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This fifth edition, of nearly 1300 pages, is a comprehensive guide to the complete field of surgery for undergraduate medical students.

The book covers surgical procedures for disorders in all systems of the body and includes discussion on surgical anatomy. Each topic has been fully revised and expanded to include the very latest information in the specialty.

The new edition is highly illustrated with nearly 3000 clinical photographs and figures. Key physical signs for each disorder are highlighted in boxes with different colour shades.

Key Points

Comprehensive guide to complete field of surgery for undergraduate medical students

Fully revised and expanded fifth edition with many new topics

Highly illustrated with nearly 3000 clinical photographs

Previous edition (9789350259443) published in 2012
JP Medical Ltd
ISBN 13:
PDF, 66.12 MB
다운로드 (pdf, 66.12 MB)

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Just loved the book. So simple and precise
14 August 2020 (19:15) 

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1. General Surgery
A. Wounds and Wound Healing 1

Wounds 1; Classification of Wounds 1; Wound Healing 6; Compartment Syndrome 10; Crush Injury 11;
Crush Syndrome 11; Degloving injuries 12; Scar 12; Keloid 12; Hypertrophic Scar 13; Problems with
Wound Healing 14

B. Ulcer 15

Ulcer 15; Granulation Tissue 18; Investigations for an Ulcer 9; Management of an Ulcer 20; Traumatic
Ulcer 22; Trophic Ulcer (Pressure Sore/Decubitus Ulcer) 22; Ulcer Due to Chilblains 23; Ulcer Due to
Frostbite 24; Martorell’s Ulcer 24; Arterial/Ischaemic Ulcer 24; Bairnsdale Ulcer 24; Carcinomatous Ulcer
(Epithelioma, Squamous Cell Carcinoma) 24; Marjolin’s Ulcer 25; Rodent Ulcer 25; Melanotic Ulcer 25;
Diabetic Ulcer 26; Meleney’s Ulcer (Postoperative Synergistic Gangrene) 27; Lupus Vulgaris 27; Tuberculous
Ulcer 28; Bazin’s Disease (Erythrocyanosis Frigida/Erythema Induratum) 28; Tropical Ulcer 28; Venous
Ulcer (Gravitational Ulcer) 29; Syphilitic Ulcer 29; Soft Chancre/Soft Sore/Ducrey’s Ulcer/Chancroid/Bubo 29;
Climatic Bubo/Tropical Bubo 29

C. Sinus and Fistula 31

Sinus 31; Fistula 31; Median Mental Sinus 33; Sequestrum 34; Preauricular Sinus 35

D. Infectious Diseases 36

Surgical Infection 36; Cellulitis 36; Erysipelas 39; Erysipeloid Disease 39; Lymphangitis 39; Abscess 40;
Metastatic and Pyaemic Abscess 45; Bacteraemia 45; Septicaemia 45; Pyaemia 45; Boil (Furuncle) 46;
Hidradenitis Suppurativa 46; Carbuncle 47; Pott’s Puffy Tumour 48; Pyogenic Granuloma (Granuloma
Pyogenicum) 48; Impetigo 49; Erythrasma 49; Scrum Pox 49; Tetanus 49; Gas Gangrene 53;
Tuberculosis 55; Leprosy 56; Syphilis (Great Pox) (French Disease) 56; Actinomycosis 57; Madura
Foot (Mycetoma Pedis) 58; Rabies (Hydrophobia) 59; Rabies in Dogs 61; Anthrax 62; Nosocomial
and Opportunistic Infections 62; Necrotising Fasciitis 63; Acute Pyomyositis 64; Surgical Site infection
(SSI) 65; HIV Infection and AIDS 67

E. Swellings 71

Lipoma 71; Cysts 74; Dermoids 75; Sebaceous Cyst (Wen, Epidermoid Cyst) 78; Glomus Tumour 81;
Papilloma 81; Warts 82; Fibrom; a 82; Bursae 83; Semimembranosus Bursa 85; Morrant Baker’s
Cyst 85; Lymph Cyst (Lymphatic Cyst) 86; Lymphangioma 86; Calcinosis Cutis 86; Neuroma 87;
Neurofibroma 87; Neurilemmoma (Schwannoma) 89; Ganglion 90; Chordoma 90; Epignathus 90

F. Electrolyte and Nutrition 92

Normal Physiology 92; Water Loss (Volume Loss) 92; Water Excess (ECF Volume Excess) 92; ECF
Loss 93; ECF Excess 93; Hyponatraemia 93; Hypernatraemia 94; Hypokalaemia 94; Hyperkala­
emia 94; Hypermagnesaemia 95; Hypomagnesaemia 95; Acid-Base Balance 95; Metabolic
Alkalosis 96; Respiratory Alkalosis 96; Metabolic Acidosis 96; Respiratory Acidosis 97; Anion Gap 97;
Fluid Therapy 97; Nutrition 101; Gastrostomy 102; Jejunostomy 103; Total Parenteral Nutrition
(TPN) 104; Refeeding Syndrome 105; Obesity and Morbid Obesity 105; Different Surgeries 106

G. Shock 110

Shock 110; Stages of Shock 111; Effects of Shock 111; Clinical Features of Shock (Hypovolaemic Shock) 114;
Assessment, Investigations and Monitoring 114; Central Venous Pressure (CVP) 115; Pulmonary
Capillary Wedge Pressure (PCWP) 116; Systemic Inflammatory Response Syndrome (SIRS) 116;
Multiple Organ Dysfunction Syndrome (MODS) 117; Oxygen Therapy 117; Topical O2 Therapy 117;



SRB's Manual of Surgery
Cardiac Arrest 117

H. Haemorrhage and Blood Transfusion 119

Haemorrhage 119; Blood Transfusion 122; Massive Blood Transfusion 124; Autologous Blood Transfusion 124;
Artificial Blood 124; Erythropoietin 125; Tourniquets 125; Disseminated intravascular Coagulation 126;
Mechanism of Blood Coagulation (Haemostasis) 126

I. Burns 128

Burns 128; Management of Burns 132; Eschar 134; Contracture in Burn Wound 135; Electrical Burns 136;
Inhalation injury 137; Chemical Burns 138

J. Trauma 139

Triage 139; Concepts in Trauma Management 141;
Injuries 142; Blast Injuries 143; Penetrating Injuries
Abdomen 146; Duodenal Injury 148; Pancreatic Injury
Liver Injury 149; Splenic Injury 149; Renal Injury
Compartment Syndrome 150; Seat-Belt Injuries 151

Spinal Injury 142; Neck injuries 142; Bullet
143; Abdominal Trauma 144; Blunt Trauma of
148; Small Bowel Injury 148; Colonic Injury 149;
150; Urinary Bladder Injury 150; Abdominal

K. Hand and Foot 152

Hand 152; Hand Infections 153; Acute Paronychia 156; Chronic Paronychia 156; Apical Subungual
Infection 156; Terminal Pulp Space Infection (Felon) 157; Infection of Web Spaces 158; Deep Palmar
Space Infection 158; Space of Parona Infection 160; Acute Suppurative Tenosynovitis 160; Compound
Palmar Ganglion 161; ORF 161; Milker’s Nodes/Nodules (Milkmaid Blisters) 161; Hand Injuries 161;
Dupuytren’s Contracture 163; Volkmann’s Ischaemic Contracture 164; Syndactyly 164; Mallet Finger
(Base Ball Finger) 165; Heberden’s Nodes 165; Spina Ventosa 165; Foot 165; Callosity 165; Corn 166;
Plantar Fasciitis (Policeman’s Heel) 166; Ingrowing Toe Nail (Onychocryptosis) 166; Onychogryphosis 167;
Onychomycosis 167; Athlete’s Foot 167; Hallux Valgus 167

L. Arterial Diseases 169

Surgical Anatomy of Thoracic Outlet 169; Arteries of Upper Limb 169; Arteries of Lower Limb 169;
Arterial Diseases 170 ; Intermittent Claudication 170 ; Rest Pain 170 ; Limb Ischaemia 171 ;
Pregangrene 171; Gangrene 171; Different Levels of Arterial Obstruction 172; Other Features
of Poor Circul­ation 173; Investigations for Arterial Diseases 174; Diseases of the Arteries 176;
Atherosclerosis 176; Thromboangiitis Obliterans (TAO) Syn. Buerger’s Disease 178; Takayasu’s Pulseless
Arteritis 182; Raynaud’s Phenomenon 182; Temporal Arteritis 184; Treatment of Arterial Diseases 184;
Subclavian Steal Syndrome 189; Acute Arterial Occlusion 189; Traumatic Acute Arterial Occlusion 190;
Embolism 190; Reperfusion Injury 192; Saddle Embolus 193; Embolectomy 193; Fat Embolism 194;
Air/Gas Embolism 195; Therapeutic Embolisation 195; Caisson’s Disease or Decompression Disease 195;
Aneurysm 195; Mycotic Aneurysm 197; Abdominal Aneurysm 197; Abdominal Aortic Aneurysm
(AAA) 198; Peripheral Aneurysm 201; Carotid Artery Aneurysm (Extracranial) 202; Dissecting
Aneurysm 203; Erythromelalgia (Erythralgia) 204; Livedo Reticularis 204; Polyarteritis Nodosa 204;
Scleroderma/Systemic Sclerosis 204; Acrocyanosis (Crurum Puellarum Frigidum) 204; Gangrene 205;
Diabetic Foot and Diabetic Gangrene 206; Trophic Ulcer 207; Bedsores (Decubitus Ulcer) (Pressure
Sores) 208; Frostbite 208; Ainhum 208; Endovascular Surgeries 208; Upper Limb Ischaemia 209;
Arterial Substitutes 211

M. Vascular Lesions and Hamartoma 213

Vascular Anomalies 213; Haemangioma 213; Vascular Malformations 216; Cirsoid Aneurysm 217;
Arteriovenous Fistula (AVF) 217; Campbell De Morgan Spots 220; Parry-Romberg Disease 220;
Hamartomata 220

N. Venous Diseases 221

Anatomy of Veins of Lower Limb 221; Physiology of Venous Blood Flow in Lower Limb 222; Deep Vein
Thrombosis 222; Varicose Veins 226; Venous Ulcer (Gravitational Ulcer) 238; Compression Therapy
for Varicose Veins 241; Thrombophlebitis 241; Klippel-Trenaunay Syndrome 242; Anticoagulants 242;
Heparin (Unfractionated/UFH) 242; Low Molecular Weight Heparin (LMWH) 242; Oral Anticoagulants 242;
Warfarin 243; Direct Thrombin Inhibitors 243; Antiplatelet Drugs 243; Pulmonary Embolism 243

O. Lymphatics 245

Surgical Anatomy 245; Lymphangiography 246; Isotope Lymphoscintigraphy 247; Lymphoedema 247;
Lymphomas 253; Hodgkin’s Lymphoma (HL) 254; Non-Hodgkin’s Lymphoma (NHL) 258; Mantle Cell
Lymphoma 259; Malt Lymphoma (Maltoma) 259; Burkitt’s Lymphoma (Malignant Lymphoma of Africa) 260;
Cutaneous T Cell Lymphoma 260; Chylous Ascites 261; Chylothorax 261; Chyluria 261; Sarcoidosis 262

P. Peripheral Nerves 263

Peripheral Nerve Injuries 263; Tinel’s Sign 265; Brachial Plexus Injuries 265; Causalgia 265; Median
Nerve Injury 266; Carpal Tunnel Syndrome 266; Ulnar Nerve Injury 268; Claw Hand 268; Radial Nerve
Injury 269; Common Peroneal Nerve Injury 270; Foot Drop 270; Medial Popliteal Nerve Injury 270;
Axillary Nerve Injury 271; Long Thoracic Nerve Injury (Nerve of Bell) 271; Meralgia Paraesthetica 271

Q. Neoplasm 272

Definition 272; Dysplasia 273; Carcinoma In Situ 273; Aetiologic Factors 273; Spread of Malignant
Tumours 274; Grading of Tumour 274; Staging of the Tumour 275; Paraneoplastic Syndromes 275;
Investigations for Neoplasm 275; Management Strategy for Cancers 280

R. Skin Tumours 282

Anatomy 282; Classification of Skin Tumours 283; Skin Adnexal Tumours 283; Dermatofibroma
(Sclerosing Angioma or Subepithelial Benign Nodular Fibrosis) 284 ; Dermatofibrosarcoma
Protuberans 285; Keratoacanthoma (Molluscum Sebaceum) 285; Rhinophyma (Potato Nose) (Bottle
Nose) 286; Seborrhoeic Keratosis (Seborrhoeic Wart, Basal Cell Papilloma) 286; Squamous Cell
Carcinoma (Epithelioma) 287; Marjolin’s Ulcer 290; Basal Cell Carcinoma (Rodent Ulcer) 290; Turban
Tumour 292; Naevi 292; Melanoma 294

S. Sarcomas 302

Sarcoma 302; Liposarcoma 308; Fibrosarcoma (11%) 308; Malignant Fibrous Histiocytoma (MFH) 310;
Leiomyosarcoma 310; Rhabdomyosarcoma 310; Chondrosarcoma 310; Haemangiosarcoma 310;
Lymphangiosarcoma 311; Synovial Sarcoma (7%) 311; Malignant Peripheral Nerve Sheath Tumour
(MPNST) (3%) 311; Kaposi’s Sarcoma 311

T. Amputations 312

Amputation 312; Complications of Amputations 318; Prosthesis 320

U. Reconstruction 321

Graft 321; Skin Grafts 321; Flaps 324; Tendon 330; Tendon Repair 331; Tendon Transfer 331; Tendon
Graft 331

V. Transplantation 332

Preoperative Evaluation 332; Organ Procurement 332; Graft Rejection (Transplant Rejection) 333;
Immunosuppressive Agents 334; Renal Transplantation 335; Liver Transplantation 336; Bone Marrow
Transplantation 338; Pancreatic Transplantation 338; Small Bowel Transplantation 338; Dialysis 339;
Cimino Fistula (Cimino-Brescia) 340

W. Stings and Bites 341

Snake Bite 341; Spider Bite 341; Bee Bite 342; Mammalian Bite 342

X. Pain 343

Gate Control Theory 343

2. Faciomaxillary Diseases


Diseases of the Palate 346; Orthopantomogram (OPG) 346; Cleft Lip and Cleft Palate 347; Maxillofacial
Injuries 350; Primary Care (Early Care) in Maxillofacial Injuries 351; Fracture Middle Third Area 352;
Zygomatic Complex Fracture 353; Fracture of the Mandible 355; Dislocation of the Mandible 357; Jaw
Tumours 358; Epulis 358; Ameloblastoma (Adamantinoma, Eve’s Disease, Multilocular Cystic Disease
of the Jaw) 359; Dentigerous Cyst (Follicular Odontome) 360; Dental Cyst (Radicular Cyst, Periapical
Cyst) 361; Osteomyelitis of Jaw 361; Alveolar Abscess (Dental Abscess) 362; Fibrous Dysplasia of
Bone/Jaw 362; Cherubism 364

3. Oral Cavity




SRB's Manual of Surgery
Ranula 365; Sublingual Dermoids 366; Stomatitis 367; Cancrum Oris (Noma) 367; Syphilitic Lesions
of Oral Cavity 368; Leukoplakia 368; Erythroplakia 369; Oral Submucosal Fibrosis 369; Premalignant
Conditions of Oral Cavity 369; Oral and Upper Aerodigestive Cancers 370; Cheek 372; Carcinoma
Cheek/Buccal Mucosa 372; Lip 383; Neoplasm of Lip 384; Carcinoma Lip 384; Tongue 387; Tongue
Ulcers 388; Benign Tumours of Tongue 389; Tongue Fissure 389; Glossitis 390; Tongue Tie 391;
Carcinoma Tongue 391; Carcinoma of Posterior One-third/Base of the Tongue 394; Nasopharyngeal
Carcinoma 395; Maxillary Tumours 395; Malignant Tumours of Tonsil 398; Carcinoma Hard Palate 398;
Laryngeal Tumours 399; Malignant Tumours of Larynx 399; Trismus 402

4. Salivary Glands


Anatomy 403; Saliva 406; Sialography 406; Salivary Calculus and Sialadenitis 406; Sialosis 409;
Sialectasis 409; Recurrent Childhood Parotitis 409; Parotid Abscess (Suppurative Parotitis) 409; Parotid
Fistula 410; Sjögren’s Syndrome 411; Mikulicz Disease 412; Salivary Neoplasms 412; Pleomorphic
Adenoma (Mixed Salivary Tumour) 413; Adenolymphoma (Warthin’s Tumour, Papillary Cystadenoma
Lymphomatosum) 415; Oncocytoma (Oxyphil Adenoma) 416; Basal Cell Adenoma 416; Mucoepidermoid
Tumour 416; Adenoid Cystic Carcinoma (10% of Salivary Tumours) 417; Acinic Cell Tumour 417;
Malignant Mixed Tumour (MMT) 417; Adenocarcinoma of Salivary Glands 417; Squamous Cell Carcinoma
of Salivary Glands 417; Submandibular Salivary Gland Tumours 417; Management of Malignant Salivary
Tumours 418; Minor Salivary Gland Tumours 420; Parotid Lymphoma 421; Parotidectomy 421; Frey’s
Syndrome (Auriculotemporal Syndrome, Gustatory Sweating) 423; Facial Nerve Injury (Lower Motor
Nerve Lesion, Surgically Related) 424

5. Neck


Anatomy of Lymphatics of Head and Neck 426; Thoracic Outlet Syndrome (TOS) 427; Cervical Rib 428;
Branchial Cyst 431; Branchial Fistula 432; Pharyngeal Pouch (Zenker's) 433; Laryngocele 434;
Cystic Hygroma (Cavernous Lymphangioma) 435; Ludwig’s Angina 436; Parapharyngeal Abscess 437;
Retropharyngeal Abscess 437; Subhyoid Bursitis (Retrohyoid Bursa/Boyer’s Bursa) 438; Carotid Body
Tumour (Potato Tumour, Chemodectoma, Nonchromaffin Paraganglioma) 438; Torticollis (Wry Neck) 440;
Sternomastoid Tumour 440; Tuberculous Lymphadenitis 441; Cold Abscess 444; Secondaries in Neck
Lymph Nodes 445; Chemotherapy for Head and Neck Cancers 452

6. Thyroid


Development 453; Anatomy 453; Physiology 455; Congenital Anomalies 455; Thyroid Function Tests 458;
FNAC of Thyroid 458; Classification of Goitre 459; Diffuse Hyperplastic Goitre 460; Multinodular Goitre
(MNG) 460; Discrete Thyroid Nodule 462; Solitary Thyroid Nodule 463; Retrosternal Goitre 466;
Thyrotoxicosis and Hyperthyroidism 467; Radioactive Iodine 477; Thyroid Neoplasms 478; Differentiated
Thyroid Carcinoma (DTC) 478; Papillary Carcinoma of Thyroid (PCT) 480; Follicular Carcinoma of
Thyroid (FCT) 482; Anaplastic Carcinoma of Thyroid 485; Medullary Carcinoma of Thyroid (MCT) 486;
Malignant Lymphoma 488; Hashimoto’s Thyroiditis (Struma Lymphomatosa) 488; De-Quervain’s Subacute
Granulomatous Thyroiditis 489; Riedel’s Thyroiditis (0.5% Common) 489; Thyroid incidentaloma 489;
Thyroidectomy 490; Emil Theodor Kocher 495; Kocher’s Test 495; Hypothyroidism 495; Recurrent
Laryngeal Nerve Palsy 496

7. Parathyroids and Adrenals


Anatomy 499; Calcium 499; Hyperparathyroidism (HPT) 500; Parathyroidectomy 503; MEN Syndrome
(MEA Syndrome) 505; Apudomas 505; Hypoparathyroidism 505; Tetany 506; Adrenals 507; Adrenal
Cortical Tumours 507; Adrenocortical Carcinoma 507; Cushing’s Syndrome 508; Conn’s Syndrome 508;
Virilising Syndrome or Adrenogenital Syndrome 509; Neuroblastoma 509; Phaeochromocytoma 510

8. Breast
Anatomy 512; Mammography 515; Aberration of Normal Development and Involution (ANDI) of The
Breast 516; Fibroadenoma 516; Fibrocystadenosis (Fibrocystic Disease of the Breast/Mammary
Dysplasia/Cyclical Mastalgia with Nodularity) 518; Sclerosing Adenosis 519; Phylloides Tumour
(Cystosarcoma Phylloides/Serocystic Disease of Brodie) 520; Mastalgia (“Pain in the Breast”) 521;
Traumatic Fat Necrosis 521; Galactocele 522; Mastitis 522; Antibioma 524; Duct Ectasia 525; Mondor’s
Disease 525; Tuberculosis of the Breast 525; Breast Cysts 526; Galactorrhoea 527; Gynaecomastia 527;


Duct Papilloma 528; Zuska-Atkins Disease 529; Mammary Fistula of Atkins 529; Carcinoma Breast 529;
TNM Staging of Carcinoma Breast 539; Management of Early Carcinoma Breast 553; Advanced
Carcinoma Breast 557; Prognostic Factors in Carcinoma Breast 559; Prophylactic Mastectomy 560;
Carcinoma of Male Breast 560; Breast Reconstruction 561; Breast Implants 563; Nipple Retraction 564

9. Peritoneum


Anatomy 565; Physiology 565; Acute Peritonitis 566; Primary Peritonitis 566; Secondary Peritonitis 566;
Tertiary Peritonitis 566; Spontaneous Bacterial Peritonitis 572; Sclerosing Peritonitis 573; Biliary Peritonitis 573;
Postoperative Peritonitis 573; Other Forms of Peritonitis 573; Pelvic Abscess 574; Subphrenic Spaces
and Subphrenic Abscess 575; Mesenteric Cysts 577; Mesenteric Panniculitis 578; Acute Mesenteric
Lymphadenitis 578; Mesenteric Malignancy 578; Mesenteric Trauma 579; Peritoneal Malignancy 579;
Omental Cyst 580; Omental Torsion 580; Omental Tumour 580

10. Abdominal Tuberculosis


Abdominal Tuberculosis 581; Ileocaecal Tuberculosis 582; Ileal Tuberculosis 587; Peritoneal
Tuberculosis 587; Tuberculous Mesenteric Lymphadenitis 590; Ano-recto-sigmoidal Tuberculosis 591;
Tuberculosis of the Omentum 591

11. Liver


Surgical Anatomy of Liver 592; Liver Function Tests (LFT) 593; Alpha Fetoprotein (AFP) 594; Liver
Biopsy 594; Liver injury 594; Infections of Liver 596; Liver Tumours 605; Liver Cysts 613; Congenital
Liver Cysts 613; Portal Hypertension 614; Oesophageal Varices 617; Emergency Management
in Severe Haemorrhage 619; Portal Hypertensive Gastropathy 624; Ascites 624; Ascites in Portal
Hypertension 626; Budd-Chiari’s Syndrome 626; Hepatic Failure 627; Hepatic Encephalopathy 627;
Hepatorenal Syndrome 628; Hepatic Resection 628; Portal Biliopathy 630

12. Gallbladder


Surgical Anatomy 631; Oral Cholecystogram (OCG; Graham-Cole Test) 633; IV Cholangiogram 633;
Endoscopic Retrograde Cholangio-pancreatography (ERCP) 633 ; Percutaneous Transhepatic
Cholangiography (PTC) 634 ; Magnetic Resonance Cholangio-pancreato­g raphy (MRCP) 634 ;
Radioisotope Scan Study 635; Peroperative Cholangiogram 635; Postoperative T-tube Cholangiogram 635;
Congenital Anomalies of Gallbladder 635; Choledochal Cysts 636; Caroli’s Disease 638; Biliary
Atresia 638; Gallstones 640; Acute Cholecystitis 643; Acute Acalculous Cholecystitis (5%) 645; Mirizzi
Syndrome 645; Empyema Gallbladder 646; Mucocele of The Gallbladder 647; Chronic Cholecystitis 647;
Murphy’s Sign 648; Gallstone Ileus 648; Cholecystoses 649; Dissolution Therapy for Gallstones 650;
Choledocholithiasis 650; Sump Syndrome 653; Courvoisier’s Law (Sign) 654; Surgical Jaundice
(Obstructive Jaundice) 654; CBD Strictures (Biliary Strictures) 657; Sclerosing Cholangitis 658;
Gallbladder Polyp 658; Benign Biliary Papilloma 658; Carcinoma Gallbladder 659; Cholangiocarcinoma
(Bile Duct Carcinoma) 661; Klatskin Tumour 661; Biliary Fistulas 662; Hemobilia 662; White Bile 663;
Cholecystectomy 663; Open Approach Cholecystectomy 663; Laparoscopic Cholecystectomy 664;
Single Incision Laparoscopic Surgery (SILS) in Cholecystectomy 665; Bile Duct Injuries 666; Postcholecystectomy Syndrome (15%) 667; Biliary Dyskinesia 667

13. Spleen


Surgical Anatomy 668; Functions of the Spleen 668; Splenunculi (30%) 669; Splenic Injury (Rupture
Spleen) 669; Splenomegaly 672; Hereditary Spherocytosis 673; Immune Haemolytic Anaemia 673;
Thalassaemia (Mediterranean Anaemia/Cooley’s Anaemia/Erythroblastic Target Cell Anaemia) 674;
Sickle Cell Disease 674; Idiopathic (Immune) Thrombocytopaenic Purpura (ITP) 674; Thrombotic
Thrombocytopaenic Purpura (TTP) 675; Splenectomy 676; Overwhelming Post-splenectomy Infection
(OPSI) 677; Splenic Artery Aneurysm 677; Splenic Abscess 678; Hypersplenism 678; Splenic Cyst 678;
Atraumatic Rupture of Spleen 679

14. Pancreas




SRB's Manual of Surgery
Anatomy 680; Serum Amylase 681; Serum Lipase 682; Magnetic Resonance Cholangio-pancreatography
(MRCP) 682; Pancreatitis 682; Acute Pancreatitis 683; Complications of Acute Pancreatitis 689;
Pseudocyst of Pancreas 690; Chronic Pancreatitis 692; Pancreatic Tumours 700; Exocrine Pancreatic
Tumours 700; Carcinoma Pancreas 702; Endocrine Pancreatic Tumours 708; Insulinomas 709;
Gastrinomas 709; Glucagonomas 710; Zollinger-Ellison Syndrome 711; Cystic Fibrosis 711; Annular
Pancreas 711; Ectopic (Accessory) Pancreatic Tissue 712; Pancreatic Divisum 712; Pancreatic
Calculus 712; Pancreatic Ascites 713; Pancreatic Fistulae 713; Pancreatic Necrosis 714; Pancreatic
Trauma 714; Cystic Lesions of Pancreas 715; Pancreatic Exocrine Insufficiency (Exocrine Pancreatic
Disease) 715

15. Retroperitoneal Space
Anatomy of Retroperitoneum 717; Retroperitoneal Fibrosis 717;
Retroperitoneal Tumours 718; Psoas Abscess 722

Retroperitoneal Swellings 718;

16. 	Differential Diagnosis of Mass Abdomen


Mass in the Right Hypochondrium 726; Mass in the Epigastrium 727; Mass in the Left Hypochondrium 728;
Mass in the Lumbar Region 729; Mass in the Umbilical Region 730; Mass in the Right Iliac Fossa 731;
Mass in the Left Iliac Fossa 731; Mass in the Hypogastrium 731; Digital Rectal Examination for Prostate
and Other Conditions 733

17. Abdominal Wall and Umbilicus


Diseases of the Umbilicus 736; Omphalitis 737; Umbilical Granuloma 737; Anomalies of Vitellointestinal
Duct 738; Umbilical Sinus 738; Umbilical Adenoma (Raspberry Tumour) 739; Umbilical Fistula 739;
Patent Urachus 739; Burst Abdomen (Abdominal Wound Dehiscence) (Acute Wound Failure) 740;
Abdominal Wall Tumours 742; Desmoid Tumour 742; Exomphalos (Omphalocele) 743; Gastroschisis
(Belly Cleft) 744; Rectus Sheath Haematoma 744; Abdominal Wall Abscess 745; Meleney’s Progressive
Synergistic Bacterial Gangrene of Abdominal Wall 745; Divarication of Recti (Diastasis Recti) 746

18. Hernia


Aetiology 748; Parts of Hernia 749; Classification of Hernia 750; Inguinal Hernia 751; Surgical
Anatomy of Inguinal Canal 751; Classification of Inguinal Hernia (Earlier) 753; Indirect (Oblique)
Inguinal Hernia 754; Direct Inguinal Hernia 762; Incarcerated Hernia 768; Strangulated Hernia 768;
Sliding Hernia (Hernia-En-Glissade) 770; Pantaloon Hernia (Double Hernia, Saddle Hernia, Romberg
Hernia) 771; Femoral Hernia 771; Ventral Hernia 774; Incisional Hernia 775; Umbilical Hernia 778;
Paraumbilical Hernia (Supra- and Infraumbilical Hernia) 779; Epigastric Hernia (Fatty Hernia of Linea
Alba) 780; Spigelian Hernia 781; Obturator Hernia 782; Richter’s Hernia 782; Lumbar Hernia 783;
Phantom Hernia 783; Sciatic Hernia 783; Complications of Hernia Surgery 783; Parastomal
Hernia 784

19. Oesophagus


Anatomy 786; Lower Oesophageal Sphincter (LOS) 788; Dysphagia 788; Contrast Study of
Oesophagus 789 ; Oesophagoscopy 790 ; Oesophageal Endosonography 790 ; Third Space
Endoscopy 790; Gastro-Oesophageal Reflux Disease (GORD/GERD) 790; Hiatus Hernia 795; Rolling
Hernia (Paraoesophageal Hernia) 795; Reflux Oesophagitis 796; Barrett’s Oesophagus 796; Barrett’s
Ulcer 797; Oesophageal Motility Disorders 797; Achalasia Cardia (Cardiospasm) 797; Plummer-Vinson
Syndrome (Paterson-Kelly Syndrome) 800; Corrosive Stricture of Oesophagus 800; Schatzki’s Rings 802;
Boerhaave’s Syndrome 802; Mallory-Weiss Syndrome 803; Tracheo-oesophageal Fistula (Oesophageal
Atresia) 803; Oesophageal Diverticulum 804; Carcinoma Oesophagus 804; Benign Tumours of the
Oesophagus 811; Oesophageal Perforation 812

20. Stomach
Anatomy 814; Blood Supply of Stomach 815; Nerve Supply of Stomach 815; Histology 815; Lymphatic
Drainage of Stomach 815; Duodenum 816; Gastric Physiology 816; Gastric Function Tests 817;
Gastrin 817; Barium Meal Study 818; Gastroscopy 818; Helicobacter pylori 819; Congenital (Infantile)
Hypertrophic Pyloric Stenosis 820; Gastritis 822; Acute Peptic Ulcer (Duodenal or Gastric Ulcer) 822;


Gastric Ulcer 823; Duodenal Ulcer 825; Pyloric Stenosis Due to Chronic Duodenal Ulcer 828; Perforated
Peptic Ulcer 830; Bleeding Peptic Ulcer 833; Haematemesis 836; Complications of Gastric Surgery 837;
Trichobezoar (Rapunzel Syndrome) 840; Chronic Duodenal Ileus (Wilkie’s Syndrome) 841; Dunbar ‘s
(MALS) Syndrome (Harjola—Marable Syndrome) 841; Acute Gastric Dilatation 842; Gastric Volvulus 842;
Gastric Polyp 843; Menetrier’s Disease 843; Duodenal Diverticula 844; Carcinoma Stomach 844;
Gastric Lymphoma 855; Gastric Sarcomas 857; Gastrointestinal Stromal Tumours (GISTS) 857;
Pyloroplasty 858; Gastrostomy 858; Gastrectomy 859; Gastrojejunostomy (GJ) 860; Retrograde
Jejunogastric Intussusception 860; Vagotomy 860

21. Small Intestine


Anatomy 862; Meckel’s Diverticulum 863; Regional Enteritis (Crohn’s Disease) 865; Surgical
Complications of Typhoid 868; Surgical Complications of Roundworm (Ascaris lumbricoides) 869;
Pneumatosis Cystoides Intestinalis 870; Mesenteric Vessel Ischaemia 871; Necrotising Enterocolitis 872;
Small Bowel Tumours 873; Benign Tumours of Small Bowel 874; Malignant Tumours of Small Bowel 876;
Carcinoid Tumour 877; Short Bowel Syndrome (Short Gut Syndrome) 879; Small Bowel Enema
(Enteroclysis) 880; Capsule Endoscopy 881; Small Bowel Enteroscopy 881; Enteric/Gastrointestinal
Fistula 881

22. Large Intestine


Anatomy 885; Hirschsprung’s Disease (Congenital Megacolon) 886; Diverticular Disease of the Colon 888;
Ulcerative Colitis 891; Ischaemic Colitis 896; Pseudomembranous Colitis 896; Surgical Complications
of Intestinal Amoebiasis 896; Tumours of Colon 897; Benign Tumours/Polyp of the Colon 897; Juvenile
Polyps 898; Metaplastic/Hyperplastic Polyp 898; Peutz-Jeghers Polyp 898; Adenoma of Colon 898;
Familial Adenomatous Polyp (FAP) 899; Carcinoma Colon 900; Angiodysplasia of Colon 909; Ogilvie’s
Syndrome 909; Colostomy 910; Stoma Care 912; Stoma Appliances 913; Faecal Fistula 913;
Preparation of Large Bowel for Surgery 914; Surgical Pouches 915; Barium Enema 915

23. Intestinal Obstruction


Intestinal Obstruction: Types 917; Dynamic Obstruction 918; Duodenal Atresia 924; Small Intestine
Atresia (Intestinal Atresia) 925; Malrotation 926; Meconium Ileus 927; Intussusception (ISS) 928;
Volvulus 931; Sigmoid Volvulus (Volvulus of Pelvic Colon) 931; Paralytic Ileus (Adynamic Intestinal
Obstruction) 933; Adhesions and Bands 933; Internal Hernias 936

24. Appendix


Surgical Anatomy 937; Acute Appendicitis 938; Incidental Appendicectomy 945; Appendicular Mass
(Periappendicular Phlegmon) 946; Appendicular Abscess 946; Faecal Fistula After Appendicectomy 947;
Mucocele of Appendix 948; Neoplasms of the Appendix 948; Laparoscopic Appendicectomy 949

25. Rectum and Anal Canal


Anatomy 951; Per-rectal Examination (Digital Examination of the Rectum) 952; Proctoscopy (Kelly’s) 953;
Sigmoidoscopy 953; Colonoscopy 953; Carcinoma Rectum 954; Solitary Ulcer Syndrome 960; Rectal
Prolapse 961; Anorectal Malformations (ARM) 965; Pilonidal Sinus/Disease (Jeep Bottom; Driver’s
Bottom) 967; Piles/Haemorrhoids 969; Anal Fissure (Fissure-in-Ano) 976; Anorectal Abscess 978;
Fistula-in-Ano 980; Anorectal Strictures 985; Condyloma Acuminata 986; Anal Intraepithelial Neoplasia
(AIN) 986; Malignant Tumours of Anal Area 986; Sacrococcygeal Teratoma 987; Anal incontinence 988;
Descending Perineal Syndrome 988; Proctitis 989; Proctalgia Fugax 989; Hidradenitis Suppurativa of
Anal Region 989; Pruritus Ani 989; Gastrointestinal Haemorrhage (GI Bleed) 989

26. Urology
A. Kidney 993

Anatomy of Kidney and Ureter 993; Kidney—Anatomy 993; Ureter—Anatomy 994; Plain X-ray—Kidney,
Ureter and Bladder (KUB) 994; Intravenous Urogram (IVU) 995; Retrograde Pyelography (RGP) 996;
Renal Angiogram 997; Micturating Cystourethrography (MCU) 997; Ascending Urethrogram 997; Isotope
Renography 998; Cystoscopy 998; Catheters 999; Foley’s Catheter 1000; Malecot’s Catheter 1000;




SRB's Manual of Surgery
Red Rubber Catheter 1001; Nephrostomy 1001; Suprapubic Cystostomy (SPC) 1002; Haematuria 1002;
Horseshoe Kidney 1003; Cystic Diseases of the Kidney 1004; Polycystic Kidney Disease (PCKD) 1004;
Duplication of Renal Pelvis and Ureter 1005; Retrocaval Ureter 1006; Ureterocele 1006; Injuries to
Kidney 1007; Renal Tuberculosis 1008; Hydronephrosis (HN) 1010; Pyonephrosis 1014; Carbuncle of
Kidney (Renal Carbuncle) 1014; Perinephric Abscess 1015; Renal Calculus 1015; Ureteric Calculi 1019;
Staghorn Calculus 1021; Benign Tumours of Kidney 1022; Wilms’ Tumour (Nephroblastoma) 1022; Renal
Cell Carcinoma (RCC) 1024

B. Urinary Bladder 1028

Anatomy 1028; Ectopia Vesicae (Extrophy of the Bladder) 1029; Urachal Anomalies 1029; Vesical
Calculus 1029; Cystitis 1031; Recurrent Cystitis 1032; Interstitial Cystitis (Hunner’s Ulcer, Elusive
Ulcer) 1032; Schistosoma Haematobium (Endemic Haematuria, Urinary Bilharziasis) (Swimmer’s
Itch) 1032; Thimble or Systolic Bladder 1033; Bladder Tumours 1033; Transitional Cell Carcinoma
(TCC) 1033; Ureterosigmoidostomy 1036; Rupture Bladder (Bladder Injury) 1037; Residual Urine 1038;
Malakoplakia 1038; Neurogenic Bladder 1038; Vesicoureteric Reflux 1039; Bladder Diverticula 1039;
Urinary Diversion 1040; Urinary Fistulas 1041

C. Prostate 1043

Anatomy 1043; Acid Phosphatase 1043; Prostate Specific Antigen (PSA) 1043; Benign Prostatic
Hyperplasia (BPH) 1044; Prostatitis 1047; Bladder Outlet Obstruction (BOO) 1047; Carcinoma
Prostate 1048

D. Urethra 1051

Anatomy 1051; Urethral Injury 1051; Rupture of Membranous Urethra and/or Prostatic Urethra
(Posterior Urethra) 1051; Rupture of Bulbous Urethra (Anterior Urethra) 1052; Stricture Urethra 1053;
Hypospadias 1055; Epispadias 1056; Posterior Urethral Valve 1056; Urethral Calculi 1056; Urethritis 1057;
Extravasation of Urine 1057; Retention of Urine 1058

E. Penis 1060

Phimosis 1060; Paraphimosis 1061; Circumcision 1061; Balanoposthitis 1062; Chordee (Cordee) 1062;
Priapism 1063; Peyronie’s Disease (Induratio-Penis Plastica) 1063; Ram’s Horn Penis 1063; Carcinoma
Penis 1063; Buschke-Löwenstein Tumour 1067

F. Scrotum 1068

Anatomy 1068; Fournier’s Gangrene 1068; Hydrocele 1069; Primary Vaginal Hydrocele 1070;
Secondary Vaginal Hydrocele 1071; Haematocele 1073; Pyocele 1074; Cyst of Epididymis 1074;
Spermatocele 1075; Varicocele 1075

G. Testis 1078

Anatomy 1078; Undescended Testis 1078; Ectopic Testis 1081; Retractile Testis 1081; Torsion of the
Testis 1081; Testicular Tumours 1083; Paratesticular Tumours 1087; Orchitis 1087; Epididymitis 1088

27. Neurosurgery


Head Injuries 1090; Extradural Haematoma 1095; Subdural Haematoma 1096; Subarachnoid
Haemorrhage (SAH) 1097; Fracture Skull 1098; Depressed Skull Fracture 1099; CSF Rhinorrhoea 1099;
Hydrocephalus 1100; Intracranial Abscess 1101; Intracranial Aneurysms 1102; Intracranial Tumours 1102;
Pituitary Tumours 1105; Craniopharyngiomas 1106; Spinal Dysraphism 1106; Meningocele 1106; Spina
Bifida 1107; Intervertebral Disc Prolapse (IVDP) 1108; Tuberculosis of Spine (Caries Spine) 1109; Spinal
Tumours 1111

28A. Thorax
Chest Injuries 1112; Fracture Ribs 1114; Flail Chest and Stove in Chest 1115; Pneumothorax 1116;
Tension Pneumothorax 1116; Haemothorax 1117; Pleural Tap 1117; Bronchoscopy 1118; Empyema
Thoracis 1118; Empyema Necessitans 1119; Lung Abscess 1120; Intercostal Tube Drainage 1121;
Shock Lung (Stiff Lung) 1123; Pulmonary Embolism (PE) 1123; Surgical Emphysema 1124; Lung
Cysts 1124; Mediastinal Tumours 1125; Thymomas 1127; Lung Cancers 1127; Pancoast Tumours
(Superior Sulcus Tumour) 1128; Chest Wall Tumours 1128; Pericarditis 1129; Acute Pericarditis 1129;


Chronic Constrictive Pericarditis (Pick’s Disease) 1129; Pericardial Tap 1129; Cardiac (Pericardial)
Tamponade 1130; Diaphragmatic Hernia 1130; Pulmonary Complications During Postoperative
Period 1133; Surgical Management of Pulmonary Tuberculosis 1133; Video-assisted Thoracoscopic
Surgery (VATS) 1133

B. Cardiac Surgery 1134

Anatomy 1134; Preoperative Assessment and Preparation of the Cardiac Patient 1135; Cardiopulmonary
Bypass 1135; Congenital Heart Diseases 1136; Patent Ductus Arteriosus (PDA)—10% 1136; Coarctation
of Aorta—5% 1136; Atrial Septal Defect (ASD)—7% 1137; Ventricular Septal Defect (VSD)—15% 1137;
Pulmonary Stenosis 1138; Transposition of Great Vessels 1138; Tetralogy of Fallot 1138; Acquired
Heart Disease 1139; Mitral Regurgitation 1139; Aortic Stenosis 1140; Aortic Regurgitation 1140; Valve
Replacement Surgery 1140; Ischaemic Heart Disease (IHD) 1140; Cardiac Pacemakers 1141; Postoperative Care 1141

29. Adjuvant Therapy


Radiotherapy 1142; Chemotherapy 1144; Cell Cycle 1145; Antimalignancy Drugs 1145; Hormone
Therapy in Cancer 1145; Immunosuppression 1146; Immunotherapy 1147; Hybridoma 1147; Gene
Therapy 1147

30. Anaesthesia


Preoperative Assessment 1148; General Anaesthesia 1149; Anaesthetic Agents 1149; Oxygen 1149;
Muscle Relaxants 1149; Reversal Agents 1149; Instruments in Anaesthesia 1149; Complications
of General Anaesthesia 1151; Postoperative Care 1151; Monitoring the Postoperative Patient 1151;
Regional Anaesthesia 1152; Topical Anaesthesia 1152; Infiltration Block 1152; Field Block 1152; Nerve
Block 1152; Intravenous Regional Anaesthesia (Bier’s Block) 1152; Spinal Anaesthesia 1152; Saddle
Block 1153; Epidural Anaesthesia 1153; Caudal Anaesthesia 1153

31. Advanced Imaging Methods


Ultrasound 1154; Doppler 1156; CT Scan 1156; Magnetic Resonance Imaging (MRI) 1158; Radionuclide
Imaging 1159; Positron-Emission Tomography (PET Scan) 1159

32. Operative Surgery
A. Asepsis and Sterilisation 1160

Sterilisation 1160; Disinfection 1160; Antisepsis 1160; Asepsis 1160; Different Methods of Disinfection/
Sterilisation 1160

B. Instruments 1163

Cheatle’s Forceps 1163; Sponge Holding Forceps (Rampley’s) 1163; Mayo’s Towel Clip 1163; Artery
Forceps (Haemostat) 1163; Right Angle Forceps 1164; Kocher’s Forceps 1164; Allis’ Tissue Holding
Forceps 1164; Babcock’s Forceps 1164; Lane’s Tissue Holding Forceps 1165; Morant-Baker’s Appendix
Holding Forceps 1165; Volkmann’s Retractor 1165; Langenbeck’s Retractor 1165; Czerny’s Retractor
(Hernia Retractor) 1165; Morris’ Retractor 1165; Deaver’s Retractor 1165; Doyen’s Retractor 1166;
Self-retaining Retractor 1166; Single Hook Retractor 1166; Plain Non-toothed Dissecting Forceps 1166;
Toothed Dissecting Forceps 1166; Surgical Needles 1166; Needle Holder 1167; Joll’s Thyroid
Retractor 1167; Moynihan’s Occlusion Clamp 1167; Payr’s Crushing Clamp (Gastric) 1167; Desjardin’s
Choledocholithotomy Forceps 1167; Bake’s Dilator 1167; Sinus Forceps (Lister’s) 1168; Scissors 1168;
Volkmann’s Scoop 1168; Tracheostomy Tube 1168; Drains 1168; Foley’s Catheter 1170; Malecot’s
Catheter 1170; Simple Red Rubber Catheter 1170; Lister’s Urethral Dilator 1170; Ryle’s Tube 1170;
Infant Feeding Tube 1171; Kehr’s ‘T’ Tube 1171; Proctoscope 1171; Flatus Tube 1171

C. Suture Materials 1172

Classification I 1172; Classification II 1173; Classification III 1173; Classification IV 1173; Classification
V 1173

D. Diathermy (Electrocautery) 1174
Types 1174

E. Operative Procedure 1175




SRB's Manual of Surgery
Abdominal Incisions 1175; Vasectomy 1176; Circumcision 1176; Hydrocele 1177; Inguinal Hernia 1177;
Appendicectomy 1178; Thyroidectomy 1178; Tracheostomy 1179; Cryosurgery 1180; Lasers in
Surgery 1180; Staplers in Surgery 1181; Nasojejunal Tube Feeding 1182; Gossypiboma 1182

F. Laparoscopic Surgery 1183

Advantages of Laparoscopic Surgery 1183; Laparoscopic Cholecystectomy 1184; Laparoscopic
Appendicectomy 1185; Advanced Laparoscopic Surgeries 1185; Diagnostic Laparoscopy 1185;
Retroperitoneoscopy 1186
Natural Orifice Transluminal Endoscopic Surgery (Notes) 1186

G. Dressings and Bandages 1187
Dressings 1187; Bandages 1187

H. Day Care Surgery 1189

Day Care Surgery 1189; Surgical Audit 1190; Surgeon and Law 1191

33. Miscellaneous


Fascinating Signs in Surgery 1192
Triads in Surgery 1201
Misnomers in Surgery 1202
Triangles in Surgery 1203
Drugs at a Glance 1204

Antibacterials 1204; Sulfonamides 1204; Quinolones 1204; Penicillin 1204; Ampicillin/Amoxycillin/
Talampicillin/ Pivampicillin 1205; Methicillin 1205; Cloxacillin/Dicloxacillin/Flucloxacillin 1205; Carbenicillin/
Ticarcillin 1205; Piperacillin/Azocillin/Mezlocillin 1205; Clavulanic Acid 1205; Sulbactum 1205;
Tazobactum 1205 ; Carbapenem/Imipenem/Meropenem 1205 ; Lincomycin/Clindamycin 1205 ;
Vancomycin/Teicoplanin 1205;
Cephalosporins 1206; Macrolides 1206; Aminoglycosides 1206;
Tetracyclines 1206; Chloramphenicol/Thiamphenicol 1207; Drugs for Tuberculosis 1207; Antiamoebic
Drugs 1207; Important Antihelminthics 1208; Anticoagulants 1208; Other Drugs 1209

Further Reading






General Surgery
A. Wounds and Wound Healing
One having a wound in his eyebrow. An ailment which I will treat. Treatment [of a wound in the eyebrow]: Now
after thou hast stitched it, [thou shouldst bind] fresh meat upon [it] the first day. If thou findest that the stitching of
this wound is loose, thou shouldst draw it together for him with two strips (of plaster), and thou shouldst treat it
with grease and honey every day until he recovers.
—[Anonymous], circa 2500 BC


Classification of Wounds
Wound Healing
Compartment Syndrome


Crush Injury
Crush Syndrome
Degloving Injuries

™™ Hypertrophic Scar
™™ Problems with Wound Healing

Wound Definition
A wound is a break in the integrity of the skin or tissues often,
which may be associated with disruption of the structure and
Wound is simply a disruption of any tissues—soft tissue or bone
or internal organs. Ulcer is disruption or break in the continuity
of any lining—may be skin, mucous membrane or others. Ulcer
is one of the types of wounds.

I. Rank and Wakefield classification
a. Tidy wounds
 They are wounds like surgical incisions and wounds
caused by sharp objects.

Fig. 1.1A: Tidy wound

 It is incised, clean, healthy wound without any tissue loss.
 Usually primary suturing is done. Healing is by primary


I dressed him and God healed him.— Ambroise Pare


SRB's Manual of Surgery
b. Untidy wounds
 They are due to:
–– Crushing.
–– Tearing.
–– Avulsion.
–– Devitalised injury.
–– Vascular injury.
–– Multiple irregular wounds.
–– Burns.
 Fracture of the underlying bone may be present.
Wound dehiscence, infection, delayed healing are common.
 Liberal excision of devitalised tissue and allowing to heal
by secondary intention is the management.
 Secondary suturing, skin graft or flap may be needed.


Fig. 1.1B: Untidy wound

II. Classification based on the type of the wound
Clean incised wound: It is a tidy, simple, clean cut wound with
linear cut edges; usually due to a sharp object like blade, glass
piece or knife. It is treated by primary suturing.

Fig. 1.2: Clean incised wound.

Lacerated wound: It has ragged edges with some part of the
tissues getting devitalized; viability of the tissues may be
impaired; depth of the injury and tissue damage should be
carefully assessed. Proper adequate wound excision, thorough
warm saline wash and suturing of the wound layer-by-layer is

Figs 1.3A and B: Lacerated wounds.

Bruise or contusion: It is due to blow or blunt force to the
skin and tissues underneath wherein blood vessels or capillaries are damaged underneath. There is skin discolouration
without breaking of the skin; broken vessels cause seepage
of blood underneath; minor soft tissue injury crushes small
vessels without breaking the skin accumulating trapped blood
underneath. It is more on the skin over the bones; lax area like
face, scrotum, eyes; vascular areas; children, old aged, fair
skin people.
Haematoma: It is a localized collection of blood after
blunt trauma or after surgery. Collected fluid blood in few
minutes to hours gets clotted; later eventually it gets liquefied and shows discoloured fluid. It may be subcutaneous/
intramuscular/subfascial/intra-articular. Large haematoma
may get infected to form an abscess; so large haematoma
needs drainage under general or regional anaesthesia. Small
haematoma usually gets absorbed (like scalp haematoma).
Often haematoma contains reddish plasmatic fluid which
should be aspirated using wide bore needle. Complications
are—pressure effects and abscess formation; both needs
incision and drainage under anaesthesia. Haematoma causing
cosmetic problems may require needle aspiration. Haematoma can occur spontaneously in coagulation disorders
(haemophilia) or in individuals who are on anticoagulant
drug therapy.

Wounds and Wound Healing

Fig. 1.4: Haematoma of eyelid.

Fig. 1.7: Typical look of abrasion in face.

Fig. 1.5: Haematoma in the groin being aspirated. Haematoma may
get infected or can compress adjacent structures.

Fig. 1.8: Multiple abrasions.

Fig. 1.6: Subungual haematoma. Often nail may need to be
removed to evacuate the blood clot.

Abrasion: It is superficial injury (scratch/graze/pressure/
contact) and is due to shearing of the skin where the surface
is rubbed off. This tangential force causes loss of epidermis
exposing dermal vessels and nerves leading into profuse painful
oozing. Abrasion heals by epithelialisation. Any dirt or foreign
body on the abrasion should be removed to avoid formation of
poor tattoo like scar.
Puncture wounds and bites: It is usually a stab wound with a
pointed object; here depth of the wound is more than the width.
Deeper vital structures or organs may be injured, so should be
assessed; foreign body or object may be present in the depth
of the wound. Wound should be explored under general or
regional anaesthesia to assess the depth and severity of the
injury and sutured layer by layer after through saline wash.

Fig. 1.9: Penetrating wound of the abdomen.

Penetrating wounds: They are similar like puncture wounds;
due to stab. Abdomen and chest are common sites. Liver,
bowel, spleen, major vessels and other visceral organs may be

A great part, I believe, of the art of medicine is the ability to observe.—Hippocrates, Father of Medicine



SRB's Manual of Surgery
involved. Ultrasound and CT scan should be done to evaluate
deeper organ injuries. Under general anaesthesia wound should
be explored properly.
Traction and avulsion injuries: these are complex injuries
with tissues getting displaced from its normal anatomical
position and alignment. It can occur in single plane like in
subcutaneous tissue or in multiple planes like in machinery
injuries, major injuries or degloving injuries. Ischaemia,
bleeding, sepsis, loss of wide tissue area are common problems. Open traction injury occurs on the surface. Closed
traction injury can occur in deeper plane like brachial plexus
injury or traction bowel injury. After initial resuscitation,
definitive treatment like skin graft or nerve repair should
be done.

III. Classification based on thickness of the wound
xx Superficial wound involving only epidermis and dermal papillae.
xx Partial thickness wound with skin loss up to deep dermis with
only deepest part of the dermis, hair follicle shafts and sweat
glands are left behind.
xx Full thickness wound with loss of entire skin and subcutaneous
tissue causing spacing out of the skin edges.
xx Deep wounds are the one extending deeper, across deep fascia into
muscles or deeper structures.
xx Complicated wounds are one associated with injury to vessels
or nerves.
xx Penetrating wound is one which penetrates into either natural
cavities or organs.
IV. Classification based on involvement of structures
xx Simple wounds are one involving only one organ or tissue.
xx Combined/complex wounds are one involving mixed tissues.

Crush injury: It is due to major wounds, war wounds,
natural disaster like earth quake injuries, tourniquet injury. It
leads into—compartment syndrome; muscle ischaemia; loss
of tissues; gangrene; sepsis. Muscle will lose its viability
which is identified by its colour (dark coloured with loss
of shining); loss of contractility; turgid, and will not bleed
on cutting.

Fig. 1.11: Complex wound exposed tendons.
Fig. 1.10: Severe crush injury leg.

Gunshot injuries: These injuries may be superficial or deep.
Usually entry wound and exit wound will be present. It causes
explosive and destructive injuries along with burn injuries in
the deeper planes and organs. It can be high velocity injuries
with massive bleeding and major organ injuries.
Injuries to bones and joints: It is common in all major injuries;
should be identified clinically and confirmed radiologically.
It needs specialized management like reduction, plating etc.
Injuries to nerves, arteries, veins (major vessels), deeper
organs: It needs initial resuscitation, later staged management
as per individual patient basis depending on the severity and
extent of injury and loss of function.
Closed blunt injury: It may be due to fall, blunt injury wherein
no obvious external injury may be seen but deeper injury
occurs; it may be often severe enough to cause major injury
like in blunt abdominal injury causing bowel/liver/spleen/
renal injuries.

wound may be closed (bruise, haematoma, blunt injury); open (abrasion,
incised, lacerated, penetrating) or complex (traction/avulsion, crush or
gunshot injuries).

V. Classification based on the time elapsed
Acute wounds are generally defined as those that progress through
the normal phases of healing and typically show signs of healing
in less than 4 weeks; examples are—surgical or traumatic or burn
wounds; progress through the healing phases in a timely and orderly
fashion - haemostasis, inflammation, proliferation, and remodeling
or maturation.
Chronic wounds are defined as those that do not follow the normal
healing process and show no signs of healing in 4 weeks. It fails to
progress through the normal phases of healing but with prolonged
inflammatory phase. Diabetes, venous/arterial diseases, nutritional
deficiencies are the causes. Hypoxia initially is a potent stimulus
for fibroblast activity and angiogenesis; persisting hypoxia impedes
fibroblast and collagen activity and also allows bacterial invasion
to make wounds chronic. Chronic wounds are chronically infected
with biofilms which interfere mainly with the inflammatory phase
of healing, contributing to the non-healing. A biofilm is a complex
structure of microorganisms contained in an extracellular matrix
of proteins and polysaccharides that adhere to a surface, creating a
protected environment for the organisms. Chronic ulcers are unresponsive to dressing treatment; it requires biopsy, culture study, definitive
treatment like wound debridement, VAC (Vacuum Assisted Closure)
therapy, skin grafting or flap. Specific conditions like tuberculosis if
present should be treated. Malignancy if confirmed is treated by wide
local excision and skin graft.

Wounds and Wound Healing

Fig. 1.14: Appendicectomy wound, which is a clean
contaminated wound.
Fig. 1.12: Chronic wounds over the scalp
vi. Classification of surgical wounds
a. Clean wound
 Surgeries of the brain, joints, heart, transplant.
 Infective rate is less than 2%.
b. Clean contaminated wound
 Bowel surgeries, gastrojejunostomy.
 Gallbladder, biliary and pancreatic surgeries.
 Infective rate is 10%.
c. Contaminated wound
 Acute abdominal conditions.
 Open fresh accidental wounds.
 Infective rate is 15–30%.
d. Dirty infected wound
 Abscess drainage.
 Empyema gallbladder.
 Faecal peritonitis.
 Infective rate is 40–70%.

Fig. 1.15: Contaminated wound—burst appendicitis.

Wound classifications
• Simple wounds: Only skin is

• Tidy wounds

• Complex wounds: Vessels,
nerves, tendons or bones are

• Untidy wounds

• Closed wounds:

• Clean wound.

–– Contusion

• Clean contaminated wound

–– Abrasion

• Contaminated wound

–– Haematoma

• Dirty wound

• Open wounds:
–– Incised wounds
–– Lacerated wounds
–– Crush injuries

Fig. 1.13: Clean wound of thyroidectomy surgery.

–– Penetrating wounds

Start by doing what’s necessary, then do what’s possible and suddenly you are doing the impossible.



SRB's Manual of Surgery
Wound healing is complex method to achieve anatomical and
functional integrity of disrupted tissue by various components like
neutrophils, macrophages, lymphocytes, fibroblasts, collagen; in
an organised staged pathways—haemostasis → inflammation →
proliferation → matrix synthesis (collagen and proteoglycan ground
substance) → maturation → remodelling → epithelialisation →
wound contraction (by myofibroblasts).

Types of Wound Healing
Primary Healing (First Intention)
xx It occurs in a clean incised wound or surgical wound.

Wound edges are approximated with sutures. There is
more epithelial regeneration than fibrosis. Wound heals
rapidly with complete closure. Scar will be linear, smooth,
and supple.


Secondary Healing (Second Intention)
xx It occurs in a wound with extensive soft tissue loss like in

major trauma, burns and wound with sepsis. It heals slowly
with fibrosis. It leads into a wide scar, often hypertrophied
and contracted. It may lead into disability.
xx Re-epithelialisation occurs from remaining dermal elements
or wound margins.

Figs 1.16A and B: Acute peritonitis with frank pus in peritoneal
cavity due to bowel perforation is a dirty wound.

Fig. 1.17: Wound causing extensive skin loss and necrosis.

A scab is a beautiful thing—a coin the body has minted, with
an invisible motto: In God We Trust. Our body loves us, and, even
while the spirit drifts dreaming, works at mending the damage
that we do.
—John Updike, 1984

Fig. 1.18: Wound in the abdomen healing with second intention
which requires secondary suturing once it granulates well. Secondary
suturing is done after 10–14 days, once wound granulates well
with proper control of infection. Scar in such type is prone to form
incisional hernia.

Healing by Third Intention (Tertiary Wound Healing or
Delayed Primary Closure)
After wound debridement and control of local infection,
wound is closed with sutures or covered using skin graft.
Primary contaminated or mixed tissue wounds heal by tertiary

Wounds and Wound Healing
Stages of wound healing
Stage of inflammation.
Stage of granulation tissue formation and organi­sation. Here due
to fibroblastic activity synthesi­sation of collagen and ground
substance occurs.
™™ Stage of epithelialisation.
™™ Stage of scar formation and resorption.
™™ Stage of maturation.

Phases of Wound Healing
Inflammatory phase (Lag or Substrate or Exudative Phase)
xx It begins immediately after formation and lasts for 72 hours.
xx There is initial arteriolar vasoconstriction, thrombus formation,
platelet aggregation due to endothelial damage and release of
adenosine diphosphate (ADP).
xx Later vasodilatation and increased vascular permeability develops.
xx Here haemostasis, coagulation and chemotaxis occur.

Coagulation begins at wound haematoma → formation of platelet
fibrin thrombus → release of cytokines, PDGF (platelet-derived growth
factor), epidermal growth factor (EGF), transforming growth factor β
(TGF – β), platelet activating factor and platelet factor IV, fibrin, serotonin. Chemotaxis causes first neutrophil migration, and then activation of macrophages, lymphocytes leading into phagocytosis, wound
debridement, matrix activation, angiogenesis. Chemotaxis factors are
complement factors, interleukin-1, TNF-α (tumour necrosis factor-α)
TGF–β and platelet factor. Activated macrophages produce free radicals and nitric oxide; release cytokine to activate lymphocytes which
release interferon and interleukin (called as lymphokines). These factors
attract polymorpho nuclear leucocytes (PMN—poly morphonuclear
cells–neutrophills) in 48 hours secreting inflammatory mediators and
bactericidal oxygen derived-free radicals. Injured tissues and platelet
release histamine, serotonin and prostaglandins which increases the
vascular permeability by vasodilatation. These actions are reduced
in diabetes mellitus, Cushing’s syndrome and immunosuppression
increasing the sepsis rate.

Remodelling phase (Maturation Phase)
xx It begins at 6 weeks and lasts for 6 months to 1 or 2 years.
xx There is maturation of collagen by cross linking and realignment
of collagen fibers along the line of tension, which is responsible
for tensile strength of the scar. There is reduced wound vascularity.
Fibroblast and myofibroblast activity causes wound contraction. Type
III collagen is replaced by type I collagen causing maturation of the
collagen. Ratio of type I collagen to type III collagen becomes 4:1.
xx Early extracellular matrix contains fibronectin and collagen type
III; eventually it contains glycosaminoglycans and proteoglycans;
final matrix contains type I collagen.
xx Scar strength is 3% in 1 week; 20% in 3 weeks; 80% in 12 weeks.
Final matured scar is acellular and avascular.
Initially fibrin, fibronectin, proteoglycans deposition occurs; later
collagen protein develops to form scar. Normal dermal skin contains
80% type I (20% type III) collagen; granulation tissue contains mainly
type III collagen; scar contains both type I and III collagen, initially
in equal proportion, later becomes 4:1. Basic essential components
of collagen are proline and lysine. Hydroxylation of lysine and later
glycosylation of this hydroxylysine decides the type of collagen
molecule. Hydroxylation of both proline and lysine as essential step
needs adequate concentration of vitamin C, iron and α ketogluteric
acid. Collagen deposition in the wound is assessed by quantity of
hydroxyproline excreted in urine. There is a balanced activity of
collagen production and degradation of collagen (collagenolysis).
Collagen is broken down by collagenase and MMPs (matrix metalloproteinases). Procollagen through procollagenase → collagen fibril →
cross linking → collagen fiber → deposition. Deposited collagen →
through collagenase → degradation and collagenolysis.

Points to be remembered


xx All these cause features of acute inflammation—rubor, calor,
tumour, dolor and loss of function.

Proliferative phase (Collagen/fibroblastic phase)
xx It begins from 3rd day and lasts for 3–6 weeks. There will be formation of granulation tissue and repair of the wound. Granulation
tissue contains fibroblasts, neocapillaries, collagen, fibronectin
and hyaluronic acid.
xx (1) Initial angiogenesis (growth of new blood vessels) occurs
by release of vascular endothelial cell growth factor (VEGF)
by keratinocytes; by release of TNF-α, TGF–β, PDGF, FGF by
macrophages. (2) Eventual fibroplasia develops by fibroblast
activity with formation of the collagen and ground substance/
glycosaminoglycans. Type III collagen is deposited initially in
a random fashion. (3) Later re-epithelialisation of the wound
surface occurs by migration of basal layer of the retained
epidermis which proliferates, differentiates and stratifies to form
wound closure.



PMN cells survive only for 24 hours; so after 48 hours PMNs won’t
be found in the wound significantly; PMNs are not needed for
wound healing.
Activated monocytes called macrophages predominate after 48
hours which will persist until completion of the wound healing.
Macrophages are the main cells of wound healing. Macrophages
secrete TNF - α, interleukin -1, fibroblast growth factor (FGF),
proteinases (MMPs – matrix metallo proteinases).
B lymphocyte will not have any role in wound healing; T
lymphocytes produce stimulatory cytokines like interleukin – 1
supporting the fibroblast activity.
Collagen and glycosamines are produced by fibroblasts. Tropocollagen is produced which aggregates to form collagen fibrils.
Hydroxyproline and hydroxylysine are synthesized by specific
enzymes using iron, α ketoglutarate and vitamin C.
Fibroblast requires vitamin C to produce collagen.
Granulation tissue and early scar contains type III collagen.
Final scar contains type I collagen mainly.
Final extra cellular matrix contains type I collagen and proteoglycans.
Collagen production decreases after 4 weeks of wound healing
(declines in 28-42 days).
Eighty per cent of tensile strength of normal skin will be achieved
finally but not 100%

Clinical diagnosis is an art, and the mastery of an art has no end: you can always be a better diagnostician
—Logan Clendening



SRB's Manual of Surgery
Wound infection: Infection prolongs inflammatory phase, releases
toxins and utilizes vital nutrients thereby prevents wound epithelialisation. The β-haemolytic streptococci more than 105 per gram of tissue
prevent wounds healing. Formation of biofilms on the wound surface
by microorganisms prevents wound healing.
Anaemia: Haemoglobin less than 8g % causes poor oxygenation of
tissues preventing healing of the wounds.
Hypoxia: Hypoxia prevents fibroblast proliferation and collagen
synthesis; it also promotes bacterial invasion into the wound. Causes
of hypoxia are—arterial diseases, cardiac failure, respiratory causes,
hypotension, smoking, tobacco, infection, diabetes mellitus and
Fig. 1.19: Healing ulcer with healthy granulation tissue which is
ready for skin grafting.

Factors affecting Wound Healing
Age: In younger age group wound healing is faster and better. In
elderly healing is delayed due to reduction in collagen synthesis,
epithelialisation, growth factors and angiogenesis. But final scar will
be excellent in old individuals.
Nutrition: Adequate vitamin, trace elements, fatty acids and proteins
are essential for wound healing. Vitamin A deficiency affects monocyte activation, inflammatory phase, collagen synthesis and growth
factor actions. Vitamin K deficiency affects synthesis of prothrombin
(II), factors VII, IX and X. Vitamin E, being an antioxidant stabilizes
the cell membrane. Vitamin C deficiency impairs collagen synthesis,
fibroblast proliferation and angiogenesis; increases the capillary
fragility and susceptibility for infection. Zinc is an essential cofactor
for RNA and DNA polymerase; magnesium is a co-factor for synthesis
of proteins and collagen; copper is a required co-factor for cytochrome
oxidase, for cytosolic anti-oxidant superoxide dismutase, and for the
optimal cross-linking of collagen; Iron is required for the hydroxylation of proline and lysine. Glutamine is the most abundant amino acid
in plasma; is a major source of energy for rapidly proliferating cells
such as fibroblasts, lymphocytes, epithelial cells, and macrophages.
The serum concentration of glutamine is reduced after major surgery,
trauma, and sepsis, and supplementation of this amino acid improves
nitrogen balance and diminishes immunosuppression. Glutamine
stimulates the inflammatory immune response in early wound healing.
Oral glutamine supplementation improves wound breaking strength
and of mature collagen. Arginine is a semi-essential amino acid that
is required in growth, severe stress, and injury. Arginine modulates
immune function, wound healing, hormone secretion, vascular tone,
and endothelial function. Arginine is a precursor to proline; supports
collagen deposition, angiogenesis, and wound contraction. Under
psychological stress situations, the metabolic demand of arginine
increases, and its supplementation hastens the wound healing. Serum
albumin level less than 2 g/dl causes prolonged inflammatory phase,
decreased fibroplasia, neovascularisation and cell synthesis and
wound remodeling and hence decreased wound healing. Wounds in
patients who remain in catabolic state will not heal. Collagen is the
major protein component of connective tissue; it contains mainly
glycine, proline, and hydroxyproline. Collagen synthesis requires
hydroxylation of lysine and proline, and co-factors such as ferrous
iron and vitamin C. Polyunsaturated fatty acids which cannot be
synthesized de novo by mammals, consist mainly of omega-6 (found
in soybean oil) and omega-3 (found in fish oil—fatty acids such as
eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]). They
affect pro-inflammatory cytokine production, cell metabolism, gene
expression and angiogenesis; improve the systemic immune function
of the host, thus reducing infectious complications.

Radiotherapy: Both external radiotherapy or ionizing radiation cause
endarteritis, fibrosis and delay in wound healing. Radiation may itself
cause local tissue necrosis, sepsis and hypoxia.
Systemic and metabolic causes: Diabetes mellitus affects all stages
of wound healing. Cardiac, renal, hepatic, respiratory diseases prevent
wound healing. Tissue oedema impairs wound healing. HIV and
immunosuppression of varying causes, malignancy leads into poor
wound healing. Jaundice interferes with wound healing. Obesity
causes hypoperfusion, reduced microcirculation, increased wound
tension and hence prevents wound healing.
Drugs: Steroids interfere with activation of macrophages, fibroblasts and angiogenesis in the early phase of healing (proliferative).
Non-steroidal anti-inflammatory drugs (NSAIDs) decrease collagen
production. Chemotherapeutic agents used in oncology inhibit cellular
proliferation, protein synthesis. Alcohol consumption decreases the
phagocyte response and pro-inflammatory cytokine release; diminishes
host response and thus increasing the infection rate.
Local factors

Presence of necrotic tissue and foreign body
Poor blood supply
Venous or lymph stasis
Tissue tension
Large defect or poor apposition
Recurrent trauma
X-ray irradiated area
Site of wound, e.g. wound over the joints and back has poor
Underlying diseases like osteomyelitis and malig­nancy
Mechanism and type of wound—incised/lacerated/crush/
Tissue hypoxia locally reduces macrophage and fibroblast activity

General Factors
™™ Age, obesity, smoking, alcohol, stress
™™ Malnutrition, zinc, copper, manganese
™™ Vitamin deficiency (Vit C, Vit A)
™™ Anaemia, hypoxia
™™ Malignancy
™™ Uraemia
™™ Jaundice
™™ Diabetes, metabolic diseases
™™ HIV and immunosuppressive diseases
™™ Steroids and cytotoxic drugs
™™ Neuropathies of different causes

Wounds and Wound Healing
Management of Wounds
Wound cleaning
Wound cleaning is needed to optimize the healing environment. It is achieved by removing visible devitalized tissues or
dressing materials or excess exudates or crusts.
Absolute aseptic technique should be used while cleaning
the wound; warm sterile isotonic normal saline (37°C—this
is optimum temperature to support cellular activity) is ideal;
normal exudates in the wound should be removed; gentle
cleaning of the wound is important to minimize the interference of the wound-healing process. Cleaning agent should be
of neutral pH and nontoxic; delipidising agents, antiseptics,
alkaline soaps should be avoided. Gentle irrigation of warm
saline using a sterile syringe on the wound surface is ideal;
rubbing with undue force using cotton or gauze may cause
mechanical damage on the process of wound healing.
Wound is measured either in two dimensions (length and
width) or in three dimensions (length, width and depth).

has to be dealt with accordingly. Fractured bone is also
identified and properly dealt with.
xx Antibiotics, fluid and electrolyte balance, blood transfusion,
tetanus toxoid (0.5 ml intramuscular to deltoid muscle), or
antitetanus globulin (ATG) injection.
Later definitive management is done with:
Wound debridement (wound toilet, or wound excision) is liberal
excision of all devitalised tissue at regular intervals (of 48-72
hours) until healthy, bleeding, vascular tidy wound is created.
Types of wound suturing
Primary suturing means suturing the wound immedia­tely within
6 hours. It is done in clean incised wounds.
™™ Delayed primary suturing means suturing the wound in 48 hours
to 10 days. It is done in lacerated wounds. This time is allowed
for the oedema to subside.
™™ Secondary suturing means suturing the wound in 10–14 days or
later. It is done in infected wounds. After the control of infection,
once healthy granulation tissue appears, secondary suturing is

Specific management
xx Wound is inspected and classified as per the type of wounds.
xx If it is in the vital area, then:

The airway should be maintained.
The bleeding, if present, should be controlled.
Intravenous fluids are started.
Oxygen, if required, may be given.
Deeper communicating injuries and fractures, etc.
should be looked for.
xx If it is an incised wound then primary suturing is done after
thorough cleaning.
xx If it is a lacerated wound then the wound is excised and
primary suturing is done.
xx If it is a crushed or devitalised wound there will be oedema
and tension in the wound. So after wound debridement
or wound excision by excising all devitalised tissue, the
oedema is allowed to subside for 2–6 days. Then delayed
primary suturing is done.
xx If it is a deep devitalised wound, after wound debridement
it is allowed to granulate completely. Later, if the wound is
small secondary suturing is done. If the wound is large a
split skin graft (Thiersch graft) is used to cover the defect.
xx In a wound with tension, fasciotomy is done so as to prevent
the development of compartment syndrome.
xx Vascular or nerve injuries are dealt with accordingly.
Vessels are sutured with 6-zero polypropylene nonabsorbable suture material. If the nerves are having clean cut
wounds it can be sutured primarily with polypropylene
6-zero or 7-zero suture material. If there is difficulty in
identifying the nerve ends or if there are crushed cut ends
of nerves then marker stitches are placed using silk at the
site and later secondary repair of the nerve is done.
xx Internal injuries (intracranial by craniotomy, intrathoracic by
intercostal tube drainage, intra-abdominal by laparotomy)


Figs 1.20A and B: Delayed primary suturing is done once oedema
over the wound subsides. It is done as single layer interrupted deep
sutures using monofilament polypropylene or polyethylene.

Fig. 1.21A

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SRB's Manual of Surgery
Features are—It compromises circulation and function mainly
of muscles and nerves. It often maintains the normal colour and
temperature of the fingers and distal pulses may not be obliterated in spite of severe muscle ischaemia. Muscle ischaemia
more than 4 hours causes muscle death and myoglobinuria.
Irreversible nerve damage develops if ischaemia persists for 8
hours. Progressive, persistent severe pain which is aggravated
by passive muscle stretching is the diagnostic sign. Tense tender
regional lymph node is typical. Pulse will be usually normally
felt in compartment syndrome; but may become absent if there
is associated arterial injury. Compartment pressure more than
30 mmHg is an indication for fasciotomy.

Fig. 1.21B

Figs 1.21A and B: Secondary suturing is done once wound is
healthy after control of wound infection.
Principles of wound suturing



Primary suturing should not be done if there is oedema/infection/devitalised tissues/haematoma
Always associated injuries to deeper structures like vessels/
nerves or tendons should be looked for before closure of the
Wound should be widened by extending the incision whenever
needed to have proper evaluation of the deeper structures—
proper exploration
Proper cleaning, asepsis, wound excision/debridement
Any foreign body in the wound should be removed
Skin closure if it is possible without tension
Skin cover by graft/flap—immediate or delayed
Untidy wound should be made tidy and clean before suturing
Proper aseptic precautions should be undertaken
Antibiotics/analgesics are needed
Sutured wound should be inspected in 48 hours
Sutures are removed after 7 days

Wound toilet is washing the wound thoroughly using normal
™™ Wound debridement (french-letting loose) is allowing content
to come out by release incisions or facio­tomies. But commonly
debridement is used for wound excision
™™ Wound excision is actually correct terminology for excision of
devitalised tissues once or serially
™™ Radical wound excision is (pseudotumour approach) is excising
entire devitalised tissues leaving tissues with visible bleeding
from all layers

Compartment syndrome is a special entity; common in leg,
forearm, thigh and arm; is a syndrome due to increased intracompartmental pressure within a limited space area.
Causes are—narrowed space due to tight dressings/plaster
cast, lying on one limb in comatous patient; increased content
within the compartment due to trauma like fractures, oedema,
ischaemic injury, haematoma, positioning after trauma, burn
injury, etc.; high pressure injection injuries like gun injury,
oil based material injury, extravasation of chemotherapeutic
drugs; snake bite.

Fig. 1.22: Necrotizing fasciitis with extensive skin involvement which
requires adequate wound excision and eventual skin coverage.

Fig. 1.23: Fasciotomy for compartment syndrome should be
longitudinal, deep and lengthy and should decompress the
compartment to expose the underlying muscle. It should be done early.

It is common in calf and forearm. Closed injuries cause
haematoma leading to increased pressure. It is often associated
with fracture of the underlying bone which in turn compresses
the major vessel further aggravating the ischaemia causing
pallor, pulseless­ness, pain, paraesthesia, diffuse swelling
and cold limb.
If allowed to progress it may eventually lead to gangrene
or chronic ischaemic contracture with deformed, disabled
Problems with the compartment syndrome

Infection, septicaemia and abscess formation
Renal failure
Gangrene of the limb
Chronic ischaemic contracture
Disabled limb, Volkmann's ischaemic contracture

Muscle necrosis releases myoglobulin which is excreted
in the urine, damages the kidneys leading into renal failure.

Affected muscle when passively stretched worsens the pain—the most
reliable clinical sign.

Wounds and Wound Healing
xx Compartment pressure will be persistently more than 30 mm

Hg. It can be measured by placing a fine catheter in the compartment and using a pressure monitor. This is an indication for
fasciotomy. Adequate lengthy incision involving skin, fat and
deep fascia should be done until underneath muscle bulges out
properly. Multiple incisions should be made if needed. Separate
incision in each compartment should be done.

Fasciotomy done in forearm anterior compartment is a specific method.
Carpal tunnel should be released by cutting flexor retinaculum. Incision begins at the junction of the thenar and hypothenar area; extends
proximally initially transverse across flexion crease of the wrist at the
ulnar border; then across forearm towards radial side of forearm; then
in proximal forearm towards medial side creating convex flap towards
lateral side. In the elbow it crosses along the medial border to reach the
arm where it runs in arm along the medial part of the anterior arm. Injury
to major nerves, palmar cutaneous branch of median nerve should be
avoided while placing the incision. Incision should be deepened by cutting
the deep fascia along the entire length of the incision. Dorsal fasciotomy
should be added by placing longitudinal lengthy incision in the midline.
Two longitudinal incisions on the dorsum of the hand also should be made.

Fig. 1.25B

Figs 1.25A and B: Traumatic crush injury pelvis exposing testis and
iliac vessels. Patient underwent hemipelvectomy.

It is due to crushing of muscles causing extravasation of blood
and release of myohaemoglobin into the circulation leading to
acute tubular necrosis and acute renal failure.

Fig. 1.24: Incision for fasciotomy in upper limb begins at flexor
retinaculum extending into the forearm with a convex flap towards radial
side eventually leading towards medial epicondyle of the elbow joint.

Mannitol or diuretics to cause diuresis, so as to flush the kidney.
Fresh blood transfusion.
Hyperbaric oxygen.

Crush injury is one where a part of the body is being squeezed/
compressed between two high force or pressure systems. It causes extensive lacerations, bruising, compartment syndrome, crush syndrome,
fractures, haemorrhage, etc. with extensive tissue destruction and
devitalisation. Renal failure, hypovolaemic shock and sepsis are the
most dreaded problems in crush injuries.

Fig. 1.25A

Mining and industrial accidents.
Air crash.
Initially tension increases in the muscle compart­ment
commonly in the limb, which itself impedes the circulation
and increases the ischaemic damage. In 3 days, urine becomes
discoloured and scanty, patient becomes restless, apathy and
delirious with onset of uraemia. Crush syndrome is often lifethreatening. Injury is much worser than initial look.
Effects of crush syndrome

Renal failure
Disability with extensive tissue loss
Gas gangrene

xx Tension in the muscle compartment is relieved by placing

multiple parallel deep incisions in the limb so as to prevent
further damage—Fasciotomy.
xx Rheomacrodex, or mannitol is given to improve the urine
output by improving the renal function.
xx Alkalisation of urine is done by giving sodium citrate
or sodium bicarbonate. It increases the solubility of acid
haematin in the urine and so promotes its excretion. Urinary
pH should be above 6.5 until urine does not show any
myoglobin. Mannitol-alkaline diuresis should be 8 litre/day.
xx Initial aggressive volume load using saline about 1-1.5 litres/
hour is ideal in these patients.
xx Haemodialysis is done sometimes as a life-saving procedure.

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SRB's Manual of Surgery
xx Other measures:

Oxygen therapy.
Blood transfusion.
 Correction of severe hyperkalaemia.


Doing fasciotomy several days after crush injury may not be safe as it
may lead to sudden release of myoglobulin causing myoglobulinuria
and renal failure.

xx It occurs due to shearing force between tissue planes as traction—
avulsion injury. It usually occurs between subcutaneous tissue
and deep fascia or between muscle and bone. It can be localised
or circumferential.
xx Avulsion injury strips off the superficial tissues exposing the
neurovascular bundle, muscles, tendons, and bone. Degloving
injury can be open or closed.

Types of scar
A mature scar is paler, acellular, softer, flat, with reduced blood
vessels and fibroblasts, without itching (diminishes).
™™ An atrophic scar is pale, flat and stretched.
™™ A hypertrophic scar is excess scar but will not extend beyond
the margin of the scar of the original wound; there is prolonged
inflammatory phase of wound healing. It develops in 1 to 3
months after trauma. It improves spontaneously.
™™ Keloid is persistent excessive growth of the scar beyond its
margin into the adjacent skin; occurs in a triangular area between
two shoulder points and xiphisternum. It develops 3 months
to years after the trauma; progressive. Presternal area is the
commonest site.
™™ A linear scar is supple, thin, soft occurs after healing by primary
™™ A wide, irregular firm scar occurs after healing by secondary
intention or when there is infection


KELOID: ‘Like a claw’
xx Keloid is common in blacks. Common in females.
xx Genetically predisposed. Often familial. Very rare in Cauca-

xx There is defect in maturation and stabilization of collagen

fibrils. Normal collagen bundles are absent.

xx Keloid continues to grow even after 6 months, may be for many

Fig. 1.26: Degloving injury wherein skin often with soft tissues gets
avulsed off the deeper plane to create extensive raw area which may
bleed/get infected.
xx It can be in one plane or multiple planes.
xx It is commonly observed in machinery injuries or major road traffic
accidents. It is much more extensive than of on initial presentation.
xx Under anaesthesia fluoroscein is injected intravenously and viable
skin is visible as fluorescent yellowish—green colour under ultraviolet light. As injection of fluoroscein is not fully safer, serial
excision is better to look for dermal punctate bleeding.
xx It needs examination under general anaesthesia, wound excision/
radical excision, flap coverage, microflap surgeries, skin grafting,
with proper asepsis, and blood transfusion as there is significant
blood loss in these injuries.

Initially immature scar is formed during remodeling phase; this scar
is disorganized contains type III collagen. Such scar is itchy, raised,
hard and pink in colour. Over the pan of 12 months scar gets matured
fully by making disorganised collagen getting aligned along the stress
lines and formation of more type I collagen. This matured scar is soft,
supple, pale and flat without any itch. Hypertrophic scar and keloid
persists to have more type III collagen than type I collagen unlike in
matured scar.

years. It extends into adjacent normal skin. It is brownish black/
pinkish black (due to vascularity) in colour, painful, tender and
sometimes hyperaesthetic; spreads and causes itching.
xx Keloid may be associated with Ehlers-Danlos syndrome or
xx When keloid occurs following an unnoticed trauma without
scar formation is called as spontaneous keloid, commonly
seen in Negroes.
xx Some keloids occasionally become non-progressive after
initial growth.
xx Pathologically keloid contains proliferating immature
fibroblasts, proliferating immature blood vessels and type
III thick collagen stroma.
Site: Common over the sternum. Other sites are upper arm,
chest wall, lower neck in front.
Differential diagnosis: Hypertrophic scar.
Treatment: Controversial.
xx Steroid injection—intrakeloidal triamcinolone, is injected at
regular intervals, may be once in 7–10 days, of 6–8 injections.
xx Steroid injection—excision—steroid injection.
xx Triamcinolone reduces the fibroblast proliferation and
collagen synthesis; it is the first line of therapy for keloid
xx Methotrexate and vitamin A therapy into the keloid.
xx Silicone gel sheeting; topical retinoids.
xx Laser therapy.
xx Vitamin E/palm oil massage.
xx Intralesional excision retaining the scar margin may prevent
recurrence. It is ideal and better than just excision.

Wounds and Wound Healing
xx Excision and irradiation or irradiation alone.
xx Excision and skin grafting may be done.

Excision and primary suturing has got high recurrence rate; hence it is
not usually practiced.

Recurrence rate is very high—more than 50%.


Occurs anywhere in the body.
Not genetically predisposed. Not familial.
Growth usually limits up to 6 months.
It is limited to the scar tissue only. It will not extend to
normal skin.
xx Spontaneous improvement with time occurs commonly.



Figs 1.27A and B: Keloid over the sternum (butterfly shaped;
commonest site) and upper part of the arm near shoulder—common
sites of occurrence.

Fig. 1.30: Diagrammatic representation of linear,
hypertrophic and keloid scar.
xx It is pale brown in colour, not painful, nontender.
xx Often self-limiting also. It responds very well for steroid

xx Recurrence is uncommon.
xx It is common in wounds crossing tension lines, deep dermal

burns, wounds healed by secondary intention.


Figs 1.28A and B: Keloid in the ear lobule and chest
wall near shoulder.

xx Often this scar breaks repeatedly and causes infection,

xx After repeated breakdown it may turn into Marjolin’s


xx It is controlled by pressure garments or often revision exci-

sion of scar and closure, if required with skin graft.
xx Triamcinolone injection is the 2nd line of therapy for hyper-

trophic scar.

Fig. 1.29: Keloid in the upper part of the scar. It is the previous
parotidectomy scar.

Fig. 1.31A

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SRB's Manual of Surgery
Differences between keloid and hypertrophic scar
Chest wall, upper arm, lower neck, ear


Genetic predisposition
Site of occurrence




Collagen synthesis


Relation of size of injury and


Natural history

Continues to grow without time limit
Extends to normal skin
Poor response
Very high
20 times more than normal skin (Type III thick)
No relation. Small healed scar can form large
Adolescents, middle age
Common in females
More in blacks (15 times)
Thick collagen with increased epidermal
hyaluronic acid
Vascular, tender, itching
Hyperaesthesia, ulceration

Hypertrophic scar
Anywhere in the body, common in flexor
Growth limits for 6 months
Limited to scar tissue only
Good response to steroids
Is uncommon
3-6 times more than normal skin (Type III fine
Related to size of injury and duration of healing
Equal in both
No racial relation
Fine collagen with increased alpha actin
Not vascular, nontender, no itching
Shows regression
Not much

Fig. 1.31B

Figs 1.31A and B: Different contractures in hypertrophic scars over
forearm, finger and neck.
Fig. 1.33: ‘Z’ plasty is very useful method to release small


Fig. 1.32: Hypertrophied scar in the abdominal healed wound

xx Wound infection is common in devitalized deep difficult wounds.
Diabetes, immunosuppression, cytotoxic drugs, anaemia, malnutrition, malignancy increases the chances of wound infection.
xx Wound dehiscence is common in all above said adverse factors.
Wound suddenly gives away with pain causing copious serosanguineous discharge. After laparotomy when done specially as an
emergency in trauma, acute abdomen and also in malignancy,
abdominal closed wound may burst in 5–7 days. Usually all layers
of abdomen give away causing discharge, occasionally bowel will
extrude out. It needs emergency closure of the abdominal wound
using specialized sutures or retention sutures.
xx Hypertrophic scar or keloid formation due to altered collagen
synthesis in the wound healing process. Collagen synthesis is
increased 3–6 times in hypertrophic scar and 20 times in keloid.
xx Deeper wound will cause specified problems like paraesthesia,
ischaemia, paralysis, etc.

B. Ulcer
™™ Ulcer

™™ Bairnsdale Ulcer

™™ Bazin’s Disease

™™ Granulation Tissue

™™ C
 arcinomatous Ulcer

™™ Tropical Ulcer

™™ Investigations for an Ulcer

™™ Marjolin's Ulcer

™™ Venous Ulcer

™™ Traumatic Ulcer

™™ Rodent Ulcer

™™ Syphilitic Ulcer

™™ Trophic Ulcer

™™ Melanotic Ulcer

™™ S oft Chancre/Soft Sore/Ducrey’s

™™ Ulcer due to Chilblains

™™ Diabetic Ulcer

™™ Ulcer due to Frostbite

™™ Meleney’s Ulcer

™™ Martorell’s Ulcer

™™ Lupus Vulgaris

™™ Arterial/Ischaemic Ulcer

™™ Tuberculous Ulcer

™™ Climatic Bubo/Tropical Bubo

An ulcer is a break in the continuity of the covering epithelium,
either skin or mucous membrane due to molecular death.

Parts of an Ulcer
a. Margin: It may be regular or irregular. It may be rounded or oval.
b. Edge: Edge is the one which connects floor of the ulcer to the
margin. Different edges are:
Sloping edge. It is seen in a healing ulcer.
Its inner part is red because of red, healthy granulation tissue.
Its outer part is white due to scar/fibrous tissue.
Its middle part is blue due to epithelial prolife­ration.
Undermined edge is seen in a tuberculous ulcer. Disease process
advances in deeper plane (in subcutaneous tissue) whereas (skin)
epidermis proliferates inwards.
Punched out edge is seen in a gummatous (syphilitic) ulcer and
trophic ulcer. It is due to endarteritis.
Raised and beaded edge (pearly white) is seen in a rodent ulcer
(BCC). Beads are due to proliferating active cells.
Everted edge (rolled out edge): It is seen in a carcino­matous ulcer
due to spill of the proliferating malignant tissues over the normal
c. Floor: It is the one which is seen. Floor may contain discharge,
granulation tissue or slough.
d. Base: Base is the one on which ulcer rests. It may be bone or soft

Fig. 1.35: Ulcer edges.

Induration of an Ulcer
Induration is a clinical palpatory sign which means a specific type
of hardness in the diseased tissue. It is obvious in well-differentiated
carcinomas. It is better felt in squamous cell carcinoma. It is also
observed in long standing ulcer with underlying fibrosis. It is
absent or less in poorly differentiated carcinomas and malignant
melanoma. Less indurated carcinoma is more aggressive. Specific
types of indurations are observed in venous diseases and chronic
deep venous thrombosis. Brawny induration is a feature of an
abscess. Induration is felt at edge, base and surrounding area of an
ulcer. Induration at surrounding area signifies the extent of disease
(tumour). Outermost part of the indurated area is taken as the point
from where clearance of wide excision is planned.

Classification I (Clinical)

Fig. 1.34: Parts of an ulcer.

1. Spreading ulcer: Here edge is inflamed, irregular and
oedematous. It is an acute painful ulcer; floor does not
contain healthy granulation tissue (or granulation tissue
is absent) but with profuse purulent discharge and slough;
surrounding area is red and edematous. Regional (draining)

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SRB's Manual of Surgery
lymph nodes are enlarged and tender due to inflammation.
There will be associated fever, pain, impairment of functions with local tissue destruction and with little evidence
of regeneration.

Fig. 1.38: Non-healing ulcer with pale unhealthy
granulation tissue with slough.

Fig. 1.36: Spreading ulcer copious purulent discharge with slough.

2. Healing ulcer: Edge is sloping with healthy pink/red
healthy granulation tissue with scanty/minimal serous
discharge in the floor; slough is absent; regional lymph
nodes may or may not be enlarged but when enlarged
always non-tender. Surrounding area does not show any
signs of inflammation or induration; base is not indurated.
Three zones are observed in healing ulcer. Innermost red
zone of healthy granulation tissue; middle bluish zone of
growing epithelium; outer whitish zone of fibrosis and scar

4. Callous (stationary) ulcer: It is also a chronic non-healing
ulcer; floor contains pale unhealthy, flabby, whitish yellow
granulation tissue and thin scanty serous discharge or often
with copious serosanguinous discharge, with indurated nontender edge; base is indurated, nontender and often fixed.
Ulcer does not show any tendency to heal. It lasts for many
months to years. Tissue destruction is more with absence
of or only minimal regeneration. Induration and pigmentation may be seen in the surrounding area. There is no/less
discharge. Regional lymph nodes may be enlarged; are firm/
hard and nontender. It is callousness towards healing; word
callous means—insensitive and cruel; and also it means—
hard skinned.

Fig. 1.39: Callous ulcer without any sign of healing and, without
any granulation tissue.

Classification II (Based on Duration)
Fig. 1.37: Healing ulcer with healthy granulation tissue in the floor.

3. Non-healing ulcer: It may be a chronic ulcer depending on
the cause of the ulcer; here edge will be depending on the
cause—punched out (trophic), undermined (tuberculous),
rolled out (carcinomatous ulcer), beaded (rodent ulcer);
floor contains unhealthy granulation tissue and slough,
and serosanguineous/purulent/bloody discharge; regional
draining lymph nodes may be enlarged but non-tender.

1. Acute ulcer—duration is less than 2 weeks.
2. Chronic ulcer—duration is more than 2 weeks (long).

Classification III (Pathological)
1. Specific ulcers:
 Tuberculous ulcer.
 Syphilitic ulcer: It is punched out, deep, with “wash-leather”
slough in the floor and with indurated base.
 Meleney’s ulcer.



Fig. 1.42: Basal cell carcinoma of face (rodent ulcer). Ulcer edge is
raised and beaded in appearance.

Figs 1.40A and B: Maggots seen in a chronic ulcer

Fig. 1.41: Tuberculous ulcer ankle area. Note the undermined edge.
Discharge study, biopsy and later antituberculous drugs are the
treatment. They are usually painless.
2. Malignant ulcers:
 Carcinomatous ulcer
 Rodent ulcer.
 Melanotic ulcer.
3. Non-specific ulcers:
 Traumatic ulcer: It may be mechanical, physical, chemical—
 Arterial ulcer: Atherosclerosis, TAO

Fig. 1.43: Squamous cell carcinoma (SCC/epithelioma) leg with
typical everted edge. SCC can be ulcerative, ulceroproliferative or
proliferative ulcer on clinical look.

Fig. 1.44: Squamous cell carcinoma in the arm with secondaries in
the axillary lymph node. Friable tumour tissues in the floor cause
bleeding after trauma. Secondaries are fixed with ulceration. It is
advanced disease.

Venous ulcer: Gravitational ulcer, post-phlebitic ulcer.
Trophic ulcer/Pressure sore.
Infective ulcers: Pyogenic ulcer.
Tropical ulcers: It occurs in tropical countries. It is callous type
of ulcer, e.g. Vincent’s ulcer.
 Ulcers due to chilblains and frostbite (cryopathic ulcer).
 Martorell’s hypertensive ulcer.

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SRB's Manual of Surgery
 Bazin’s ulcer.
 Diabetic ulcer.
 Ulcers due to leucaemia, polycythemia, jaundice, collagen

diseases, lymphoedema.
 Cortisol ulcers are due to long-time application of cortisol

(steroid) creams to certain skin diseases. These ulcers are
callous ulcers last for long time and require excision and skin

Fig. 1.48: Large ulcer in the foot and leg with exposed tendon.

Fig. 1.45: Ischaemic ulcer foot. Middle three toes are already
amputated because of gangrene.

Fig. 1.49: Nonhealing ulcer foot in a diabetic patient with Pseudomonas
infection. Note the greenish discharge in the wound. Pseudomonas
infection is commonly hospital acquired.

Wagner’s Grading/Classification of Ulcer
Grade 0
Grade 1
Grade 2
Grade 3
Grade 4
Grade 5

– Preulcerative lesion/healed ulcer
– Superficial ulcer
– Ulcer deeper to subcutaneous tissue exposing soft
tissues or bone
– Abscess formation underneath/osteomyelitis
– Gangrene of part of the tissues/limb/foot
– Gangrene of entire one area/foot
Stages of ulcer healing

1. Stage of extension: Ulcer floor is covered with slough, purulent
discharge and inflamed edge and margin.
2. Stage of transition: Floor shows separated slough; healthy granulation tissue; serous discharge.

Fig. 1.46: Venous ulcers in both feet. Site is around ankle (Gaiter’s
zone). There are healthy granulation tissues. It needs skin grafting and
definitive procedure for varicose veins after evaluation.

3. Stage of repair: Fibrosis, collagen deposition, scar formation

It is proliferation of new capillaries and fibroblasts intermingled with red blood cells and white blood cells with thin fibrin
cover over it.

Fig. 1.47: Infective ulcer in the foot. Note the quantity of slough,
exposed tendon and gangrenous toes. Patient requires below or
above knee amputation.

xx Healthy granulation tissue: It occurs in a healing ulcer. It has got
sloping edge. It bleeds on touch. It has got serous discharge. 5 Ps
of granulation tissue—Pink, Punctate haemorrhages, Pulseful,

Painless, Pin head granulation. Skin grafting takes up well with
healthy granulation tissue. Streptococci growth in culture should
be less than 105/gram of tissue before skin grafting.
Different discharges in an ulcer (as well as from a sinus)
a. Serous: In healing ulcer
b. Purulent: In infected ulcer
Staphylococci: Yellowish and creamy
Streptococci: Bloody and opalescent
Pseudomonas: Greenish colour due to pseudocyanin
c. Bloody: Malignant ulcer, healing ulcer from healthy granulation
d. Seropurulent
e. Serosanguinous: Serous and blood
f. Serous with sulphur granules: Actinomycosis
g. Yellowish: Tuberculous ulcer

Fig. 1.52: Pyogenic granuloma.

xx Study of discharge: Culture and sensitivity, AFB study,

Fig. 1.50: Healing ulcer with healthy granulation tissue. Note the
sloping edge.
xx Unhealthy granulation tissue: It is pale with purulent discharge.
Its floor is covered with slough. Its edge is inflamed and oedematous. It is a spreading ulcer.
xx Unhealthy, pale, flat granulation tissue: It is seen in chronic
nonhealing ulcer (callous ulcer).
xx Exuberant granulation tissue (Proud flesh): It occurs in a sinus or
ulcer wherein granulation tissue protrudes out of the sinus opening
or ulcer bed like a proliferating mass. It is commonly associated
with a retained foreign body in the sinus cavity.
Fig. 1.53: Typical greenish coloured ulcer due to
Pseudomonas infection.

Fig. 1.51: Exuberant granulation tissue (proud flesh) in an ulcer. It
should be scooped out using Volkmann’s scoop prior to skin grafting.
xx Sprouting granulation tissue of sinus.
xx Pyogenic granuloma: It is a type of exuberant granu­lation tissue.
Here granulation tissue from an infected wound or ulcer bed
protrudes out, presenting as a well-localised, red swelling which
bleeds on touching.
Differential diagnosis: Papilloma, skin adnexal tumours.
Treatment: Antibiotics, excision and sent for biopsy.

Fig. 1.54: X-ray showing osteomyelitis with sequestrum inside.
Osteomyelitis prevents ulcer healing. Bone thickening on clinical
examination is typical.

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SRB's Manual of Surgery
xx Wedge biopsy: Biopsy is taken from the edge because edge

contains multiplying cells. Usually two biopsies are taken.
Biopsy taken from the centre may be inadequate because
of central necrosis.
xx X-ray of the part to look for periostitis/osteomyelitis.
xx FNAC of the lymph node.
xx Chest X-ray, Mantoux test in suspected case of tuberculous
xx Haemoglobin, ESR, total WBC count, serum protein estimation (albumin).


Ulcer will not granulate if haemoglobin is less than 8 gm% and serum
albumin is <3 gm%.

Assessment of an ulcer



Cause of an ulcer should be found—diabetes/venous/arterial/
Clinical type should be assessed
Assessment of wound is important—anatomical site; size and
depth of the wound; edge of the wound; mobility; fixity; induration; surrounding area; local blood supply. Wound perimeter may
be useful in assessing this
Wound imaging is done by tracing it on a transparent acetate
sheet at regular intervals
Presence of systemic features; regional nodal status; function of
the limb/part; joint movements; distal pulses; sensations should
be assessed
Severity of infection should be assessed—culture of discharge
Specific investigations like wedge biopsy; X-ray of part; blood
sugar; arterial/venous Doppler; angiogram


Cause should be found and treated.
Correction of the anaemia, deficiencies like of protein and vitamins.
Proper investigation as needed.
Transfusion of the blood if required.
Control the pain and infection.
Rest, immobilization, elevation, avoidance of repeated trauma.
Care of the ulcer by debridement, ulcer cleaning and dressing.
Desloughing is done either mechanically or chemically. Mechanically it is done using scissor by excising the slough. Hydrogen
peroxide which releases nascent oxygen is used as chemical
agent. Acriflavine is antiseptic and irritant and so desloughs the
area and promotes granulation tissue formation. Eusol (Edinburgh
University Solution) which contains sodium hypochlorite releases
nascent chlorine which forms a water soluble complex with slough
to dissolve it. Use of povidone iodine in ulcer cleaning is controversial (open wound is not suitable; it is mainly for cleaning the
surgical field prior to incision). Maggots if present in the wound
will cause crawling sensation and are removed using turpentine
xx Removal of the exuberant granulation tissue is also required when
xx Ulcer cleaning and dressing is done daily or twice daily or once
in 2–3 days depending on the type of ulcer and type of dressing
used. Normal saline is ideal for ulcer cleaning. Various dressings are available. Films (opsite/semipermeable polyurethane),
hydrocolloids (duoderm), hydrogels (polyethylene oxide with
water), hydroactives (nonpectin-based polyurethane matrix), foams




(polyurethane hydrophilic or hydrophobic non-occlusive), impregnates (non-adherent fine mesh impregnated with antibacterials),
calcium alginates etc.
Topical antibiotics for infected ulcers are not essential but like
framycetin, silver sulphadiazine, mupirocin may be used.
Vacuum assisted closure (VAC) therapy: It is by creation of negative pressure (25–200 mmHg), continuous or intermittent over
the wound surface; it causes reduced fluid in the interstitial space,
reduces oedema, increases the cell proliferation and protein matrix
synthesis, promotes formation of healthy granulation tissue. Sterile
foam is placed over the ulcer bed covering widely; tube drain
with multiple holes is kept within it and end of the tube comes out
significantly away; foam is sealed airtight using a sterile adhesive
film. Tube is connected to suction system. Suction is maintained
initially continuously later intermittently. Redressing is done only
after 4–7 days.
Therapy using infrared/short wave/ultraviolet rays to decrease the
ulcer size is often used but their benefits are not proved. Amnion to
promote re-epithelialisation, chorion to promote granulation tissue
formation is also often used.
Antibiotics are not required once healthy granulation tissues are
Maggot debridement therapy: It is used as biotherapy (but not
commonly) by placing cultured live disinfected maggots. Maggots
are larvae of the green bottle fly, also known as the green blowfly
(Lucilia sericata). They act by dissolving and engulfing dead
necrotic tissues; they may reduce the bacterial content in the
wound. They can inhibit many bacteria including MRSA (methicillin resistant bacteria), anaerobic and aerobic bacteria. They
secrete proteolytic enzymes to have mechanical effects; secretion
of ammonia alters the pH in the ulcer bed which inhibits bacterial
growth. They increase the granulation tissue formation also.
Once ulcer granulates, defect is closed with secondary suturing,
skin graft or flaps.
Autologous bone marrow monocytes injection into the ulcer area is
new concept by Professor Sribatsa Mohapatra but yet to confirm.


Figs 1.55A and B: Ulcer in the foot, initially with slough; later after
slough excision and regular dressings. Area requires skin grafting.

Debridement of an ulcer



It is removal of devitalised tissue
Small ulcers are debrided in the ward
Large ulcers are debrided in operation theatre under general
All dead, devitalised, necrotic tissues are removed
Slough should be separated adequately before debridement
Often devitalised tissue separates on its own by autolysis
Enzymes like collagenase are used for debridement
Hydrotherapy and dressings are mechanical nonselective
method of debridement

Dressing of an ulcer is done

Figs 1.56A to C: Ulcer leg with exposed bone. Patient underwent local
rotation flap to cover. Area from where flap is rotated is covered with
split skin graft. When the bone is exposed, skin grafting is not possible.


To keep ulcer moist
To keep surrounding skin dry
To reduce pain
To soothen the tissue
To protect the wound
As an absorbent for the discharge

Debridement can be surgical, mechanical, autolytic or enzymatic.

Ulcer dressings




Cotton dressing—cheap but traumatic
Paraffin dressing
Polyurethane dressings used in clean wounds
Alginates (seaweed) dressing used when there are heavy exudates
Type 1 collagen dressings cause haemostasis, proliferation of
fibroblasts and improve the blood supply
Foam dressings are highly absorbent, decrease the wound
maceration, and reduce the frequency of dressing­—hydrophilic
polyurethane foam
Hydrocolloid dressings help in separation of slough and autolysis
of dead tissues
Transparent film dressings are waterproof, permit oxygen and
water vapour across and prevent contamination
Hydrogel dressings used for clean wounds

Causes of formation of chronic/nonhealing ulcer
Local causes:
™™ Recurrent infection
™™ Trauma, presence of foreign body or sequestrum
™™ Absence of rest and immobilization
™™ Poor blood supply, hypoxia
™™ Oedema of the part
™™ Loss of sensation
™™ Periostitis or osteomyelitis of the underlying bone
™™ Fibrosis of the surrounding soft tissues
™™ Lymphatic diseases

Figs 1.57A and B: Solutions commonly used for ulcer and surrounding
area cleaning and dressing—povidone iodine (brownish); EUSOL
(colourless); hydrogen peroxide and normal saline. Note the EUSOL
bath. Dilute EUSOL solution in a basin is used wherein ulcer foot is
dipped and kept in place for 20–30 minutes. EUSOL removes the slough
and cleans the ulcer bed. Hydrogen peroxide releases nascent oxygen
and helps in removing necrotic material. Povidone iodine is not used
for open wound; it is only a surface antiseptic

General/Specific causes:
™™ Anaemia, hypoproteinaemia
™™ Vitamin deficiencies
™™ Tuberculosis, leprosy
™™ Diabetes mellitus, hypertension
™™ Chronic liver or kidney diseases
™™ Steroid therapy locally or systemically
™™ Cytotoxic chemotherapy or radiotherapy
™™ Malignancy

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SRB's Manual of Surgery
xx Such ulcer occurs after trauma. It may be mechanical—dental ulcer
along the margin of the tongue due to tooth injury; physical like
by electrical burn; chemical like by alkali injury.
xx Such ulcer is acute, superficial, painful and tender. Secondary
infection or poor blood supply of the area make it chronic and deep.
xx Footballer’s ulcer is a traumatic ulcer occurring over the

shin of males due to direct knocks on the shin. It is staphylococcal infection with a chronic and deep ulcer.
xx Traumatic ulcers can occur anywhere in the body due to trauma.

Fig. 1.58: Traumatic ulcers in the upper limb.

It is due to:
xx Impaired nutrition.
xx Defective blood supply.
xx Neurological deficit.


Over the ischial tuberosity.
In the heel.
In relation to heads of metatarsals.
Over the shoulder.
Due to the presence of neurological deficit, trophic
ulcer is also called as neurogenic ulcer/neuropathic ulcer.
Initially it begins as callosity due to repeated trauma and
pressure, under which suppuration occurs and gives way
through a central hole which extends down into the deeper
plane up to the underlying bone as perforating ulcer
(penetrating ulcer).
Bedsores are trophic ulcers.
Factors causing pressure sore
Normal stimulus to relieve the pressure is absent in anaesthetised patient
™™ Nutritional deficiencies worsens the necrosis
™™ Inadequate padding over the bony