

Bazin's Ulcer SS Associated

with 'Erythrocyanosis frigida'. Frigida is a disease exclusively occurs in young women with thick ankles (due to increased subcutaneous fat), characterized by diminished arterial supply to the ankle skin as a result of absence or small perforators arising from posterior tibial and peroneal arteries.

SS E.

SS Clinically

presents as blue, tender, cold ankle in cold weather and hot, swollen, tender ankle in hot weather. SS Superficial, tender nodules around the ankle develops, which breakdown to form small, multiple ulcers. SS Sympathectomy is necessary, particularly if patient lives in a cold climate. SS Tuberculosis is responsible in many of these patients. ATD is effective in that patients.

Martorell's Ulcer SS These

ulcer develop in patients of older age group with history of hypertension or atherosclerosis. SS Ulcer develops due to sudden obliteration of end arterioles of the skin of outer or back side of calf ⇓ Skin and soft tissue sloughs away ⇓ Punched-out ulcer SS Patients present with painful ulcer in calf of one side or both sides and it takes months to heal.

Cryopathic Ulcer Cryopathic ulcer

Chilblains

Frost bite

Ulcer, Sinus and Fistula 

923

Chilblains (perniosis)

Meleney's ulcer SS These

ulcers seen in the postoperative wounds after surgery for peritonitis or after drainage of empyema thoracis SS Caused by symbiotic action of microaerophilic nonhemolytic streptococci and hemolytic Staph. aureus ⇓ Infection causing endarteritis of skin of postoperative wounds ⇓ Ulcer formation SS Undermined ulcer with plenty of granulation tissue in the floor SS Patient presents with painful ulcer with features of toxemia.

924 

Illustrated Surgery—A

Road Map

Tropical Ulcer SS Acute

ulcerative lesion of the skin found in patients of tropical regions (Africa, India) SS Usually caused by Vincent's organisms (Fusobacterium fusiformis) and Borrelia vincentii.

SS Ulcer with undermined and slightly raised edge, copious serosangineous discharge, significant pain—Characteristic



features. [Ulcer refuses to heal for months and even years.]

Syphilitic Ulcer Syphilis has 3 stages

Primary

Secondary

Tertiary

Ulcer develops in all 3 stages.

In primary syphilis SS Hard chancre or Hunterian chancre develops at the site of entry of Treponema pallidum after 3–4 weeks of exposure.

Ulcer, Sinus and Fistula 

925

SS They

usually develops in external genital areas, but may also found in extragenital sites, e.g. lip, tongue, nipple and perianal region. SS They are usually single, nontender, oval or round shaped, raised hyperemic margin with an indurated base. SS Regional lymph nodes are enlarged which are nontender and firm.

In secondary syphilis SS Ulcers

develop in the form of white mucous patches, snail-track ulcers (narrow, curved and shallow ulcers), or as condyloma lata (fleshy, warty growth at the mucocutaneous junction). SS Nontender, generalized lymphadenopathy—Particularly epitrochlear and suboccipital group of lymph nodes are enlarged.

In tertiary syphilis SS Gummatous

ulcer develops (typically present over subcutaneous bones, e.g. tibia, sternum, ulna, skull and anterior surface of scrotum). SS It develops due to delayed hypersensitivity reaction with endartitis obliterans and vasculitis. SS The ulcer is nontender, punched-out edge with wash leathers slough in the floor. SS After healing, silvery 'tissue paper' scar develops. SS Lymph nodes are not enlarged.

Soft Chancre (Ducrey's Ulcer) SS Caused

by Haemophilus ducreyi.

926 

Illustrated Surgery—A

SS Regional

Road Map

lymph nodes become enlarged and tender.

Actinomycosis by gram-positive mycelia (Actinomyces israelii). ulcer develops which discharge granules ('sulfur granules') SS Commonly found in— Facio cervical region (most common) – Thorax – Liver. SS Presence of 'sulfur granules' in the discharge is almost diagnostic. On microscopy, the granules consist of gram positive mycelia. SS Caused

SS Multiple

Basic Priniciples of Ulcer Dressing SS Primary

aim of ulcer dressing— zz To remove the dead, necrotic tissues zz To hasten the granulation process zz To accelerate the healing. SS During dressing, followings must be kept in mind: zz Excess exudate to be removed zz All dead and necrotic tissues should be excised zz Dressing must be permeable to oxygen, CO , moisture and impermeable to microorganisms 2 zz Dressing must be such that there will be minimal trauma during dressing change.

Ulcer, Sinus and Fistula 

927

Sinuses and Fistula Sinus SS A

blind track lined by granulation tissue from an epithelial surface into surrounding tissues.

Fistula SS A

communicating track lined by granulation tissue between two epithelial surfaces. may develop between hollow viscus and skin (external fistula) and between two hollow viscus (internal fistula).

SS Communication

928 

Illustrated Surgery—A

Road Map

Causes of Peristence of Sinus or Fistula SS Presence

of foreign body or necrotic tissue (e.g. suture material, sequestrum, tuft of hair) of distal obstruction SS Chronic infection (e.g. tuberculosis, actinomycosis) SS History of radiotherapy SS Nondependant drainage SS Malignancy. SS Presence

CHAPTER 25

Urology

Important Topics

z

Urinary Symptoms

zCongenital zCystic

Malformations

Disease of Kidney

zHydronephrosis zRenal

Stone

zInfections

of Kidney

zTuberculosis zKidney

of Kidney

Tumors

zUreferal

Calculi

zUrethelial

Tumors of Renal Pelvis and Ureter

zCongenital zBladder

Anomalies of Urinary Bladder

Calculi

zSchistosomiasis zBladder

Tumor

zDiseases zUrethral

of the Urinary Bladder

of Prostate

Stricture

zHypospadias zPriapism zPeyronie's

Disease

zCarcinoma

of Penis

zTesticular

Neoplasm

‘The person who never made a mistake never tried anything new.’

Urology

931

Diseases of the Kidney

Urinary Symptoms 1. Hematuria S Presence

of blood in the urine is called hematuria. [In adults, hematuria of any degree must be regarded as symptom of urologic malignancy until proved otherwise.] S Evaluation—Search the answers of following queries:

S Gross

hematuria is commonly associated with significant pathology in comparison to microscopic hematuria.

932

Illustrated Surgery—A

Road Map

Hematuria associated with pain is commonly due to obstruction by clots or due to inflammation. „ Malignancies of kidney and bladder usually present with painless hematuria. [Patients with gross painless hematuria have a urinary tract malignancy until proved otherwise.] z Clot indicates significant degree of hematuria „ Amorphous clot—Bladder or prostatic urethral origin „ Vermiform clot—Upper urinary tract origin. z

Causes of Hematuria

Other causes of discoloration of urine—Must be excluded S Paroxysmal hemoglobinuria S Excess beetroot consumption S Porphyria.

2. Pain a. Renal Pain S Caused by acute distension of renal capsule due to obstruction or inflammation. S Pain due to inflammation is steady; pain due to obstruction is colicky.

Urology

933

Pain is usually located in the ipsilateral renal angle (junction of lateral border of erector spinae and 12th rib)

Renal pain may be associated with GI symptoms due to— S Reflex stimulation of celiac ganglion S Proximity of organs of GI system.

b. Ureteral pain S Acute colicky pain in the loin that usually radiates to the ipsilateral groin and genitalia. The patient rolls around in agony. Pain-free periods persist between each attack. S Site of radiation of pain is determined by site of obstruction. In obstruction of right midureter, pain is referred to right iliac fossa (simulate appendicitis) and in obstruction of left midureter, pain is referred to left iliac fossa (simulate diverticulitis). In midureter obstruction, pain may also referred to scrotum and labium. In obstruction of lower ureter, patient may experience pain that radiates along the urethra to the tip of penis, along with frequency, urgency. S Pain is due to hyperperistalsis of the ureter to relieve the obstruction.

934

Illustrated Surgery—A

Road Map

c. Vesical pain S Usually caused by overdistension of urinary bladder or by inflammation of urinary bladder. S Pain is felt at suprapubic region and is most severe when bladder is full. S Sometimes, in cystitis, patient may complain sharp, stabbing suprapubic pain at the end of micturition—called 'Strangury'. d. Prostatic pain S Usually caused by distension of prostatic capsule as a result of inflammation. S Patient experiences a penetrating ache in perineum or rectum that is poorly localized and usually associated with dysuria and frequency. e. Urethral pain S Scalding or burning sensation in penis or vulva during voiding due to inflammation of bladder or urethra.

3. Irritative Symptoms

Nocturia without frequency— S CHF and in peripheral edema (intravascular volume along with urine output increases in supine position). S Geriatric patient (renal blood flow is increased in recumbent position, renal concentrating ability is decreased in older age). S Consumption of caffeinated and alcoholic beverages in evening (due to diuretic effect).

4. Obstructive Symptoms

Urology

935

5. Incontinence

a. Continuous incontinence S Due to vesicovaginal fistula secondary to gynecological procedure, radiation, after obstructed labor S Due to ectopic ureter that enters the urethra or female genital tract.

b. Stress incontinence: Leakage of urine with coughing, sneezing or other activities that increase intraabdominal pressure. S Develops in women after childbearing or menopause [due to weakening of pelvic tissues]. S After radical prostatectomy. d. Overflow incontinence—

c. Urgency incontinence: Strong urge to void followed by passage of urine. S Found in cystitis, neurogenic bladder and in bladder outlet obstruction.

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6. Enuresis Urinary incontinence during sleep. Children older than 6 years with enuresis warrants thorough urologic evaluation.

Diseases of Kidney and Ureter Congenital Malformations Anomalies in number

Anomalies of ascent

Anomalies of form and fusion

Congenital malformations

Cystic diseases

Anomalies of renal vasculature

Other malformations

Anomalies in number

Bilateral renal agenesis

Unilateral renal agenesis

Supernumerary kidney

Duplication of ureter

Duplication of renal pelvis

Urology

937

Bilateral Renal Agenesis S Children

who born alive can't survive beyond 48 hours due to associated pulmonary hypoplasia. S Presence of oligohydramnios and Potter facies (prominent fold and skin crease beneath eyes, blunt nose, depression between lower lip and chin, low set ears) are pathognomonic.

Unilateral Renal Agenesis

S Occurs

once in 1100 births. GI system and musculoskeletal systems are affected. S Unilateral agenesis with contralateral normal kidney can lead to normal life. S Contact sports or strenuous physical exertion must be avoided. S Sometimes

Supernumerary Kidney S Very

rare anomaly (about 100 cases have been reported). kidney has its own collecting system, blood supply and distinct capsule. S The kidney is located either separately or loosely attached to the main kidney of the ipsilateral side, commonly caudal to the dominant kidney. S Supernumerary

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Duplication of Renal Pelvis S Most

common congenital deformity of upper renal tract.

Duplication of Ureter S In

most of the cases, the ureters join in the lower third of their course. Sometimes, the ureters open independently into the bladder. Ureter from the upper pelvis opens distal and medial to the ureter from lower pelvis.

S Infection,

stone formation and PUJ obstruction are more common in duplication of renal pelvis or ureter. male, the aberrant opening may be above the external urethral sphincter, at the apex of bladder trigone, in the posterior urethra (most common site of termination of ectopic ureter), in seminal vesicle or ejaculatory duct. S In female, ectopic opening may be below the urethral sphincter or into the vagina [urethra and vestibule are the most common site of termination of ectopic ureter.] S In

Urology

939

Treatment S If

atrophic or nonfunctioning chronically infected segment of kidney is present—Partial nephrectomy S Incontinence due to ectopic ureter—Implantation of ureter into bladder or into the fellow ureter.

Anomalies of ascent

Simple renal ectopia

Cephalad renal ectopia

Thoracic kidney

Simple Renal Ectopia S Kidney

S Usually

fails to reach its normal location (renal fossa) from pelvis and arrest at any level along its path of ascent.

smaller than normal kidney, renal pelvis is anterior to the parenchyma. About half of the ectopic kidneys have dilated pelvicalyceal system due to ureteropelvic or ureterovesical junction.

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S Associated

genital anomalies are usually present. S More susceptible for development of hydronephrosis and stone formation. No increased risk for malignant transformation.

Cephalad Renal Ectopia S Both

kidneys are located just beneath the diaphragm. S Ureters are excessively long and origin of renal arteries are more cephalad.

Thoracic Kidney S Partial

or complete protrusion of kidney through the diaphragm into the posterior mediastinum (through foramen of Bochdalek).

Anomalies of form and fusion

Crossed renal ectopia with and without fusion

Horseshoe kidney

Urology

941

Crossed Renal Ectopia with and without Fusion S When

a kidney located on the side opposite from which its ureter inserts into the bladder, it is called Crossed ectopia.

Different types of crossed ectopia

S About

ninety percent of crossed ectopic kidneys are fused with the normally positioned kidney anomalies (genitalia and skeletal system) are common in solitary crossed renal ectopia S Most of the patients have normal prognosis. S Associated

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Horseshoe Kidney S Most

common of all renal fusion anomalies. medial subdivisions of the mesonephric bud meet and fuse in the midline. The fusion occurs before the rotation on their long axis. S The kidneys usually fused at their lower poles. The inferior mesenteric artery prevents ascent by obstructing the isthmus. S Most

S As

kidneys fail to rotate, the calyces are pointed posteriorly. The ureter may insert high on the pelvis and a characteristic angulation while crossing over and anterior to isthmus. Ureter enters the bladder normally. S The blood supply is variable. Sometimes duplicate and triplicate renal arteries supply the kidneys. Isthmus is supplied by main renal artery or artery originating from aorta and sometimes branches arising from inferior mesenteric artery or common iliac artery. S Associated anomalies present—Genitourinary, skeletal, cardiovascular and CNS defects. S Patient may presents with vague abdominal pain radiated to lumbar area. Sometimes, patient may present with midline abdominal mass. Many of the patients with ureteropelvic junction obstruction. As a result, increased incidence of infection and calculus formation. S Classic radiologic features (in Urogram) — Lower pole calyces on both sides are directed towards midline — Ureters have vase-like curves. S Division of isthmus is not indicated for relief of pain.

Anomalies of Renal Vasculature [Accessory, Aberrant, Multiple Vessels] S Accessory

vessel— Two or more arterial branches supplying the same renal segment. S Aberrant vessel— Kidney supplied by vessels originate from other than aorta or main renal artery. S Multiple vessels—Any kidney supplied by more than one vessel.

Urology

Cystic Disease of Kidney

Cystic diseases of kidney

Congenital/Acquired

S Most S Most

Nonneoplastic/Neoplastic

of the cystic lesions are congenital and nonneoplastic of the cystic lesions arise from nephrons and collecting ducts.

Autosomal Dominant (Adult) Polycystic Kidney Disease (ADPKD) S An

important cause of end-stage renal failure. of inheritance is autosomal dominant with mutation in PKD gene. Three PKD genes are identified: 1. PKD1 gene (in 85% cases)—Located in chromosome 16 2. PKD2 gene (5–10% cases)—Located in chromosome 4 3. PKD3 gene—About 5% cases. S Symptoms and signs usually manifest between 30 to 50 years. A number of associated anomalies are present: z Multiple cysts in liver, pancreas; spleen, lungs (appears later than renal cysts). z Aneurysm of the circle of Willis. z Colonic diverticula. z Aortic aneurysm. z Mitral valve prolapse. S Patients present with— z Dull aching pain in the lumbar region z Irregular abdominal mass z Hematuria z Infection z Hypertension. z Subarachnoid hemorrhage (due to rupture of berry aneurysm) z End-stage renal failure. S Pattern

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CT scan showing multiple cysts in liver, spleen and kidneys

S Kidneys

are bilaterally enlarged and lobulated appearance due to underlying cyst. Cysts are of varying sizes, from few mm to 4–5 cm in diameter. Cysts do not communicate with the pelvis of the kidney. Cysts derived from entire nephron. [Only 1% of nephrons changed into cysts].

S For

diagnosis, positive family history is important but not essential. Bilateral renal cysts associated with 3 or more hepatic cyst, presence of berry aneurysm or solitary cyst in pancreas or spleen are sufficient enough for establish the diagnosis. S Ultrasonography and CT abdomen reveals multiple cysts in both kidneys and sometimes cysts in liver, pancreas. On intravenous urography — Bilateral renal enlargement — Calyceal distortion (like spiders' legs) — Swiss cheese appearance in nephrogram phase. MRI is helpful when patient is in compromised renal function. S Treatment — According to symptoms — No definite surgical procedure is helpful. [50% of the children of patient will be affected. The children should be screened by ultrasonography.]

Urology

945

Autosomal Recessive (Infantile) Polycystic Kidney Disease (ADPKD) S A

rare disease— 1 of every 40,000 live births. of inheritance is autosomal recessive. Mutations of a single gene PKHD1, located on chromosome 6 is responsible. S Age of presentation may be— z Perinatal z Neonatal [Earlier the disease presents, more severe the disease.] z Infantile z Juvenile. S Clinical manifestations depend on when the disease presents. Newborn presents with huge, normal reniform-shaped, nonbosselated, hard flank mass and sometimes history of difficult delivery due to the mass. Also history of oligohydramnios. If disease appears later in childhood, patient may present with renal failure and hypertension. All affected individuals have associated congenital hepatic fibrosis, which may lead to portal hypertension and splenomegaly. S Cysts are formed from dilatation of collecting tubules. S Pattern

S The

disease may be suspected during prenatal USG screening. Newborn presenting with ARPKD can be diagnosed by USG. In delayed films of IVU—Functioning kidneys with characteristic radial streaking (sunburst pattern). S Patients to be treated for hypertension, renal and hepatic failure. Hemodialysis and renal transplantation may be considered in some of these patients.

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Road Map

Simple Cyst of the Kidney S A

common incidental finding in USG imaging of abdomen. seen in infants and children. S If cyst causes pain or pressure effects, laparoscopic unroofing either transperitoneally or retroperitoneally, is the treatment. [A simple cyst must be differentiated from a cystic neoplasm or early stage of ADPKD.] S Rarely

Other Malformations Congenital Megaureter

Urology

947

Postcaval Ureter (Also Termed Retrocaval Ureter or Preureteral Vena Cava) S Right

ureter passes behind the IVC instead of right of it. this disorder, the right ureter deviates medially behind the IVC, winding about and crossing in front of it form a medial to lateral direction, then follows the normal course to drain in the bladder.

S In

S Most

of the patients present in 3rd or 4th decades. Patient may present with pain in the flank or hydronephrosis. is superior to demonstrate the course of IVC and ureter in comparison to CT and retrograde pyelography. S Treatment is excision of retrocaval segment of ureter followed by ureteral relocation. S MRI

Ureteroceles S A

cystic dilatation of the intramural part of ureter, associated with stenotic ureteral opening. S Found mostly in females (4 :1). S Large ureterocele can obstruct the bladder neck or contralateral ureteral orifice resulting in hydroureter and hydronephrosis. S The 'adder head' finding in IUV is typical. Voiding cystourethrography can delineate the size and location of ureterocele and also can detect the presence or absence of vesicoureteral reflux. S Treatment is indicated for symptomatic ureterocele (bilateral hydronephrosis). Endoscopic incision (transverse incision) through the full thickness of ureterocele using cutting diathermy is the preferred surgical approach.

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Hydronephrosis S Aseptic

dilatation of the calyces and pelvis of the kidney due to partial or complete obstruction to the outflow of

urine.

Cause of Hydronephrosis

Unilateral hydronephrosis Tumor infiltrating the ureter e.g. carcinoma cervix, rectum, colon prostate. z Retrocaval ureter. z Congenital PUJ stenosis. z Calculus in renal pelvis or ureter. z Ureterocele. z Neoplasm of ureter. z Neoplasm of bladder involving ureteric orifice. z

Pathophysiology

Bilateral hydronephrosis Carcinoma bladder. z Bladder neck contracture. z Prostatic enlargement (benign or malignant). z Urethral stricture. z Posterior urethral valve. z Retroperitoneal fibrosis. z

Urology

949

Clinical Features S Insidious

onset of dull, persistent aching pain in the loin is the commonest symptom S Sensation of dragging heaviness S Pain or heaviness may be exacerbated by taking excess water or alcohol. S Intermittent hydronephrosis—After attack of pain, swelling appears in loin S Few

 

hours later, after passage of large amount of urine, the pain relieved and swelling disappears – Also called 'Dietl's crisis'.

Diagnosis S USG

imaging— z Initial screening test for detection of hydronephrosis z Can also detect hydronephrosis in utero. S Intravenous urography—Pelvis appears dilated and calyces lose their cupping and become clubbed.

(diethylenetriaminepentaacetic acid) Renography—99mTC labelled DTPA is injected intravenously. If there is distal obstruction, the marker is trapped in renal pelvis and will not be washed out even after diuresis.

S DTPA

Treatment S Indications

for surgical intervention: Recurrent episodes of pain z Progressive hydronephrosis z Pyonephrosis z Evidence of parenchymal damage. S Surgical options— Management of hydronephrosis + definite management of cause of hydronephrosis. z

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Renal Stone S Stone

disease is one of the common urologic diseases S Commonly affects adult men than adult women S How stone develops?

Stone formation process is a complex cascade of events

Urology

951

What is Randall’s plaque? S According to Randall, initial event may be an erosion at the tip of a renal papilla. Deposition of calcium on this erosion produces a lesion called ‘Randall’s plaque’.

Risk Factors 1.

2.

3. Hyperuricosuria to nn dietary purine intake S Diseases associated with hyperuricosuria: z Gout z Myeloproliferative disorders z Multiple myeloma z Hemolytic disorders. S Due

4. Low urine pH ( 1 cm require fragmentation by intracorporeal lithotripters.

Urology

5. Introduction of nephrostomy tube—

Open Surgery for Renal Stone S Indicated

only where multiple PNL or ESWL may needed.

1. Pyelolithotomy

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2. Nephrolithotomy

3. Partial Nephrectomy S Stone

in the lowermost calyx and that part of renal parenchyma is damaged.

4. Nephrectomy S Poorly

functioning kidney with staghorn calculi with contralateral normally functioning kidney.

Urology

Prevention of Recurrence S Obesity

is an independant risk factor sodium restriction is helpful to prevent recurrence S Fluid intake must be such that urine output > 2 liters/day S Avoid— z High protein, low carbohydrate diet z Excess milk products z Oxalate-rich foods (e.g. spinach, beet, chocolate and nuts) z Vit C over intake (should be < 2 gm/day) z Red meat, fish— in patient with hyperuricemia. S Citrus juice (particularly lemon juice) intake prevents recurrence. S All patients with bilateral and recurrent stone formers should be investigated: 1. Serum calcium—Three occasions 2. Serum uric acid 3. 24 hours urinary excretion of urate, calcium, phosphate and cystine. S Dietary

Infections of Kidney

Different Routes of Infection

963

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Acute Pyelonephritis S Acute

Causes

suppurative inflammation of kidney and renal pelvis.

Urology

2. Hematogenous infection

S Susceptibility

of infection increased in — Diabetes mellitus — Pregnancy — After instrumentation

Pathology

Clinical presentation S Patient

present with abrupt onset of fever, chill, pain and tenderness in renal angle S Dysuria, increased frequency and urgency are often present.

Sequelae of acute pylonephritis

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Diagnosis

Treatment

S If

fever persists more than 72 hours, radiologic investigation (USG/CT) have to be done to rule out obstructive uropathy, anatomic abnormalities or perirenal infections. S Repeat urine culture on 5th–7th day, on 10th–14th day and 4th–6th week.

Urology

967

Chronic Pyelonephritis S A

chronic tubulointerstitial disease resulting from repeated attacks of inflammation and healing. S According to etiology, 2 types—

According to etiology

5HÀX[DVVRFLDWHGS\HORQHSKULWLV >UHÀX[QHSKURSDWK\@

Chronic obstructive pyelonephritis

Obstruction at different levels of urinary tract results in recurrent episodes of infection

Fibrosis

Major cause of chronic pyelonephritis. z Reflux may be unilateral or bilateral. z VUR is common in girl child, due to absence or shortening of intramural past or ureter. VUR is also associated with UTI. z

Scarring of cortex

S Generalized

characteristics of chronic pyelonephritis: z One or both kidneys may affected. Either kidney is diffusely or scatteredly involved. z Grossly, the kidney is small, contracted with irregular scarring. z Chronic interstitial inflammation is present. z Tubules show varying degrees of atrophy and dilatation. Glomeruli are usually unaffected except in advanced stage. [Hyaline casts are sometimes present in the tubules resembling thyroid colloid— Renal thyroidization.]

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Clinical features S Usually

no symptoms are present until chronic renal failure develops. S If it is a sequele of recurrent attacks of acute pyelonephritis, then symptoms like fever, loin pain and dysuria may be present. S Hypertension is present in about 40% of patient and may be of malignant type.

Diagnosis S Urine

culture commonly reveals presence of E.coli, Proteus, Pseudomonas. Urine culture may be negative. are usually absent. Plenty of WBCs are found in microscopical examination of urine. S IVU findings are almost diagnostic. The usual findings are: z Asymmetrical kidney outline. z Blunting or dilatation of one or more calyces and cortical scars at the corresponding site. S Casts

Treatment of bacterial infection (emperical o then according to C/S report) S Prevention of future infections S Treatment of causative factors (stone/VUR) S Nephrectomy/partial nephrectomy S Renal transplantation (in patient with end stage renal failure). S Treatment

Urology

969

Perinephric Abscess Causes Mycobacterial perinephric abscess may develop from a nearby spinal tuberculous focus.

Symptoms and signs S High

swinging pyrexia or flank mass S Tenderness in loin. [Psoas abscess is to be differentiated by limping gait and flexion and externally rotated ipsilateral hip.] S Abdominal

Diagnosis Laboratory investigation— S Leukocytosis S Serum creatinine. Urine examination— S Pyuria S Culture of urine– E.coli, Proteus, S. aureus are found in most of the cases. Plain X-ray of KUB— S Absence of psoas shadow S Reactionary scoliosis—Concavity of vertebral column toward the abscess S Elevated and immobile diaphragm on the affected side. CT is specifically helpful to identify the abscess as well as detailed information about the spread of infection. This is very much helpful for planning surgical drainage.

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Treatment Antimicrobial therapy + Drainage of abscess + Treatment of cause of abscess

USG or CT guided drainage (for small abscess)   Pus sent for C/S

Surgical drainage (through lumbar incision)   Pus sent for C/S

[Nephrectomy is indicated for pyonephrosis of nonfunctioning kidney.]

Pyonephrosis S Pyonephrosis

is infected hydronephrosis along with suppurative destruction of renal parenchyma S Patient looks toxic, high rise of temperature with chill, flank pain, tenderness in loin, swelling in loin S History of urinary tract calculi, UTI may be present S USG reveals dilated pelvicalyceal system S CT is nonspecific S IVU shows a poorly functioning or nonfunctioning hydronephrotic kidney.

Urology

971

Antimicrobial therapy (parenteral) + Surgical intervention (urgent)

Drainage of pus through percutaneous nephrostomy Ÿ Treatment of cause of obstruction and source of infection

[Nephrectomy to be considered in a nonfunctioning kidney where the contralateral kidney is functioning normally.]

Renal Abscess or Carbuncle S Collection

of purulent material confined to renal parenchyma.

Etiopathogenesis Etiopathogenesis

Hematogenous spread

Ascending infection (associated with obstruction/stasis)

Due to calculi, pregnancy

Due to neurogenic bladder

[Commonly seen in diabetic patients, IV drug abusers, immunosuppressive patients.]

VUR

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S Fever

with chill, flank pain, tender swelling in loin are the usual symptoms and signs. S Diagnosis Lab investigations • Marked leukocytosis • Positive blood culture Imaging • Urine culture Gram + ve (if hematogenous spread)

Gram –ve (if ascending infection)

S USG

and CT helps to differentiate renal abscess from other inflammatory renal diseases is the investigation of choice. S Treatment Parenteral antimicrobial therapy (selection of antimicrobial agent according to presumed source of infection) Abscess < 3 cm Abscess > 3 cm Abscess in immunosuppressed patient S CT

Parenteral antibiotic therapy

patient not responding

Tuberculosis of Kidney Etiopathogenesis

Drainage of abscess (CT/USG guided or open drainage)

Urology

How the Tubercular Ulcer Develops?

Different Types of Tubercular Lesion in Kidney

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Clinical Features S Usually

common in 20–40 years of age. [Genitourinary TB is very uncommon in children.] S More common in men (2 :1) S Right kidney is more affected S Increased frequency of micturition—Often the earliest symptom S Hematuria S Dull aching pain in loin S Constitutional symptom—Weight loss, evening rise of temperature. [Suspect genitourinary TB if patient presenting with vague, persistent urinary symptoms without any obvious cause.]

Diagnosis S Diagnosis

Imaging • Plain X-ray—Calcification in kidney. • IVU— Distortion of calyx, calyceal and parenchymal destruction. • CT—Imaging modality of choice. 3D reconstruction of CT image is helpful to identify calyceal abnormalities, hydronephrosis, hydroureter. • Chest X-ray—To exclude an active lung lesion.

Urine examination • Sterile pyuria is the classic finding on routine urinalysis and culture.

• Z–N staining rarely shows presence of acid-fast bacilli. • Urine culture—Culture on Lowenstein- Jensen medium take 6–8 weeks as the bacteria is slow growing. 3–5 consecutive early morning samples of urine should be cultured [because the organism is intermittently excreted].

• Fluorescence microscopy. • Radiometric culture method. • PCR of DNA or rRNA.

Treatment S Prognosis

is good if patient completes the course of ATD (6–9) months S Surgical intervention—Aim is to preserve the organ and reconstruction rather than excision z Surgery should be done at least after 4–6 weeks of chemotherapy z Nephrectomy or partial nephrectomy may be indicated.

Urology

975

Kidney Tumors

Kidney tumors

Malignant

Benign

Epithelial tumor of renal parenchyma z z

Adenoma Oncocytoma

z

Renal cell carcinoma

z

Transitional cell carcinoma

z

Wilms' tumor

Epithelial tumor of renal pelvis

z

Transitional cell papilloma

Embryonal tumor

z

Mesoblastic nephroma

Nonepithelial tumor

z

Angiomyolipoma Metastatic tumor Most common malignant tumor of kidney. z Usually, hematogenous route of spread. z Lung, breast, GI tumors, malignant melanoma are the common primary sites. z

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Benign Renal Tumor They are usually an incidental finding during radiological imaging, after nephrectomy or at autopsy.

Oncocytoma S A

benign epithelial tumor arising from collecting ducts. S Ultrastructurally, these tumors are packed with numerous large mitochondrias. [Most of the oncocytomas cannot be differentiated from RCC by clinical or radiological means.] That is why, most urologists treat this tumor aggressively (thermal ablation, partial nephrectomy, radical nephrectomy).

Angiomyolipoma S A

benign clonal neoplasm that contains mature adipose tissue, smooth muscle and thick-walled vessels. S This tumor is often associated with tuberous sclerosis (20–30%) [Tuberous sclerosis syndrome—An autosomal dominant disorder is characterized by mental retardation, epilepsy, adenoma sebaceum] S AML associated with tuberous sclerosis is more likely to be bilateral and multicentric. Their growth rate is higher in comparison to solitary AML. S Its fat content gives it a characteristic appearance in CT. On CT scan, presence of fat within a renal lesion is diagnostic of AML and excludes RCC. S Positivity to HMB–45, a monoclonal antibody is characteristic for AML. S Small (< 4 cm), asymptomatic AML can be observed expectantly with close surveillance. Solitary, large, symptomatic (e.g. life-threatening hemorrhage) AML needs total nephrectomy. S In tuberous sclerosis patients, bilateral AML, patients with pre-existing renal insufficiency— A nephron-sparing approach) selective embolization/partial nephrectomy) should be considered.

Renal Cell Carcinoma (Hypernephroma, Grawitz Tumor) S Most

lethal of all the urologic malignancies S Common in elderly patients— in 6th and 7th decades S Male-female ratio 3:2 S Most of the RCCs are sporadic S These tumors are derived from tubular epithelium. So they are located predominantly in the cortex S Usually arises from poles of the kidney, usually from the upper pole S Most sporadic RCCs are unilateral and unifocal.

Urology

Risk factor

Pathology S Most

RCCs are round to avoid in shape, golden yellow in color, usually varies in size from 5–8 cm, circumscribed by a pseudocapsule (composed of compressed parenchyma and fibrous tissue). z Cut section shows areas of necrosis, hemorrhage and cystic changes. [RCC with cystic degeneration is associated with better prognosis than solid RCC.]

977

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Road Map

on cytogenetics, RCC is classified into: z Clear cell type (70%) — „ Most common type. „ The cells contain lipid, glycogen which are removed during processing of tissues, thus appears as cells with clear cytoplasm (clear cell). z Papillary type (10–15%)— „ The tumor cells arranged in papillary pattern over fibrovascular stalks. „ They tend to be bilateral and multiple. z Chromophobe type (5%)— „ Arise from intercalated cells of collecting ducts. „ Stains more darkly than clear cell type. „ Perinuclear halo and presence of numerous microvesicles are distinctive features. „ Better prognosis. z Granular cell type (8%)— „ Abundant acidophilic cytoplasm with marked atypia present. z Sarcomatoid type— Most anaplastic variety of RCC. z Collecting duct type (45 gm, resection time> 90 minutes, Irrigant fluid > 70 cm H O. 2 „ Syndrome is manifested as mental confusion nausea, vomiting, hypertension, bradycardia and visual disturbance. „ Treatment includes— Diuretic (furosemide) + Decreasing the fluid overload In severe cases, 200 ml of 3% saline (very slow infusion) z Hemorrhage— „ After completion of TURP procedure, the color of irrigation fluid should be light pink. „ Arterial bleeding must be controlled with electrocoagulation. „ Venous bleeding can be controlled by placing the catheter on traction for few minutes and over inflating the balloon of the catheter. 2. Transurethral needle ablation of the prostate (TUNA)— z Low-level Radiofrequency energy (490KHZ) is delivered by needles into the prostatic tissue causing localized necrosis. z

Urology

3. Transurethral microwave therapy (TUMT)— z Microwave therapy uses heat energy thus resulting in hemorrhagic necrosis and sympathetic nerve degeneration.

4. Transurethral ultrasound-guided laser-induced prostatectomy (TULIP)— z Different types of laser— „ Nd-YAG laser „ KTP laser „ Ho: YAG laser „ Diode laser. Laser works on the prostatic tissue either by coagulation or vaporization.

5. Transurethral incision of the prostate (TUIP)— z Incision is made at 5 and 7 o'clock positions, starting just distal to ureteral orifice and end just proximal to verumontanum.

Open prostatectomy S Indications

for prostatectomy

TURP is the gold standard approach for prostatectomy

{

1. 2. 3. 4.

Acute retention Recurrent UTI Recurrent hematuria IPSS symptom severtiy— moderate to severe, but patient not responding to medical therapy 5. Renal insufficiency

Open approach is only indicated when— 1. Prostate size > 75 gm 2. Associated bladder diverticula 3. Associated large bladder calculi.

1007

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Road Map Different approaches for open prostatectomy

Retropubic prostatectomy (Millin)

Retropubic prostatectomy

Transvesical prostatectomy (Frayer's)

Urology

Suprapubic prostatectomy (transvesical)

S Complications—

Hemorrhage Perforation of bladder or prostatic capsule z Incontinence z Urethral stricture z Bladder neck stricture z Retrograde ejaculation. z z

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Prostate Prostatitis Types of Prostatitis S Different

types

S Traditional

classification z Acute bacterial prostatitis z Chronic bacterial prostatitis z Nonbacterial prostatitis z Prostatodynia

{ { { {

NIH classification Category I Category II Category III A (inflammatory CPPS) Category III B (noninflammatory CPPS) Category IV (asymptomatic inflammatory prostatitis)

[CPPS– chronic pelvic pain syndrome]

Clinical Presentation S Category I— Acute onset of perineal or suprapubic pain associated with irritative and obstructive urinary symptoms

along with systemic symptoms (e.g. fever, malaise, nausea, vomiting). S Category II—History of recurrent UTI. S Category III A and B— z Pain in the perineum, suprapubic area and penis. z Pain during or after ejaculation. S Category IV— z Asymptomatic z Evidence of prostatitis detected during workup for other prostatic pathologies.

Assessment of Symptoms S Objective

assessment of symptoms— By NIH—CPSI (The National Institutes of health-chronic prostatitis symptom Index) z This symptom index covers 3 domains: „ Pain (location, frequency, severity) „ Urinary symptoms (irritative and obstructive symptoms) „ Quality of impact. z

Urology

1011

Diagnosis S In

acute prostatitis, on DRE, prostate gland presents as a hot, boggy and exquisitely tender swelling. [DRE is better avoided due to sphincter spasm.] S 4-glass test (Meares Stamey test)— A four-glass collection technique to differentiate between urethral, bladder and prostate infections. S Urine culture—E. coli, Klebsiella, Proteus, Pseudomonas are the most common uropathogens found in prostate specimens. Gram-positive enterococci are the next common organisms. S Cytology.

Treatment S Antibiotics—

Fluoroquinolones are effective in chronic prostatitis caused by Enterobacteriaceae, but not against P. aeruginosa or enterococci. S D-adrenergic blockers— May improve outflow obstruction and thereby intraprostatic ductal reflux is diminished.

Carcinoma of Prostate S Carcinoma

of prostate is the most common malignant tumor in men of 65 years or more. is predominantly a disease of older males. S Prostate carcinoma is unique among solid tumors—it exists in two forms — (1) Histologic (Latent) form and (2) Clinically evident form. S It

Risk Factors S Genetic

factors— Various susceptibility genes have been identified. Among them, HPC1 is best characterized. Others are – SR–A/MSR and MIC–1 gene. S Chronic inflammation— There is a significant association of prostate carcinoma with history of sexually transmitted disease. S Androgen— A variable lifetime exposure of prostate to androgens have important role in carcinogenesis. No doseresponse relationship is yet established. S Estrogen— Estrogen increases risk by initiating inflammation and producing mutagenic metabolites. S Vitamin D— Vitamin D deficiency is associated with increased risk of prostate carcinoma. S Dietary factors— Diects rich in fat particularly polyunsaturated fat are associated with n risk. S Obesity—Higher BMI is associated with nrisk.

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Pathology

Adenocarcinoma is the most common histologic type. z The tumor may show variable degrees of differentiation and based on that, a grading system was devised– Gleason system. z

[Presence of osteoblastic metastases in older male—Suspect prostate carcinoma with bony metastases.]

Urology

Clinical Features S In

early stage, patient become asymptomatic. S Incidentally, it is detected during histologic examination of prostatic tissue excised for BPH. S Clinically, it may be detected as hard nodular prostate during routine DRE. S In locally advanced stage, patient may present with symptoms of LUTS, hematuria, local discomfort. S In the stage of metastases, patient may present with bone pain. S On DRE—Stony hard consistency with obliteration of median sulcus.

Staging S TNM

T1—

staging Clinically inapparent lesion

T1a T1b T1c T2—

Palpable cancer confined to prostate

T3—

Extraprostatic extension (seminal vesicles) T3a— Unilateral extracapsular extension T3b— Bilateral extracapsular extension

T4— Extension to adjacent structures (not seminal vesicles) T4a— Tumor invades bladder neck, external sphincter and /or rectum T4b— Tumor invades levator muscle and/or fixed to pelvic wall.

1013

1014

Illustrated Surgery—A

Road Map

S Investigations

for diagnosis and staging— S Triad of investigation for diagnosis

DRE Serum PSA TRUS guided prostatic biopsy

[Bone scan is an additional investigation (if needed)] 1. DRE — n serum PSA along with DRE improves the positive predictive value of DRE. 2. PSA— (Prostate specific antigen)— z A proteolytic enzyme produced by normal and neoplastic prostate epithelium. z PSA is secreted in high concentration (mg/ml) in seminal fluid and maintains the seminal secretions in a liquid phase. z Serum PSA is elevated when normal prostatic architecture is disrupted and PSA is diffused from prostatic tissue to circulation. z Serum PSA is elevated in

Prostate disease After prostate manipulation – BPH – Prostate massage – Prostate carcinoma – Prostate biopsy – Prostatitis – Transurethral resection z Men with PSA > 4 ng/ml should undergo a TRUS-guided prostate biopsy. z PSA velocity (rate of change of PSA values with time), PSA density (ratio of serum PSA value and volume of prostate gland) and free versus bound forms of PSA— are the most useful tests when PSA is in between 4–10 ng/ml (Gray zone). 3. TRUS–guided prostate biopsy— z TRUS is not helpful to detect early prostate carcinoma. z TRUS is helpful to locate the suspicious lesions targeted for biopsy. z A 18-gauge core biopsy device is attached to the ultrasound probe and biopsy is taken (sextant biopsy).

4. Bone scan— z Standard imaging modality for detecting bony metastases. z Bone scan is not necessary if PSA < 10 ng/ml. z Bone scan is indicated if PSA> 20 ng/ml or patient presents with bone pain.

Urology

1015

Treatment S Treatment

of localized disease (T1a, T1b, T2)— 1. Active monitoring— is particularly indicated formen with life expectancy 10 years and without any comorbid illness. Different techniques

Open (retropubic/perineal prostatectomy) Minimally invasive (laparoscopic/robotic) „ Radical prostatectomy includes complete removal of prostate along with seminal vesicles + modified pelvic lymph node dissection „ Complications

Early Late • Nerve injury (obturator nerve) • Erectile dysfunction • Ureteral injury • Urinary incontinence • Rectal injury • Urethral stricture • Urinary fistula 3. Radiotherapy—Radical radiotherapy to the prostatic bed and pelvic lymph nodes. 4. Cryotherapy. S Treatment of locally advanced disease (T , T )— 3 4 1. Radical prostatectomy—Most of the patients are not benefited by this treatment modality 2. Adjuvant radiotherapy—Improves local control after radical prostatectomy 3. Androgen deprivation. S Treatment of metastatic disease—

Androgen ablation

By ablating the source

Antiandrogens

LHRH/RH inhibition

– Bilateral subcapsular orchiectomy

– Cyproterone acetate – Flutamide – Bicalutamide

– Goserelin – Leuprolide – Cetrorelix – Aborelix

Inhibition of androgen Synthesis – Aminoglutethimide – Ketoconazole

1016

Illustrated Surgery—A

Road Map

Urethra Urethral Stricture S Classically,

urethral stricture means scarring involving the anterior urethra and sometimes along with spongy erectile tissue of corpus spongiosum.

Etiology S Congenital—Rarest

of all cases. S Traumatic—following straddle trauma. S Inflammatory— z Postgonorrheal (less common nowadays) z Lichen-sclerosus-balanitis xerotica obliterans. S Iatrogenic— z Indwelling catheter z Endoscopic procedure.

Clinical Features S Straining

during micturition urinary stream S Increased urinary frequency S Recurrent UTI S Acute retention of urine S In well-developed stricture, the stricture can be palpated along the line of urethra. S Poor

Evaluation S

Location, length, depth and density of the stricture must be determined to make appropriate line of management.

Urology

Depth

Determined by— USG z Dynamic retrograde urethrogram z Urethroscopy z

Determined by— Clinical examination z Elasticity felt during urethroscopy z

Treatment S Dilatation S Internal S Urethral

urethrotomy stents

S Laser S Reconstruction.

1. Dilatation—Strictured urethra is stretched using graduated series of dilators.

[During dilatation, be cautious about making false passage.]

Density

{

Length

{

Location

1017

1018

Illustrated Surgery—A

Road Map

2. Internal urethrotomy— Urethrotomy— Transurethral incision through the scar to healthy tissue.

3. Urethral stents z Temporary z Permanent.

4. Laser

5. Reconstruction a. Excision and reanastomosis b. Primary urethral reconstruction with the help of graft.

Excision and reanastomosis

Urology

1019

Hypospadias S A

congenital abnormality in which urethral meatus open on the ventral aspect of the penis, scrotum or perineum. S Commonly associated anomalies are— z Abnormal ventral curvature of the penis (chordee). z Abnormal distribution of foreskin—presence of dorsal hood and deficient ventral foreskin.

1020

Illustrated Surgery—A

S Classification—Level

Road Map

of hypospadias can be accurately determined by only after correction penile curvature

(orthoplasty).

Hypospadias with chordee

S Development—Due

to incomplete fusion of urethral plate during development of penis. factor— Risk is increased by history of maternal intake of estrogen or progesterone during pregnancy. S Associated anomalies include— Cryptorchidism — Inguinal hernia Syndromes where hypospadias is one of the features— S Aniridia-Wilms' tumor association S Beckwith-Wiedemann syndrome. [Penoscrotal or perineal hypospadias may represent intersex state. Hypospadias along with cryptorchidism also may represent intersex disorder. So chromosomal study must be done in these conditions.] S The ideal age of surgery is between 6–12 months of age. [Newborn with hypospadias should not be circumcised.] S Principles of hypospadias repair— 1. Correction of penile curvature 2. Urethroplasty z Correction of penile curvature is done by 2 steps— Step 1 — Assessment of penile curvature—By inducing erection S Risk

By injecting normal saline into corpora cavernosa

By injecting arterial vasodilator (prostaglandin E1) into corpora cavernosa

Urology

1021

Urethroplasty S For

distal hypospadias middle hypospadias S For proximal hypospadias. S For

For distal hypospadias S Meatoplasty and glanuloplasty (MAGPI)— All glanular and some coronal hypospadias are repaired by this technique. S Tubularization

technique— is a Snodgrass modification of Thiersch-Duplay technique.

Critical steps are: z A 'relaxing' incision of the urethral plate distal to the hypospadias opening. z Tubularization of the relaxed urethral plate.

For middle and proximal hypospadias: Onlay island flap is a useful technique z Transverse preputial island flap (TPIF). z

1022

Illustrated Surgery—A

Road Map

Priapism S An

erection that is unrelated to sexual activity or persists beyond that.

Urology

Types

Priapism

/RZÀRZSULDSLVPLVFKHPLF 7\SH,

+LJKÀRZSULDSLVPQRQLVFKHPLF 7\SH,,

•Due to venous occlusion and ĹLQWUDFDYHUQRVDOSUHVVXUH •Characterized by erect painful penis ZLWKHQJRUJHGJODQV •Causes— –Sickle cell disease –Leukemia –Spinal cord injury –0HGLFDWLRQV HJ VLOGHQD¿O FKORUSURPD]LQHWUD]RGRQH  –,QWUDFDYHUQRVDO LQMHFWLRQV IRU erectile dysfunction –,GLRSDWKLF [/RZÀRZSULDSLVPVKRXOGEHWUHDWHG DVPHGLFDOHPHUJHQF\@ >/RZÀRZSULDSLVPLVEDVLFDOO\FRPSDUWPHQWV\QGURPHRISHQLV@

•'XH WR LQFUHDVHG DUWHULDO LQÀRZ DQG LQFUHDVHGYHQRXVRXWÀRZ • &KDUDFWHUL]HGE\QRQWHQGHUHUHFWLRQ*ODQV LVVRIW • &DXVHV²$UWHULRYHQRXV ¿VWXOD VHFRQGDU\ WRSHQLOHRUSHULQHDOWUDXPD

Diagnosis S Low-flow

priapism can be differentiated from high-flow priapism by corporal blood gas analysis. In high-flow priapism, corporal blood gas analysis is similar to arterial blood gas. In low-flow priapism, corporal blood gas analysis is similar to venous blood (hypoxia, hypercapnia and acidosis). High-flow priapism also can be confirmed by perineal Doppler USG.

Management of Low-Flow Priapism irrigation with D-adrenergic agonist (e.g. phenylephrine, epinephrine, ephedrine).

S Intracorporal

1023

1024

Illustrated Surgery—A

Road Map

Repetition of this sequence every 5 minutes interval until detumescence. BP and pulse should be monitored during this procedure.

,ILQWUDFRUSRUHDOLQMHFWLRQIDLOVVKXQWLV necessary

Corporoglandular (Winter shunt)

Corporospongiosal (Sacher shunt)

Corporosaphenous *UD\KDFNVKXQW

*=J=CAIAJPKB%ECDŃKS-NE=LEOI S Can

be treated expectantly embolization of A-V fistula is effective. If this fails, the fistula is surgically ligated.

S Selective

Management of Priapism due to Sickle Cell Disease S Can

be managed conservatively with hydration, alkalinization with bicarbonate and oxygenation S Chance of recurrent priapism is high, so transfusion or exchange transfusion should be considered.

Peyronie's Disease S Dense

fibrous plaque on the tunica albuginea, causing curvature of the penis. S Exact etiology is unknown. Plaque represents scar tissue resulting from buckling trauma of the penis usually during intercourse. S Clinical presentation— z Painful erection z Deformity in penis (both in flaccid and erect state) z Well-defined plaque or induration on the dorsal surface of the penis.

Urology

1025

In most of the cases, curvature is noted during erection, not in flaccid state. S Efficacy of medical management is doubtful. Therapy with Vitamin E, colchicines. Tamoxifen may be effective in some cases. S Surgical interference is indicated if erectile dysfunction develops or curvature interferes with sexual intercourse. Plication and corporoplasty. Incision and grafting have excellent results. Significant erectile dysfunction in Peyronie's disease warrants penile prosthesis. z

Carcinoma of Penis S Commonly

presents in the sixth decode of life, but may develop in earlier age.

S Etiology—

Phimosis—Definitive role of smegma in carcinogenesis is still lacking. Neonatal circumcision is protective for invasive penile carcinoma, not so much protective for CIS. Circumcision at puberty or at adult life do not have any protective role. z HPV infection—particularly HPV-16 z Exposure to tobacco products —cigaret smoking, chewing tobacco, snuff— all are associated with increased risk. z Ultraviolet light exposure. z Balanitis xerotica obliterans z Premalignant lesions of penis— „ Leukoplakia of the glans „ Erythroplasia of Querat. S Pathology—Lesion usually arises in prepuce and glans, but extends to involve the shaft. Two forms of growth—Exophytic and ulcerative. z

1026

Illustrated Surgery—A

Road Map

S Distant

metastases to lungs, liver, bone and brain are uncommon than 90% of carcinomas are squamous cell carcinoma. Squamous cell carcinoma are graded using Broder's classification: Low grade (Grade I and II)—Tumors are usually confined to prepuce and glans High grade (Grade III)—Tumors are usually involve the shalf of penis. [Verrucous carcinoma—An exuberant variety of squamous cell carcinoma with extremely low potential for lymph node metastases.] S More

Clinical Presentation S Patient

may present with small papular, warty growth or in advanced cases, an exophytic lesion. [Phimosis may obscure the tumor.] S Patient may present with inguinal lymph nodes or ulceration in the inguinal region. S Urethral involvement is very rare. S On clinical examination, location, fixity, involvement of corporal bodies must be assessed. [Bilateral palpation of inguinal area must be done to assess lymphadenopathy.]

KJłNI=PEKJKB!E=CJKOEO=J@0P=CEJC S For

confirmation of diagnosis, assessment of depth of invasion and presence of vascular invasion, for histologic grading— biopsy is essential. S A dorsal slit is often necessary for adequate exposure for biopsy. S In early-stage, small sized lesion in glans—No further radiologic workup is necessary. S High grade lesions suspected of involving corporal bodies, and if partial penectomy is being considered—Contrast enhanced MRI is helpful to give additional information. S For assessment of inguinal lymph nodes, clinical assessment is sufficient enough. Abdominal and pelvic CT is recommended in obese patients and in patients where inguinal lymphadenectomy is indicated.

Urology

1027

Treatment S Treatment

of primary tumor S Treatment of regional lymph nodes.

Treatment of primary lesion Different treatment options Depending on the stage of tumor, different treatment options

Circumcision

Local resection

Laser ablation

Mohs micrographic surgery

Partial penectomy

In CIS S Circumcision

(if preputial lesion) S Topical 5-FU cream (minimal systemic absorption) S Nd: YAG laser S Mohs micrographic surgery S Radiotherapy.

In invasive carcinoma Different treatment options

Partial penectomy •Distal penile lesion

Total penectomy

Radiotherapy

•Lesion involving the midshaft and base of penis

•Young patient with small VXSHU¿FLDOOHVLRQLQGLVWDO penis who is willing to preserve his organ • 3DWLHQWXQ¿WIRUVXUJHU\

Total penectomy

1028

Illustrated Surgery—A

Road Map

Partial penectomy The ability to void in standing position and to perform sexual intercourse is preserved.

Urology

Total penectomy

1029

1030

Illustrated Surgery—A

Road Map

Radiotherapy S Plesiobrachytherapy

(radioactive substance is molded around the tumor) S Interstitial brachytherapy (placement of radioactive material within the tumor) S External beam radiotherapy.

Advanced penile cancer S Proximal

tumor with involvement of adjacent structures—Total penectomy with scrotectomy with bilateral orchiectomy is recommended.

Management of regional lymph nodes Inguinal lymph node metastases is a important prognostic factor. S Clinically NO– z TIS, Ta, T tumor with grade 1 or 2 tumor histology— Watchful waiting 1 z T , T with grade 3 tumor and presence of vascular invasion—Superficial inguinal lymph node dissection 2 3

Lymph nodes sent for frozen section biopsy If negative If positive Modified inguinal lymphadenectomy S Clinically

node positive (N1)— Treatment of primary tumor   4–6 weeks of antibiotic (e.g. 1st or 2nd generation antibiotics)  Lymph nodes still palpable Modified inguinal lymphadenectomy

No further procedure needed

Urology

1031

Role of Pelvic Lymphadenectomy S To

identify patient who should receive adjuvant combination chemotherapy control can be achieved.

S Locoregional

Neoplasms of Testis S About

99% of testicular neoplasms are malignant type. S About 95% of testicular tumors arise from germ cells and all are malignant. S About 90% of germ cell tumors (GCT) arise in testicular tissue and rest are extragonadal (mediastinum, retroperitoneum). S Testicular GCT is the most common solid tumor in between 15–35 years.

Risk Factors S Cryptorchidism—Risk of testicular cancer is 3–14 times in undescended testis, less risk is also present in contralateral

normally descended testis. Orchiopexy cannot prevent the risk of carcinogenesis, but it allow the clinician to early detection of tumor growth. S Androgen insensitivity syndrome and gonadal dysgenesis— associated with increased incidence.

H=OOEł?=PEKJ S Tumors

with one histologic pattern (60%)— z Seminoma z Teratoma z Yolk sac tumor Nonseminomatous GCT z Choriocarcinoma. S Tumors of more than one histologic type (40%)— z Leydig cell tumor z Sertoli's cell tumor.

}

1032

Illustrated Surgery—A

Road Map

Seminoma S Accounts

for 50% of GCTs. frequently develops between 35–45 years of age. S Arises from seminiferous tubules. S Two variant forms— z Classic seminoma z Spermatocytic seminoma. S On cut section S Most

S Prognosis

is better among all GCTs S Highly radiosensitive.

Nonseminomatous GCT S Comprises

about 50% of all GCTs. S Different types— z Teratoma z Choriocarcinoma z Yolk sac tumor z Embryonal carcinoma.

Teratoma S Composed

of two or more germ cell layers—Ectoderm, mesoderm, endoderm. types— z Mature teratoma z Immature teratoma z Teratoma with malignant transformation.

S Different

Urology

S On

1033

cut section

S Usually

develop in younger age.

Sex cord-stromal tumor S Two

types— Leydig cell tumor—Secretes androgen, thereby causes sexual precocity z Sertoli cell tumor—Secretes estrogen, thereby causes gynecomastia and loss of libido. z

Clinical Presentation of Testiclular Neoplasm S The

pathognomonic presentation is painless testicular mass. S May present with features of epididymoorchitis. S In advanced stage, patient may present with distant metastases (iliac and paraaortic lymph nodes, liver and lungs). S On clinical examination, testis is enlarged and firm. Testicular sensation is lost. Lax secondary hydrocele may present. All testicular swellings are suspicious, particularly if persists after antibiotic treatment.

Diagnosis Clinical findings, imaging studies and tumor markers are to be considered for diagnosis All suspected testicular malignancies must be approached through an inguinal approach.

1034

Illustrated Surgery—A

Road Map

Radical inguinal orchiectomy (testis and spermatic cord en bloc) with early, high ligation of spermatic cord at the deep inguinal ring is the only accepted diagnostic as well as initial therapeutic procedure.

The orchiectomy specimen must be examined by the pathologist for histologic type and subtype, T stage of the tumor as well as lymphatic and vascular invasion.

Staging Staging is important for planning the proper management.

AJCC staging system (TNMS)

Tumor (T)

Node (N)

Meastasis (M)

Serum tumor marker (S)

Staging is done by 1. Radical inguinal orchiectomy—to know the 'T' status 2. Imaging— to know the 'N' and 'M' status z Chest X-ray— PA and lateral view of chest X-ray should be done to detect pulmonary metastasis. If high index of suspicion is present, chest CT to be considered. z Abdominal CT— Most effective imaging modality to defect retroperitoneal lymph node involvement. z MRI or PET— Offers no added value.

Urology

1035

3. Tumor markers— a. D–fetoprotein— „ Increased level of D–fetoprotein are never found in pure seminoma. „ Nonseminomatous GCT (containing elements of yolk sac) produce AFP. „ So, n AFP is a indicator of presence of nonseminomatous component in GCT. [Persistently elevated AFP after orchiectomy—Think of liver metastases.] b. Human chorionic gonadotropin (HCG)— „ Produced by syncytiotrophoblasts. „ In all choriocarcinomas, about 50% of patients with embryonal carcinoma and few percentage of patients with seminomas have n level of HCG. c. Lactate dehydrogenase (LDH) „ Due to its low specificity, serum LDH level should be corroborated with other findings „ A direct relationship is present between tumor burden and LDH level „ Most useful surveillance marker to detect persistence as well as recurrent tumors.

Treatment S Treatment

of seminoma of nonseminomatous GCT.

Treatment of seminoma

6WDJH,710 S) •Radiation therapy is the VWDQGDUGWUHDWPHQW • Standard dose is  *\ WR SDUDDRUWLF QRGHVRQO\ • Role of chemotherapy LVFRQWURYHUVLDO $OPRVWRISDWLHQW are cured after adjuvant UDGLRWKHUDS\

6WDJH,,DDQG,,E •6WDJH ,,D 1 ± 1  DUH best treated by adjuvant UDGLRWKHUDS\ •5DGLDWLRQ¿HOGLQFOXGHV –Bilateral common iliac nodes –Paracaval –Paraaortic •6WDJH ,,E 1) disease are better managed by cisplatin EDVHGFKHPRWKHUDS\

6WDJH,,FDQG,,, •Cisplatin-based chemotherapy • Radiation therapy is reserved in treatment failure cases

Treatment of nonseminomaWRXV*&7

6WDJH,DQG,,D

{

S Treatment

Low-stage disease

6WDJH,,E

6WDJH,,FDQG,,,

1036

Illustrated Surgery—A

S Treatment

Road Map

of stage I and IIa— 1. Modified (template) retroperitoneal lymph node dissection through a transabdominal approach is the treatment. [In modified RPLND, postganglionic nerve fibers are spared.] 2. Retroperitoneal lymph node irradiation—Radiation to paraaortic and ipsilateral pelvic lymph nodes. 3. Chemotherapy—Chemotherapy with bleomycin, etoposide and cisplatin. S Treatment of stage IIb— 1. Modified RPLND 2. Chemotherapy—Usually considered with nodes > 3 cm and patients with relapse. S Treatment of stage IIc and stage III— 1. For good-risk patients—3 cycles of chemotherapy (bleomycin, etoposide, cisplatin) 2. For poor-risk patients— 4 cycles of chemotherapy (same regime).

Chapter 26

Minimally Invasive Surgery, Robotic Surgery

Important Topics

zzDifferent

Minimal Access Techniques

zzPhysiology

of Pneumoperitoneum

zzLaparoscopic zzPort

Access

Placement

zzInstrumentation zzAdvantages zzNew

and Disadvantages of MIS

Techniques of MIS

zzRobotic

Surgery

‘The mind likes a strange idea as little as the body likes a strange protein and resists it with a similar energy. It would not perhaps, be too fanciful to say that a new idea is the most quickly acting antigen known to science.’ Wilfrid Batten Lewis Trotter (1872–1939) British Surgeon and Sociologist

Minimally Invasive Surgery, Robotic Surgery 

1039

Minimally Invasive Surgery

SS It

is not a discipline of surgery, rather a philosophy of surgery. philosophy— zz Small incision zz Use of miniaturized sophisticated instuments and imaging techniques zz Performing basic to complex surgical interventions zz Less sufferings of the patient.

SS The

Different Minimal Access Techniques Laparoscopy Access to the inflated peritoneal cavity (pneumoperitoneum) through sleeve (metal or plastic)

Extracavitary Endoscopy Body planes (retroperitoneal space, space of Retzius, extraperitoneal space, subfascial space of leg) are accessed, but needs inflation to develop the working space. Examples: TEP repair of inguinal hernia, Laparoscopic nephrectomy, subfascial perforator ligation.

1040 

Illustrated Surgery—A

Road Map

Endoluminal Endoscopy Rigid or flexible endoscopes are introduced into the urinary tract (e.g. cystoscopy), gastrointestinal tract (upper and lower gastrointestinal endoscopy), respiratory tract (e.g. bronchoscopy).

Thoracoscopy Thoracic cavity is accessed through a rigid endoscope.

Minimally Invasive Surgery, Robotic Surgery 

Physiology of Pneumoperitoneum

1041

1042 

Illustrated Surgery—A

Road Map

Access SS Laproscopic

access and subcutaneous access SS Hand-assisted laparoscopic access. SS Extraperitoneal

Laparoscopic Access Two techniques for abdominal access

Direct puncture (with Veress needle)

Open technique (Hasson technique)

Direct puncture techique SS Measures

to be taken— zz Site of incision—Umbilicus is one of the preferred point of access, because the abdominal wall is quite thin in this location, even in obese patient.

Trajectory of Veress needle

Minimally Invasive Surgery, Robotic Surgery  Force and depth of insertion of needle— Veress needle is inserted after lifting the abdominal wall with towel clips or firm hand grip.



Surgeon can feel two pops as the needle penetrate the fascia and peritoneum. Confirmation of proper placement of needle—

1043

1044 

Illustrated Surgery—A

Road Map

Then the Veress needle is connected to the insufflation tubing.

Open technique (Hasson technique) Particulary indicated in patient who have undergone abdominal operations previously.

Extraperitoneal and Subcutaneous Access Extraperitoneal and subcutaneous access

Access to retroperitoneum • For nephrectomy, ureterolithotomy, adrenalectomy

Access to preperitoneal space • For TEP repair of inguinal hernia

Access to subcutaneous space • For subfascial perforator ligation • Minimally invasive thyroid surgery • Saphenous vein harvesting

Minimally Invasive Surgery, Robotic Surgery 

1045

Hand-assisted Laporoscopic Access SS In

laparoscopy, a 'port' for the hand is created in such a way that the pneumoperitoneum is preserved SS Tactile advantages of open surgery can be achieved due to use of hand SS Particularly indicated in advanced colon surgery.

Port Placement Ideal trocar orientation will create an equilateral triangle between the surgeon's right hand, left hand and the telescope. Each arm will be about 10–15 cm.

Instrumentation 1. Imaging system zz

Telescope—Standard laparoscope is a metal shaft containing a series of quartz-rod lenses and optical fibers.

1046 

Illustrated Surgery—A

Road Map

SS Length

of laparoscope—24 cm SS Diameter of laparoscope— zz 10 mm (most commonly used) zz 5 mm (can be used through the 5 mm working ports) zz 1.1 mm (used in pediatric laparoscopy). SS End of laparoscope— zz Flat-end (0°)—provides straight view zz Angled end (30° or 45°)— Provides oblique view as well as provides wider field of view. When diameter of the rod lens telescope is doubled, the illumination is 4 times greater.

SS

Video camera: Video camera is attached to the eyepiece of the telescope zz For perfect color representation, three-chip camera is required—Red, green and blue (RGB) input zz In minimally invasive techniques— Priority is on— Illumination — 1st priority Resolution — 2nd priority Color — 3rd priority. zz

Minimally Invasive Surgery, Robotic Surgery 

SS

1047

Light source: zz zz

Bulbs of mercury, halogen vapor or xenon— 150–300 watt In large cavity, in procedure where bleeding may encountered, bright light source is indicated.

SS

Video monitor:



To display the image. [High definition monitors have a resolution of upto eight times more than a standard NTSC/ PAL monitors.] zz

2. Energy sources a. Radiofrequency electrosurgery— „„ Most popular energy source in minimally invasive surgery. „„ RF electrosurgery delivers an alternating current of 500 000 cycles/s (Hz). This causes tissue heating that results in coagulation (60°C), dessication (100°C) and carbonization (> 200°C). „„ The RF can be delivered by monopolar and bipolar electrodes.

A short, high voltage current (coagulation current) is used for coagulation necrosis of bleeding sources. Lower voltage, higher-wattage current (cutting current) is used for tissue division. „„ Complications: ––Capacitive coupling ––Direct coupling. „„

1048 

Illustrated Surgery—A

Road Map

Ligasure— A newer bipolar device—Both coagulates (larger vessels) as well as divides the tissue. „„ Argon beam coagulation— ––A special type of monopolar electrosurgery. ––Uniform field of electrons is delivered across a tissue surface with the help of a jet of argon gas. ––Not preferable in laparoscopic surgery because the argon gas increases the chance of gas embolism. „„

b. Ultrasonic shears (harmonic scalpel)— „„ Can coagulate and divide the blood vessels. „„ A generator produces an current (55,500 Hz) that transmits to the piezoelectric crystal stack (in the transducer). The crystal stack converts the electrical energy to mechanical vibration at the same frequency. This vibration is further amplified as it traverses the active blade of the harmonic scalpel. The shearing force separates the tissue and produces heat, results in coagulation of bleeding vessels. „„ Damage to adjacent tissues is minimal.

Minimally Invasive Surgery, Robotic Surgery 

1049

3. Hand instruments They are larger and narrower than conventional hand instruments (in open surgery). zz Standard hand instruments are 30 cm long and 5 mm in diameter. zz Shorter and narrower instruments are required for pediatric (2–3 mm) laparoscopy, whereas longer instruments are required for bariatric surgery. zz

4. Ports

zz

All ports have attachments for insufflation and valves to prevent gas leaks.

5. Insufflator zz zz

Rapid-flow insuflator supplies the CO2 and maintains the pneumoperitoneum. It maintains the gas-flow according to present pressure values.

Advantages and Disadvantages Advantages



Disadvantages



•

Smaller incisions

•

Two dimensional representation of the operative field makes the depth perception difficult

•

Cosmetically better

•

Hand-eye coordination is required.

•

Decreased tissue trauma

•

Loss of tactile feedback

•

Earlier return to activity

•

Technical expertise and infrastructure facility is required

•

Reduced hospital stay

• •

Video recording of the procedure is possible in all cases Decressed chance of contact with HIV and hepatitis B virus

Examples of Laparoscopic Procedures Basic

Advanced

•

Cholecystectomy

•

Bile duct exploration

•

Appendectomy

•

Nissen fundoplication

•

Hernia repair (TEP and TAPP)

•

Splenectomy

•

Diagnostic laparoscopy

•

Colectomy (hand assisted)

•

Nephrectomy

•

Adrenalectomy

1050 

Illustrated Surgery—A

Road Map

Contraindications Absolute •

×

Relative

Generalized peritonitis

•

?

Pregnancy

•

Intestinal obstruction

•

History of multiple abdominal operations

•

Cirrhosis of liver

•

Organomegaly

•

Coagulopathy

Complications Related to pneumoperitoneum

Related to port insertion

Related to procedure

Dlayed complications

• Damage to major vessels or • Injury to viscera, vessels viscera

• Diathermy related injury (direct • Port site infection (e.g. atypical mycoupling, capacitive coupling) cobacterial infection)

• CO2 embolus

• Inadvertent organ injury or liga- • Port site hernia (commonly in umtion (e.g. CBD ligation) bilical part)

• Metabolic acidosis

• Hemorrhage

• Hemorrhage

• Cardiorespiratory compromise

New Techniques of Minimally Invasive Surgery 1. Notes (Natural Orifice Transluminal Endoscopic Surgery) 2. SILS (Single Incision Laparoscopic Surgery).

Notes (Natural Orifice Transluminal Endoscopic Surgery) SS This

concept involves access within the abdominal cavity through a natural orifice (vagina, mouth, urethra) to perform surgical procedures. SS Transvaginal and transgastric approach are common in Notes. SS TV Notes is a safe alternative to traditional laparoscopic surgery in female patient. zz Appendectomy, cholecystectomy, nephrectomy, adrenalectomy, hernia repair are now performed by TV Notes. zz The advantages are better cosmetics outcome, decreased postoperative pain and shorter recovery period. SS In transgastric Notes, dual channel flexible endoscope is used and through the gastrostomy wound, the endoscope along with instruments reach to the target organ. zz The site of gastrostomy depends on the type of surgery. zz Cholecystectomy, appendectomy are performed by transgastric NOTES.

Minimally Invasive Surgery, Robotic Surgery 

1051

Single Incision Laparoscopic Surgery (SILS) SS SILS

involves use of single port device with multiple port sites. Umbilicus is often the site of single incision and port insertion. SS The challanges in this technique are close proximity of the instruments, difficulty in retraction of organs, increased cost.

Robotic Surgery SS Still

now, robotic surgery is performed by a surgeon with the help of robotic arms, not by a preprogramed robots. 'surgeon with robotic arms'. SS Two surgical robotic system— zz Zeus robotic surgical system zz da Vinci surgical robotic system (the robotic system now used.) SS How da Vinci surgical robotic system works? zz Its working principle is based on the master-slave concept. zz Made up of 3 components.

1052 

Illustrated Surgery—A

Road Map

Components of da Vinci Robotic System SS Surgeon



console: Viewing a 3-D image of the operative field, the surgeon moves the master controllers at the console. These movement, are exactly translated to the robotic arm, but with more degree of movement, more preciseness and without any tremor or fatigue.

SS The

patient (robotic) cart: Consists of 4 arms—One for the camera and others for the instruments.

––

Each arm has 3 joints (resembling the human arm) Setup joint (shoulder) Instrument clutch button (elbow) Effector instrument (wrist) –– Each instrument have a wrist—The wrist provides six degrees of freedom at the tip and the seventh degree of freedom is by the instrument itself.

Minimally Invasive Surgery, Robotic Surgery 

1053

SS Vision

cart: Consists of 3-D high resolution endoscope, camera (3-chip) with camera control unit, high intensity illuminators.

––This

system provides 3-D stereoscopic vision to the surgeon.

Advantages SS 3-D

stereoscopic vision to the surgeon—Depth perception of binocular vision can be achieved. SS More degrees of freedom of instruments. SS Improved hand-eye coordination due to visual and spatial alignment, the surgeon feel as though his hands are inside the patient's body. SS Motion scaling—A unique feature of da vinci system. It scales down coarse movements of the surgeon (master) to smaller and finer movements made by the robotic arm (slave) and instrument tip. SS Useful in difficult anatomic areas (e.g. pelvis) where extremely fine dissection is warranted (e.g. nerve sparing dissection).

Disadvantages SS Higher

cost SS Needs expertise proper training SS Needs adequate setup.

Chapter 27

Nerve Injury

Important Topics

zzClasification zzPrinciples zzSpecific

of Nerve Injuries

of Nerve Repair

Nerve Injuries

‘Look at the sky. We are not alone. The whole universe is friendly to us and conspires only to give the best to those who dream and work.’

1056 

Illustrated Surgery—A

Road Map

Introduction

SS A

peripheral nerve trunk is made up of many nerve fibers. SS Each nerve fiber consists of an axon which is surrounded by myelin sheath formed by Schwann cells. SS Axon is the process of a nerve cell (neuron). Each neuron consists of a cell body, dendrites and one axon.

SS Group



of nerve fibers form fascicles. Each fascicle is surrounded by a layer of connective tissue, the perineurium. Many such fascicles are surrounded by connective tissue sheath, called the epineurium. Fascicles surrounded by the epineurium form the nerve fiber.



[Connective sheath of peripheral nerve are very much strong.]

Classification of Nerve Injuries SS Seddon's

classification zz Neuropraxia zz Axonotmesis zz Neurotmesis. SS Sunderland's classification zz 1st degree zz 2nd degree zz 3rd degree zz 4th degree zz 5th degree.

Nerve Injury 

Neuropraxia SS Local

block of conduction of nerve fibers due to localized demyelination of axon. SS Caused by compression of the nerve, mild stretching, etc. SS Recovery occurs spontaneously (takes days to weeks).

Axonotmesis SS Disruption

of axons and myelin sheath but perineurium and epineurium is intact degeneration occurs distal to the site of injury, so distal conduction is lost SS Recovery occurs by spontaneous regeneration (1–2 mm/day) SS Restoration of motor and sensory function is almost normal SS Caused by severe stretch injury of the nerve. SS Wallerian

1057

1058 

Illustrated Surgery—A

Road Map

Neurotmesis SS The

nerve is completely severed SS No recovery is possible unless surgical repair is undertaken SS Recovery is not so perfect, in aspect of both motor and sensory function SS Caused by cut injury (after trauma or iatrogenic), severe traction injury.

Sunderland's Classification degree ≡ Neuropraxia SS 2nd degree ≡ Axonotmesis SS 3rd degree ≡ Disruption of axon and endoneurial tube, intact perineurium and epineurium [Schwann cell basement membrane along with endoneurial collagen fiber form the endoneurial tube] SS 4th degree ≡ Only epineurium is intact SS 5th degree ≡ Epineurium is also disrupted. SS 1st

Clinical Features SS In

neuropraxia, paralysis of specific muscle groups but sensory and autonomic function is preserved. SS In axonotmesis, complete paralysis of specific muscle groups, sensory function and autonomic function (e.g. sweating) is also lost.

Nerve Injury 

1059

Management of Nerve Injury in Closed Injury SS A

loss of nerve function in a closed injury is usually due to stretch or compression. SS The type of injury is usually neuropraxia a axonotmesis. SS These type of injuries recover spontaneously, but you have to wait for few weeks if it is axonotmesis. SS If any doubt about neurotmesis, the wound should be explored for surgical repair of the nerve, as early repair carries better prognosis.

Management of Nerve Injury in Open Injury SS After

control of hemorrhage, the surgical exploration should be continued for search of injured nerve, if any clinical evidence of nerve injury is present. SS Routine exploration without any evidence of neurological deficit should be done in flexor compartment of forearm (in this region, nerves are vulnerable to damage.

Principles of Nerve Repair SS Timing

of repair zz Primary repair is indicated if— „„ Clean, incised wound „„ Surgeon has proper expertise „„ Proper instruments (e.g. loupes, operating microscopes) available. zz Secondary repair is perferable if— „„ Highly contaminated wound „„ Proper expertise and instruments not available. SS Type of repair zz Nerve suturing „„ Clean division of the nerve „„ After mobilization, suturing is technically not possible. zz Nerve grafting „„ Length of nerve is lost „„ After mobilization, suturing is technically not possible. SS Choice of suture material zz Fine (8/0 or fine), nonabsorbable (e.g. prolene or nylon) suture is preferable for median nerve, 6/0 for sciatic nerve and 10/0 for digital nerve.

1060 

Illustrated Surgery—A

Road Map

SS Basic

steps of primary suturing zz Minimal trimming of nerve ends. zz Correct orientation of the nerve ends to minimise crossover during recovery (pattern of nerve fascicles and surface blood vessels act as guide for proper alignment). zz Sutures are placed in the epineurium (epineurial repair). No need of interfascicular repair. zz Sufficient suturing to provide epineurial cover. zz Excessive suturing must be avoided.

SS Basic

steps of secondary repair— During wound exploration, it primary repair is technically not feasible, secondary repair to be planned. zz The severed ends should be fixed to surrounding tissue to prevent further retraction. zz During secondary repair, first to identify the nerve before dissecting the scar tissue. zz The neuroma of both ends must be excised until nerve bundles sprout from the cut surface. zz Orientation and suturing techniques are same as primary suturing. zz

Nerve Injury 

1061

SS Nerve

grafting— zz When direct nerve suturing is technically not feasible (defect > 3 cm), nerve grafting (cable grafting) is indicated. zz The nerves that can be used as graft are sural nerve, saphenous nerve, medial cutaneous nerve of forearm (these are nerves of long length carries sensation of small areas).

SS Postoperative

management— Immobilization for 3 weeks to protect the suture line from undue tension zz Regular physiotherapy to prevent contracture and muscle atrophy zz Tinel's sign is regularly elicited to monitor axon regeneration. zz

SS Specific

nerve injuries Facial nerve— „„ Neuropraxia after superficial parotidectomy is not uncommon. Recovery within few days is the rule. „„ If nerve is damaged or sacrificed for treatment purpose (involvement of facial nerve in carcinoma parotid), nerve graft is indicated (great auricular nerve is the preferable nerve for grafting). zz Recurrent laryngeal nerve— „„ Chance of injury is more in thyroid surgery (particularly in total thyroidectomy or re-do thyroid surgery). „„ Neuropraxia due to dissection recovers spontaneously. „„ In unilateral axonotmesis or neurotmesis, force of voice is reduced. „„ In bilateral injury, both vocal cords is shifted medially. Thereby, tracheostomy is indicated to maintain the airway. zz Brachial plexus— „„ Caused by— –– Traction injuries (in motor cycle accidents) –– Penetrating injuries in axilla –– Iatrogenic (during axillary lymph node dissection). „„ In traction injury, any grade of injury like neuropraxia, axonotmesis, neurotmesis, preganglionic injury (avulsion of the roots from the spinal cord) may occur. „„ According to degree of injury, the neurological deficit varies from paralysis and sensory loss of whole upper limb to only a specific group of muscles. zz Median nerve— „„ Usually injured at elbow (fracture distal humerus or dislocation of elbow joint) or at wrist (laceration or fracture distal radius). „„ Paralysis of pronators and flexor muscles of wrist and fingers (except flexor carpi ulnaris and medial part of flexor digitorum profundus). Thenar muscles are also paralyzed. „„ Sensory loss over the palmar aspect of thumb, index, middle finger and radial half of ring finger. zz

1062  zz

zz

zz

Illustrated Surgery—A

Road Map

Radial nerve— „„ Commonly injured in the radial groove in fracture of humeral shaft. „„ Recovery after repair is satisfactory. „„ 'Saturday night palsy' is neuropraxia or axonotmesis of radial nerve due to pressure over the nerve, as arm is placed over the sharp back of a chair in deep sleep. „„ Paralysis of brachioradialis, extensor digitorum and extensors of wrist. „„ Sensory loss over the dorsum of the thumb and first webspace.

Ulnar nerve— „„ Commonly injured following lacerations in forearm „„ Paralysis of small muscles of hand (except thenar muscles and lateral two lumbricals) „„ Sensory loss over the medial one and half of the ring finger.

Sciatic nerve— „„ Rarely injured after posterior dislocation of hip and fracture pelvis „„ Prognosis after repair is poor.

Chapter 28

Surgery of Hand

Important Topics

zzPrinciples

of Hand Surgery

zzInfections

in Hand

zzHand

Injuries

‘However many holy words you read, however many you speak, what good will they do you if you do not act on upon them?’

Surgery of Hand 

Introduction

SS Anesthesia

in hand surgery.

Different types anesthesia

Digital nerve block (without adrenalin)

SS Tourniquet—To

Brachial plexus block

General anesthesia

make a bloodless operative field for better visualization of structures.

SS Incisions—

Shorter incision in palmar aspect is better placed through flexion crease zz If longer exposure is needed, a 'mid-lateral incision' is preferable zz To prevent scar contracture formation, the incision should not cross the skin creases at right angle zz Incision should not cross the wrist at right angles. zz

1065

1066 

Illustrated Surgery—A

Road Map

SS Instrumentation—

General instruments are used but that must be of delicate variety (e.g. scissors, forceps) Bipolar diathermy is preferable zz Loupes and sometimes microscopes are required. zz zz

SS Position

of immobilization—

The position of immobilization is maintained by boxing glove dressing along with plaster back slab.

SS Measures

to prevent swelling and stiffness— zz Elevation—Hand must be elevated in a high sling. zz Position of immobilization— Previously described. zz Early joint movement—Movement of the joints should be stored as early as possible.

Surgery of Hand 

1067

Infections in Hand SS Acute paronychia—

Acute infection of the nail fold. Mild infection can be treated by antibiotics. zz If any pus collection, it must be drained by either separating the nail from nail bed or by partial excision of proximal part of nail. zz zz

SS Chronic paronychia—

A chronic fungal infection of the nail fold zz Treatment–keep the hands dry and application of antifungal ointment. SS Pulp space infection— zz Infection of the terminal pulp space does not spread proximally into the other pulp spaces due to fibrous septa, but it causes a rapid rise of pressure with sloughing of skin and osteomyelitis of terminal phalanx. zz Incision is made over the maximum point of tenderness. zz

SS Web space infection—

The web spaces are connected with the dorsum of the hand and proximal pulp spaces of the fingers. Natatory ligament is a fascial support in web space and acts as a partial barrier between volar and dorsal web space. zz At the stage of cellulitis, antibiotic therapy is sufficient. zz If abscess develops, it must be drained. The abscess should be drained through the most direct route. Incision should be in such position that digital nerves and vessels will least likely injured. zz

1068 

Illustrated Surgery—A

Road Map

Flexor tendon sheath infection— „„ The synovial sheath of the flexor tendons, those of index, middle and ring finger end proximally at the level of metacarpophalangeal joints. The synovial sheath of thumb is continuous with the radial bursa and synovial sheath of little finger is continuous with ulnar bursa. zz

Infection in the tendon sheath of index, middle and ring finger can't spread to the palm or forearm. Infection in the tendon sheaths of thumb and little finger can spread to the palm and forearm. „„ Patient complains of throbbing pain and swelling of the fingers. Passive movements cause severe pain. Infection of synovial sheath of thumb or radial bursa causes swelling of thumb and thenar eminence and makes the thumb slightly flexed. Infection of the ulnar bursa causes swelling of the whole hand, sometimes involvement of the wrist. „„ Surgical exploration of the affected tendon sheath or infected bursa is mandatory if the infection has not subsided after 48 hours of antibiotic management.

Surgery of Hand 

zz

1069

Palmar space infection— „„ The deep fascial spaces are consist of hypothenar, midpalmar and thenar spaces. „„ These spaces are prone to infection by penetrating trauma or from spreading from a neighboring compartment. „„ The characteristic presentation is loss of normal concavity of the palm along with swelling of the dorsum of the hand. „„ Passive movements of the fingers cause extreme pain. „„ Drainage of the pus is done through appropriate lumbrical canal.

Injuries in Hand SS Nerve

injury: zz Median nerve injury— „„ Wasting of thenar eminence „„ Inability to abduction and opposition of thumb „„ Absence of flexion of terminal interphalangeal joint of index finger. zz Ulnar nerve injury— „„ Wasting of hypothenar eminence „„ Inability to flexion of little and ring fingers „„ Inability to adduct and abduct the fingers. zz Radial nerve injury— „„ Inability to extend the wrist „„ Inability to extend the MCP joint of digits and interphalangeal joint of thumb.

1070 

Illustrated Surgery—A

Road Map

Tests to check the integrity of median, ulnar and radial nerve—

Tendon injury zz

Injury of extensor tendons— „„ Repair is done by classic tendon suturing technique. (with nonabsorbable, monofilament suture— Polypropylene). „„ Recovery is satisfactory.

Surgery of Hand 

zz

1071

Injury of flexor tendons— „„ Injury in zone 2 and 4— Primary repair should not be attempted, repair should be done by a tendon graft of palmaris longus or plantaris. „„ Injury in zone 1, 3 and 5— Primary repair is satisfactory.

Vascular Injury

Chapter 29

Neck Swelling

Important Topics

zzAnatomy zzNeck

of Neck

Swellings

‘Technology is just a tool. In terms of getting the kids working together and motivating them, the teacher is the most important.’

1074 

Illustrated Surgery—A

Road Map

Neck

Anatomy of Neck SS Neck

is divided into two triangles:

SS Neck

is divided by multiple fascial layers:

Neck Swelling  SS Neck

1075

is divided into seven lymphatic levels:

Neck Swellings [Among 800 lymph nodes in the body, about 300 of them are present in the neck]

Lymphadenopathy SS Enlargement

of the cervical lymph node is the most common cause of neck swelling

SS Causes—

Infection: Tuberculosis, tonsillitis, infective focus in oral and nasal cavity, larynx, pharynx, ear, face, toxoplasmosis. zz Metastatic deposit: Carcinoma in head-neck region (nasopharynx, tonsil, piriform fossa, supraglottic larynx), carcinoma in chest and abdomen. zz Primary neoplasms of lymphatic system: Hodgkin's lymphoma and nonhodgkin's lymphoma. zz Sarcoidosis zz

1076 

Illustrated Surgery—A

Road Map

Nonspecific lymphadenitis SS Due

to infective focus in oral and nasal cavity, larynx, pharynx and face SS Enlarged lymph nodes are tender SS Systemic symptoms like fever, malaise are usually present SS Treatment is— zz Treatment of the infective focus with appropriate antibiotics zz If abscess develops, then incision and drainage is indicated along with antibiotics.

Tuberculous lymphadenitis SS Common

cause of cervical lymphadenopathy in developing countries. SS Both human and bovine strain may be responsible. SS Tubercular bacilli can enter the body through the tonsil, from where it enters the cervical lymph nodes. SS In most of the cases, disease is limited to clinically affected cervical lymph nodes. Associated pulmonary and renal tuberculosis is rare. If any suspicion, then it have to be investigated. SS Common in children and young adults, but can occur at any ages. SS The upper deep cervical lymph nodes are most commonly affected. SS In the early stage, the nodes are appeared firm and discrete. If no treatment is instituted, caseation increases, infection spreads beyond the capsule of nodes. The nodes now become coalesce and appear as matted. Abscess develops in the center of the matted glands. Initially, the pus is confined by the deep cervical fascia, but later it bursts through it and reach the subcutaneous tissue. Now it has two compartments, one on either side of the deep fascia connected by a track. This is now called 'collarstud abscess'. The superficial abscess gradually enlarges, the skin overlying the abscess becomes eroded and then the discharging sinus develops.

Neck Swelling  SS Treatment

is antitubercular chemotherapy.

Metastatic deposit in cervical lymph node SS Commonest

cause of cervical lymphadenopathy in adults. SS The primary one is most oftently present in the buccal cavity (tongue, lip, buccal mucosa) and larynx. Other sites that have to be searched for— zz Skin of scalp, ear and external auditory meatus zz Nose, nasopharynx and maxillary antrum zz Thyroid zz Upper limb and both sides of chest wall zz Lungs zz Breast zz Stomach, pancreas, ovaries zz Testis.

SS Presents

as painless lump in neck. They are hard, irregular, tethered to the surrounding structures. SS Enlarged left supraclavicular lymph node is called Virchow's node. SS Presence of Virchow's node is called Troisier's sign. SS Treatment— Treatment of the primary disease. Radiotherapy/neck dissection for the lymph node.

1077

1078 

Illustrated Surgery—A

Road Map

Primary neoplasm of lymph node SS Malignant

lymphoma (Hodgkin's lymphoma and Non-Hodgkin's lymphoma) are most common primary tumor of lymphoid tissue. SS Painless lymphadenopathy, particularly in the posterior triangle along with systemic symptoms (e.g. fever, malaise, weight loss, pallor). SS Lymph nodes are smooth, discrete and rubbery in consistency. SS Other groups of lymph nodes (e.g. inguinal, axillary) are commonly enlarged. SS Chemotherapy is the treatment of choice.

Branchial Cyst SS It

is a remnant of a branchial cleft, usually the second branchial cleft. SS It is lined by squamous epithelium and contains turbid, thick white fluid full of fat globules and cholesterol crystals secreted by sebaceous glands of epithelial lining. SS Presents in adult life, a painless cystic swelling in upper lateral part of neck, appears beneath the junction of upper one-third and lower two-third of sternomastoid at its anterior border. SS USG and FNAC are useful methods for diagnosis. SS Excision is the treatment of choice.

Neck Swelling 

1079

Incision over the cyst along the skin crease. Incision should be atleast 2 cm below the angle of jaw to avoid the injury of marginal mandibular branch of facial nerve. zz The anterior (superficial) part of the cyst can be easily enucleated. If deep extension is present, then it must be excised with careful dissection. zz The deeper part of the cyst extends backwards and upwards in between the internal and enternal carotid artery to the region of tonsillar fossa. The hypoglossal and spinal accessory nerves are encountered during dissection of deeper extension of cyst. zz

Branchial Fistula SS It

is due to persistence of second branchial cleft. SS The external opening is near the lower third of sternomastoid at its anterior border, the internal opening in the tonsillar fossa.

SS The

tract is lined by ciliated columnar epithelium. SS Patient presents with small dimple in the lower part of the neck that discharges mucous or mucopurulent discharge with recurrent interval. SS If the upper end of the fistula obliterates, then it is called branchial sinus. SS Treatment is excision of sinus.

1080 

Illustrated Surgery—A

Road Map

Carotid Body Tumor (Chemodectoma) SS It

is the tumor of the chemoreceptor tissue of the carotid body. SS Carotid body usually presents on the posterior aspect of the bifurcation of common carotid artery, and adherent to the carotid wall. SS Patient presents with nontender, slowly growing lump. On examination, the lump is palpable at the level of hyoid bone, beneath the anterior border of sternomastoid muscle. Most of these tumors are hard, pulsatile. The common carotid artery is below the lump and the external carotid artery may pass over the lump. SS Carotid body tumors are also called 'Potato tumor', because of its shape and firm consistency. Most of these tumors are mistaken as cervical lymphadenopathy. SS Duplex study is to be done to delineate the nature of tumor. Carotid angiogram is indicated to demonstrate the carotid bifurcation and its relationship with the tumor. [FNAC is contraindicated.]

Neck Swelling 

1081

Cystic Hygroma SS Congenital

cystic abnormalities of lymphatic channels, develops due to failure of a cluster of lymphatic channels (jugular lymph sac) to connect into normal lymphatic pathways. SS It is composed of multiple uni and multiloculor cysts, each cyst contain clear lymph. SS Other sites of cystic hygroma—Axilla Groin Mediastinum. SS It may present at birth, may be so large to obstruct the delivery of the baby. May present in early infancy. SS Commonly located in the lower third of neck, at the base of the posterior triangle.

SS Treatment

is—Excision of all of the cyst. This excision demands a meticulous neck dissection. Injection of sclerosant before planning the surgery may diminish the size of the tumor, but it destroys the normal tissue planes, makes further surgery more cumbersome.

Sternomastoid Tumor SS Swelling

in the middle third of sternomastoid muscle, found in the neonates. is due to infarcted segment of muscle following trauma of birth. SS Mother notice a lump in neck with slight torticollis. SS If muscle damage is more and causes fibrosis, the tilting of head to one side will become prominent as the child grows. SS It

1082 

Illustrated Surgery—A

Road Map

Thyroglossal Cyst SS Most

common congenital anomaly of the neck. cyst represents the persistence of a part of thyroglossal duct, which begins at the foramen cecum and ends at the thyroid isthmus.

SS The

SS The

cyst can present anywhere between base of tongue and isthmus of thyroid. The two sites are common–subhyoid and suprahyoid at the midline. SS The swelling moves with deglutition as well as with protrusion of tongue. [Thyroglossal cyst may be the only thyroid tissue present in the body. So, before excision, thyroid scan should be done.]

SS Treatment

is excision of cyst along with whole thyroglossal tract including the body of hyoid bone. This is called Sistrunk's operation.

Chapter 30

Cleft Lip and Palate

Important Topics

zzClassification

of Cleft Lip

zzManagement

of Cleft Lip

zzClassification

of Cleft Palate

zzManagement

of Cleft Palate

‘When books are opened, we discover that we have wings.’

Cleft Lip and Palate 

1085

Cleft Lip SS Congenital



defects in head and neck is one of the common pathologies encountered by Pediatric and Plastic surgeons. Among head-neck defects, cleft lip and palate is the most common problem encountered.

SS During

embryogenesis, the five facial elements (one frontonasal, two lateral maxillary and two mandibular segments) merge to form the face and jaw. The frontonasal process forms the nose, the nasal septum, the nostrils, the philtrum of the upper lip and the premaxilla. The maxillary process form the cheek, the upper lip (except the philtrum), the upper jaw and palate. The mandibular processes form the lower jaw and lower lip. SS In classic theory, failure of fusion of the maxillary process and frontonasal process causes the cleft.

SS Incidence—

Racial difference is noted in prevalence zz Cleft lip and palate—45% zz Isolated cleft lip—15% zz Isolated cleft palate—40% zz Cleft lip and other malformations is about 14% zz In cleft lip, the deformity in left side is about 60%. zz

Etiology

1086 

Illustrated Surgery—A

Classification

Road Map

Cleft Lip and Palate  SS Defects

in cleft lip (unilateral)— zz Ill-defined philtral ridge on the cleft side zz Columella shorter on cleft side zz Lateral inferior and posterior displacement of the alar cartilage zz Vermilion thining zz Nasal floor defect zz Hypoplastic muscles and abnormal muscle insertions. SS Defects in cleft lip (bilateral)— zz Premaxilla is outwardly rotated and projected zz Prolabium is devoid of muscle zz Short columella.

1087

1088 

Illustrated Surgery—A

Road Map

Treatment multidisciplinary team consists of plastic surgeon, pediatric dentist, otorhinolaryngologist, speech therapist, pediatrician and psychologist is necessary for highest level of care. SS Timing of repair— Usually follow the 'rule of tens' 10 weeks of age 10 lbs body weight Hb% 10 mg/dl. SS Presurgical procedure— Presurgical orthodontics such as nasoalveolar segment alignment. SS Goal of repair—To make the appearance of lip, nose and face normal and also to make the development of speech, dentition and facial growth almost normal. SS Principles of cleft lip repair— zz Layered repair of skin, muscles and mucous membrane to restore symmetric shape and function zz To level cupid's bow and reconstruct the central philtrum of the lip zz Primary closure of the alveolar cleft (gingivoperiosteoplasty) at the time of primary lip repair zz Primary nasoplasty at the time of lip repair. SS The Millard rotation—Advancement flap technique is widely used for unilateral cleft lip repair. SS Delaire technique is another option. SS Mulliken technique is commonly used for bilateral cleft lip repair. SS A

Cleft Palate SS Due

to failure of fusion of the two palatal processes SS Etiology—Multifactorial.

Classification

Cleft Lip and Palate 

1089

SS Problems

due to cleft palate— zz Ineffective suckling and feeding (due to failure of creating negative intraoral pressure because of nasal and oral cavity continuity). zz Speech difficulties (due to velopharyngeal incompetence). zz Improper facial growth. zz Recurrent otitis media. SS Timing of repair— Before speech development (6– 18 months of age) SS Goal of surgical repair—To separate the oral and nasal cavities and formation of tight velopharyngeal valve. SS Different techniques of repair— zz Furlow palatoplasty—Double opposing z-plasty of soft palate. zz Von Langenbeck repair—Bipedicled hard palate mucoperiosteal flap repair. zz Wardill-Veau-Kilner repair—Unipedicled hard palate mucoperiosteal flap repair.

SS Secondary

management— zz Hearing difficulty—Child with cleft lip and palate are at increased risk of sensorineural deafness and conductive deafness (due to secretory otitis media). All children with cleft lip and palate should undergo assessment for deafness by auditory brainstem responses (ABR) and tympanometry before 1 year of age. Sensorineural deafness are treated with hearing aid and treatment of conductive deafness is controversial. zz Speech difficulty—Speech assessment should be started from 1½ years of age and at regular interval. Assessment is done by— „„ Videofluoroscopy „„ Aerophonoscopy „„ Nasoendoscopy. Difficulties are managed by— „„ Speech therapy „„ Veloplasty „„ Pharyngoplasty. SS Dental abnormalities— zz Child with cleft lip and palate should undergo regular dental examination. zz Delayed eruption, variation in number and ill health teeth may present. zz Preventive measures, e.g. fluoride supplements, maintenance of dental hygiene is essential for disease-free dentition. SS Orthodontic management—By alveolar bone graft/maxillary osteotomy.

Chapter 31

Anesthesia

Important Topics

zzTypes zzLocal

of Anesthesia Anesthesia

zzSpinal

Anesthesia

zzEpidural zzGeneral

Anesthesia Anesthesia

zzPreoperative zzComplication

Evaluation of GA

‘I keep six honest serving men; they taught me all I know. Their names are what, why, when, how where and who.’

1092 

Illustrated Surgery—A

Road Map

Introduction

SS The

discipline of anesthesia mainly controls three components during any surgical procedure: zz Pain zz Consciousness zz Movement.

Types of Anesthesia Anesthesia

Local

Regional (spinal/epidural)

General

Local Anesthesia SS Local

anesthesia reversibly block impulse conductions along nerve axons by blocking voltage-gated sodium channels (small-diameter unmyelinated fibers, such as type C pain fibers are most sensitive whereas heavily myelinated, thicker fibers are least). SS 2 classes of local anesthetics (according to chemical structure).



Amides • Lidocaine • Bupivacaine • Prilocaine • Ropivacaine

Esters • Cocaine • Procaine • Benzocaine

Anesthesia 

1093

SS Amides

are metabolized in the liver SS Esters are hydrolyzed in the blood by pseudocholinesterase.

Local anesthetics can be used in various routes

Nerve block

EMLA cream is composed of 2.5% lidocaine and 2.5% prilocaine. Its topical use is very much useful for anesthetizing the skin before minor vascular access, superficial laser skin treatment.

1094 

Illustrated Surgery—A

Road Map

Systemic toxicity

CNS manifestations • Sleepiness • Circumoral and tongue numbness • Metallic taste • Tinnitus • Visual disturbances • Slurred speech • Seizures

SS Treatment

of toxicity— zz Oxygen and airway support zz For seizure—Bezodiazepine or thiopental zz Cardiovascular support. SS Precautions to be taken to avoid toxicity— zz Before injecting local anesthetic, always aspirate to exclude vascular entry. SS Calculation of the toxic dose of the local anesthetic— zz Toxic dose of lidocaine 5 mg/kg [1% = 10 mg/ ml] zz Toxic dose of bupivacaine 3 mg/kg.

CVS manifestations • Hypotension • ↑P–R interval • Bradycardia • Cardiac arrest [Bupivacaine is more cardiotoxic than other local anesthetics.] [Inadvertent IV injection of bupivacaine results in profound hypotension, VT, VF, complete A–V block that is refractory to treatment.]

Anesthesia 

1095

SS Epinephrine

as an additive: zz Advantages „„ Reduces local bleeding „„ Absorption of local anesthetic from injection site is delayed, so the anesthetic will work for a longer period „„ Systemic absorption is delayed, so chance of toxicity will be less. Epinephrine containing anesthetics should not be injected in body parts which are supplied by end arteries.

Spinal Anesthesia SS Local

anesthetics is injected into the CSF surrounding the spinal cord, in the subarachnoid space resulting in sensory, motor and sympathetic blockade below the level of block. SS Site of injection is usually below L1 or L2 (needle is passed between two lumbar spinous processes). SS Lidocaine, bupivacaine are the commonly used anesthetic agents. SS Indicated in lower abdominal operations, in urologic surgery, surgery in perineum and lower extremity.

Advantages SS Complications

of general anesthesia can be avoided SS Patient is awake.

Complications SS Hypotension

(particularly if patient is not adequately prehydrated)

SS Bradycardia SS Postdural SS Radicular

puncture headache (is related to diameter of spinal needle, female gender, younger age) neuropathy (temporary)

SS Backache SS Cardiorespiratory

compromise (if more cephaled spread).

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Road Map

Spinal anesthesia

Epidural anesthesia

Epidural Anesthesia SS Local

anesthetic is injected into lumbar or thoracic epidural space SS A epidural catheter is placed into epidural space after locating the space with needle SS Catheter can be used for repeated dosing SS Postop analgesics can be administered for several days through this catheter.

Advantages SS The

onset of sympathetic blockade and hypotension is slower in comparison to spinal anesthesia.

Anesthesia 

Complications SS Similar

to spinal anesthesia.

Specific complications SS Epidural

hematoma (in patient receiving oral or parenteral anticoagulants) SS Epidural abscess.

General Anesthesia General anesthesia produce three separate effects:

Effect of general anesthesia

Unconsciousness and amnesia

Analgesia

General anesthesia

SS General

anesthesia is achieved by both intravenous and inhalational agents. agents—Used for induction of anesthesia.

SS Intravenous

Muscle relaxation

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Road Map

SS IV



agents (causing unconsciousness and amnesia)— 1. Barbiturates— Thiopental is a barbiturate that is commonly used. They act on GABA receptor, resulting in inhibition of excitatory synaptic transmission. „„ Barbiturates are anticonvulsants and reduces cerebral metabolism „„ In higher doses, it is myocardial depressant. 2. Propofol— It acts on GABA receptor resulting in inhibition of synaptic transmission. „„ It has bronchodilator property „„ It may cause hypotension. Anesthesia of choice for ambulatory surgery. 3. Etomidate— It acts on GABA receptor. 4. Ketamine— zz It acts on NMDA receptor zz It is a dissociative anesthetic, producing analgesia also zz Patient may present with delirium and hallucinations while regaining consciousness zz It increases heart rate and BP zz It can maintain BP in hypovolemic patients by sympathetic stimulation zz It is myocardial depressant.

IV Agents (Causing Reduction of Anxiety as well as Amnesia) Benzodiazepines SS Acts

on GABA receptor SS Commonly used benzodiazepines are—Diazepam, lorazepam, midazolam SS Cause peripheral vasodilation and hypotension SS They are also good anticonvulsants SS When it is combined with opioid analgesics, it may cause respiratory depression.

IV Agents (Causing Analgesia) Opioid analgesics on μ-receptor in brain and spinal cord used opiod analgesics are: morphine, codein, fentanyl (Synthetic opiod). [Remifentanil (a fentanyl analog) undergo rapid hydrolysis that is not affected by age, weight, renal or hepatic function.] SS Acts

SS Commonly

Anesthesia 

Nonopioid analgesics SS Ketamine—Previously

described SS Ketorolac—Acts by inhibiting both COX-1 and COX-2.

IV Agents (Causing Neuromuscular Block) SS Acts

on postsynaptic receptors in the neuromuscular junction to antogonize the effects acetylcholine. SS 2 types of neuromuscular blockers— zz Nondepolarizing agents „„ Vecuronium „„ Pancuronium „„ Atracuronium. zz Depolarizing agents „„ Succinylcholine. SS Succinylcholine— zz Rapid acting (< 60 seconds) depolarizing neuromuscular blocker. Also rapid offset (5–8 minutes). zz Rapidly hydrolyzed by plasma cholinesterase. zz Causes hyperkalemia. Patient with severe burn or trauma may develop arrhythmia or cardiac arrest. zz Can cause increase in intraocular, intracranial and intragastric pressures. zz Malignant hyperthemia—A rare but fatal complication. SS Vecuronium— zz Intermediate duration ( 1 hour) nondepolarizing blocker. zz Excreted by kidneys in unchanged form. SS Atracurium— zz Intermediate-acting (