Surgery - Principles in General

I SBN

969- 8295- 09- 7

SURGERY PRINCIPLES IN GENERAL FIRST EDITION

Muhammad Shuja Tahir Muhammad Abid Bashir

SURGERY

First Edition

“PRINCIPLES IN GENERAL” 2006 I

Shuja Tahir Abid Bashir

SURGERY

COPYRIGHT NOTICE: January 2006

First Edition .......... Jan 2006

Muhammad Shuja Tahir

ISBN No. 969-8295-11-9 Pak Rupees. 300/Overseas US $ 10/-

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form, by any means without prior permission of the copyright owner.

Published by:

Independent Publishing House

Jinnah Colony, Faisalabad.

Tel: 092-41-617122-24, 623412, Fax: 092-41-623413 indpubho@yahoo.com, editor@fsd.paknet.com.pk

II

SURGERY

Muhammad Shuja Tahir MBBS, FRCS, FCPS

“PRINCIPLES IN GENERAL”

Professor of Surgery

Muhammad Abid Bashir MBBS, FCPS Assistant Professor of Surgery

III

SURGERY

Dedicated to my dear younger colleagues; “The future surgeons”.

Shuja Tahir

IV

PREFACE This book has been written to make it easier and simple to understand principles of surgery; the basis of surgery.

The surgery is a dynamic subject which is improving and changing all the time. The technical developments are making the progress and bringing changes at such a high pace that even books can’t keep up.

The younger surgeons will be better equipped to deal with surgical problems after deep insight into the basis of surgical principles.

I hope all doctors, surgeons or non surgeons will be benefitted from this book. Patients whether having a surgical or non surgical problem will also be served better.

May God Almighty heal and cure all the ailing people.

Muhammad Shuja Tahir

V

FOREWORD This book on Principles of Surgery has been written by Professor Muhammad Shuja Tahir and his colleagues recently to give a simple and up to date understanding of the scientific basis of surgery and critical care to the undergraduates, post graduates and practicing junior and senior doctors.

It will be of great help in the surgical management of various problems to all of us practicing surgery at various levels. It is problem solving, up to date and very simple to understand and follow.

I wish that it helps the patients maximally (Amen).

A. G. Rehan, FRCS, FCPS Professor of Surgery Principal Punjab Medical College, Faisalabad

VI

CONTRIBUTORS Dr. Mahnaaz Roohi, FRCOG Professor of Gynaecology & Obstetrics Punjab Medical College, Faisalabad Dr. Muhammad Yousaf Shah, FRCS Professor of Surgery Punjab Medical College, Faisalabad Dr. Faisal Bilal Lodhi, FCPS Assistant Professor Punjab Medical College, Faisalabad Dr. Muhammad Abid Bashir, FCPS Assistant Professor of Surgery Independent Medical College, Faisalabad Dr. Tariq Mahmood, FCPS Assistant Professor of Surgery Punjab Medical College, Faisalabad Dr. Sohail Amer, FCPS Senior Registrar Allied Hospital, Faisalabad Dr. Ata-ul-Lateef, FCPS Senior Registrar Allied Hospital, Faisalabad

VII

ACKNOWLEDGMENTS Thanks to God Almighty who blessed me to complete the manuscript of this book. I wish and hope to achieve objectives of writing this book. This book will help the surgeons of all stages (learning, training, teaching and supervising) to understand the basic principles of surgery.

I thank all my nears and dears specially Prof. Mahnaaz Roohi who never noticed that I was writing the book or did not disturb me knowingly. I am under a great deal of obligation to Faqir Hussain and Waseem Zafar for typing, retyping, designing and redesigning the manuscript to its final shape. I hope all of you like it.

I wish to thank all the contributors, most of them are very clearly our future. I wish them the best of luck and best of future. I wish to thank every body who helped in completing the manuscript.

I would like to thank the future readers of this book who will be benefitted and will learn the basis of surgery.

I am grateful to my friends, colleagues both seniors and juniors for their valuable advice, analytical criticism and proof reading. They are so many and their contribution is so much that I can’t thank them enough. I would like to put their names in the list of acknowledgments;

VIII

Mahnaaz Roohi, FRCOG Professor of Gynaecology & Obstetrics Punjab Medical College, Faisalabad Dr. Muhammad Yousaf Shah, FRCS Professor of Surgery Punjab Medical College, Faisalabad Dr. Tariq Mehmood, FCPS Assistant Professor of Surgery Punjab Medical College, Faisalabad.

Dr. Faisal Bilal Lodhi, FCPS Assistant Professor of Surgery Punjab Medical College, Faisalabad.

Dr. Ata-ul-Latif, FCPS Senior Registrar Surgery Allied Hospital, Faisalabad.

Dr. Muhammad Abid Bashir, FCPS Assistant Professor of Surgery Independent Medical College, Faisalabad.

Dr. Muhammad Awais Shuja, MRCS Resident Medical Officer, United Kingdom.

IX

Dr. Quddus ur Rehman, FCPS Assistant Professor of Anatomy Independent Medical College, Faisalabad.

Dr. Ghulam Murtaza, FCPS Assistant Professor of Anatomy Independent Medical College, Faisalabad.

Dr. Irfan Ahmad Mughal, MBBS, M.Phil, Ph.D, MBA Professor of Anatomy Independent Medical College, Faisalabad.

Dr. Usman Latif, FCPS Assistant Professor Independent Medical College, Faisalabad.

Dr. Kashif Jameel, FCPS Assistant Professor Independent Medical College, Faisalabad.

Dr. Rizwan Ahmad, MBBS Registrar Punjab Medical College, Faisalabad.

Dr. Ayesha Rana, MBBS Medical Officer Shaffee Medical Centre, Faisalabad.

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Dr. Ghazala Noor, MBBS Medical Officer Shaffee Medical Centre, Faisalabad.

Dr. Lubna Imtiaz, MBBS Medical Officer Shaffee Medical Centre, Faisalabad.

Dr. Nausheen Bano, MBBS Medical Officer Shaffee Medical Centre, Faisalabad.

Mr. Muhammad Atif and Mr Muhammad Khalid for beautiful binding.

I am extremely grateful to my wife Prof. Mahnaaz Roohi, Awais, Nadia, Hajra and Noor, my lovely children who spared me for the long period required for this publication.

I am sorry for omissions and shortcomings although these are not intentional.

I am most grateful to God Almighty for all blessings which made this publication possible and pray for more and more blessings in future.

Amen.

Prof. Muhammad Shuja Tahir

XI

CONTENTS WOUNDS 01 02 03 04 05

1

Wounds Wound Healing Factors Affecting Normal Healing Prevention of Wound Infection Wound Care (Treatment of Wounds)

PS-001 PS-002 PS-003 PS-004 PS-005

2 11 21 27 35

PS-006 PS-007 PS-008 PS-009

45 51 55 59

SURGICAL PRACTICE 06 07 08 09

43

Cryo Surgery Lasers in Surgery Tourniquets Surgical Drains

INFECTIONS 10 11 12

63

Acute Abscess Tetanus Aseptic Surgery and Sterilization

PS-010 PS-011 PS-012

65 75 83

PS-013 PS-014 PS-015 PS-016 PS-017 PS-018 PS-019 PS-020 PS-021 PS-022 PS-023

91 99 109 117 127 139 143 149 155 161 165

CRITICAL CARE 13 14 15 16 17 18 19 20 21 22 23

89

Pre-Operative and Intra Operative Care Haemorrhage Blood Transfusion Shock Sepsis Syndrome (SS) Fluid and Electrolyte Balance - 1 (Fluid Compartments) Fluid and Electrolyte Balance - 2 (Fluid Balance) Fluid and Electrolyte Balance - 3 (Sodium Balance) Fluid and Electrolyte Balance - 4 (Potassium Balance) Fluid and Electrolyte Balance - 5 (Calcium Balance) Fluid and Electrolyte Balance - 6 (Magnesium Balance)

BURNS 24 25

167

Burns Split Skin Graft

PS-024 PS-025

169 185

PS-026 PS-027 PS-028 PS-029

189 191 193 195

BENIGN TUMORS 26 27 28 29

Epidermal Inclusion Cyst Lipoma Dermoid Cyst Fibroma

187

XII

CONTENTS 30

Junctional Naevus

31 32 33 34

Malignant Tumors Non Melanoma Skin Cancer -1 (Squamous Cell Carcinoma) Non Melanoma Skin Cancer -2 (Basal Cell Carcinoma) Malignant Melanoma

35 36 37

Supraclavicular Gland Enlargement Enlargement of Lymph Glands Hodgkin’s Disease

38 39 40 41 42

Peripheral Ischaemia Peripheral Arterial Aneurysms Gangrene Gangrene of the Big Toe Leg Ulcer

43 44

Varicose Veins Deep Vein Thrombosis

PS-030

197

PS-031 PS-032 PS-033 PS-034

201 209 215 219

PS-035 PS-036 PS-037

233 237 241

PS-038 PS-039 PS-040 PS-041 PS-042

251 269 277 283 289

PS-043 PS-044

299 307

MALIGNANT TUMORS

199

LYMPHATICS

231

ARTERIAL SYSTEM

249

VENOUS SYSTEM

297

INDEX 44

313

Index

PS-045

XIII

315

Wounds

WOUNDS

2

OBJECTIVES To assess the type and site of wound (To have the initial photograph for future reference).

To assess the class of wound.

To assess the associated damage.

To plan adequate management of wound.

To prevent wound infection.

To have serial photographs of wound at various stages of healing.

SURGERY - PRINCIPLES IN GENERAL

2

3

WOUNDS

PS-001

WOUNDS Shuja Tahir, FRCS, FCPS Ata-ul-Latif, FCPS Cutaneous wound is defined as any break in skin (epithelial lined surface) caused by injury, operation or infection. It requires nursing intervention to promote healing. The nursing approach focuses on psycho-social and physical factors affecting wound care1.

The wounds can be; Acute wounds Chronic wounds ACUTE WOUNDS Acute wounds are wounds which follow surgery or any kind of injury. These wounds usually resolve and heal within 7-10 days.

occurs spontaneously, rapidly and in predictable phases.

Surgical wound is a wound produced in the hospital electively or accidently during any procedure. It is produced under strict aseptic conditions.

Wounds may be described depending upon their type such as; Bruise.

Abrasion.

Surgical (wound).

Lacerated wound.

Penetrating wound.

Degloving wound.

War wound.

Burn wound.

Incised wound.

BRUISE It is the type of wound with minimum visible disruption of skin integrity. It is caused by crush injury to skin and underlying tissue. It presents with hemorrhage in subcutaneous tissue or in dermal and epidermal layers of the skin.

Acute wound is the loss of integrity of the healthy tissue either immediately after surgery or accident or trauma. It heals quickly and completely. The healing SURGERY - PRINCIPLES IN GENERAL

The subcutaneous hemorrhages are absorbed in a few days or few weeks. It usually heals on its own or may require analgesics and antiseptics to relieve symptoms and enhance recovery.

3

WOUNDS

ABRASION It is the type of wound which shows disruption of integrity of superficial layers of the skin. It follows minor crush injuries or friction injuries. It requires antiseptics to prevent infection and further worsening of the wound. It heals on its own. It may require local antiseptics for early recovery.

LACERATED WOUNDS These are common type of wounds which follow most of injuries. The edges are not clean cut but irregular in nature. The loss of skin integrity is variable. The skin loss is partial at some areas and complete at other areas.

SURGERY - PRINCIPLES IN GENERAL

4

These wounds require debridment, suturing of wound edges, use of local antiseptics, dressings, antibiotics and analgesics to relieve symptoms.

SURGICAL WOUNDS It is a clean cut wound made by sharp instrument (knife) under complete asepsis.

Usually surgical wound is closed by various methods such as; Suturing.

Stapling.

Steri-strips (Strip approximation).

4

WOUNDS

5

STAB WOUNDS Stab wounds are caused by sharp edged objects such as knife, nails, pointed objects, daggers, broken and pointed glass pieces. Ice-pick injuries are common in our society.

GUN SHOT WOUNDS Gun shot wounds are caused by various types of low and high velocity weapons. These may show wound of entry and wound of exit.

PENETRATING WOUNDS These are the wounds caused by pointed or sharp objects. These have small superficial opening but penetrate up to variable depths depending upon the sharpness, length of injuring object and force applied.

Mechanism of penetrating injury helps to assess the involvement of anatomical areas. These may be; Stab wounds.

Gun shot wounds.

Missile wounds.

SURGERY - PRINCIPLES IN GENERAL

MISSILE WOUNDS These wounds are caused by various types of missiles following accidents. The damage caused depends upon the velocity of missile and the distance between firearm and victim.

WAR WOUNDS These are the wounds which follow warfare or violence leading to various injuries.

These are multiple lacerated and penetrating wounds. These may be soiled and dirty. These may need adequate debridement, antiseptic care, antibiotics and symptomatic treatment. These wounds must be left open to heal initially. These may 5

6

WOUNDS

be sutured secondarily for achieving first degree healing.

chapter.

The wounds can be described depending upon the site of injury such as;

DEGLOVING WOUNDS These wounds are caused by machine injuries, accidents and friction injuries. There is larger area of skin loss which is usually of full thickness. It needs debridement and use of blood transfusion, antiseptic dressing, antibiotics and symptomatic treatment.

Skin cover is to be provided for proper recovery and healing by first degree.

Facial wounds.

Neck wounds.

Chest wounds.

Abdominal wounds.

Perineal wounds.

Limb wounds (Peripheral wounds).

BURN WOUNDS These are the wounds following burn injuries of various types. These are described in a separate

FACIAL WOUNDS These wounds are present on the face of the patient.

The healing is good in these wounds due to better

SURGERY - PRINCIPLES IN GENERAL

6

WOUNDS

vascular supply of the area. The suturing is to be performed cosmetically to avoid disfigurement. The sutures are removed in 3-4 days to prevent suture marks.

NECK WOUNDS These wounds are present any where in the neck.

These heal quickly due to good vascular supply like facial wounds.

CHEST WOUNDS The wounds in the chest if present near or over sternum show hypertrophic scarring or keloid formation. The healing is otherwise satisfactory.

SURGERY - PRINCIPLES IN GENERAL

7

Occasionally these may be complicated by extension into the pleural cavity.

ABDOMINAL WOUNDS These wounds are present anywhere over the abdomen. These heal within normal time.

PERINEAL WOUNDS These wounds are difficult to dress because of their position. The prevention of infection is difficult as areobic and anaerobic perineal contamination continues. Mechanical cleaning helps to achieve adequate healing and prevention of infection.

7

8

WOUNDS

Healing wound peri anal region

PERIPHERAL WOUNDS (LIMB WOUNDS) These wounds are present on the limbs. Hand wounds present problems of management and may lead to functional disabilities and lower limb wounds heal slowly. These may even change into chronic wounds in the presence of co-morbid factors.

CHRONIC WOUNDS Chronic wounds are the wounds which fail to heal over period of months. These follow non healing acute wounds with larger skin loss or the complicated wounds commonly associated with diabetes mellitus, neurological loss, ischemia and venous hypertension due to varicose veins. These require special care and treatment and take long time to heal.

Chronic wound is the wound which fails to heal over extended duration or presents with frequent recurrences. These are; Pressure ulcers.

Diabetic ulcers.

Lower leg ulcers.

Vascular ulcers.

Post operative open wounds.

Entero cutaneous fistulae.

SURGERY - PRINCIPLES IN GENERAL

These non healing wounds are seen in older patients with multiple systemic problems, poor medical care and inadequate health habits. Common co-morbid factors are diabetes mellitus, immune disorders, malignancy, liver, renal, chronic gastro intestinal illnesses, smoking, hypertension, obesity and immobility. The chronic wound is due to variable micro-environment of the wound5.

Most of the acute and chronic wounds are polymicrobial involving both aerobic and anaerobic organisms.

The surgical wound can be described as following classes2,3.

CLASSES OF WOUNDS 1. Clean.

2. Clean contaminated.

3. Contaminated.

4. Septic or Dirty.

CLEAN or potentially clean wounds are the ones which are made on non infected tissue and these have no organisms or normal flora present in the wound or its vicinity.

8

WOUNDS

9

tissue, atmosphere of the operation room, instruments or surgeon's hands. These wounds do not show any sign of infection (presence of signs of inflammation and pus discharge)4.

EXAMPLE Surgery for acute appendicitis and colon etc. The risk of post operative wound infection in these wounds is five times more than with clean wounds2,3.

Prophylactic use of peri-operative antibiotics for aerobes and anaerobes is mandatory to avoid post operative infection in these wounds.

EXAMPLE Surgical wound for hernial repair and breast lump excision.

SEPTIC or infected wounds are the ones which show all the features of inflammation and presence of pus (infection).

The risk of postoperative infection is minimum in these wounds2,3.

No antibiotics are required for prevention of infection in these wounds.

CLEAN CONTAMINATED wounds are the ones which are made on a clean and non infected tissue. These carry organisms in the vicinity of wound but not in the wound itself.

EXAMPLE: Surgical wounds for surgery of gall bladder, prostate and ureter etc.

The risk of post operative infection is three times as compared with clean wounds2,3. In these wounds prophylactic use of peri-operative antibiotics prevents the post operative infection significantly.

CONTAMINATED wounds are the ones which carry the organisms in the wound either from the surrounding SURGERY - PRINCIPLES IN GENERAL

EXAMPLE Surgery for gastrointestinal perforations and generalized or pelvic peritonitis and intestinal obstruction etc.

The risk of post operative infection is maximum and is about six times more than with clean wounds2,3.

Appropriate antibiotic cover is essential for 9

10

WOUNDS

prevention and treatment of infection from aerobes and anaerobic organisms in these patients.

REFERENCES 1. Teare J, Barrett C. Using quality of life assessment in wound care. Nurs stand Oct 2002; 23;17(6): 5960,64, 67-8.

2. Cortale M. Gobessi V. Calligaris L. The role of the environment in postoperative infections. [ITALIAN] Annali Italiani Di Chirurgia. Nov-Dec 1989; 60(6):547-50: discussion 550-1.

3. Ojiegbe GC. Njoku-obi AN. Ojukwu JO. Incidence and parametric determinants of post operative wound infections in a university hospital. Captral African Journal of Medicine. March 1990; 36(3):63-7.

4. Deviatov VA. Petrov SV. Causes of suppurative complications after appendicectomy. [Russian] Khirurgiia. March 1991; (3):103-6.

5. Cooper S. Wicke C. Feffer F. Koucker G. Beker HD. Documentation of 7051 Chronic wounds using a new computerized system within a net work of wound care centre. Arcr Surg. March 2004; 139(3): 251-8.

SUMMARY Wounds Acute wounds ! Bruise ! Abrasion ! Lacerated wounds ! Surgical wounds Penetrating wounds ! Stab wounds ! Gunshot wounds ! Missile wounds War wounds Degloving wounds Burn wounds Regional Wounds ! Facial wounds ! Neck wounds ! Chest wounds ! Abdominal wounds ! Perineal wounds ! Limb wounds Chronic wounds Classes of wounds ! Clean ! Clean contaminated ! Contaminated ! Septic

SURGERY - PRINCIPLES IN GENERAL

10

WOUND HEALING

1

PS-002

WOUND HEALING Shuja Tahir, FRCS, FCPS

WOUND1 The wound is disruption of normal anatomical structure and function resulting from pathological processes beginning internally or externally to the involved organ.

Cutaneous wound is defined as any break in the skin integrity caused by injury, operation or infection.

WOUND HEALING1 Wound healing is restoration of the tissue continuity after injury. It involves wound closure and restoration of function of the damaged tissue.

Injured tissue heals by partial or complete regeneration or by repair.

1

REGENERATION Regeneration is complete re-establishment of the original tissue structure. It heals to normal function of the tissue. Its examples are epithelial tissue epidermis, gastro intestinal tract epithelium, respiratory tract epithelium, liver parenchyma, bone, smooth muscle and some skeletal muscles.

tissue holds the injured tissue together. It is functionally less effective due to reduced tensile strength and energy absorbing capacity.

Cutaneous wound healing occurs both by regeneration of epidermis and repair of dermis.

BIOLOGY OF WOUND HEALING Wound healing occurs by primary or first intention (primary healing) or by second intention.

Most surgical wounds are categorized as acute wounds. Healing occurs within expected time and without complications. Healing is affected by intrinsic and extrinsic factors causing complications2.

Understanding of wound healing has moved from cellular to molecular level. Several molecular explanations for altered healing and treatment of chronic wounds are available3.

Dermis is incapable of regeneration. It heals by repair.

PRIMARY HEALING The normal healing process in a simple or closed wound is also called healing by primary intention or primary union or first degree healing. This is seen in the healing of clean, well perfused, incised wound with edges in apposition such as the surgical wound4.

REPAIR1 The original tissue is replaced by non specialized connective tissue forming an inferior scar. The scar

Epithelialization occurs early (within 24 hours) in these wounds. Epithelium grows from basal cells of epidermis and minimum granulation tissue is formed.

PRINCIPLES OF SURGERY

11

WOUND HEALING

Wound contraction has minimum role to play in the healing of such wounds.

SECOND DEGREE HEALING Open Wound Healing Healing By Second Intention The healing of an open wound or a wound with edges apart is called healing by second intention or healing by second degree. It heals by granulation tissue formation and maximum cicatrization.

The epithelium has to grow over larger areas in these wounds. In this wound contraction is more to allow growth of intact overlying epithelium. It leads to more scar tissue formation, distortion and cosmetically unsatisfactory scar. It is associated with impairment of functions due to repair process.

SECONDARY HEALING It is the healing in a wound which has been resutured. It heals at faster speed than by second intention. It achieves less scaring and better cosmetic results. It happens due to continuity of fully established healing process in the wound at the time of re-suturing (products of healing already present).

NORMAL WOUND HEALING Wound healing is an active process. The whole process consists of series of phases. These phases are continuous and overlapping. These may not occur in orderly fashion5. These involve the stages of hemostasis, inflammation, and repair.

Healing process consists of multiple integrated networks of cell-matrix-cytokine interactions. The cells at the wound site produce or alter various cytokines and extracellular matrix. These in turn alter the behavior of producer cells(autocrine response) or neighbouring cells (paracrine response)7.

PRINCIPLES OF SURGERY

2

PHASES OF HEALING Three distinct and continuous phases are seen during wound healing process5.

PHASE OF PREPARATION Inflammatory phase Early phase It is the localized protective tissue response initiated by injury or destruction of tissues. It helps to destroy, dilute or wall off the injurious agent and injured tissues.

Inflammation brings nutrients to the area of the wound, removes debris and bacteria and provides chemical stimuli for wound repair.

It is the earliest phase and it starts immediately after the wound is made. It lasts for few days (approximately upto 4th day of healing). The cellular and enzyme activity is seen during this phase.

Objectives of inflammation are removal of debris and necrotic tissue and reduction of local infection. The inflammatory process has an early phase and a late phase. Foundations of the repair are laid during this phase. This phase does not provide strength to the wound.

HAEMORRHAGE & CLOT FORMATION1 Tissue injury causes cell death and vessel disruption.

Clot formation occurs both within the damaged vessels resulting in cessation of haemorrhage and within wound to provide provisional matrix of fibrin, fibronectin, von Willibrand factor (vWF) and thrombospondin.

Hemostasis with fibrin formation creates a protective wound scab. The scab provides a surface beneath which cell migration and movement of the wound 12

WOUND HEALING

edges can occur.

The small initial haemorrhage leads to formation of clot which is rich in fibrin content. This fibrin coagulum contains red cells and polymorphs which increase in number about eight hours after the injury or incision. Fibrinous exudate thus produced, helps to cement the cut margins of the wound.

The clot formation in the wound helps in early migration of cells, stimulates fibroblast proliferation (via thrombin). It shields mitogenic and chemotactic factors for inhibitors. The blood clotting involves humoral aspects of coagulation and cellular response.

The ultimate effect of coagulation is the conversion of protein fibrinogen into an insoluble fibrin network stabilizing the initial haemostatic plug.

Following biological active substances are released to stimulate synthesis of extracellular matrix (ECM) which initiates the phase of repair; Platelet derived growth factor (PDGF).

Platelet factor-4 (PF4).

Transforming growth factor Âľ (TGF alpha).

Transforming growth factor âb (TGF beta).

Blood clotting activates Hageman factor and leads to generation of bradykinin and initiation of classical and alternative complement cascades generating complement derived anaphylatoxins C3a and C5a.

These changes increase permeability of injured vessels and cause release of plasma protein and formation of extravascular clot.

PRINCIPLES OF SURGERY

3

The anaphylatoxins stimulate release of vasoactive mediators histamine and leukotriens (LT) C4 and D4 from mast cells. This phase is neutrophil rich.

LT B4 is released by activated neutrophils (FMP) formyl methionyl peptides are cleaved from bacterial proteins. Platelet activating factor (PAF), tumour necrosis factor a (TNF a ), Platelet factor-4 (PF4) and Platelet derived growth factor (PDGF), interleukin -8, growth related protein and melanoma growth stimulating activity G&P (MGSA).

Monocytes are influxed by beta chemokine family such as monocytes, chemoattractant protein-I (MC P-1) and macrophage inflammatory protein-I alpha (MIP-1 Alpha). Other factors attracting monocytes are platelet derived endothelial cell growth factor (PD-ECGF), thrombin, Transforming Growth Factor beta (TGF beta) and fragments of collagen, elastin and fibronectin.

Neutrophil adherence to micro-vascular endothelium is initial step in diapedesis (leucocyte migration into wound and surrounding tissue). Its is facilitated by chemical mediators (chemoattractants).

These are ; 1. Immunoglobulin (Ig) gene suppressor family (Intercellular adhesion molecule-I (ICAM) and ICAM-2 and vascular cell adhesion molecule-I (VCAM-I).

2. The integrin family beta integrins, lymphocyte function associated antigen-I (LFAA-1) 3. Selectin family L-selectin, P & E selectins.

The main function of neutrophils that infiltrate the wound bed is the phagocytosis of pathogenic bacteria and dead tissue. The inflammatory environment stimulates release of toxic reactive 13

4

WOUND HEALING

oxygen intermediates which destroy the bacteria and damage the surrounding normal healthy tissue.

Although exact factors for this change are not known but following may be responsible;

Leukocytosis ceases within a few days when the wound is not infected. It indicates end of early phase of inflammation.

1.

2.

3.

4.

5.

The vasodilatation of inflammation occurs during first half an hour of injury due to release of histamine. Then Kinins and Prostaglandins, PGE1 and PGE2 take up this function. Aspirin and indomethacin inhibit their action. These are anti-inflammatory drugs. Acute inflammatory reaction follows the initial haemorrhage. All vessels around the injured or wounded area dilate after initial constriction.

Insoluble fibronectin.

Low oxygen tension.

Chemotactic agents.

Bacterial lipopolysaccharides.

Interferons.

Macrophages not only remove the dead and degenerate tissue but also generate chemotactic factors which are responsible for the recruitment of additional inflammatory cells or release of collagenases.

Proteins and plasma leaks into the wound due to increased permeability of dilated vessels. The white cells adhere to the capillary endothelium and migrate actively to the site of injury.

These also synthesize and release growth and regulatory factors critical for granulation tissue formation including Platelet derived growth factor (PDGF), Transforming growth factors (TGF) beta, TGF alpha and fibroblast growth factor (FGF) and IL-1.

Increased blood supply to the area provides nourishment and phagocytes which remove the dead and degenerating tissue.

The macrophages play an important and significant role in transition from inflammatory phase to proliferative phase of wound healing.

The inflammatory reaction in the early period of wound healing is essential for proper wound healing.

RE-EPITHELIALIZATION1 Re-epithelialization starts rapidly and soon after injury. It continues throughout the proliferative phase of repair.

If steroids or any other drug is used to suppress the inflammatory reaction, the wound healing is compromised.

Neutrophils infiltrate ceases by the end of early phase of inflammation. Macrophages continue to accumulate. Monocytes differentiate into macrophages after migration from vessels to wound site. Monocytes and few fibroblasts are usually seen by the end of twenty four hours.

PRINCIPLES OF SURGERY

In the skin wounds, the epidermis immediately adjacent to the wound edge thickens within 24 hours after injury.

Epidermal cells reconstitute into an organized keratinized, stratified epithelium which covers the wound defect and restores functions of skin minimizing morbidity and mortality after cutaneous injury.

14

WOUND HEALING

5

Some of the basal cells present at the margin loose their firm attachment with dermis. These cells migrate into the defect and enlarge in size.

After wound healing, the epithelial and mesenchymal repair occurs but it never attains normal tissue architecture.

The epithelial cells from the adjacent epidermis of the wound migrate into the wound within first 24 hours of the injury. These epithelial cells lie between dermis and the clot. The surface is covered with crust or scab of dried clot overlying these cells during first twenty four hours.

The intercellular attachments (desmosomes) are dissolved. Basement membrane attachment (hemidesmosomes) is also dissolved. The peripheral cytoplasmic actin filaments are for med.

Pseudopodia are projected and cells are able to move. The calcium is associated with signaling of these cell movements1.

In the next 24-48 hours, the epidermal cells grow into the space where connective tissue will develop eventually and thus form a spur.

The migrating cells of epidermis do not divide. The mitotic activity occurs only in the basal cells very near to the edge of the wound. Epithelial cells also grow along the suture line. The stimulus for epithelialization is loss of contact between the epithelial cells.

The epithelial migration is stimulated by ; ! ! !

Orientation of components of substrate such as fibrin and fibronectin.

Chemotactic factors generated during clotting and platelet.

Loss of contact inhibition by adjacent cells.

The rate of migration of cells is dependent upon tissue oxygen tension. It is highest in hyper-baric environment when the rate of cell movement is 1221µm per hour. Humidity also helps cellular migration at higher rates.

Whole of the wound surface gets epithelialized within 48 hours. This epithelium divides and redivides to make normal multiple layers.

PRINCIPLES OF SURGERY

The epithelial cells migrate either by “leap frogging” or “tractor tread” mechanism or both of these mechanisms.

The subcuticular stitches injure the hair follicles and sweat glands and cause injury to the subcuticular layer of epithelial cells. These may lead to epithelial cyst formation after healing4.

Once the cells grow and make contact with each other, an inhibitory hormone (Chalone) is produced and epithelial growth and migration is stopped. This process is called contact inhibition. No other cause for this inhibition is known. Contact inhibition prevents further migration.

PHASE OF PROLIFERATION Fibroblastic phase Repair begins immediately after wounding and proceeds rapidly through the processes of epithelialization, fibroplasia and capillary proliferation into the wound area.

The wound healing or repair is performed by the connective tissue which is produced by the granulation tissue. The connective tissue is composed of matrix of cells and newly growing 15

6

WOUND HEALING

capillaries which are also called organs of repair. If it is healthy, the healing is good and satisfactory. The matrix of cells and capillaries disappear after the repair is complete4.

The cells of repair are mainly; ! !

Macrophages.

Fibroblasts.

The macrophages stimulate fibroblast activity and inward growth of new capillaries.

The fibroblasts require good supply of easily diffusible oxygen for its normal function. The fibroblasts synthesize; Collagen (Glycosaminoglycans of ground substance) Fibronectin (Glycoprotein) The fibronectin holds the structure of the ground substance.

This phase is characterized by the formation of granulation tissue which consists of; Fibroplasia Angiogenesis FIBROPLASIA Fibroplasia leads to migration of fibroblasts into the wound leading to synthesis and secretion of collagenous and non-collagenous matrix.

After the initial inflammation has settled, fibroblasts appear in the depth of wounds. These are spindle shaped cells with oval nuclei. These can attain any shape. These cells contain diffuse golgi apparatus and dilated rough endoplasmic reticulum. These PRINCIPLES OF SURGERY

cells originate from local mesenchymal tissue attached to the capillaries. These cells dominate the cell population by 10th day after the wound formation. These cells synthesize and secrete collagen molecules8.The migration of fibroblasts into the wound is achieved by; Chemotactic factors Compliment metabolites C5a derivative Growth factors such as ; PDGF (Platelet derived growth factor).

PF4 (Platelet factor-4) Growth factor (TGF beta and IL-4) Matrix factors (Collagen types I & III and fibronectin) An adhesion gradient Haptotaxis 3D arrangement of ECM fibrils within tissue.

The fibroblasts use the fibrin coagulum as a scaffolding. The fibroblasts and epithelial cells form adhesive contact with the coagulum and grow on the wound8.

This phase starts after four to five days of wound formation. The ground substance appears in large quantities. The fibroblast capillary system (organ of repair) is most active during this phase. The strength of wound increases rapidly during this phase.

ANGIOGENESIS The granulation tissue requires profuse blood supply for oxygen and nutrition. The process of new blood vessel formation starts 2-3 days after injury. The capillary buds grow into wound from the already present venules near the edge of the wound.

16

WOUND HEALING

The angiogenesis involves disruption of the basement membrane of venules due to release of plasminogen activator, collagenase and stromelysin by the endothelial cells.

The formation of new capillaries starts at the rate of 0.6 mm/day. Initially these capillaries are fragile and very permeable later on these capillaries mature up providing to well developed blood supply within the granulation tissue.

The fibroblast capillary system synthesizes the collagen and ground substance very actively by end of one week after the wound is made.

Collagen synthesis starts from 3rd-5th day of wound formation and continues for several weeks.

Net collagen accumulation depends upon synthesis and degradation. It is stimulated by several factors such as growth factors and cytokines. These are produced by fibroblasts and leukocytes.

7

DEMOLITION & ORGANIZATION MATURATION After 4-5 weeks of injury, the number of fibroblasts decreases. The capillary network is also decreased changing into proper capillary system. Now the collagen fibers dominate the wound area.

The collagen fiber bundles enlarge and produce massive dense collagenous structure binding several tissues tightly. It is called the scar. The scar changes in its bulk over many years. Sometimes increasing into hypertrophic scar or keloid and sometimes decreasing in thickness to hairline scar.

The pigmentation also becomes normal and scar is hardly visible. Sometimes the scar is too weak and leads to dehiscence and incisional hernia formation8.

Demolition phase follows after acute inflammation, which removes the dead and degenerating tissue.

The fibroblasts don't have fibrolytic activity.

Macrophages are found free at the edge of the wound. These remove the debris and stimulate fibroplasia.

Rapid capillary formation is a common feature. These form by budding from existing venules. The endothelial cells contain a potent plasminogen activator which causes fibrolysis8.

The cellular proliferation and migration inwards are main features of growth factors9.

The collagen content is directly proportional to the tensile strength of the wound during the first month.

GRANULATION TISSUE The dense population of macrophages, fibroblasts and endothelial cells embedded in loose matrix of collagen types I, III, fibrin, fibronectin and proteoglycans rich in hyaluronic acid is called granulation tissue. It is not covered by epidermal cells.

The granulation tissue prevents excessive migration of the epithelial tissue. The epithelial tissue forming spurs, degenerates and is replaced by the granulation tissue which later on shrinks due to devascularization. It also changes its color from red to white.

The use of adhesive tapes instead of sutures gives better cosmetic results as it avoids suture marks.

PRINCIPLES OF SURGERY

17

8

WOUND HEALING

REMODELING Remodeling of immature tissue matrix starts simultaneously with granulation tissue formation.

It is 10% of normal skin at the end of one week. It rapidly increases over next four weeks and reaches 70-80% of normal skin10.

It is regarded as the third and final phase of wound healing as it continues for many months or even years after resolution of granulation tissue formation.

BURST STRENGTH It is the measures of the load required to break the scar regardless of its cross-sectional area.

The highly vascular and cellular granulation tissue is replaced and remodeled during this phase.

It happens by migration of cells out of wound or by programmed cell death (apoptosis)1.

WOUND CONTRACTION It is reduction of part or all of the skin defect by centripetal movement of the surrounding undamaged skin.

It starts about a week after injury and reaches its peak in 2 weeks. It reduces the size of wound and its requirement for scar formation.

Its rate is 0.6 - 0.7 mm per day and it is independent on the size of the wound.

TENSILE STRENGTH OF THE SCAR It is the measure of the load per cross sectional area at rupture of the scar.

It is provided by the collagen which is produced by the fibroblasts and is the most common protein present in animal kingdom.

There is cross linking between alpha chains of adjacent molecules which provide structural stability of collagen and is a major contributor to the tensile strength of collagen.

PRINCIPLES OF SURGERY

The incised wound gains strength immediately after suture.

After two days, the burst strength is between 50-100 grams.

The burst strength rises very quickly by 3rd day when collagen fibers have appeared.

The burst strength reaches over 1 kg per linear centimeter after 3 weeks, (21 days).

The rate of gain of strength is quicker for four months then it slows and continues over years.

The repaired wound never achieves the strength of normal tissue. The elasticity is also never the same8.

The wound healing process becomes less active after a month or so.

The strength of the wound recovers more slowly. The number of cells and capillaries also diminish and the cell population also diminishes.

REFERENCES 1. Melissa Calvin. Cutaneous wound repair. Wounds, 1998; 10(1): 12-32.

2. Baxter H. Management of surgical wounds. Nurs

18

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WOUND HEALING

times. April 2003; 1-7; 99(13): 66-8.

SUMMARY WOUND HEALING

3. Cooper DM. Wound healing. New understandings.

Nurs prac forms. Jun1999; 10(2): 74-86.

4. Forester JC. Wound healing and fibrosis. Textbook of surgical physiology. Jamieson and Kay's. Ledingham IainMca. MacKay Colin. Churchill Livingstone Edinburgh. 4th edition, 1988.

5. Gilmore MA. Phases of wound healing. Dimensions of Oncology Nursing. Fall 1991; 5(3):32-4.

6. Phillips SJ, Physiology of wound healing and surgical wound care. ASAIO J. Nov-Dec 2000; 46(6): S2-5.

7. Clark RA. Basics of cutaneous wound repair journal of dermatologic surgery and oncology. [JC:hza]. Aug 1993; 19 (8); 693-706.

8. John W. Madden. Arnold J Arem. Wound healing.

Biologic and clinical features. David Sabiston, JR Text book of surgery. WB Saunders company London 14th edition. 1991; 168-175.

9. Skoken SJ. Davis RH. Principles of wound healing and growth factor considerations. Journal of the American Pediatric medical association. [JC:ipa]. Apr 1993; 83(4): 2230-7.

10. Ramzi S. Cotran. Vinay Kumar. Stanley L. Robbins.

Inflammation and repair Robbins pathologic basis of disease. WB saunders company 5th edition. 1994; 85-92.

PRINCIPLES OF SURGERY

Biology of Wound Healing Types of Wound Healing

! ! !

Primary Healing Second Degree Healing Secondary Healing

Process of Normal Healing Inflammation Clot formation

! ! ! ! !

Release of Biologically active substances Synthesis of extra cellular matrix Nuetrophil rich phase Re-epithelialization Contact inhibition

Repair

! ! ! !

Fibroblastic phase Fibroplasia Angiogenesis Granulation tissue formation

Demolition & Organization Maturation Re-modelling Wound Contraction

19

1

FACTORS AFFECTING NORMAL HEALING

PS-003

FACTORS AFFECTING NORMAL HEALING Shuja Tahir, FRCS, FCPS

Different tissues have their own normal rates of growth during the process of healing. The optimal rate of healing is approached when factors advantageous to healing are present and factors having the ability to disturb or retard the healing processes are absent or controlled6.

The understanding of pathophysiological basis of healing has improved over years. Many factors affect healing positively or adversely. Identification of factors affecting a particular wound help in better management of the wound.

Guidelines are developed to achieve satisfactory wound healing.

Documentation of following features of wound is important to develop these guide lines; ! ! !

Wound characteristics.

Wound healing dynamics.

Wound care.

The factors which interfere with normal healing are ;

the treating doctor and should avoid all possible factors delaying healing.

Grading of wound depth is useful guide in predicting the possible required for adequate healing.

Healing process is delayed in elderly patients due to multiple age related factors. Healing of ulcers is delayed in patients complicated by respiratory insufficiency, diabetes mellitus and infection3.

GENERAL FACTORS AGE Wound healing is better in young patients. It is poor in old patients. Hypertrophic scar and keloids are more common in younger age group. Wound dehiscence is more common in old age group but it is more due to cardiac and pulmonary problems than wound itself4.

GENERAL HEALTH Healing is better in healthy and fit patients while in cachexic and ill patients it is poor and delayed.

SMOKING4 Smoking has been found to delay healing.

Patient compliance.

Grading of wound depth.

Age of the patient1,2.

DEHYDRATION4 Proper hydration is very essential for wound healing.

Patient compliance is a very important factor in wound healing. Patients should follow instruction of

HYPOPROTEINEMIA4,5 It delays healing when associated with 20% loss of

SURGERY - PRINCIPLES IN GENERAL

21

FACTORS AFFECTING NORMAL HEALING

2

weight. The exact cause of its negative effect on healing is not clear. Amino acids are involved in the biochemical process of wound healing. Previous view of effect of sulfur containing amino acid on wound healing is without any proof.

HORMONES Steroids inhibit normal inflammatory reaction, limit capillary budding, inhibit fibroblast proliferation and minimize epithelialization. Thus the healing is delayed6.

ANAEMIA It leads to delayed wound healing or non healing in severely anaemic patients. The low oxygen tension over prolonged periods leads to significant impairment of healing.

Steroids affect wound healing adversely. These increase collagen lysis and decrease collagen synthesis. The steroids also inhibit the inflammatory reaction which is essential for proper wound healing.

Haemorrhage and anaemia have no direct effect on wound healing. Indirectly, these effect by lowering oxygen tension locally due to decreased oxygen carrying capacity, vasoconstriction, hypovolemia and elevated blood viscosity.

VITAMIN 'A' Its deficiency also delays wound healing. Its demand is increased in early post operative period probably due to the increased cortisol level.

VITAMIN C5 Ascorbic acid (vit-C) is important for synthesis of collagen. It holds three alpha chains after hydroxylation thus promoting wound healing and wound strength.

ZINC COPPER AND FERROUS5 Zinc is important for wound healing. It increases fibroblastic activities. Its deficiency leads to limited growth and delayed puberty. Copper and ferrous are required for normal collagen metabolism.

GENERAL DISEASES4 Diabetes mellitus, jaundice, respiratory illness, malignancy and renal impairment delay healing.

SURGERY - PRINCIPLES IN GENERAL

Anabolic hormones like testosterone have positive effect on the healing process.

CYTOTOXIC DRUGS3 The cellular activity is essential for wound healing.

The cytotoxic drugs delay healing by impairing cellular activity. These should be avoided during first four weeks of wound healing.

TEMPERATURE The wound healing is better when atmospheric temperature is about 30 degrees centigrade. The raised temperature doesn't accelerate healing directly. It probably acts by raising the subcutaneous oxygen tension which improves wound healing.

MISCELLANEOUS Many other nutrients such as amino acids, thiamine and magnesium are involved in the biochemical process of wound healing. Their deficiency will also lead to poor or defective healing.

LOCAL FACTORS RE-SUTURING OF WOUNDS When the wound bursts and is resutured, it gains more strength at a shorter period. It is probably due to increased rate of new collagen deposition.

22

3

FACTORS AFFECTING NORMAL HEALING

The secondary healing of a wound is quicker1,5.

patients with varicose veins leads to slow healing.

EXUDATE Wound fluid from acute wound may have beneficial effect on wound healing and that of chronic wounds may inhibit healing.

EXPOSURE OR DRYNESS Exposure or dryness of the wound surface kills the surface cells and destroys normal blood flow in the superficial vessels6,9.

Changes in nature and volume of exudate provide information on underlying state of wound and may give indication of increasing bacterial load and presence of infection and healing process. Careful monitoring of exudate can provide information for application of systemic and local therapies7.

Moisture provides a positive influence on the mechanical and hormonal aspects of the wounds.

GROWTH FACTORS Growth factors are essential for regulating the cellular events involved in the formation of granulation tissue and in wound healing.

Growth factors attract cells into the wound, stimulate their proliferation and have a preformed influence on extra cellular matrix (ECM) deposition. Growth factors have positive influence on wounds with impaired healing8.

ANOXIA3 Tissue oxygenation is very important for the healing of wounds. It is true that fibroblasts can survive tissue anoxia to some degree. They cannot synthesize proper collagen under anoxic conditions and their bactericidal function is also diminished.

Wounds of areas having better oxygen supply heal quicker. Ischaemia and poor blood supply leads to bed sores in bed ridden patients.

ADHESION TO THE BONY SURFACE This may delay the wound healing as in tibial fractures. It is because the adequate apposition of the wound is not possible.

DEPTH & WIDTH OF WOUND Depth of wound and size of wound is important in affecting the healing process. Deeper the wound, longer is the period of healing, greater width of wound needs longer time period for healing and the scar formation is poorer.

TIGHT STITCHES, EDEMA These minimize tissue perfusion locally. External pressure of tight bandage and internal pressure of edema also decrease local tissue perfusion and delay healing.

REGIONAL BLOOD SUPPLY The wounds of face heal much quickly due to better blood supply.

Wounds stitched under tension or when the wounds get edematous and tense due to operation or injury, heal poorly.

Wounds in the areas with poor blood supply heal slowly such as pre-tibial area. The poor circulation in

The presence of one piece of sterile silk stitch leads to one thousand times higher risk of staphylococcal infection.

SURGERY - PRINCIPLES IN GENERAL

23

4

FACTORS AFFECTING NORMAL HEALING

DRESSINGS Repeated dressings delay healing by disrupting the granulation tissue formation and removing the newly formed epithelial tissue.

MISCELLANEOUS Foreign bodies, local irritants and mobility of the wound, all delay healing by breakdown of healing tissue.

Wet dressing leads to infection and thus delay healing.

Foreign bodies, dead tissue, debris in the wound are mechanical barriers to the fibroblasts, preventing their entry into the wound.

Closed dressing (sealed dressing) is better as it avoids infection and disruption of the granulation tissue.

USE OF ANTISEPTICS Epidermis with its thickness protects underlying tissues from effect of antiseptics when these are used for antisepsis. When these are applied on openwounds, all the cells are killed on contact5.

4

INFECTION It delays healing by causing continuous tissue breakdown. It also retards collagen synthesis and leads to defective healing. The healing process becomes static at the phase of inflammation in the presence of bacteria in the wound.

TRAUMA Local tissue injury in crushed wounds delays healing due to local tissue anoxia. There is greater incidence of infection in such wounds and healing is further delayed.

RADIOTHERAPY It delays healing because of cell destruction and irreversible damage to capillaries. It also leads to local tissue anoxia and cell destruction. It stops the fibroblastic activity. If it is given during first three days of wound healing, there is significant delay in gain of strength.

These also prolong inflammatory reaction and cause infection. These delay wound healing and gain in wound strength.

Wound surface washing with normal saline irrigation or adequate debridement is essential to improve healing process6.

Use of binders to support the abdominal wounds delay healing.

Neoplasia delays healing.

Ultrasound and pulsed magnetic energy also improve healing.

REFERENCES 1. Shuja Tahir; Surgery “TMA Selected Questions� UroObs Publishers, 3rd edition. 1997; 14-21.

2. Cooper S, Wicke C, Pfeffer F, Kovcker G, Beker HD. Documentation of 7051 chronic wounds using a new computerized system with in a net work of wound care centers. Arch Surg. Mar 2004; 139(3): 251-8.

3. Mendez Eastman S. Use of hyperbaricand negative pressure therapy in multi-disciplinary care of a patient with non healing wounds. J wound, ostomy continence Nurs. Mar 1999; 26(2): 67-76.

4. Gilmore MA. Phases of wound healing. Dimensions of

SURGERY - PRINCIPLES IN GENERAL

24

5

FACTORS AFFECTING NORMAL HEALING

Oncology Nursing. Fall 1991; 5(3):32-4.

5. Utley R. Nutritional factors associated with wound healing in the elderly. Ostomy wound management.

April 1992; 38(3):22. 24. 26 -7 .

6. John W. Madden. Arnold J Arem. Wound healing.

Biologic and clinical features. David Sabiston, JR Text book of surgery. WB Saunders company London 14th edition. 1991; 168-175.

7. Vowden K, Vowden P. Understanding exudate management and role of exudate in the healing process. Br.J. Community Nurs. 2003; 8(11 Suppl): 4-13.

8. Declair V, The importance of growth factors in wound healing. Ostomy wound manage. Apr 1999; 45(4): 64-8, 70-2, 74.

9. Skoken SJ. Davis RH. Principals of wound healing and growth factor considerations. Journal of the American Pediatric medical association. [JC:ipa]. Apr 1993; 83(4): 2230-7.

SURGERY - PRINCIPLES IN GENERAL

SUMMARY Factors affecting wound healing General factors ! Age ! Health ! Smoking ! Dehydration ! Hypoproteinamea ! Aneamia ! Vitamin A ! Vitamin C ! Copper and ferrous ! General diseases ! Hormones ! Cytotoxic drugs ! Temperature ! Miscellaneous Local factors Re-suturing of wounds Exudate Growth factors Depth and width of wound Regional blood supply Exposure or dryness Anoxia Adhesion to bony surface Tight stiches Edema Dressings Use of antiseptics Infections Local trauma Miscellaneous

! ! ! ! ! ! ! ! ! ! ! ! ! ! !

25

1

PREVENTION OF WOUND INFECTION

PS-004

PREVENTION OF WOUND INFECTION Shuja Tahir, FRCS, FCPS Tariq Mahmood, FCPS

Progress in the field of surgery has continued over centuries. Its quality has improved with the progress in anaesthesia, new surgical techniques, new technology in instrumentation and beginning of minimally invasive and micro-invasive surgery. The main progress has been made in either better care of wounds or the use of minimum wounds or total avoidance of wounds.

The prevention of hospital wound infection has revolutionized surgery in the recent era. The hospital wound infection is a major risk factor for the failure of surgical procedures, increased patient's morbidity and even mortality.

Surgical Wound Infection (SWI) surveillance is an essential part of the surgical audit in whole of the developed world. It is essential in the control and prevention of surgical wound infection (SWI)1,12.

APPROPRIATE USE OF ANTIBIOTICS The prophylactic use of antibiotics produces only a minor degree of improvement in the control of surgical wound infection. It is of very low significance2.

The antibiotics should only be used when these are indicated. These are indicated in contaminated and infected wounds. These should be used in adequate dosage and for adequate period and to cover all possible organisms (Aerobes and Anaerobes).

SURGERY - PRINCIPLES IN GENERAL

Haphazard and inadequate use of antibiotics leads to the production of resistant strains3.

The resistant strains of most of the organisms are in abundance in the hospital wards due to abuse of antibiotics. These may lead to serious infection which is not controllable with simple or even most advanced antibiotics in many situations.

The treatment of established wound infection can be achieved satisfactorily by the use of appropriate antimicrobial agents. But the prevention of wound infection is still ideal in surgical managements.

Treatment of wound infections with antibiotics and development of new and better antibiotics used to be the main priority during last few decades4.

Progress in the understanding of surgical wound infections and its pathophysiology has changed the priorities altogether.

Asepsis, better antisepsis and development of better host defence mechanisms is the main aim of preventing and treating the surgical wound infections4.

The hospital wound infection is prevented with full vigor and to do so, the pathogenesis of hospital wound infection has to be understood properly and prevention must start before the wound is actually

27

2

PREVENTION OF WOUND INFECTION

made.

Following micro-organisms have been seen commonly as a cause of hospital wound infection; 1. Staphylococcus epidermidis and Staphylococcus aureus.

2. Polymicrobial flora.

3. E. coli.

4. Pseudomonas aeroginosa.

Staphylococci are present at anterior nares and are commonly transmitted by the hands. The staphylococci multiply with great ease on the skin of the hands and perineum. These can be transmitted by direct contact or via contact of object, bedding, communal bath or towel. Type 80 of staphylococci is notorious for its virulence and speed of spread.

Surgical site infection is a major concern for all surgeons. Prevention or treatment of this infection requires identification of risk factors including host factors, perioperative wound hygiene and operative risk factors13.

RISK FACTORS Following risk factors have been found to influence the surgical wound infection significantly. These should be clearly understood to prevent the surgical wound infection2,3,6,7,8,9,10.

THE PATIENT 1. Age above 60 years.

2. Obesity.

3. Diabetes mellitus.

4. Renal failure.

5. Liver failure.

6. Radiotherapy prior to surgery.

7. Blood transfusion especially with packed cells.

SURGERY - PRINCIPLES IN GENERAL

8.

9.

10.

11.

Patients having chemotherapy.

Immuno compromised patients.

Decreased regional blood flow.

Malignancy.

TYPE OF SURGERY AND CLASS OF WOUND 1. Longer duration of surgery.

2. Emergency surgery.

3. More than two operations during same sitting.

4. Poor surgical technique.

5. Use of drains.

6. Lower wound class.

(Contaminated and infected wounds).

OPERATION ROOM AND ITS STAFF 1. Insufficient and inexperienced staff.

2. Old and inappropriate operation room.

3. Longer and mal-organized operation list.

4. Greater number of operation room staff.

5. Frequent entries into the operation room.

6. Higher temperature in the operation room.

7. Poor ventilation in the operation room.

WARD, ITS STAFF AND OCCUPANTS 1. Longer pre or post-operative stay in the hospital 2. General wards as compared to separate rooms DRESSING ROOM Its locations.

Its maintenance.

THE PATIENT The rate of wound infection has been repeatedly found to be more in older patients. Multiple factors such as nutritional deficiencies, associated diseases and aging process is probably the cause of increased rate of infection.

Obesity is another common cause of increased 28

PREVENTION OF WOUND INFECTION

hospital wound infection. It may be the poor blood supply of the fat or the general difficulty in maintaining cleanliness in the obese patients.

Although it seems simple to loose weight but practically it takes a lot of effort and perseverance on the part of patient to loose weight. Dietician, physiotherapist, social councillor and anti obesity physicians are used to offer help to reduce weight. If possible, the patients should be politely requested to lose weight before surgery.

Blood transfusion especially with packed cells is an independent risk factor. Intravenous cannulation increases the rate of surgical wound infection.

Generalized diseases such as diabetes mellitus, liver failure or renal failure lead to increased wound infection. Low resistance may be the possible cause for increased rate of infection in these patients.

The risk of surgical wound infection is also more in cases when patient has received radiotherapy preoperatively.

Local ischaemia following radiotherapy may be the cause. The decreased regional blood flow increases the wound infection. It is seen commonly in peripheral ischaemia.

The human beings have multiple organisms normally residing in their body as normal flora. Normally these are harmless but they produce pathologic (harmful) effects following metabolic changes due to surgery, disease or injuries.

AUTO INFECTION When the normal flora of patient have infected the patient due to altered circumstances, the patient is responsible for infection of his own wound.

SURGERY - PRINCIPLES IN GENERAL

3

CROSS INFECTION When the patient gets infected from other people who are carrying the organisms, the patient may get infected or pass on the infection to other patients.

This is the reason for higher risk of infection during hospital stay. Longer the hospital stay, greater is the risk of cross infection5,6,7,8.

PRE-OPERATIVE STAY IN HOSPITAL The duration of stay in the hospital pre operatively always increases the chances of hospital wound infection. It is one of the well established major risk factors of surgical wound infection. If possible, the patient should be kept in the hospital for minimum possible time to avoid cross infection and minimize the expenditure5. The patient should be investigated and prepared for surgery as an outpatient.

PERSONAL HYGIENE OF THE PATIENT The patient is kept clean pre and post operatively. His clothes, sheets and blankets are kept clean. These are boiled and washed before using again. The patient's linen is frequently changed and boiled before re-use.

The patient should have proper bath before going for surgery unless it is contra-indicated. The operation site or limb may be prepared (cleaned) with suitable antiseptic solution few times before surgery.

OPERATION ROOM CLOTHING When the patient is shifted to operation room, he/she should be wearing operation room clothes and his/her usual clothes are not allowed into the operation room. The operation room clothes are clean clothes which may not be autoclaved but are used only once. These are washed or boiled before reuse.

29

4

PREVENTION OF WOUND INFECTION

PREPARATION OF OPERATION SITE (ANTISEPTIC SKIN PREPARATION) Skin over the operation site is prepared with antiseptic solution or liquid soap few times a day before surgery. Preparation with irritating disinfectants is avoided. Skin is always cleaned with antiseptic solution half an hour and just before the operation.

Tincture of Iodine is a very satisfactory antiseptic solution. Unfortunately it is irritant which makes its use limited. The iodine solution is allowed to dry up and stay dried for at least ten to twenty minutes for proper antisepsis. Then the tincture of Iodine is cleaned and removed with the help of methylated spirit or alcohol.

Pyodine is a better preparation of Iodine as it is less irritant. It doesn't have to be cleaned or removed.

Pyodine stains the tissue deep yellow. It is not acceptable to many surgeons for this reason and has to be removed just before incision.

The method of skin preparation in some of the operation rooms with tincture of Iodine and quick cleaning of the tincture with methylated spirit does not achieve adequate antisepsis. It only wastes the money spent for antisepsis and gives false sense of antisepsis.

The use of sterile adhesive sheets during operation has improved the prevention of wound infection as it prevents the spread of organisms from the skin adjacent to the wound during surgery.

Shaving of the skin over the site of operation is performed just before the surgery so that damaged skin doesn't get infected before surgery.

SURGERY - PRINCIPLES IN GENERAL

The surgery (elective) is postponed and infection is treated before surgery if the patient has got any infected focus, such as boil and abscess etc. It is extremely essential for elective general surgical, urological, vascular or orthopaedics surgery and grafting of the tissues.

The general condition of the patient should be satisfactory. Patient should have adequate haemoglobin level and normal nutritional status.

OPERATION ROOM AND ITS STAFF The surgical wound infection in the hospital occurs either in the operation room or in the ward.

The infection occurring from operation room manifests itself within a week after operation while later infections are from the ward. Deep seated infections are usually from operation room and superficial infections can be from the operation room or the ward.

The spread of wound infection in operation room may occur; By direct contact from surgeon and staff.

From contaminated room air7.

From contaminated instruments or linen8.

The operation room is kept clean and tidy. Maximum sterility is maintained. Most of the surgical wound infections are due to air borne spread of infection from the operation room atmosphere7.

The patient, doctors, nurses and rest of the operation room staff are not allowed into the operation room without changing into operation room gear (clothes, shoes, caps and mask).

30

PREVENTION OF WOUND INFECTION

THE SURGEON The surgeon may have infection on the hands or other parts of the body. The most dangerous areas for spread of infection are the anterior nares, hands and the wrists.

Whatever the surgeon may do, he cannot sterilize his hands as some organisms are going to stay in the skin pores. Thus after proper scrubbing up with liquid soap, hexachloraphene, iodoform or 0.5% chlorhexidine for nearly five minutes and cleaning the nails with sterile brushes, the surgeon wears impermeable gloves. These gloves are changed even if slightest perforation is seen or suspected as the sweat under the gloves definitely contains some bacteria.

The surgeon is masked and capped properly so that the danger of droplet infection is minimized. The mask is used to cover both nose and mouth.

Improper wearing of the mask leads to the spread of infection.

OPERATION ROOMS The operation room is designed efficiently so that it has adequate ventilation. By no means air from ward should enter into the operation theatre. New operation rooms and new hospitals have shown lower rates of hospital wound infection11.

The operation room should be separate and away from the wards but with easy access and should be of adequate size according to the needs of the hospital.

It should be in the Cul-De-Sac of the hospital.

Preferably the operation room should be on the first or second floor and not on the ground floor or basement to avoid contamination.

The scrubbing up room and the dirty disposal rooms should be separate from the main operation room.

SURGERY - PRINCIPLES IN GENERAL

5

Their exit should not be through the main operation room.

The floor, the walls and fittings of the operation room should be smooth so that these can be cleaned easily.

Operation room temperature should be most comfortable (about 18-21 degrees centigrade) and humidity about 55% so that the ideal atmosphere for work is available. The ventilation of operation room is of paramount importance. The air of the operation room should be as sterile as possible.

Positive pressure system is essential for the operation room sterility. The filters (antimicrobial) of about 5 nm (nanometer) pores are used, so that the air in the room is sterile maximally. These filters are changed regularly for efficient filtration.

The anaesthesia room should be preferably separate but adjacent to the main operation room to minimize operation room contamination. Anaesthetic gases leakage is kept minimum and is removed as soon as possible.

Other less effective methods for the operation room sterilization are the use of ultraviolet lights and cleaning of the operation room floors and walls with potent antiseptic solutions like carbolic acid. The operation room is cleaned adequately after the operation list is finished. It is also cleaned before the operation list is started.

OPERATION LIST The operation list should not be too big to compromise the efficiency. It should be arranged in a way that infants, children, diabetics and patients on medicine for associated illnesses are managed 31

PREVENTION OF WOUND INFECTION

before the otherwise young and healthy adults. The proper organization of the operation list not only brings down the rate of infection but also lowers the overall rate of complications.

OPERATION ROOM STAFF The operation room staff is trained adequately before allowed to work in the operation room. The staff should be adequate in number. Every staff member has a designated duty and performs it in a structured manner without unorganized movements and minimum possible help in the operation.

Inexperienced staff is a definite source of wound infection. Over staffing and frequent entries into and out of operation room increase the risk of wound infection.

As the movements in the operation room cause rising of the settled organisms, the operation room staff is kept minimum and is not allowed to move un necessarily. The operation room is kept locked during surgery to avoid unwanted entries and movements of the staff.

Anybody suffering from any infection, common cold etc. should refrain from entering the operation room.

Greater the number of operation room attendants, greater is the chance of breakdown of asepsis9.

SURGICAL EQUIPMENT The operation room equipment is kept minimum but appropriate to allow efficient and smooth surgery so that accumulation of the organisms is minimum.

The gloves for the surgeon and his assisting team are pre-sterilized and disposable and are discarded after each use. If any perforation or contamination is suspected, these are discarded immediately.

SURGERY - PRINCIPLES IN GENERAL

6

The instruments are either doubly sterilized and wrapped or are sterilized or autoclaved immediately before use and are kept covered with sterile sheets.

The instruments and the operation room linen is autoclaved or sterilized with any other appropriate method. It is re-sterilized if there is any doubt of contamination. The sterilization is checked meticulously before use.

The gowns and the operation room sheets are autoclaved. These should be dry when used. These are changed immediately if get wet and soaked during prolonged surgery.

The dirty linen is disposed of to the outer exit of operation room and is not allowed back into the operation room or is not kept in any portion of the operation room for longer hours. The dirty or used instruments are also sent immediately for cleaning and autoclaving or any other suitable sterilization.

WARDS The mode of spread of the infection in the wards is not at all different than operation room except that many patients (potential sources of infection) are also present.

Patients with obvious infections, purulent exudates and chronic osteomyelitis are notorious to spread the infection and are kept isolated from rest of the clean cases of the ward. They are nursed in separate wards or at least separate bays of the same ward.

The wards are frequently cleaned, washed, scrubbed with proper antiseptic solutions and are well ventilated.

The air of the wards is sufficiently contaminated 32

7

PREVENTION OF WOUND INFECTION

during the examination and dressings of the wounds of different patients. This practice is avoided and a well organized ward dressing room is used for this purpose.

respect is likely to achieve excellent results.

REFERENCES 1. Cortale M. Gobessi V. Calligaris L. The role of the environment in postoperative infections. [ITALIAN] Annali Italiani Di Chirurgia. Nov-Dec 1989; 60(6): 547-50: discussion 550-1.

DRESSING ROOMS The dressing room is present in the ward or near the ward. It is properly disinfected and well ventilated. Its air should not exhaust in the wards. It is constructed and maintained like operation room.

2. Deviatov VA. Petrov SV. Causes of suppurative complications after appendectomy. [Russian] Khirurgiia. Mar 1991; (3):103-6.

The wounds are examined, cleaned and dressed in the dressing room. No touch technique is practiced for dressings. The dressings are performed most aseptically.

3. Ojiegbe GC. Njoku-obi AN. Ojukwu JO. Incidence and parametric determinants of post operative wound infections in a university hospital. Captral African Journal of Medicine. Mar 1990; 36(3):63-7.

The operation room dressings are the most aseptic dressings and are not removed or changed unless clearly indicated. The operation room dressings should only be changed if these are soaked with blood, fluid or discharge from the wound. These dressings may also be removed if any suspicion of wound infection is obvious such as local tenderness or fever etc.

4. Ronald L. Nichols. Bacteriology in surgery, Mastery of surgery. Lloyd M Nyhus and Robert J. Baker.

Boston Toronto: Little Brown 1984; 71-81.

The contaminated articles are adequately disposed off. Non disposable articles are properly cleaned and sterilized. Dirty linen is sent to laundry as soon as possible.

The prevention of hospital infection will only be possible if all the hospital staff and occupants work as a team for it and tough discipline is maintained.

SURGICAL WOUND INFECTION (SWI) SURVEILLANCE The surgical wound infection surveillance is performed adequately and it is computerized. A better organized and realistic approach in this SURGERY - PRINCIPLES IN GENERAL

5. Duhaime AC. Bonner K. et al. Distribution of bacteria in the operating room environment and its relation to ventricular shunt infections: A prospective study, Child's nervous system. Aug 1991; 7(4):211-4.

6. Ayeliffe G. A. Role of the environment of operating suite in surgical wound infection. Review of infectious diseases: Sep-Oct 1991; 13 suppl 10:800-4.

7. Bremmeloard A. Sorenson AM. et al. 4 year experience with computerized registration of postoperative infection and identification of risk factors. Ugeskrift for Laeger. May 1991; 153(20):1416-9.

8. Moro M.L. Sommella L. et al. Surgical infections surveillance: Results of a six month incidence study in two Italian hospitals. European journal of Epidemiology. Nov 1991; 7(6):641-8.

9. Asensio Vegas A. Monge Jodra V. et al. Surgical

33

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PREVENTION OF WOUND INFECTION

wound infection: The risk factors and a predictive model, Medicina clinica. April 1993;100(14):521-5.

10. Johnson JI. Bloomer WD. Effect of prior radiotherapy on post surgical wound infection. Head and neck.

Mar-Apr 1989; 11(2):132-6.

11. Ford C. D. VanMooral Egliem G. Menlove RL. Blood transfusions and post operative wound infection.

Surgery. June 1993; 113(6):603-7.

12. Anonymous. Consensus paper on the surveillance of surgical wound infection. The society for hospital Epidemiology of America: The association for practitioners in infection control: The centers for disease control: The surgical infection society.

Infection control and hospital Epidemiology. Oct 1992; 13(10):599-605.

13. Viviang Loo; A Peter Mclean. Infection control in surgical practice. ACS Surgery 2004.

SURGERY - PRINCIPLES IN GENERAL

SUMMARY Prevention of wound infection Appropriate use of antibiotics Risk factors ! The patient ! Type of surgery ! Class of wound ! Operation room and its staff ! Wards and its occupants ! Dressing room Auto infection Cross infection Pre-operative stay in hospital Personal hygiene Operating room clothing Preparation of operation site Care of operation room and its staff Care of surgeon Care of surgical equipment Care of dressing rooms Surgical wound infection surveillance

34

1

WOUND CARE

PS-005

WOUND CARE

TREATMENT OF WOUNDS Shuja Tahir, FRCS, FCPS

Surgery is creating wounds and caring for these properly.

treated and brought to normal range as early as possible.

The history of wound care and management closely parallels that of military surgery which has laid down the principles and dictated the practices of wound cleansing, debridement and coverage.

The wounds are managed on their own merits as efficiently as possible.

Successful wound care means achievement of healing in minimum prescribed period without any scarring and deformity.

Complete epithelialization of the wound is accepted as end point of healing.

CARE OF ACUTE WOUNDS The importance of wound care, wound assessment, debridement, pre and post operative management and subsequent skin care is known to all involved in wound management.

The wound care is never satisfactory in isolation.

Assessment of general condition of patient is essential for management of acute and chronic wounds.

There are essentially two types of wounds from a treatment standpoint; ! !

It is critical to determine in the event of tissue loss whether vital structures such as bone, tendons, nerves and vessels have been exposed.

It is also important to determine the amount of soft tissue contusion and contamination.

Wound measurements, wound tracings, simple planimetery and photography of wound is used for adequate assessment. It can be performed by assessing following critical components and collecting information1; !

General health of the patient should be as optimal as possible.

!

Anaemia, hypoproteinemia, liver functions, renal functions and cardio-pulmonary status should be

!

SURGERY - PRINCIPLES IN GENERAL

Those characterized by loss of tissue.

Those in which no tissue has been lost.

Exact location of wound with correct land marks is recorded.

Wound size is measured in metric system in greatest length and width at right angle to each other.

Color, temperature and swelling of surrounding tissue is noted.

35

WOUND CARE

! ! !

Nature of wound edges and margins is clearly recorded.

Nature of wound exudate and its odour is also noted1.

Presence or absence of pain in the wound.

A photograph of wound at every visit is taken for comparison during follow up.

A delicate biochemical balance exists within a normal wound environment ensuring rapid closure. This balance can be disrupted by following external stimuli resulting in impaired wound healing; ! !

Critical bacterial colonization.

Increased host inflammatory response.

Efforts are directed to prevent infection, facilitate wound healing, promote comfort and maintain optimal function and minimize deformaties2,3.

Whether the wound is acute or chronic, essential principles of wound care must be observed in order to avoid wound sepsis and achieve rapid and optimal wound healing9.

Aseptic environment is provided to the wound.

Antiseptics are used to clean the tissue adjacent to the wound.

All devitalized tissues must be debrided either hydrodynamically, chemically, mechanically or surgically.

Tissues are handled gently.

Normal anatomy of injured tissue is restored.

Caustic solutions capable of sterilizing the skin

SURGERY - PRINCIPLES IN GENERAL

2

should never be applied to the wound. It is desirable never to put anything in the wound that cannot be tolerated comfortably in the conjunctival sac.

All dead spaces are obliterated before closure of wound to avoid fluid collection and pus formation.

Exposed vital structures are covered by well vascularized tissues.

Healing of adequately managed acute wound occurs spontaneously, rapidly and in predictable phases.

Scar is minimum and cosmetically acceptable.

Primary wound healing by early closure either primarily or with the help of grafts or flaps is preferred to secondary healing and wound contraction with subsequent contracture which interferes with range of movement and function.

Skin edges are apposed with various methods; SUTURES Non absorbable suture with eyeless needle of suitable size is used to stitch the cutaneous wound.

Multiple unnecessary pricks are avoided to achieve cosmetically good results.

STAPLERS Metallic stapling gun is used to appose the skin edges. It is quick to use and does not close the skin too tightly and causes minimum sub-cuticular injury as compared to non absorbable sutures.

STERISTRIPS (Strip Approximation) These are sterilized cotton or paper strips which are used to appose the wound edges. These can be applied over the approximated wound edges. These achieve good cosmetic results if applied properly.

Movements of wound edges may lead to poor healing if the strip is loose.

36

3

WOUND CARE

WOUND DRESSING An essential part of any wound management protocol is wound dressing.

It can not be too strongly emphasized that a wound dressing may have a profound influence on healing, particularly of second degree healing, a critical feature being the extent to which such dressing restricts the evaporation of water from the wound surface.

The key wound dressing performance indicators observed are ; ! ! ! ! ! ! ! !

Ability to promote autolytic debridement resulting in reduction of non viable tissue.

Production of granulating wound bed.

Clean wound margins.

Evidence of epithelial migration.

Wound healing.

Wound pain reduction.

Wound odour improvement.

Improved over all wound appearance.

It requires nursing intervention to promote healing.

The nursing approach focuses on psycho- social and physical factors affecting wound care4.

CARE OF CHRONIC WOUNDS Chronic wound care poses multiple problems and are very difficult to treat. These wounds fail to heal over an extended period and show frequent recurrence.

Chronic wounds may result from a deficiency in growth factors or in inhibition of their function. This deficiency may be partly the result of elevated levels of proteinase that degrades the growth factors and ECM components at the wound site.

SURGERY - PRINCIPLES IN GENERAL

37

4

WOUND CARE

The healing can be facilitated by providing exogenous growth factors or inhibiting proteinase activity at the wound site.

Advances in the wound care of chronic wounds have followed the understanding of patho-physiology of these wounds.

Successful treatment of chronic wounds requires management of underlying pathology and preparation of wound bed.

Commonly seen chronic wounds are; Pressure ulcers.

Diabetic ulcers.

Lower leg ulcers.

Vascular ulcers.

Post operative open wounds.

Entero cutaneous fistulae.

These chronic wounds may be associated with other co-morbid factors making the healing even more difficult ;

The objectives of healing of chronic wounds are ; ! ! ! !

To target the excessive wound exudate.

Debridement of devitalized tissue.

Stimulation of healthy granulation tissue formation.

Improvement in the nature of surrounding tissue and skin.

Management of chronic wounds is a very specialized field. It requires adequate assessment to predict healing process.

It is quite clear that chronic wounds develop granulation tissue much faster, re-epithelialize quicker when treated with dressings allowing moist healing.

Pain is relieved with occlusive dressings. Infection is prevented, edema is minimized and wound repair is accelerated5.

Slow release “physiologic� antiseptics to decrease the bacterial burden are useful in difficult and infected wounds. Silver and iodine ions are used successfully in overall management of these patients.

SURGERY - PRINCIPLES IN GENERAL

Old age.

Obesity.

Smoking.

Immobility.

Diabetes mellitus.

Hypertension.

Malnutrition.

Immune disorders.

Malignancy.

Compromised functions of multiple organs i.e liver, kidney, heart etc.

Increased venous pressure causes fibrinogen extravasation through endothelial gap junctions resulting in a precapillary cuff that acts as a barrier to oxygen and other nutrients in the blood contributing to ulceration.

Leukocytes trapped in the diseased veins and circulation by reduced shear stress become activated on the endothelial surface (sticky leukocytes). These release inflammatory mediators leading to tissue destruction, blockage of small capillaries causing localized ischemia6.

The therapy for venous ulcers has following 38

WOUND CARE

objectives; ! ! ! !

Lowering venous hypertension.

Increasing (fibrinolytic) activity.

Enhancement of tissue vascularity.

Compression dressing to push leaked fluid back into circulation (20-40 mm of Hg compression pressure).

Rapid correction of venous insufficiency / venous hypertension and removing the barriers to healing will help in adequate preparation of wound bed and healthy granulation tissue. Non viable tissue, bacterial burden, proteolytic imbalance, and altered composition of wound exudate is to be removed for adequate healing.

Occlusive dressings maintain wound moisture and modify wound environment. It also leads to autolytic debridement, accelerates epithelialization and reduces wound pain.

Actisorb速 Silver 220 Silver Impregnated Activated Charcoal dressing (SIAC). Antimicrobial dressing helps to improve healing of chronic wounds by reducing protease activity and not affecting cell proliferation7.

5

Topical growth factors and bio-engineered skin products are used in treatment of chronic ulcers.

These are effective in accelerating the process of re epithelialization, decreasing scarring and stimulating healing.

Topically applicable cytokines will be very helpful when available.

Better wound dressing, improved compression devices, effective debriding agents, topical growth factors, bio engineered skin products help to achieve healing of chronic wounds5.

Hyalauronan Ester is a major component of Extracellular Matrix (ECM)and plays an important role in tissue repair. It influences a number of events critical to successful wound healing including inflammation, cell migration, re-epithelialization and scar formation.

It is useful in patients who are immuno-compromised and have decreased resistance to infection4.

Human skin equivalent (apligrap速 organ ogenesis Inc, USA) helps in chronic care more effectively than standard care venous ulcers healing.

Wound infection and cross contamination can be minimized by dressings which can control infection via the absorption, effective retention and immobilization of bacteria associated with wound fluid. It can further be controlled by providing an effective barrier to the transmission of blood borne viruses8,9.

Biocellulose wound dressing is a biosynthetic matrix (xcell速 xylos corporation USA). It is hydrophilic and has excellent tensile strength. It has ability to donate or absorb fluid/moisture. It is bio-compatible, pyrogen free and non toxic. Sustained compression therapy helps in reducing the venous hypertension and leakage of fibrinogen6.

Exudate management is the key factor in achieving wound healing. Appropriate dressing applied to an exuding wound can absorb exudate and improve the underlying wound surface environment. It also conforms to the contoured surfaces presented by chronic wound. An intimate contact at wound/ dressing interface is important in minimizing dead

SURGERY - PRINCIPLES IN GENERAL

39

6

WOUND CARE

space across the intensive wound surface10.

Healing and epithelialization is better within most environment under occlusion dressing.

Topical use of glycyl-L-histidyl-L-Lysine Tripeptide Copper Complex (TCC) accelerates wound healing in ischemic open wounds and may be an effective stimulant of healing in chronic wounds11,12.

Hyper-baric oxygen therapy (HBOT) improves healing of chronic wound following radiation. It enhances neovascularization in irradiated tissue13.

A bio-synthetic cellulose material has been engineered to create a new wound dressing with dual fluid handling ability capable of maintaining an optimal moist wound healing environment by hydrating or absorbing fluid from the wound.

Combined zinc/iron solution enhances healing in acute partial thickness burn wound.

Keratinocytes and fibroblasts suspended in thrombin and cryoprotectant and a solution of fibrinogen improves wound healing by secreting a cocktail of growth factors and cyto kines14.

Low frequency ultrasonic assisted wound treatment (UAW) is emerging as an alternative method for wound bed preparation and debridement.

Deep tissue penetration of ultrasonic vibration and energy results in micro cavitations causing bacterial destruction15.

Small intestinal submucosa “SIS� is quite effective treatment in managing full thickness wound. It

SURGERY - PRINCIPLES IN GENERAL

achieves higher degree of wound closure as compared to conventional care16.

REFERENCES 1. Cyuthia A, Worley. Assessment and terminology; Critical issues in wound care. Dermatol Nurse 2004: 16(5): 451-452.

2. Cooper DM. Wound healing. New understandings.

Nurs prac forms. Jun 1999; 10(2): 74-86.

3. Dickerson P, Purduo G F, Hunt JL. Traumatic wound care. Dermatol Nurs. Feb 1999; 11(1): 53-6, 60-80.

4. Dirk A, Hollandeers, Thomas Schmandra. Joachin Windelf; A new approach to treatment of recalcitrant wounds; A case report demonstrating the use of hyaluronan esters. Wounds 2000; 12(5): 111-117.

5. Vincent falavga. Commentary advances in wound care; Are we there yet? Wounds 2000; 12(2):51-52.

6. Oscar M. Alverez.Mayant Patel, Junita Booker. Lee Markowitz. Effectiveness of a biocell use wound dressing for the treatment of chronic venous leg ulcers. Wounds 2004; 16(7):224-233.

7. Breda Cullen; Janine Macadam, Sarah Jayne Gngory.

Alicia essleer, David Greenhalgh. Effect of silver based wound dressings on protease activity and cell proliferation. Wounds 2003; 15(4):A23-34.

8. P Bowler, S Jones. Infection control properties of absorbent dressings. Wounds 2003; 15(4): A23A34.

9. Nicholas Pericone, Maris D. Kerstein, Robert S, Kirsner. Rebort A Norma. How to approach acute and chronic wound healing in elderly. Wounds 1999; 11(16):145-151.

10. M Walker, SM adams, DC Pritchard. In vitro studies to

40

7

WOUND CARE

measure intimacy of wound surface contact by models wound care products. Wounds 2003; 15(4): A23-A34.

11. Sherman O Canapp Jr, James P farese, Gregorys Schultz et al. The effect of topical TCC on healing in a chronic wound model. Wounds 2003; 15(4): A23A34.

12. Onzalo Serafica, Oscar alveraz, marie Etris. Clinical evaluation of a new bio-engineered wound dressing with a unique dual fluid handling capability. Wounds 2003; 15(4): A23-A34.

13. Richard Sample, Takkin Lo, James Anholin et al.

Hyperbaric oxygen therapy for delayed radiation injury. A seven year review. Wounds 2003; 15(4): A23-A34.

14. Chris Rinsch, Beatrice Mis, Vincent onfard, Eric Rollandspray applied living keratinocytes and fibroblasts as a biologically active wound dressing.

Wounds 2003; 15(4): A23-A34.

15. Jeffrey A, Nuzgoda, Kathleen M Nelson, Daven walek.

Clinical experience using ultrasonic assisted wound treatment. Wounds 2003; 15(4): A23-A34.

SUMMARY Acute Wound Care Sutures Staplers Steristrips Wound dressing

! ! ! !

Chronic Wound Care Lowering of venous pressure Special dressing ! Silver impregnated activated charcoal dressing ! Occlusive dressing ! Biocellulose wound dressing ! Human skin equivalent dressing ! Topical growth factors & bio-engineered skin products ! Hyalauronan ester ! Exudate management ! Topical use of copper complex ! Hyper basic oxygen therapy ! Combined zinc-iron-solution ! Keratinocytes & fibroblasts ! Low frequency ultrasonic assisted wound treatment ! Small intestine submecosa (SIS)

16. Robert H demling Jeffery A Niezgoda, G Daxin Haraway, Eliot N Mostow. Small intestinal submucosa wound matrix and full thickness venous ulcers preliminary results. Wounds 2004; 16(1): 18-22.

SURGERY - PRINCIPLES IN GENERAL

41

Surgical Practice

CRYOSURGERY

1 PS-006

CRYOSURGERY Shuja Tahir, FRCS, FCPS Abid Bashir, FCPS

Cryosurgery is the use of extremely cold temperatures to freeze and destroy abnormal tissues. It is also known as cryotherapy or cryoablation. It is a technique that involves using freezing as a form of surgery.

HISTORY Using extreme cold to treat cancer dates to the 1840s, when an English doctor used iced saline through tubes to treat tumors, Liquid nitrogen came into use after World War II for skin problems, brain tumors and some neuromuscular disorders. The first human prostate cryosurgery was performed in 1966, but there were high rates of rectovesical fistula formation. The breakthrough came in 1996, when newer equipment came out that allowed the simultaneous use of as many as eight probes.

MECHANISM OF ACTION Irreversible damage in treated tissue occurs because of intracellular ice formation (Fig-1). Rapid cooling of cells below -40oC results in formation of intracellular ice crystals that disrupts cell membrane and intra cellular organelles. The degree of damage depends on the rate of cooling and the lowest temperature achieved. Inflammation develops during the 24 hours after treatment, further contributing to destruction of the lesion through immunologically mediated mechanisms. During rapid freezing stage, blood flow to the ice ball ceases completely. During thawing, blood flow returns slowly

SURGERY - PRINCIPLES IN GENERAL

and fixed tumor antigens and intracellular enzymes leak into the circulation stimulating immune response1.

Generally, destruction of benign lesions requires temperatures of -20°C to -30°C (-4°F to -22°F).

Effective removal of malignant tissue often requires temperatures of -40°C (-40°F) to -50°C. Slow thaw time and repeated freeze-thaw cycles produce more tissue injury than a single freeze and thaw. Usually, several minutes are allowed between repeat freezethaw cycles.

Total freeze time (TFT), halo thaw time (HTT), thermocouple thaw time or total thaw time (TTT), are useful indicators of adequacy of freeze.

A number of new methods are being evaluated to enhance the efficacy of cryosurgery. These include the use of microwave2 and antifreeze protein3.

MR-guided cryosurgery with new navigation system has been developed for safe and accurate puncture with a cryoprobe4. Concept of dynamic cryosurgery has been introduced by Rewcastle et al. According to them, the probe temperature is oscillated throughout the formation of the iceball which results in the propagation of thermal waves through the frozen tissue. These thermal waves enhance the formation of lethal intracellular ice. Thermal waves rapidly attenuate with radial distance from

45

CRYOSURGERY

2

cryoprobes and distort in shape. Their velocity is independent of amplitude but dependent on frequency.

common benign lesions. However, this method is being supplemented by liquid nitrogen spray techniques.

Constructive and destructive interference between thermal waves is shown to occur and implies that control of thermal waves to focus their lethal effects on designated regions of the frozen tissue is possible with multiple cryoprobes.5

Liquid nitrogen spray equipment is easy to use, and similar techniques can be employed to manage benign, pre-malignant, and malignant lesions. Spray methods include the timed spot freeze technique, the rotary or spiral pattern, and the paintbrush method (Fig-3).

Despite latest developments in cryosurgery, there are still challenges to be addressed to improve its efficacy. Two primary challenges are determining thermal injury thresholds for various types of cell/tissues, and understanding of the mechanisms of freezing induced cell/tissue injury within a cryolesion. Recently, a cryo-injury model has been developed using tissue engineering technology.

Engineered tissue equivalents (TEs) were constructed by seeding and culturing cells in a type I collagen matrix.6 CRYOGENS First cryogens were liquid air7 and compressed carbon dioxide snow.8 Liquid nitrogen became available in the 1940s and currently is the most widely used cryogen. It is particularly useful in the treatment of malignant lesions. Temperatures of -25째C to -50째C (-13째F to -58째F) can be achieved within 30 seconds if a sufficient amount of liquid nitrogen is applied by spray or probe. Other cryogens include; solidified carbon dioxide, nitrous oxide, Freon and helium.

TYPES OF CRYO-APPLICATION There are three types of cryo-application (Fig-2); The cotton-tipped dipstick method of liquid nitrogen application has been popular in the management of

SURGERY - PRINCIPLES IN GENERAL

The timed spot freeze technique achieves temperatures that are adequate for tissue destruction in an ice field up to 2 cm in diameter. The best approach for lesions larger than 2 cm (including an adequate margin) is to use overlapping treatment fields.

A cryoprobe attached to the liquid nitrogen spray gun can provide added versatility, depending on the site and type of the lesion. Various sizes and types of cryoprobes are available. The cryoprobe is applied directly to the lesions (Fig-2).

A gel interface medium often is used between the probe and the skin surface. Cryoprobes frequently are used in the treatment of smaller facial lesions (e.g., on the eyelids), where scatter of liquid nitrogen is undesirable.

Probes are also useful in the management of vascular lesions, where the pressure of the probe can be used to remove blood from the tissues thus allowing more adequate treatment.

ADVANTAGES AND DISADVANTAGES OF CRYOSURGERY Advantages of cryosurgery include shor t preparation time, low risk of infection, and minimal 46

3

CRYOSURGERY

wound care. In addition, cryosurgery requires no expensive supplies or injectable anesthesia, and the patient does not have to return for suture removal.

Cryosurgery is particularly useful in patients receiving anticoagulants, those allergic to local anesthetics, and those who have pacemakers.

The major disadvantage of cryosurgery is the uncertainty surrounding its long-term effectiveness.

matrix of the skin may also cause scarring.

Cryosurgery is best suited for patients with light skin and for treatment of lesions in non hair-bearing areas of the body.

Benign skin lesions that are suitable for freezing include actinic keratosis, solar lentigo, seborrheic keratosis, viral wart, molluscum contagiosum, and dermatofibroma. Solar damage, acne, as well as some cosmetic defects are also amenable to freezing9. Keloids that are refractory to surgery have also been successfully treated by intra lesional cryosurgery .10

Dipstick Spray Probe Fig-2. Types of cryo application

Fig-1. Ice ball formation

INDICATIONS OF CRYOSURGERY Cryosurgery is being used for a number of skin lesions. Mild freezing leads to dermo-epidermal separation, which is useful in treating benign epidermal lesions. The more sensitive cells in the epidermis are destroyed while the dermis is left intact. Treatment may be complicated by an element of hypo-pigmentation. Disruption of the collagen SURGERY - PRINCIPLES IN GENERAL

Fig-3. Techniques of Nitrogen spray

A number of studies have been published on use of cryosurgery in the treatment of inoperable 47

4

CRYOSURGERY

carcinoma prostate and liver tumors (both primary and secondary)11. Cryosurgery has also been used to treat haemangiomata9,12. Patients of neuralgia are also being treated with cryosurgery.13 Cryosurgery has also been useful in treating ophthalmic lesions14. Even Single cryothermia applications of 3 minutes produce permanent Cavotricuspid isthmus conduction block in patients with typical Atrial flutter significantly reducing procedure duration.15 CONTRAINDICATIONS TO CRYOSURGERY16 ABSOLUTE CONTRAINDICATIONS ! ! ! ! ! !

Lesion for which tissue pathology confirmation is required. (Biopsy can be taken before cryosurgical ablation in such cases).

Lesion located in an area with compromised circulation.

Melanoma.

Patient unable to accept possibility of pigmentary changes.

Proven sensitivity or adverse reaction to cryosurgery Sclerosing basal cell carcinoma or recurrent basal cell or squamous cell carcinoma, particularly when located in a high-risk area e.g., temple and nasolabial fold.

RELATIVE CONTRAINDICATIONS. ! Cold intolerance. ! Cold urticaria. ! Collagen disease or autoimmune disease. ! Concurrent treatment with immunosuppressive drugs. ! Cryoglobulinemia.

SURGERY - PRINCIPLES IN GENERAL

! ! ! ! !

Heavily pigmented skin.

Lesions located in pretibial areas, eyelid margins, nasolabial fold, ala nasi, and hairbearing areas.

Multiple myeloma.

Pyoderma gangrenosum.

Raynaud's disease.

COMPLICATIONS AND SIDE EFFECTS OF CRYOSURGERY16 Acute ! Bleeding at the freeze site. ! Blister formation. ! Edema. ! Headache (after treatment of facial lesions). ! Pain. ! Syncope (vasovagal; rare).

Delayed ! Bleeding. ! Excess granulation tissue formation (rare). ! Infection (rare).

Protracted or permanent ! Atrophy (rare). ! Hair and hair follicle loss. ! Hypopigmentation.

Protracted but temporary ! Alteration of sensation. ! Hyperpigmentation. ! Hypertrophic scarring.

SAFETY MEASURES & PRECAUTIONS17 While using cryosurgery, protection of vital areas is essential and may utilize various modalities, but metal devices should be avoided. Areas requiring special attention for protection include the following:

48

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CRYOSURGERY

1) Eyes (plastic retractor, goggles, tongue blade) 2) Nares (cotton, tongue blade, Styrofoam) 3) Ears (cotton in canal, gauze padding, tongue blade, polystyrene plastic) REFERENCE 1.

Cushchieri A, Steele, RJC, Moossa, AR: Surgical crafts and technology In Essential surgical practice (Volume-1) Butterworth-Heinemann, Oxford. 4th edition 2000. pp 38-68

2.

Shafranov V V, Kobiatsky AV, Borkhunova EN, Taganov AV.: Method of extension of the volume of the zone of cryolesion. Proceedings of the 10th world congress on cryosurgery, November 1998.

3.

Koushafar,H., Pham,L,. Rubinsky,B.: Enhanced Cryodestruction with Antifreeze Proteins. Proceedings of the 10th world congress on cryosurgery, November 1998

4.

Mogami T, Dohi M, Harada J.: A New Image Navigation System for MR-Guided Cryosurgery. Magn Reson Med Sci. Dec 2002; 15;1(4):191-7.

5.

6.

Rewcastle JC, Sandison GA, Saliken JC, McKinnon JG, Donnelly BJ.: Dynamic cryosurgery: creating a more potent iceball with the use of thermal waves. Proceedings of the 10th world congress on cryosurgery. November 1998.

Han B, Grassl ED, Barocas VH, Coad JE, Bischof JC.; A cryoinjury model using engineered tissue equivalents for cryosurgical applications. Ann Biomed Eng. Jul 2005; 33(7):972-82.

7.

White AC. Liquid air: Its application in medicine and surgery. Med Rec 1899; 56:109-12.

8.

Pusey W. The use of carbon dioxide in the treatment of nevi and other lesions of the skin. JAMA 1907;49:1354-6.

Thai Kand Sinclair RD.: Cryosurgery of benign skin lesions.

Australasian Journal of Dermatology. 1999; 40(4):175.

9.

10. Gupta S, Kumar B.: Intralesional Cryosurgery using lumbar puncture and/or hypodermic needles for large,

SURGERY - PRINCIPLES IN GENERAL

bulky, recalcitrant keloids. International Journal of Dermatology. May 2001; 40(5):349.

11. Seifert JK, Springer A, Baier P, Junginger T. Liver resection or cryotherapy for colorectal liver metastases A prospective case control study. Int J Colorectal Dis. 2005 Jun 23, [Epub ahead of print] 12. Shafranov V.V. Butorina AN. Borkhunova E. N. Treatment Of Hemangiomas In Children By Cryomethode.

Proceedings of the 10th world congress on cryosurgery, November 1998 13. Nat,.SC.. Herzog R. Binneberg A et al.: New cryosurgical devices for cryolesion of tumors and pain elimination.

Proceedings of the 10th world congress on cryosurgery, November 1998 14. Cryotherapy for Retinopathy of Prematurity Cooperative Group.: Multicenter Trial of Cryotherapy for Retinopathy of Prematurity - Ophthalmological Outcomes at 10 Years.

Archives of Ophthalmology. 2001;119(8):1110-1118 15. Manusama R, Timmermans C, Philippens S, Crijns HJ, Ayers GM, Rodriguez LM.: Single cryothermia applications of less than five minutes produce permanent cavotricuspid isthmus block in humans. Heart Rhythm. 2004 Nov; 1(5):594-9.

16. Mark D. Andrews, M.D.: Cryosurgery for Common Skin Conditions. Am Fam Physician 2004;69:2365-72.

17. Drake LA.(Chairman), Ceilley RI. Cornelison RL et al.(Committee on Guidelines of Care): Guidelines of care for cryosurgery. J Am Acad Dermatol 1994;31:648-53 SUMMARY Cryo Surgery Cryogens Type of cryo application Advantages and disadvantages of cryo surgery Indications Contra-indications Complications Safety margin and precaution

49

LASERS IN SURGERY

1 PS-007

LASERS IN SURGERY Shuja Tahir, FRCS, FCPS Abid Bashir, FCPS

The word Laser is abbreviated form of 'Light Amplification by the Stimulated Emission of Radiation'. The name itself is self explanatory; lasers are amplified electromagnetic (light) waves. These are generated by emission of radiation when they are stimulated.

There are three components of a laser device; a vacuum chamber called resonator, a lasing material, and an energy source (electrical current or light).

Within the resonator, the molecules of lasing material are excited from there resting state by absorption of energy to higher energy levels (Stimulation).

Some of these excited molecules return spontaneously to their resting state level and in doing so, they emit extra energy in the form of photons (emission of radiation).

It is important to note that energy emitted is of the same wavelength characteristic of the lasing material. The photons also interact with other excited atoms which return to the resting state emitting more photons. The net result is the production of the waves of same wavelength, traveling in same direction and in phase with one another (spatially coherent).1 TYPES OF LASERS Lasers are classified according to the type of lasing material. The lasing material may be solid like ruby,

SURGERY - PRINCIPLES IN GENERAL

liquid (usually organic dyes in suitable solvent) or gas like CO2, helium, argon etc. Each substance produces laser beams of specified wavelength and has specific uses.

Lasers can also be classified according to the production of the beam e.g., continuous or pulsed (with or without Q-switch). Pulsing of output can reduce thermal damage .

PROPERTIES OF LASERS Laser beam have three properties. These are; ! Collimated - parallel output beam with minimum divergence resulting in little energy loss ! Coherent - waves are all in phase resulting in little loss of energy ! Monochromic all waves are of the same wave length.

EFFECT OF LASERS PHOTOCHEMICAL The laser produces chemical changes in a substance.

This property is used in photodynamic therapy. A photosensitizer (e.g., hematoporphyrin derivative) is injected into the body and sufficient time is given so that it may be taken up and retained by the target tissue (a tumor or a dysplastic lesion). Then it is irradiated by a specific laser producing highly reactive toxic species like free oxygen radicals resulting in necrosis of the tumor.

51

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LASERS IN SURGERY

PHOTOTHERMAL The lasers produce excessive heat when absorbed in tissues. This effect is used to produce photo coagulation, cutting and ablation by vaporization.

CO2 lasers are absorbed within a depth of 0.2mm.

They are ideal for cutting. Nd:YAG (yttriuym, aluminium, garnet) laser is excellent for endoscopic control of bleeding because of greater penetration (2mm).

PHOTOMECHANICAL Power densities of around 1016/m2 are required to produce localized shock waves. Q-switched pulsed lasers are used for intraluminal stone fragmentation. This effect is also used in ophthalmology for capsulotomy and iridotomy.

MEDICAL APPLICATIONS OF LASERS THERAPEUTIC USES There is an ever increasing list of therapeutic indications of lasers. These are;

have been tried by hindley et al as an outdoor procedure with encouraging results2.

Skin and Cosmetic Surgery Laser has a wide range of uses in skin and cosmetic surgery. They include removal of hair, resurfacing of scars, removal of birth marks3 (port-wine stain, hemangioma, Epidermal nevi), removal of tattoos4, cosmetic surgery (like blephroplasty5), antiwrinkle surgery and in the treatment of a number of skin lesions like acne rosacae.

Urology Lasers have an increasing role in urology as well including intraluminal stone fragmentation and thermal ablation of prostatic hyperplasia.

Stimulation of Healing Low power laser energy lasers near red or infrared region of wavelength have been shown to stimulate healing. They are helpful in wound healing and relief of chronic pain of musculoskeletal origin.

Oncology Photodynamic therapy for inoperable esophageal and bronchial carcinoma, mucosal cancers of GIT and urinary bladder and destruction of barette’s esophagus. Photothermal destructions of solid organ tumors like liver tumors.

DIAGNOSTIC INDICATIONS Photochemical effect of lasers is being used in early detection of severe dysplasia and in situ mucosal cancers of endoscopically accessible areas (GIT,bronchus and urinary bladder).

Ophthalmology Band keratoplasty, refashioning of corneal curvature for refractive errors,capsulotomy, iridotomy.

OPTICAL ALIGNMENT Low power lasers are used in optical alignment systems for patient positioning to radiotherapy.

Cardiovascular System Removal of atherosclerotic plaques from coronary and peripheral vessels.

SAFETY OF LASERS Lasers are classified according to the amount of damage they can cause.

Gynaecology Recently, MRI guided laser ablation of uterine fibroids

!

SURGERY - PRINCIPLES IN GENERAL

Class 1 - generally safe.

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LASERS IN SURGERY

Class 2 - safe within the time of the blink reflex.

Class 3 - cause blindness after short exposure from mirrored surfaces.

Class 4 - unsafe even with reflection from nonmirrored surfaces

! ! !

All medical lasers belong to class 4. Necessary precautions should be observed while using lasers and they have to be used by properly trained personnel only.

COMPLICATIONS OF LASERS6 TO PATIENT ! Excessive burning. ! Scar formation. ! Visceral perforation.

TO THE OPERATOR ! Accidental skin exposure. ! Corneal or retinal burns.

REFERENCE 1.

Cushchieri A, Steele, RJC, Moossa, AR.: Surgical crafts and technology In Essential surgical practice (Volume 1) Butterworth-Heinemann, Oxford. 4th edition 2000. pp 38-68

2.

Hindley, JT, Law, PA , Hickey, M. et al.: Clinical outcomes following percutaneous magnetic resonance image guided laser ablation of symptomatic uterine fibroids.

Hum. Reprod., Oct 2002; 17: 2737 - 2741.

3.

www.medscape.com/viewarticle/412194

4.

Kuperman-Beade M, Levine VJ, Ashinoff.: R Laser Removal of Tattoos Am J Clin Dermatol. 2001;2:21-25

5.

Biesman BS.: Blepharoplasty: Laser or Cold Steel? Skin Therapy Letter 8(7):5-7, 2003

6.

McBurney E I. Side effects and complications of laser therapy. Dermatol Clin 2002; 20: 165-176

SURGERY - PRINCIPLES IN GENERAL

SUMMARY Lasers in surgery Types Properties Effects ! Photochemical ! Photothermal ! Photomechanical Medical applications Therapeutic ! Oncology ! Opthalmology ! Cardiovascular ! Gynaecological ! Skin and cosmetic surgery ! Urology ! Wound healing Optical alignment Diagnostic indications Safety of lasers Complications of lasers ! Effects on patient ! Effects on operator

53

TOURNIQUETS

1 PS-008

TOURNIQUETS Shuja Tahir, FRCS, FCPS Abid Bashir, FCPS

The word tourniquet is derived from old French word “tourner” meaning to turn; iquet” being the diminutive form.1,2 It is a compression device used to cut off the flow of blood to a part of the body, most often an arm or leg.

It may be a special surgical instrument, a rubber tube, a strip of cloth, or any flexible material that can be tightened to exert pressure.2 Tourniquet is any type of compression device applied to the limbs in order to stop the arterial, venous and capillary flow of blood for a prescribed period (60-90 minutes).

OBJECTIVES OF USE OF TOURNIQUETS 1. To stop bleeding from limbs as first aid.

2. To stop bleeding from limbs in emergencies before wound exploration.

3. To distend the limb veins before phlebotomies.

4. To distend veins during surgery for arteriovenous fistula formation.

5. To achieve bloodless field during hand surgery, nerve repair and tendon repair.

6. To stop the flow of anesthetic agent from area of regional anaesthesia of the limb.

Tourniquets are commonly used in surgery. These have a special role in hand surgery. These also

SURGERY - PRINCIPLES IN GENERAL

provide bloodless field so that proper identification of tissues is possible. These provide excellent haemostasis. Blood loss is minimized. When used improperly, these may be dangerous. These are also used in regional anesthesia (Bayer' block). They also have a very special role in emergency and trauma.

TYPES OF TOURNIQUETS WITH THEIR USES The Esmarch introduced the first tourniquet in 1873.

A rubber band was wrapped around the limb several times. The primary problem was the high pressures generated. Pressures in excess of 1000 mmHg have been demonstrated. Twisting and stretching of skin during application promoted skin trauma. These problems produced a higher incidence of complications associated with the Esmarch tourniquet. As a result, the Esmarch has generally been abandoned except in emergency and trauma where any thing can be used as tourniquet.

RUBBER TOURNIQUET A long rubber tube about 10 cm wide and about a meter long. It is similar to Esmarch's tube. Its uses are similar but it is more traumatic to skin, vascular intima, soft tissue and nerves of area of application.

ELASTIC TOURNIQUET Small size elastic tourniquets are used for easy phlebotomies. These are about 2-3 cm wide and about 25-40 cm long. These are used to block the

55

TOURNIQUETS

venous flow only and thus making the veins prominent for easy venous puncture. These are used for; 1.

2.

3.

4.

Collection of blood sample.

Introduction of intravenous cannula.

Introduction of CVP line.

Intravenous injection for diagnostic or of therapeutic purposes.

PNEUMATIC TOURNIQUET Pneumatic Tourniquet was introduced in 1904 by Cushing. It is less traumatic to skin and vascular intima. It can be controlled easily as it can be inflated and deflated as and when required.

POSITIONS USED ! Arm. ! Forearm. ! Thigh. ! Calf. ! Other - Finger, toe, etc.

Most commonly it is used on the arm and thigh.

Forearm and calf tourniquets are being used more frequently for intravenous regional anesthesia.

Single digit tourniquets are generally discouraged.

INDICATIONS ! Emergency and trauma ! Tendon repair ! Nerve repair ! Vascular repair ! Hand surgery ! Bayer's block (regional anesthesia) TECHNIQUE In emergency, when the patient is bleeding from the limbs, a tourniquet may be made from a strong, SURGERY - PRINCIPLES IN GENERAL

2

pliable material, such as gauze or muslin bandages, clothing, or cravats. An improvised tourniquet is used with a rigid stick-like object. To minimize skin damage, ensure that the tourniquet is at least 2 inches wide. Never use material that will cut the skin, such as rope or wire. Do not cover the tourniquet; it should be in full view. As an extra precaution, The letter “T� can be written on patient's forehead along with time of application.

For application of pneumatic tourniquet before limb surgery, the limb is first elevated and exsanguinated.

Esmarch bandage is applied from distal to proximal end of the limb for tissue compression. It decreases the amount of blood distal to the cuff. This reduces blood in the surgical field and may limit peak plasma levels of local anesthetic (LA) in the case of intravenous regional anesthesia when the cuff is deflated. Exsanguination is not done in injured or infected limb for obvious reasons. Similarly, patients with poor cardiac reserves may not tolerate the acute volume shift specially from lower limbs.

Heavy cotton pad is applied. Pneumatic tourniquet is applied and pressure is elevated well above the systolic pressure to impede the arterial flow. The aim is to produce a bloodless field and/or containment of local anesthetic. Therefore, the cuff pressure needs to be high enough to prevent arterial and venous blood from passing beneath. However, the major mechanism of nerve injury related to the tourniquet is excessive pressure causing nerve compression.

Therefore, a compromise has to be made. The lowest pressure that safely assures hemostasis and arterial occlusion is the goal.

This minimum tourniquet pressure required to maintain hemostasis will depend on :

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TOURNIQUETS

!

!

!

!

Limb size - Higher pressures are required on the thigh than on the arm because a greater mass of subcutaneous tissue has to be compressed to compress the artery below.

Conversely, lower pressures are needed in thin or cachectic patients vs. obese patients.

Cuff type and cuff width - The cuff pressure required to eliminate blood flow decreases as the cuff width increases3-5. Wider cuffs provide better transmission of tissue compression and lower cuff pressures are necessary to compress the artery Peripheral vascular disease - Higher cuff pressures will be necessary in hypertensive patients and patients with calcified and less compressible vessels.

Intraoperative systolic blood pressure range More labile BP with higher SBP peaks requires higher cuff pressure for adequate hemostasis.

Time of inflation is recorded. The safe ischemia time for upper limb is 90 minutes and for lower limb is 60 minutes. If prolonged tourniquet times are necessary, then reperfusion periods should be used.

This allows correction of metabolic abnormalities in the limb and restoration of depleted energy stores. It has been observed that complete intracellular bioenergetic recovery occurs within five minutes after tourniquet release6.

PRECAUTIONS Following precautions should be observed for tourniquet surgery.

It should be applied at proper place. Proximal limb placement (thigh or upper arm) is preferred because larger amounts of tissue and muscle protect nerves from potential trauma. Place the tourniquet on the

SURGERY - PRINCIPLES IN GENERAL

point of maximal circumference of the limb. Avoid application over bony prominence or any area where skin, nerves, or blood vessels are compressed excessively against a hard bony surface. ! ! ! ! ! !

Adequate padding should be used.

Limb should be properly exsanguinated before inflation.

Time of inflation should be recorded.

Use minimal pressure - usually 100 mmHg above systolic blood pressure Use for minimal duration - no longer than 90 minutes.

Multiple inflations or deflations should be avoided.

It should be deflated after the operation. A good point is to strap the limb to the operation table, so that if one forgets to deflate the tourniquet, at the time of shifting, it is remembered.

COMPLICATIONS Following complications may be encountered while using tourniquets. ! Volume overload as exsanguinations of limb autotransfuses blood from peripheral circulation to central circulation ! Nerve injury, ! Vascular injury ! Postoperative embolic events ! Myoglobinuria ! Increased blood viscosity ! Increased postoperative pain ! Tourniquet burns, due to preparation solution getting under the tourniquet ! Rapid systemic absorption of local anesthetic drug in case of cuff failure ! Post-tourniquet Syndrome ": Swollen, stiff, pale limb with weakness but no paralysis. Duration 57

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TOURNIQUETS

1-6 weeks. Postoperative edema is the main cause.

Deflating a tourniquet leads to the release of blood with low pH and pO2 plus high pCO2, lactate, and K+. This leads to corresponding changes in systemic values : decreased pH, decreased pO2, increased pCO2, increased K+, and increased Lactate.

!

CONTRAINDICATIONS The relative contraindications to the use of tourniquet when the arterial tourniquet should be avoided are; Peripheral Vascular Disease. (Raynaud's disease) Severely injured or traumatized limb.

Peripheral neuropathy or CNS disorders.

Severe infection in the limb.

DVT in the Involved Limb.

Severe arthritic changes / Bony spurs in the involved limb.

Poor skin condition of the involved limb.

AV Fistula.

Contraindications to intravenous regional anesthesia.

Lack of appropriate equipment - especially with intravenous regional anesthesia Sickle cell hemoglobinopathy.

! ! ! ! ! ! ! ! ! ! !

cuffs. Clin Ortho Rel Res 1993; 286:257-261.

4.

Newman, R. J. and Muirhead, A., A safe and effective low pressure tourniquet. A prospective evaluation. J. Bone.

Joint. Surg. Br. 1986; 68:625-628.

5.

Pedowitz, R. A., Gershuni, D. H., Botte, M. J., Kuiper, S., Rydevik, B. L., and Hargens, A. R., The use of lower tourniquet inflation pressures in extremity surgery facilitated by curved and wide tourniquets and an integrated cuff inflation system. Clin Ortho Rel Res 1993; 287:237-244.

6.

Sapega, A. A., Heppenstall, R. B., Chance, B., Park, Y. S., and Sokolow, D., Optimizing tourniquet application and release times in extremity surgery. A biochemical and ultrastructural study. J.Bone.Joint.Surg.Am. 1985; 67:303-314.

SUMMARY Tourniquets Objectives Types ! Rubber tourniquets ! Elastic tourniquets ! Pneumatic tourniquets Indications Technique Precautions Complications Contraindications

REFERENCE: 1.

Columbia Encyclopedia, Sixth Edition, 2005.

2.

The American Heritage Dictionary of the English Language, Fourth Edition Copyright Š by Houghton Mifflin Company, 2000.

3.

Graham, B., Breault, M. J., McEwen, J. A., and McGraw, R. W., Occlusion of arterial flow in the extremities at subsystolic pressures through the use of wide tourniquet

SURGERY - PRINCIPLES IN GENERAL

58

1

SURGICAL DRAINS

PS-009

SURGICAL DRAINS Shuja Tahir, FRCS, FCPS Abid Bashir, FCPS

Surgical Drain is a device used to evacuate any potential collection from the surgical site. Drains are used to drain purulent collections, to prevent the accumulation of blood, or to indicate the possibility of a leaking surgical anastomosis.

The use of surgical drains has decreased in recent years as the evidence for benefit is questioned. Their use is not without complications and therefore, they should be judiciously used.1 There are no rigid guidelines for the indications of drains. It is matter of personal preference but it is still recommended in certain surgical procedures2,3,4.

The surgeons should understand the benefits and applications of drainage and the tissue responses to the constituent materials. The most important point is that drains are not a substitute for meticulous surgical technique.1 TYPES OF DRAINS Drains are of many types; open or close, active or passive, plastic, rubber or latex even made up of twisted nylon or prolene.

OPEN DRAINS As the name suggests, open drains do not have any closed collecting system. The drain fluid collects in gauze pad or stoma bag. It increases the risk of infection. These comprise of rubber or plastic

SURGERY - PRINCIPLES IN GENERAL

channel to drain any potential fluid collection.

Corrugated rubber drains used to be popular some years ago, but due to increased incidence of infections, their use is abandoned. Simplest example of open drain is longitudinally opened tube drain (drip set). Its use is also very limited. It is only used in small wounds for better cosmetic results.

CLOSED DRAINS These consist of a tube connected to a closed drainage system. Tube may be of variable size, depending upon the type and site of surgery. The tube is usually taken out through a separate stab incision and is anchored to the skin. It is connected to a closed drainage system, usually a bag or a bottle (in case of active suction drains).

The advantages include measurement of drainage fluid and less chances of infection. The main disadvantage is their tendency to get blocked.

Depending upon whether suction has been applied or not, these can be divided into two main types.

PASSIVE DRAINS These drains do not use any active suction system for evacuation of fluids. These simply consist of a tube drain connected to a bag that hangs by the side of the patient. These drain the fluid by gravity and by the differential pressure between body cavities and the exterior.

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SURGICAL DRAINS

ACTIVE DRAINS These drains use suction mechanism for active evacuation of fluids. The simplest form is 50cc disposable syringe attached to the draining tube with negative pressure created by pulling the plunger.

drains stimulate more inflammatory reaction than the plastic drains. This inflammatory reaction is beneficial in certain conditions like T-tube for biliary drainage. The newer soft silicon drains provoke least inflammatory reaction8.

There are many types of suction drainage system available in the market (redivac, Jackson-Pratt, hemovac etc). These provide excellent drainage system with relatively low caliber.5

! !

The main disadvantage is generation of high pressure gradient at the surgical site6 which leads to many complications like hemorrhage and trauma to the tissues. A compromise has recently been suggested by Chintamani et al by use of semi-suction drains after radical mastectomy7.

UNDER WATER SEAL Under water seal is added to the chest drains to prevent entry of air into the pleural cavity (having negative intrapleural pressure). It consists of a glass bottle with two openings. The bottle is half filled with water with antiseptic solution.

The channel connected to the draining tube is dipped in water, while other channel is kept above the water level. The air and fluid from pleural cavity drain into the bottle. The fluid settles down and the air goes out through the open channel. The reverse movement of air is prevented by under water end of the drainage channel.

COMPLICATIONS The complications of drains include; ! Inflammatory Reaction It depends upon the material of the drain. Rubber

SURGERY - PRINCIPLES IN GENERAL

! ! ! ! !

Infections injury to the tissues leading to hemorrhage (vessels) or fistula formation (gut or biliary duct). pain and discomfort to the patient. prolonged ileus. loss of fluids and electrolytes. drain site metastasis. blockage of drain.

Not very rarely, hernia may develop through a drain site.

Occasionally a drain may get struck while taking out.

CARE OF THE DRAINS Following principles should be observed while taking care of the drains.

Drains should be taken out of the wound through dependent part.

The drain should always be lower than the exit site.

This may not be strictly followed with suction drains.

There should not be bending or kinking of the tubes.

Drains should be emptied twice daily, preferably at the same time and the output properly recorded as per amount, color etc.

Any abnormal discharge should be properly investigated.

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Drains are removed when the drainage is reduced to between 20-50 ml / 24 hrs.

REFERENCE 1.

Memon MA, Memon B, Memon MI, Donohue JH.: The uses and abuses of drains in abdominal surgery. Hosp Med. 2002 May; 63(5):282-8.

2.

Petrowsky H, Demartines N, Rousson V, Clavien PA.: Evidence-based value of prophylactic drainage in gastrointestinal surgery: a systematic review and metaanalyses. Ann Surg. 2004 Dec;240(6):1074-84; discussion 1084-5.

SUMMARY Surgical Drains Types ! Open drains ! Close drains ! Passive drains ! Active drains ! Under water seal drains Complications Inflammatory reaction Infections

! !

Care of drains 3.

Torzilli G, Olivari N, Del Fabbro D, Gambetti A, Leoni P, Gendarini A, Makuuchi M.: Bilirubin level fluctuation in drain discharge after hepatectomies justifies long-term drain maintenance. Hepatogastroenterology. 2005 JulAug;52(64):1206-10

4.

Gurer A, Gomceli I, Ozdogan M, Ozlem N, Sozen S, Aydin R.: Is Routine Cavity Drainage Necessary in Karydakis Flap Operation? A Prospective, Randomized Trial. Dis Colon Rectum. 2005 Jun 24; [Epub ahead of print]

5.

Newcomb AE, Alphonso N, Norgaard MA, Cochrane AD, Karl TR, Brizard CP.: High-vacuum drains rival conventional underwater-seal drains after pediatric heart surgery. Eur J Cardiothorac Surg. 2005 Mar;27(3):395-9

6.

Grobmyer,SR, Graham D, Brennan MF, Coit D.: High pressure gradients generated by closed-suction surgical drainage systems. Surgical infections. Sep 2002, 3 (3): 245-9

7.

Chintamani, Singhal V, Singh J, Bansal A, Saxena S.: Half versus full vacuum suction drainage after modified radical mastectomy for breast cancer - a prospective randomized clinical trial. BMC Cancer. 2005 Jan 27;5(1):11

8.

Rayatt SS, Dancey AL, Jaffe W.: Soft fluted silicone drains: a prospective, randomized, patient-controlled study. Plast Reconstr Surg. 2005 May;115(6):1605-8

SURGERY - PRINCIPLES IN GENERAL

61

Infections

1

ACUTE ABSCESS

PS-010

ACUTE ABSCESS (PYOGENIC ABSCESS)

Shuja Tahir, FRCS, FCPS An abscess is a localized collection of the pus in a closed cavity of living tissue. It is caused by the pyogenic (Suppurative or pus forming) microorganisms. The abscess is usually produced by the presence of these bacteria deep into the tissue.

PATHOGENESIS The pyogenic bacteria reach the infected area by one of the following three routes;

! ! ! !

Direct infection from outside (penetrating wounds).

Local extension from some adjacent focus of infection.

Hematogenous spread (through blood stream).

Lymphatic spread (through lymphatics).

The bacteria multiply after reaching the site where local atmosphere is favourable for their growth. The micro-organisms produce significant local necrosis.

There is accumulation of neutrophils at the necrosed area.

When the infective process progresses to suppuration and resolution is not possible, the abscess is formed. This is typical of staphylococcal lesions such as boils. The events in the formation of abscess occur in following sequence;

!

Circumscribed necrosis of the tissue due to the micro-organisms, chemical agents or mechani-

SURGERY - PRINCIPLES IN GENERAL

! !

cal injury.

Marked polymorphonuclear infiltration.

The pyogenic agents kill these leukocytes. These dead and degenerating leukocytes are called “PUS CELLS”.

This necrotic material undergoes softening due to release of proteolytic enzymes of the dying leukocytes and by the autolysis mediated by tissue’s own cathepsins. This fluid material is called pus, and when present in a closed cavity forms an abscess1.

The pus is present in the tissues, organs or a confined space. The central region of the abscess in semi fluid collection of necrosed tissue and white cells. The surrounding area shows vasodilatation, organ parenchymal cells, fibroblastic proliferation and other features of inflammation.

The abscess contains;

! ! ! ! !

Pus which is made up of dead and dying leukocytes (pus cells).

Other contents of inflammatory exudate.

Edema fluid and fibrin.

Tissue debris (necrotic tissue, nucleic acid and lipids).

Organisms.

Many of the micro-organisms are living and can be cultured but pus due to chemical agents is sterile and

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ACUTE ABSCESS

doesn’t contain organisms.

The abscess cavity is lined by pyogenic membrane which in the beginning consists of acutely inflamed tissue and is heavily infiltrated with polymorphs. The copious fibrinous exudate is soon organized into granulation tissue.

The tension in the abscess cavity rises due to increased exudation of plasma. It gives typical throbbing pain of the abscess.

FEVER The rise in temperature is the important clinical feature in all abscesses. The deep seated or organ abscesses are usually diagnosed due to typical pattern of the fever in these patients. The fever is swinging a step ladder type.

In many situations, it may be the only feature for diagnosis of occult abscesses7.

CLINICAL FEATURES PAIN / TENDERNESS The abscess is very painful. The pain is continuous and throbbing in nature. It increases in severity in a pulsatile fashion. It increases on movements and due to gravitational effect. Sever pain is experienced on touching the abscess or even sometime on pointing towards the abscess.

105

SWELLING The abscess presents as swelling when it is superficial and subcutaneous in its site.

99

103

101

97

Deep seated abscesses or the abscesses present in various organs don’t present as obvious swellings.

Abscesses presenting in deep tissue or internal organs exhibit tenderness which can be assessed with various clinical tests7.

The abscess of some organs presents with their enlargement. The liver abscess may present as large diffuse swelling in the right hypochondrium.

Pancreatic abscess may present as a diffuse soft and cystic swelling in the epigastrium.

SURGERY - PRINCIPLES IN GENERAL

WEIGHT LOSS The abscess and its effects may lead to loss of appetite, nausea and vomiting . The fever and toxaemia also leads to loss of weight and generalized weakness.

ANOREXIA This is an effect of large size abscess or intra peritoneal abscesses. The bacteremia, septicaemia and toxaemia may be the cause of loss of appetite.

The actual disease may also cause anorexia.

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ACUTE ABSCESS

3

ANAEMIA It is usually seen in patients with abscesses which are untreated or inadequately treated.

inflammatory exudate in its base. This slough becomes detached and ulcer heals by repair and regeneration.

FATE OF THE ABSCESS RESOLUTION It may occur after complete proteolytic digestion of the necrosed tissue, pus cells and dead microorganisms.

ANTIBIOMA Sometimes when abscess is not drained and patient is treated conservatively with antibiotics, the abscess becomes sterile and its walls are organized into fibrous tissue. This cystic mass with organized walls containing sterile fluid is called an antibioma.

SPONTANEOUS DRAINAGE When the abscess points at the surface, it bursts and drains its contents spontaneously. Resolution follows which may be complete or incomplete requiring surgical intervention.

SURGICAL DRAINAGE The abscess is anticipated or diagnosed at an earlier time in clinical practice. Surgical drainage is performed under appropriate anaesthesia. It takes lesser time to heal. It achieves cosmetically better results. The morbidity and mortality is much less.

SINUS FORMATION A large quantity of pus is formed and its drainage into a hollow viscus or to exterior from the closed abscess cavity leading to a sinus formation and continuous discharge of pus. It is usually seen when necrotic material is present in the abscess cavity.

CHRONIC ABSCESS Acute abscess may lead to chronic inflammation due to persisting infection and chronic abscess formation results. Then its wall is composed of fibrous tissue, heavily infiltrated by polymorphs, macrophages, lymphocytes and plasma cells.

ABSCESSES IN SPECIALIZED SITUATIONS BRAIN ABSCESS It is presence of pus in the brain matter. It has all of the general features of an abscess. It presents as a space-occupying lesion of the intra cranial cavity. It also produces secondary brain damage.

CALCIFICATION Sometimes if the abscess is not drained, it may not burst, but its walls become organized into thick fibrous tissue. The pus becomes thick due to absorption of water and it may undergo calcification.

ULCERATION Occasionally epithelial surface is involved and develops ulceration which has necrotic and SURGERY - PRINCIPLES IN GENERAL

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ACUTE ABSCESS

It has symptoms due to pressure over the involved area of the brain leading to loss of function of that part of brain such as hemiplegia, hemianaesthesia or impairment of consciousness, focal seizures or even death of the patient2.

It may follow direct extension from mastoiditis or penetrating injuries of skull or open fracture of skull or through other predisposing conditions such as acute bacterial endocarditis, cyanotic heart disease and chronic pulmonary sepsis which tend to produce multiple abscesses. Common organism are streptococci and staphylococci.

right lobe of liver.

PANCREATIC ABSCESS It is the collection of pus in the pancreatic parenchyma. It may present as a mass in the epigastrium and with all the gross features of intraperitoneal abscess.

General features of raised intra cranial pressure are seen. The C.S.F. pressure is raised, white cell count and protein level is also raised but glucose level is normal2.

LIVER ABSCESS It is the collection of pus in the liver parenchyma. It may be solitary or multiple. It may be amoebic or pyogenic abscess. The pyaemic abscesses are usually multiple but parasitic amoebic abscesses are usually solitary. These may be present in any part or lobe of the liver, but more commonly tend to occur in SURGERY - PRINCIPLES IN GENERAL

EMPYEMA OF GALL BLADDER It is the collection of pus in the gall bladder. It may follow an attack of acute cholecystitis. It is usually seen in the patients suffering from chronic cholecystitis or cholelithiasis or infection of a mucocele of the gall bladder. It presents with all features of abscess in the right hypochondrium. It necessarily occurs in patients having obstruction in cystic duct.

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APPENDICULAR ABSCESS It is the collection of pus in the periappendicular area. It follows an attack of acute appendicitis. If it is not treated in time and a mass is formed which may later on lead to local necrosis, perforation and localized collection of pus in right iliac fossa in the periappendicular area.

SUBPHRENIC ABSCESS It is the localized collection of pus in the peritoneal cavity under the dome of diaphragm. It presents after generalized peritonitis due to typhoid perforations and post-operatively if the infection is virulent or drainage has been improper. It leads to decreased diaphragmatic movements. It is associated with sympathetic pleural effusion.

5

LUNG ABSCESS It is the collection of pus in any part of the lung parenchyma or a cavity which is formed due to localized necrosis of the lung tissue.

The liquefaction of the necrotic material occurs. Its symptoms are related to the diminished lung function. The features of septicaemia and altered lung function will depend upon the size of the abscess, its duration and the virulence of the organisms.

INTERLOOP ABSCESS It is the localized collection of pus in between the adherent loops of bowel. It is seen in patients who have suffered from generalized peritonitis or occasionally in post-laparotomy sepsis.

PARACOLIC ABSCESS It is the localized collection of pus in the paracolic spaces. It may follow operations when the infection is already uncontrolled or after bowel perforations or peritonitis.

EMPYEMA THORACIS It is collection of pus in the pleural cavity. It may also be called as pleural abscess. It leads to collapse of lungs and loss of its function. It also leads to septic shock syndrome and death of the patients. It should be drained through an underwater seal drainage system activity and at an early stage to protect the lungs from collapsing.

SURGERY - PRINCIPLES IN GENERAL

Staphylococci, gram negative and anaerobic organisms such as bacteroids are the usual organisms involved in lung abscess formation.

The predisposing factors are; 69

ACUTE ABSCESS

! ! ! !

6

Aspiration of infective material.

Primary bacterial infection (post pneumonic or klebsiella infection).

Septic embolism from neoplasia.

Miscellaneous such as direct penetrating injuries, suppuration from oesophagus, spine and subphrenic abscess.

Primary cryptogenic lung abscess is the one when no other predisposing factor of lung abscess is known5.

BREAST ABSCESS It is the collection of pus in the breast. Commonly it is seen in the lactating breast. The abscess remains contained in the lobes of breast localized by the fibrous septa. The induration lasts longer.

The bacterial access is through the lactiferous ducts when there is inspissation of secretions in the ducts or cracks and fissures in the nipple during early periods of nursing. These changes follow dermatitis of nipple.

The inflammatory process leads to cellulitis with localized subcutaneous, sub-areolar, interlobular, peri-ductal and retro mammary collection of pus.

The abscess typically occurs within first few weeks of lactation and breast feeding.

It is most often staphylococcal in nature. Bacterial invasion of the breast tissue leads to development of acute mastitis. The localization of abscess occurs easily. Multi-locular abscess is typically staphylococcal. Streptococcal infection tends to cause diffuse spreading infection and involves larger areas. It is localized at a later stage.

SURGERY - PRINCIPLES IN GENERAL

Commonly the breast abscess is unilateral, it may be unicentric or multi centric collection. It may be a single abscess or multiple abscesses may be present.

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The abscess presents with painful localized area overthe breast. The erythema over the breast becomes clearly visible. The area of breast becomes tender, red and hot over next few days if not treated in time.

The area is indurated initially but becomes soft and fluctuant within next few days. Overlying skin gets necrosed. The abscess may drain spontaneously.

The axillary glands may be tender and enlarged on the same side.

MANAGEMENT Objectives of management are;

! ! ! !

Assessment of general condition of the patient.

Confirmation of diagnosis.

Immediate treatment for relief of symptoms.

Definitive treatment of the cause.

The patient is investigated thoroughly for general assessment and confirmation of diagnosis. Complete urine examination and blood examination is performed and ultrasound of the breast is performed.

CONSERVATIVE TREATMENT ! Analgesia can be given both by mouth or parenterally to relieve the pain. ! Focal heat compresses are used. ! Parenteral or oral antibiotics against gram positive cocci are used in adequate doses.

The conservative treatment is continued for 2-3 days. If the symptomatic relief is obtained, the treatment may be continued for few days till complete relief.

SURGERY - PRINCIPLES IN GENERAL

!

Ultrasound guided aspiration of pus collection is then performed.

SURGICAL TREATMENT Fluctuation becomes elicitable at a late stage. The skin necrosis occurs by the time fluctuation is positive. The breast abscess is drained at an early period when it is still in the induration stage through a cosmetically acceptable incision.

Incomplete drainage leads to healing with fibrosis and scarring. It may occasionally be mistaken as malignancy. It should be completely drained by breaking all the loculi to avoid residual abscess formation.

Surgical drainage of abscess with complete breakage of all loculi is the adequate treatment of breast abscess. Thorough Debridement of the abscess is required for good cosmetic results and prevention of recurrent abscess. Discontinuation of the lactation by using anti prolactin drugs (Bromocriptine) helps to resolve the inflammatory process by regression of lactation.

Breast suction with the help of breast suction pump helps to get rid of the thick milk secretion but stimulates further lactation and may not be always helpful in resolution of inflammatory process.

Breast abscess may resolve or be cured with adequate treatment. It may progress to form chronic or recurrent abscess with improper or inadequate treatment.

Chronic or recurrent abscess is investigated for acid fast bacilli, fungi, aerobic and anaerobic bacteria.

Thorough debridement and use of appropriate antibiotics for longer period may be necessary.

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Simple mastectomy may be required in worse cases to treat and avoid the chronic infection.

NON LACTATIONAL BREAST ABSCESS It is usually seen in 30-60 years age group, these are manifestations of duct ectasia/periductal mastitis.

Causative organisms are anaerobes e.g. bacteroides, anaerobic streptococci.

These often present as a slightly tender periareolar mass. Spontaneous resolution is common but these may progress to an abscess. Systemic features are less marked.

Treatment is aspiration and obtaining pus for culture & sensitivity. A combination of flucloxacillin and metronidazole is recommended.

Repeated aspirations may be helpful. Occasionally drainage is required and must be done through smallest possible incision.

Definitive treatment is major duct excision and nipple eversion when acute inflammation has settled. It should be performed under proper antibiotic cover.

MASTITIS NEONATORUM Breast abscesses can rarely occur in neonates due to infection of milk induced by transplacental passage of maternal hormones.

Treatment is antibiotics. Occasionally, surgical drainage is necessary and may lead to distortion of breast contour in later life.

PERIANAL ABSCESS It is the collection of pus in the perianal space. It also becomes fluctuant at later stage. It should also be drained as early as possible when it is still indurated.

SURGERY - PRINCIPLES IN GENERAL

8

PERI URETHRAL ABSCESS It is the collection of pus in peri-urethral space. It has also communication with urethra. It should be drained and urethra should be protected by catheterization prior to surgery. It is more common in males as their urethra is longer.

Treatment is incision and drainage by sparing urethra.

PELVIC ABSCESS It is the localized collection of pus in the pelvis. It is intra-peritoneal abscess. It presents with severe general symptoms.

It should be treated actively and surgically. It may present with diarrhoea in a post operative patients or a post peritonitis patient.

On rectal examination a soft globular bulge is felt in the rectum due to presence of pus in rectovesical pouch or pouch of Douglas. It may be drained through rectum, vagina, percutaneously.

SATELLITE ABSCESSES These are micro-abscesses present in the granulomas of lymphogranuloma venereum which coalesce to form bigger abscesses. These are irregular or branching abscesses.

BRODIE’S ABSCESS It is localized collection of pus in the bones. It is a small intra osseous abscess. It frequently involves the cortex and is walled off by reactive bone.

It follows acute or chronic osteomyelitis. Usually it is 4 staphylococcal in nature .

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SUMMARY

REFERENCES 1. Walter JB. Israel MS. Hospital (Nosocomial) infection.

General pathology 6th edition. Churchill. Living stone London. 1987; 225-260.

2. Umberto De. Girolami. Mathaw P. Frosch. Douglas C. Anthony. The central nervous system. Robbins pathologic basis of disease. Cotran. Kumar. Robbins 5th edition W.B. Saunders Company London. 1994; 1316-131.

3. Cortan. Kumar, Robbins The breast: Robbins pathologic basis of disease, 5th edition W.B. Saunders Company London. 1994; 1092-93.

4. Andrew E. Rosedberg. Skeletal system and soft tissue tumors. Robbins pathologic basis of disease 5th edition W.B. Saunders Company London. 1994; 1230-31.

5. Lester Kolezik J. Schoen. The lung. Robleims pathologic basis of disease. Cotram, Kumar Robbins 5th edition W.B. Saunders Company London. 1994; 699-700.

6. Widjaya P. Bilic A. Babic . Z et al. Amoebic liver abscess: ultrasonographic characteristics and results of different therapeutic approaches. Acta Media Iugoslavica [JC:10s]. 1991; 45(1):15-2.

Acute abscess (Pyogenic abscess) Fate of abscess ! Resolution ! Spontaneous drainage ! Surgical drainage ! Sinus formation ! Calcification ! Ulceration ! Antibioma formation ! Chronic abscess formation Specialized abscesses Brain abscess Liver abscess Pancreatic abscess Empyema gall bladder Appendicular abscess Subphernic abscess Interloop abscess Paracolic abscess Empyema thorasis Lung abscess Breast abscess Peri anal abscess Peri uretheral abscess Pelvic abscess Satellite abscess Brodie’s abscess

! ! ! ! ! ! ! ! ! ! ! ! ! ! ! !

7. Maltz G. Krauer CM. Amoebic liver abscess: a 15 year s experience. American jour nal of gestroenteology [JC:3he]. June 1991; 86(6):70410.

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1 PS-011

TETANUS Shuja Tahir, FRCS, FCPS Tetanus is an acute emergency. It is a very serious life threatening disorder. It is characterized by convulsive contractions of the voluntary muscles. It is a preventable disease which can have a very fulminating course and may be fatal even after adequate treatment1.

BACTERIOLOGY It is caused by clostridium tetani which is a gram positive, slender motile rod. It is about five microns in length. It has drum stick or tennis racket appearance.

The organism is an anaerobe and requires other organisms, foreign bodies and dead tissue which can provide anaerobic atmosphere for its growth. It is spore forming and its spores can survive under most unfavorable circumstances. Anaerobic atmosphere (low oxygen tension), previous tissue damage and poor phagocytic defence helps the spores to grow and produce powerful exotoxin.

It produces following exotoxins ; TETANOLYSIN It is a haemolysin which causes haemolysis.

TETANOSPASMIN It is an exotoxin which is a neurotoxin. This is the most violent poison known to mankind. It is the cause of all the symptoms which are very lethal.

SURGERY - PRINCIPLES IN GENERAL

The incubation period is usually one to two weeks but it may be shorter to few days or longer upto few months depending upon ; Suitability of local environment.

Germination of spores.

Distance from contaminated wound to central nervous system for toxin to travel.

PATHOLOGY The clostridium tetani most commonly gets access into the body through a punctured or lacerated wound, through abrasions, burns or any other injuries.

Usually the entry is from external environment such as contaminated wound, dressings, hands or instruments but many times it may be endogenous in origin. Intravenous drug abusers are commonly affected.

No matter what is the mode of entry the disease is a disaster for the patient.

The exotoxins (Tetanospasmin and Tetanolysin) are produced by the organism when favorable anaerobic atmosphere is available. The release of toxin requires germination of spores and proliferation without competing flora. The exotoxin is absorbed from the site of infection. It travels through the blood stream and attaches to the peripheral nerve endings

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mainly to motor neurones. It is fixed in motor neurones and central nervous system. Some of the toxin stays in circulation as free exotoxin. The organism itself does not cause any tissue damage.

The exotoxin has dual action ; It interferes with acetyl-choline-cholinesterase balance at peripheral motor end plates. The persistent presence of acetyl choline produces sustained tonic muscular spasm.

2

LOCK JAW (TRISMUS) It is the spasmodic stiffness of muscles of mastication. It causes difficulty in opening the jaw.

It is usually the first and most common symptom.

SARDONIC SMILE (RISUS SARDONICUS) It is smiling and fixed expression (mask like) of the face. It is typical of this disease.

It appears little later. It presents due to the rigidity and tonic spasms of the facial muscles.

It causes extreme hyperexcitability of motor neurons of anterior horn cells which result in explosive, widespread reflex spasms of muscles even after minor stimuli.

DYSPHAGIA It is also one of the most common features. It is the difficulty in swallowing. It is noticed early while eating.

Only when the exotoxin passes across the synapses into the pre-synaptic terminals of inhibitory spinal interneurons, the sustained spasmodic contractions appear.

DIFFICULTY IN BREATHING It occurs due to severe and sustained spasm of respiratory muscles. The muscles fail to relax. It leads to sudden respiratory arrest and death.

The toxin does not cross blood brain barrier and the patient always remains alert even just before death.

NUCHAL RIGIDITY It is felt in the neck due to spasmodic contractions of the extensor muscles of the neck

The toxin, producing all these effects, is fixed to the neuronal tissue and cannot be neutralized. The free toxin can be neutralized by using anti tetanus serum.

Gross examination of the wound reveals nonspecific inflammatory changes and tissue necrosis. The neurologic changes are also nonspecific such as swelling of the motor ganglion cells of the spinal cord and medulla with nuclear swelling and chromatolysis.

CLINICAL FEATURES The clinical feature are due to the sustained convulsive contractions of the voluntary muscles.

There is some degree of sympathetic over activity as well. The common features are as follows3,4 : SURGERY - PRINCIPLES IN GENERAL

OPISTHOTONUS (STIFFNESS IN EXTENSION) It is the spasmodic contraction of the extensor muscles of the back and abdomen. It is a typical feature of tetanus. The patient is stiff in extension CONVULSIONS The tonic muscle spasms spare the limbs in early disease.

The violent spasmodic contractions of voluntary muscles are seen following even minimal stimulation such as putting the light on, blowing of the wind, producing noise, slight movements and changing of 76

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clothes or sheets.

Later on the reflex convulsions start which may lead to the rupture of the muscles. Severe muscle spasms may cause arrest of breathing and death.

FEVER The temperature is elevated.

AUTONOMIC INSTABILITY There is some degree of sympathetic over activity and autonomic instability which leads to instability of cardio vascular system. Due to loss of sympathetic inhibition, the heart rate rises (Tachycardia), blood pressure rises and arrhythmias are encountered2.

Death follows in few weeks due to chest infection, aspiration pneumonia and respiratory failure. Even sudden cardiac arrest may occur in severe cases.

DIAGNOSIS The diagnosis is usually based on clinical features. It may not be always confirmatory specially in elderly people. Laboratory investigations offer minimum help to confirm the diagnosis3,4. It definitely helps in excluding similar diseases such as meningitis and cerebral melaria.

INVESTIGATIONS No investigation is confirmatory for diagnosis.

Diagnosis is most of the time clinical based on history and clinical examination. Although following investigation may be needed depending upon clinical examination of patient.

URINE EXAMINATION It is a general and nonspecific investigation for tetanus.

SURGERY - PRINCIPLES IN GENERAL

BLOOD COMPLETE EXAMINATION It is also a general and nonspecific investigation. As the infection of the wound is present, leuckocytosis and raised sedimenttation rate is seen.

ARTERIAL BLOOD GASES This is an investigation required to monitor the patient during attacks of anoxia.

CSF EXAMINATION It shows raised protein level which is also nonspecific.

X-RAY CHEST It shows aspiration pneumonia or other changes if present.

ECG EXAMINATION It shows increased heart rate and arrhythmias.

EEG EXAMINATION It shows abnormalities in the record.

ULTRASOUND AND CT SCANNING These show complications of spasmodic muscles contractions such as hematomas.

PREVENTION All population should be protected against this highly fatal but preventable disease.

Pregnant mothers should be vaccinated actively during last trimester of pregnancy. This helps both mother and the baby and it has brought down the risk of tetanus neonatorum.

The delivery should always be conducted by fully trained and qualified staff under optimal aseptic conditions. The dressing of the cord should be clean and sterilized10.

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ACTIVE IMMUNIZATION Every body should be actively immunized against tetanus. A very well organized campaign should start at all levels. Tetanus toxoid is used for this purpose.

Three doses are required for proper immunity to develop.

One milliliter of tetanus toxoid should be injected intramuscularly. The second dose is given after 4-6 weeks. The third dose is given after one year interval.

The booster dose is given on yearly basis. This covers the patient against tetanus.

The booster dose of toxoid (1 ml intramuscularly) should be given every year and at every injury time which ever is earlier.

PASSIVE IMMUNIZATION This can be achieved by injecting human anti tetanus globulin (A.T.G.) after testing against allergic reaction (Allergic reactions are less common after A.T.G.).

This immunity is achieved at the same time while active immunity takes some time to develop.

The use of anti tetanus serum (ATS) has been abandoned due to severe anaphylactic reactions.

Even manufacture of bovine anti tetanus serum which was quite common during last century has been completely stopped.

Long acting penicillin or other suitable antibiotics should be used to treat the superimposed infection.

TREATMENT OF TETANUS The tetanus should not be allowed to occur. Rigorous prevention measures should be used for total eradication of the disease.

Once the tetanus has occurred the aims of treatment are ; IMMEDIATE Prevention of spasms.

Prevention of respiratory embarrassment.

Prevention of metabolic complications.

Neutralization of toxin.

EARLY Prevention of pulmonary embolism.

Prevention of aspiration pneumonia.

LATE Prevention of malnutrition.

Prevention of pressure sores9 MANAGEMENT OF POST OPERATIVE TETANUS ISOLATION As soon as the first symptom of tetanus is seen in any post operative patient, the patient is isolated from rest of the ward patients.

The best thing in case of injury to non immunized patient is to provide passive immunity by A.T.G. and give a dose of tetanus toxoid to start the active immunization.

The tetanus can be fatal even after adequate treatment1.

Wound toilet should always be done and every effort should be made to avoid any anaerobic environment at the wound site.

All the syringes and other utensils are separated and the patient is kept in a dark, quiet and well ventilated room.

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The patient should be treated as an established case of tetanus.

The operation theater should be closed and the source of tetanus infection is searched. Proper cleaning and sterilization of the operating theater is very essential before further operations are performed in that operation theater. The tetanus may be caused from endogenous source which should be suspected if gastro-intestinal surgery have been performed.

TREATMENT OF ESTABLISHED CASE OF TETANUS ISOLATION The patient should be isolated in dark, quite room which should be well ventilated.

SEDATION In mild cases sedation is given by sparine, valium, largactil or amylbarbitone can be used. These drugs should be repeated at regular intervals.

Intrathecal Baclofen (1 mg/hr) relieves the spasticity8.

MUSCLE RELAXANTS The patient should have parenteral muscle relaxant and patient should be kept in the intensive care unit in case assisted respiration is required.

AIRWAY This should be kept clear. If there is any difficulty in breathing either endotracheal intubation or tracheostomy should be performed. If tracheostomy is done, It should be looked after properly by regular suction and proper humidification.

If the patient is dangerously ill and has major cyanotic

SURGERY - PRINCIPLES IN GENERAL

5

convulsions, he should have artificial respiration.

High frequency controlled ventilation keeps the 7 patient well oxygenated .

IMMUNIZATION 100,000 units antitetanus serum A.T.S. is used to neutralize free toxin but it may cause severe allergic reaction. Even anaphylactic reaction and death of the patient can occur.

Human antitetanus globulin(ATG) is preferable because of less severe hypersensitivity reactions.

These should be given through intravenous route.

WOUND MANAGEMENT The wound responsible for tetanus should be managed actively. Thorough wound debridement should be done. The wound should be preferably left unstitched. In case of retained products of conception, evacuation should be done at an early stage.

The wound dressings should be done regularly. All dead and necrotic tissue should be removed immediately.

ANTIBIOTICS These should be used to prevent the super-imposed infection.

These should be used against gram positive, gram negative and anaerobic organisms. Massive specific antibacterial therapy is given intravenously to prevent and treat the infection9.

FEEDING Nasogastric feeding with proper provision of calories (2000 kcal/day) is essential. Liquid balanced diet should be given daily and if blood urea is raised, 79

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proteins can be with held temporarily.

FLUIDS AND ELECTROLYTES Fluid and electrolytes balance should be properly maintained by strict intake and output records.

Estimation of urea and electrolytes should be performed regularly and abnormalities should be corrected.

Plenty of fluids should be given to keep the effective vascular volume well compensated9.

CARE OF THE BLADDER As the patient is heavily sedated, care of the urinary bladder is essential. An indwelling catheter may be required.

CARE OF THE BOWEL These patients should not be allowed to get constipated. Suppositories and enemas can be used to keep the bowel working normally.

PHYSIOTHERAPY As these patients are heavily sedated, their cough reflex is depressed. The chest infection could become a very serious problems. Regular chest physiotherapy and aspiration of tracheo-bronchial tree should be carried out. Physiotherapy of limbs is given to prevent contractures. Frequent change of posture is done to prevent bed sores.

These intensive efforts can decrease the mortality to less than 20% in established cases of tetanus.

COMPLICATIONS Following common complications are seen in patients of tetanus3,4 ;

SURGERY - PRINCIPLES IN GENERAL

Cardiac arrhythmias.

Blood pressure lability.

Increased hemorrhagic tendencies.

Increased thrombotic complications.

Rectus abdominus hematoma.5 Aspiration pneumonia.

Pulmonary embolism.

Anoxic periods.

Malnutrition.

Pressure sores.

Urinary tract infection.

Respiratory arrest.

Death.

OUTCOME Mortality rate has been brought down from 60% to 20% at good intensive care units. The disease if cured, leaves very little residual damage.

REFERENCES 1. Kefer M.P. Tetanus. American Journal of Emergency Medicine [JC:aa2]. Sep 1992; 10(5):445-8.

2. King WW, Cave DR. Use of esmobol to control autonomic instability of tetanus. American Journal of Medicine. [JC:3ic]. Oct 1991; 91(4): 425-8.

3. Luisto M. Tetanus is final and diagnostic problems and complications. Annals of medicine [JC:and]. Feb 1990; 22(1):15-9.

4. Chao CH. Yu KW Lie CY et al. Tetanus: 20 Yousaf clinical Chung Hua 1 Hsueh Tsa Chil Chinese medical Journal. [JC:cha]. Aug 1991; 46(2):110-5.

5. Suhr G.M Green. AEJr. Rectus abdominus sheath hematoma as a complication of tetanus. Diagnosis by computed tomographic scanning clinical imaging [JC:cin]. March 1989; 13(1):82-6.

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6. Franz Von Lichlenberg M.D. Infection diseases patholic basis of disease, Robbins, Cotreme, Kumar 3rd edition W.B. Saunder's company Philadelphia. 1984; 324-325.

7. Knight AL. Richardson JP. Management of tetanus in the elderly. Journal of American board of family practice [JC:127]. Jan-Feb 1992; 5(1):43-9.

8. Kapoor SK. Reddaiah VP. Lobo J. Control of tetanus neonatorum in a rural area. Indian Journal of paediatrics. [JC:gkt]. May-Jun 1991; 58(3):341-4.

SUMMARY Tetanus Diagnosis Prevention ! Active immunization ! Passive immunization Management Complications Outcome

9. Saissy JM. Rauxo. et al. Severe tetanus and intrathecal baclofen annuls francaises D Anaesthesia et De Reanimation. [JC:42t]. 1990; 9(2):183-4.

10. Egoror VM. Verbukam. Kazakov DP. A case of successful treatment of an 11 years old child with a fulminating form of tetanus. Anestezrolozinia I Reanimatologica. [JC:4st]. Sep-Oct (5):66-7.

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ASEPTIC SURGERY AND STERILIZATION

PS-012

ASEPTIC SURGERY AND STERILIZATION Shuja Tahir, FRCS, FCPS ASEPTIC SURGERY (ASEPSIS DURING SURGERY) The surgical procedures conducted under conditions and environments with total protection from sepsis are termed as Aseptic Surgery.

The surgical procedures are carried out in a way that wounds and other susceptible sites are prevented from contamination by ensuring that only sterile hands, instruments, clothes and material make contact with the wound.

All necessary precautions are taken to avoid bacterial invasion and bacteremia.

are the foci of bacterial growth in patients with inadequate defence mechanism2.

SEPTICAEMIA It is the presence of septic foci and necrosed cells of monocytic phagocytic system (MPS) in the blood stream. It usually follows bacteremia. It has following typical features;

! ! !

Associated severe clinical features of the primary disease.

Large number of micro organisms.

Host resistance against the micro organisms is inadequate or has completely failed1,2.

Air borne transmission of the organisms is prevented or minimized by providing sterile atmosphere during surgery.

SYSTEMIC INFLAMMATORY RESPONSE (SIRS) It is manifested by two or more of the following;

The prevention of the hospital infection is another vital part of the aseptic surgery1,2.

1.

2.

3.

4.

5.

BACTEREMIA Bacteremia is the transient presence of bacteria in the blood stream of patients whose body defence mechanism is adequate. It causes very few clinical feature such as rigors1,2.

SEPSIS Sepsis is a Greek word and it means "putrefaction". It is the presence of septic foci in the body. Septic foci

SURGERY - PRINCIPLES IN GENERAL

Temperature more than 38oC or less then 36oC. Heart rate more than 90/min.

Respiratory rate more than 20/min PACO2 more than 4.3 Kpa White cell count more then 12000/cmm or less then 4000/cmm.

Severe SIRS is SIRS with documented infection having hypoperfusion, hypotension and organ dysfunction.

ANTISEPSIS It is the inhibition of bacterial growth in vitro and in

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vivo when various substances are applied to the surface of living tissue under suitable conditions of 2 contact . In Greek it means "against putrefaction".

ANTISEPTICS These are the substances which inhibit bacterial growth in vitro and in vivo when applied to the surface of living tissue under suitable conditions of contact.

The antibacterial action depends upon;

! ! !

Concentration.

Duration of contact.

Temperature2.

DISINFECTANTS These are the substances which kill the microorganisms in inanimate environments (non living substances). Ideally these are ;

! ! ! ! ! ! !

Able to kill organisms in high dilutions.

Non injurious to tissue.

Inexpensive.

Stable.

Non staining.

Odourless.

Rapidly acting.

STERILIZATION Sterilization include following;

! ! ! ! ! ! !

The patient.

Operation towels and sheets.

Scalpels & Needles.

Suture material.

Surgeon's hands.

Instruments.

Cystoscope.

SURGERY - PRINCIPLES IN GENERAL

!

Endoscopes.

SURGEON'S HANDS Surgeon’s hands can not be sterilized. No living tissue can be sterilized. No matter what is done, one can only reduce the resident flora from surgeon's hands. These can never be completely eliminated.

The hands should be gently scrubbed upto mid forearm for 3-5 minutes with liquid soap or any other liquid antiseptic solution such as pyodine scrub.

Gentle brushing under the nails once at the beginning of the operation list is enough and then 2-3 minutes scrubbing with liquid antiseptics helps to achieve maximum hand sterilization.

A six minute scrub up with soap and water reduces bacterial flora by about 50% only. 2-3 minute scrub up with liquid 0.5% chlorhexidine, hexachlorophene or iodoform causes reduction of flora to 1%.

The use of antiseptic solutions for hand preparation is not better than the use of liquid soaps3,4.

Prolonged washing of hands and injury to the skin during over-enthusiastic brushing of the hands causes more harm than good to the skin sterilization.

The hands should be kept lifted up and dried with sterile towel before putting on the sterile gown and gloves.

The presence of organisms on surgeons hands can be isolated by using non porous sterilized surgical gloves. These are used to perform aseptic surgery and for double protection against any contamination during surgery.

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Damaged gloves should be discarded immediately as these can spread the infection from surgeon to patient or from patient to surgeon.

STERILIZATION OF PATIENT'S BODY SKIN The skin carries an innumerable number of micro organisms normally. These are called normal commensals. The most common micro organism is staphylococcus. The micro organisms are present on the skin surface and in the ducts of the skin glands.

There is no method to sterilize patient's body totally without causing death of the patient. Skin of the patient can be prepared by using antiseptics.

The skin gets cleaned and most of the surface micro organisms can be removed by washing with clean and fresh water mechanically.

Detergents such as solid or liquid soaps when used to wash the skin, get rid of most of the micro organisms from skin surface and distal parts of the ducts of the skin glands temporarily.

It is far more effective to wash and clean the abrasions and superficial wounds with soap and water than topical antiseptics2. Pyodine scrub and Hibi scrub are used to clean the skin with equally good results.

Pre-operative cleaning and washing of the operative site or total body definitely minimizes wound infection4.

The skin can stay sterile only for less than one hour after preparation as the organisms from depths of ducts start coming out to the surface and may cause infection.

SURGERY - PRINCIPLES IN GENERAL

3

The surgical wounds may be protected by use of sterilized adhesive tapes over the area to be used for surgical wound and the surrounding tissue. The adhesive tapes keep the transfer of micro organisms to the surgical wound in check.

Following antiseptic agents can be used preoperatively for skin preparation and minimizing the post operative wound infection.

TINCTURE OF IODINE It is a powerful skin antiseptic solution but is very irritant. It should be applied and allowed to stay dried for ten minutes before surgery is undertaken. Many patients can be allergic or hypersensitive to it, so it should not be used at delicate areas like face, breast, external genitalia and over the skin of babies.

It stains the body tissues deep yellow which ensures complete preparation of the desired area of the skin.

This staining of the skin is undesirable during surgery. It can be removed with the help of methylated spirit or alcohol.

70% ETHANOL It is a good disinfectant. It is less irritant.

It is colorless and area prepared can not be demarcated easily. Chances of improper skin preparation are more. A colour can be added to ensure complete preparation of the desired area.

0.5% CHLORHEXIDINE IN 70%ETHANOL It is a very good disinfectant. It is also less irritant. It is of light color and one can miss certain areas of skin from cleaning as demarcation is not obvious.

POVIDONE IODINE SOLUTION (PYODINE & PLASODINE) It is a refined and better form of iodine solution. The 85

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antiseptic qualities are equally good but it is less irritant and causes lesser number of allergic reactions.

It contains 10% iodine. It is also an effective disinfectant. It stains the body tissues deep yellow which may be undesirable during surgery.

HEXACHLOROPHENE LIQUID SOAP It is also very effective antiseptic solution. It is less irritant than Iodine preparations.

The skin is best prepared by cleaning it with disinfectants (pyodine scrub) half an hour before surgery and then preparing it with pyodine solution before the operation. It should be kept painted for nearly ten minutes before the incision is made to ensure adequate antisepsis.

OPERATION TOWELS (LINEN) AUTOCLAVING Autoclaving is the use of steam under pressure to ensure adequate sterilization.

The autoclave temperature should be maintained at 120 degrees centigrade for half an hour. Twenty pounds (20 lbs) pressure should also be maintained throughout autoclaving. The autoclaving should be checked with the use of marking tapes.

The autoclaving should be redone every day or after suspicion of breakdown of sterilization. The linen should be dry at the end of autoclaving otherwise it should be redone properly.

Autoclaving requires at least two hours for cleaning, packing and autoclaving and it has to be redone every 24 hours.

Operating theatre linen should be preferably SURGERY - PRINCIPLES IN GENERAL

4

autoclaved properly. The drums should not be overfilled with linen and the linen should be loosely packed for definite excess of steam to all parts of the linen. The drums should be kept securely closed all the time.

GAMMA RAYS IRRADIATION It is the use of penetrating irradiation with gamma rays to sterilize various objects.

It can also be used for sterilization of the towels (Linen). The linen is doubly packed in non porous paper material. The sterilization remains effective for the prescribed period unless coverings are damaged.

This is the best method for sterilization. It does not damage the fabrics. It can be done economically but only in bulk which can only be done commercially.

This is the method used at most of the advanced places these days. It requires larger number of linen and instruments sets to be sterilized.

SCALPELS AND NEEDLES These instruments loose their sharpness due to oxidation during autoclaving. Extreme care should be taken to autoclave these.

Gamma irradiation is an excellent method to sterilize them. It doesn't blunt the edges and is available commercially. This is the method of choice these days. The only disadvantage is that it requires larger number of instrument sets to be sterilized for adequate availability.

SUTURE MATERIALS Most of the suture materials are sterilized by Gamma irradiation as it is effective and doesn't damage the 86

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material.

0.5%. Its efficacy only lasts for two weeks.

Catgut can also be sterilized by keeping it in Lugol's iodine solution for one week. Other sutures can be autoclaved as well.

The chemical sterilization is expensive and irritant to the patient's body, so instruments have to be washed very carefully with sterilized water before use.

Pre-sterilized suture materials are commercially available in all sizes and brands and with various size needles.

This method is very satisfactory. It is commonly used these days. The new chemical substances last longer than two weeks and are relatively economical.

INSTRUMENTS Instruments can be autoclaved and it should be done properly.

REFERENCES

Gamma rays irradiation is also very effective method of sterilization as it doesn't damage the instruments and doesn't blunt them.

This is the method of choice these days. The only disadvantage is that a large number of instrument sets have to be kept pre sterilized because it takes longer time to transport and get back the instrument sets from Gamma irradiation plant. The sets of instruments remain sterilized till the packing is not damaged. These can be used in emergency situation without wasting time.

CYSTOSCOPE As these instruments are very delicate and may be damaged during autoclaving, these should be disinfected by pasteurization in water at 75 degrees centigrade for 10-40 minutes. All gram negative organisms are killed but spores survive.

Low temperature steam can also be used for shorter periods.

Chemical disinfectants can also be used. More commonly used substance is glutaraldehyde (cidex) SURGERY - PRINCIPLES IN GENERAL

1. Julio HO. Chberg MD. Gordon F. Antisepsis sabiston.

Text book of surgery murray 14th edition W.B Saunders London. 1991; 210-236.

2. Earnst jawetz. Disinfectants and antiseptics. Basic and clinical pharmacology. Bertrams G Katzung 5th edition. APPELTON and LANGE. Norwalk Connectiant USA. 1992; 690-94.

3. Walter JB. Israel MS. Hospital (Nosocomial) infection.

General pathology 6th edition. Churchill. Livingstone London. 1987; 255-260.

4. Ayeliffe G. A. Role of the environment of operating suite in surgical wound infection. Review of infectious diseases: Sep-Oct 1991; 13 suppl (10):800-4 .

SUMMARY Aseptic surgery Bacteremia Sepsis Septicaemia Systemic inflammatory response (SIRS) Antisepsis Antiseptics Disinfectants Sterilization

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Critical Care

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PRE-OPERATIVE AND INTRA OPERATIVE CARE

PS-013

PRE-OPERATIVE AND INTRA OPERATIVE CARE Shuja Tahir, FRCS, FCPS Nauman Ahmad FRACS Surgical management of the patient is life saving in many conditions. It offers relief of symptoms and cure of disease process on one hand and poses lots of risks on the other hand.

OBJECTIVES OF PRE & INTRA OPERATIVE CARE ! To identify features in patient which may have poor effects of anaesthesia or surgery. ! To treat associated diseases prior to surgery. ! To organize appropriate pre-medication. ! To prevent DVT (Deep Vein Thrombosis). ! To prescribe prophylactic antibiotics if required. ! To plan pre and intra operative management and monitoring strategies.

Most of the surgical procedures require anaesthesia of one type or the other. For safe anaesthesia, preanaesthetic evaluation and preparation is very important.

!

General anaesthesia is a state of reversible loss of consciousness for the duration of surgery.

Local and regional anaesthesia is reversible loss of sensation of the part of body to be operated upon.

Management of anaesthesia begins with the preoperative psychological preparation of the patient and administration of a drug selected to elicit specific pharmacologic responses.

This initial psychological and pharmacological component of anaesthetic management is referred to as preoperative medication.

The aims of a preoperative visit can be summarized as ;

!

The benefit/risk ratio is to be balanced before surgery is under-taken. The patient is assessed very carefully before surgery. Difficult situations are anticipated and corrected before surgery such as;

! ! ! !

Peri operative difficulties.

Operation room facilities and equipment.

Adequate expertise and assistance for required surgical procedure.

Patient safety measures.

SURGERY - PRINCIPLES IN GENERAL

Adequate counseling of the patient.

! !

Assessment of the patient for fitness for anaesthesia, be it general or regional.

To allay anxiety and fear by explanation of the whole process and reassurance of the patient.

To prescribe pre-medicants if necessary.

Pre-operative medication is an aid, not a substitute for sympathy and re-assurance.

Ideally all patients should enter the preoperative period free from apprehension, well sedated but easily arousible and fully cooperative.

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The importance of this visit cannot be over emphasized, not only that the anesthetist may study the patient's physical problems, but also that he may give him psychological support for his forthcoming operation.

Explanation and reassurance are of great importance, followed by specific drug therapy if necessary.

Confidence results not from the indiscriminate use of drugs with unwanted side effects but from the rapport established with hospital staff. It may or may not require to be reinforced by the judicious use of drugs.

Psychological pre-medication is provided by the anaesthetist's preoperative visit and interview with the patient.

Important aspects of preoperative evaluation performed by anaesthetist include history, physical examination, review of current drug therapy.

The important aspect is to inform the patient and his family members about events to expect on the day of surgery.

Planned management of anaesthesia discussed with the patient and informed consent obtained.

The visit is then summarized and recorded in his/her file with details of history taking notes of previous general anaesthetic, reaction to drugs and coexisting diseases if present.

Current drug therapy is noted to avoid any adverse interaction.

SURGERY - PRINCIPLES IN GENERAL

Physical examination is primarily directed towards cardiovascular system, respiratory system, upper airways to recognize difficult intubation.

Laboratory data should be available such as urine analysis, Hb%, serum electrolytes, urea level, chest x-ray, ECG., pulmonary function tests etc.

The balanced or good general anaesthesia should achieve ;

! ! !

Sleep.

Relaxation.

Analgesia.

Combination of drugs are used to achieve this triad with out any adverse or toxic effects of the drugs used for this purpose.

RISKS OF ANAESTHESIA There are many hazards of anaesthesia which should be anticipated and prevented.

Partial or complete airway obstruction is possible after general anaesthesia.

Laryngeal mask or tracheal intubation are required to prevent in airway obstruction.

Unconscious patient loses gag and cough reflexes which prevent aspiration of regurgitated gastric contents. The aspiration of contents by anaesthetized patient may lead to bronchial or alveolar inflammation or severe ARDS. Patients should fast for at least 4-8 hours before proposed surgery to avoid the preventable complications. Many patients are at higher risk of complications due to aspiration of gastric contents 92

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such as;

! ! ! ! ! ! !

necessary elective surgery is deferred till patient's condition is improved.

Pregnancy specially 2 & 3rd trimester.

Hiatus hernia.

Gastric outlet obstruction.

Inadequate fasting (Emergencies).

Small gut obstruction.

Acute abdomen.

Gastric emptying delaying medicine such as opioids.

PREOPERATIVE PHYSICAL STATUS CLASSIFICATION A physical status classification is then assigned according to American Society of Anaesthesiologist (ASA) and a technique of anaesthesia chosen.

Preoperative physical status classification of patients.

Pharmacological premedication is typically administered in patient's hospital room one to two hours before the anticipated induction of anaesthesia.

The goals for pharmacological premedication are multiple and must be individualized to meet each patient's unique requirements.

The ideal premedicant should;

! ! ! !

Class

Definition

1

A normal healthy patient

2

A patient with mild systemic disease and non functional limitations A patient with moderate to severe systemic disease that results in some functional limitation A patient with severe systemic disease that is a constant threat to life and functionally incapacitating A moribund patient who is not expected to survive 24 hours with or without surgery A brain dead patient whose organs are being harvested If the procedure is an emergency the physical status is followed by "E" (for example 2E)

3 4 5 6 E

In case of the patient not being in optimal medical condition prior to elective surgery, it should be discussed with the patient's primary physician and if SURGERY - PRINCIPLES IN GENERAL

Allay fear and anxiety, without producing side effects.

Cause minimal depression of the respiratory and circulatory systems.

Be simple and pleasant to take and should act over a reasonably long period of time.

Be safe and effective in all patients.

Such a drug or combination of drugs, has yet to be discovered, but regimens have been involved which are valuable in a wide variety of patients and circumstances.

Premedication may be used to modify anaesthesia in various ways.

A great deal is now known about the drugs commonly used in premedication but often this knowledge is not applied in helping the tense and anxious patients who are awaiting surgery with the result that patient's psychological needs receive much less attention than their physical ones.

Premedication has become a ritual, taking little in account of individual's needs. The main purpose of premedication can be summarized; 93

PRE-OPERATIVE AND INTRA OPERATIVE CARE

! ! ! ! ! !

To reduce fear and anxiety and enable the patient to face his operation with calmness and confidence.

To achieve anti-sialagogue effect.

To eliminate side effects of anaesthetic agents.

To achieve facilitation of induction of anaesthesia.

To reduce unwanted reflex activity.

To produce amnesia and ensure a smooth recovery.

However, many of these aims are better achievable by incorporating drugs into the anaesthetic technique itself, rather than by using them as premedicants.

DRUGS USED FOR ALLAYING ANXIETY The predominant aim is the relief of anxiety.

Anxiety is a complex subjective response which is influenced by various factors such as a person's temperament, his home, his attitude to illness and his cultural and religious background.

Most important it is effected by his understanding or lack of understanding of his condition and its treatment.

Many drugs are effective in relieving anxiety, but have side effects which are some times worse than the symptoms they purpose to remove.

Many popular premedicants cause dizziness, nausea or disorientation, while the discomfort of a dry mouth is a common complaint.

The regimen chosen should be a compromise between the effectiveness of the drug and its liability to produce undesirable side effects.

SURGERY - PRINCIPLES IN GENERAL

4

OPIATES These are usually combined with vagolytic drugs.

These have been popular since 19th century. These have the disadvantage of causing respiratory depression and reducing the response to a rise in arterial CO2 tension, whilst these also cause some loss of circulatory reflexes, resulting in postural hypotension if the patient is placed in a head up position.

These also cause nausea, vomiting. Inspite of these disadvantages, in clinical practice the morphine or papaveretum with hyoscine are amongst the most effective drugs for allaying anxiety with a low incidence of side effects.

BARBITURATES These are generally central nervous system depressants producing marked calmness. The margin between sedation and uncontrolled excitement with the use of these drugs is narrow.

These have been largely replaced by the neuroleptic and anxiolytic drugs which have more specific actions on the brain.

PHENOTHIAZINE DERIVATIVES These have good sedative and antiemetic properties. Combining these with opiates enhance the good effects of the latter and diminishes their emetic effects but this is obtained only with an increased incidence of the more serious side effects of phenothiazine themselves and recovery from the anesthesia is usually delayed.

BUTYROPHENONES Haloperidol and deoperidol have been used in neuroleptic analgesia in combination with fentanyl and phenoperidine as these are largely devoid of 94

PRE-OPERATIVE AND INTRA OPERATIVE CARE

cardio-vascular depression. The use as premedicants is however short lived due to their unpleasant psychotic effects and extra-pyramidal dystonic effects.

BENZODIAZEPINES These have anti-convulsant and central muscle relaxant effect and are selective in depressing emotional responses.

These have little respiratory depressant effect.

These do not delay recovery and there after followed by a period of amnesia, thus making a valuable contribution to postoperative comfort.

The evidence suggests that the benzodiazepines are closer to the ideal for allaying apprehension without producing side effects than most other drugs available.

ANTICHOLINERGIC DRUGS Routine inclusion of these drugs is not necessary.

The common reasons for administering these are;

5

Glycopyrrolate is most logical drug to select if antisialagogue response without CNS effects is desired.

H2 ANTAGONISTS These are used for increasing gastric fluid pH prior to induction. These are important in obstetrics patients and the patient's with full stomach.

TIMING, ROUTE OF ADMINISTRATION AND DOSAGE Best management seems to be by giving the patient mild tranquilizers from time of hospital admission or even before this at home.

Insomnia is most distressing and many people welcome a night's sleep while in hospital.

For premedication prior to going to operation theater, it is essential to prescribe the timing as well as the dosage as no drug is effective if given too late because of the unpredictable nature of surgical lists.

Drugs with long duration of action are most suitable.

For anti-sialagogue effect.

Production of sedation and amnesic effect e.g. scopolamine.

Prevention of reflex bradycardia.

Oral medication is preferred by most patients. Its main contraindications are before operations on upper gastrointestinal and before emergency operation when absorption is delayed.

Undesirable side effect of anticholinergic drugs are multiple and must be considered while using these drugs for premedication ;

I/M injections are usually prescribed 1-1½ hours preoperatively so that their maximum effect is seen in anaesthesia room whilst those given orally are given 1-2 hours before. All drugs should be prescribed according to the individual patient's needs.

! ! !

! ! ! ! !

CNS toxicity, Tachycardia, relaxation of lower esophageal sphincter.

Raised body temperature.

Increased physiological dead space.

Mydriasis and cycloplegia.

SURGERY - PRINCIPLES IN GENERAL

SPECIAL CIRCUMSTANCES WHICH MAY AFFECT CHOICE AND DOSAGE AGE Elderly patients are given low dosage of anaesthetic 95

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agents.

those with recent head injury.

Children have unpredictable requirements of anaesthetic agents.

Atropine is used to block bradycardia associated with traction of extra-ocular muscles in ophthalmological cases.

PHYSICAL STATUS Shocked patients require drugs which improve the tissue perfusion.

Dehydrated patients require intravenous fluids and electrolytes to improve the effective volume.

Acid-base disturbances are corrected by improving shock.

Respiratory depression may require assisted respiration.

CCF is treated conventionally.

Surgery is required as indicated.

Febrile patients require anti pyretics.

Atropine should be avoided in febrile patients.

Cardiovascular depression may occur during anaesthesia due to reduction in cardiac output or vasodilatation. Mild to moderate hypotension is compensated physiologically. Anaesthesia related hypotension has less favourable output in following condition;

DRUG INTERACTION It should be considered in patients on multi-drug therapy. Cardiac, antihypertensive, respiratory, anticonvulsant, anti-diabetic and steroid medication will need to be continued as part of pre-operative preparation.

! ! ! ! ! !

OBSTETRIC PATIENTS AND OTHER EMERGENCIES Obstetric patients and those with full stomach are at risk and neutralization of gastric acidity by an antacid should therefore be a routine part of premedication in such patients.

FLUID BALANCE DERANGEMENTS Many patients are brought to operating theatre after starvation, vomiting and blood loss. These losses may not be well compensated. These should be rectified adequately to avoid complications. Following steps are taken to improve the situation;

Sedatives are avoided in obstetrics because of the danger of causing respiratory depression in neonate.

Depressants are highly dangerous in patients with impaired consciousness and therefore premedication is omitted in neuro-surgical patients and SURGERY - PRINCIPLES IN GENERAL

Respiratory depression is a possible problem of general anaesthesia. The anaesthetist should monitor the patient very carefully. Pulse oximeter and capnograph should be used for adequate monitoring.

! ! !

Hypovoleamia.

Cardiogenic shock.

Coronary artery disease.

Aortic stenosis.

Carotid artery stenosis.

Cerebro vascular disease.

Rehydration.

Maintenance of fluid balance.

Replacement of all losses.

TEMPERATURE CONTROL Anaesthetized patient tend to lose core periphery 96

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temperature gradient. It leads in redistribution of body heat. Cold blood and fluids infusions may further deteriorate the temperature control. In cold weather it can be corrected by;

! ! ! ! !

Theatre temperature should be 22oC. Patient should be covered.

Anaesthesia gas may be warmed.

Intravenous fluids are warmed.

Monitoring through rectal probe is satisfactory.

Acute respiratory tract infection is a definite contraindication to general anaesthesia for elective surgery. But it may be used in clinical emergency situations with caution.

Chronic obstructive airway disease should be diagnosed and assessed by;

! ! ! ! !

Exercise tolerance.

Dyspnoea on flat lying.

Medication for chest problem.

ICU or hospital admission for chest problems.

Right heart failure, cyanosis of oxygen therapy.

Asthma should be diagnosed and controlled before anaesthesia.

Lung function tests and pulse oximetry is performed.

hepatotoxicity should be avoided.

Obesity and malnutrition both conditions are not very helpful for anaesthesia and surgery. These may be treated before anaesthesia if possible.

REFERENCES 1. Beecher HK. Preanaesthetic medication J. Am. med.

Ass. 157, 242-243.

2. Carpenter FA. Thompson R. Evaluation of Preanaesthetic medication Anesthesiology. 1962; (23): 141-142.

3. Cohen EN. Beecher. Narcotics in Preanaesthetic medication a controlled study, J. Am med. Ass. 1951; (147): 1664-1668.

4. Dundee JW. Moore J. Study of drug given before anaesthesia I. A method of drop assessment. Br. J. Anesth. (34): 485-463.

5. Egbert LD. Battit. The value of the preop. visit by an anaesthetist J. Am. med. Ass. (185): 553-555.

SUMMARY Pre and intra operative care Risk of anaesthesia Preoperative physical status (ASA classification)

Diabetes mellitus is controlled and fresh blood glucose levels must be obtained just before anaesthesia.

Thyroid disease, rheumatoid arthritis should be treated and controlled before anesthesia.

Renal and hepatic problems are diagnosed, assessed and all drugs having nephro or SURGERY - PRINCIPLES IN GENERAL

97

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HAEMORRHAGE

PS-014a

HAEMORRHAGE Shuja Tahir, FRCS, FCPS Haemorrhage (bleeding) is loss of blood from the circulatory system in a living person.

Haemorrhage can be described according to the etiology as ;

It could be classified depending upon the site of loss as;

(a) Primary haemorrhage (b) Reactionary haemorrhage (c) Secondary haemorrhage

(a) Arterial (b) Venous (c) Capillary ARTERIAL HAEMORRHAGE It is the blood loss from arteries. This is bright red in color. It spurts under pressure and blood loss rises and falls with the pulse. It is pulsatile in nature. It can be easily diagnosed on clinical inspection.

VENOUS HAEMORRHAGE It is the blood loss from veins. This is darker in color due to less oxygen content in it. The color becomes even darker in severe loss due to low oxygenation and stagnation. The loss may be greater in venous haemorrhage because 60-70% of total blood is present in venous system. The blood just pools out and it is not pulsatile. It requires a skillful surgeon to arrest it when it is from a larger vein.

CAPILLARY HAEMORRHAGE It is loss of blood from the capillaries. This is bright red in color and is seen as rapid ooze. It may become serious if it continues over prolonged periods as in haemophilia.

SURGERY - PRINCIPLES IN GENERAL

PRIMARY HAEMORRHAGE This is the type of blood loss which occurs at the time of injury or operation.

REACTIONARY HAEMORRHAGE This is the type of blood loss which occurs usually within 4-6 hours after injury or operation or may be within first twenty four hours.

This occurs due to slipping of the ligature or dislodgement of the clot which may be due to rise in blood pressure during recovery from shock or due to sudden rise in venous pressure due to coughing, sneezing, restlessness and vomiting. This is common after penetrating wounds (Butcher's thigh) or few hours post operatively.

SECONDARY HAEMORRHAGE This type of blood loss occurs usually 1-2 weeks after the injury or operation. It is due to infection and sloughing of the vessels. These may be predisposed by a piece of fractured bone, malignant lesion, a ligature or any foreign body in an infected area or pressure of drainage tube.

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It may occur after vascular surgery and amputation of the limb. It usually presents with small bleed in the beginning (warning haemorrhage) followed by severe and sudden haemorrhage which, if not treated adequately, may lead to death of the patient.

The haematemesis and bleeding in advanced malignancy due to erosion of the vessels are typical examples of this type of haemorrhage.

Haemorrhage can be classified depending upon its mode of presentation such as ; I. External or Revealed Haemorrhage II. Internal or Concealed Haemorrhage

REVEALED HAEMORRHAGE External Haemorrhage This is when the blood loss is visible as seen during operations or after open injuries. It is diagnosed clinically and easily. It is the loss of blood from superficial wounds such as ;

Surgical wounds.

Accidental wounds.

Homicidal wounds.

Suicidal wounds.

The blood loss could be from deeper structures such as ; Haematemesis.

Haemoptysis.

Epistaxis.

Haematuria.

Bleeding from rectum.

Melena.

SURGERY - PRINCIPLES IN GENERAL

CONCEALED HAEMORRHAGE INTERNAL HAEMORRHAGE It is the blood loss which is not visible and is only diagnosed by indirect assessment through clinical features of blood loss. This is when the blood loss is concealed in the body cavities.

Various investigations are also required to diagnose it.

It may be cerebral haemorrhage, subarachnoid haemorrhage, haemothrorax, haemopericardium or haemoperitoneum due to ruptured intra peritoneal organs such as liver, spleen or ruptured ectopic pregnancy and ruptured aortic aneurysm.

This concealed haemorrhage may become, revealed haemorrhage sometimes as haematemesis, melaena, haematuria or vaginal bleeding.

The haemorrhage can be classified according to the speed of blood loss as ; 1. Acute haemorrhage.

2. Chronic haemorrhage.

ACUTE HAEMORRHAGE This is sudden loss of blood due to any reason. It causes most dramatic effects on the patients and other people concerned.

Sudden loss of 30% blood volume may lead to death.

In nervous and sensitive patients even minor loss of blood may cause vaso-vagal attack due to fear and fright (even attendants may have vasovagal syncopal attack just by watching).

CHRONIC HAEMORRHAGE This is when blood is lost slowly in small amounts and over a longer period. This does not cause dramatic

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changes but shows all the ill effects of chronic blood loss1,2,3.

This is seen in patients with peptic ulcer, internal haemorrhoids, haematuria and malignancies. These patients are severely anaemic and have haemodilution with normal blood volume. These patients are haemodynamically compromised and any injury or surgery leading to even minor blood loss may lead to fatal results.

The haemorrhage can be described according to amount of loss ; I. Severe haemorrhage.

II. Moderate haemorrhage.

III. Mild haemorrhage.

This classification is based on the amount of blood loss. No clear demarcation is possible with the amount of haemorrhage.

SEVERE HAEMORRHAGE It is the sudden loss of blood more than 30% of the total blood volume. Unless immediate measures to stop the haemorrhage and replacement of lost blood are taken, the consequences may be fatal.

MODERATE HAEMORRHAGE It is the sudden loss of blood more than 20% of the total blood volume. Active management of such problem is required to avoid further deterioration of the patient. Early control of haemorrhage and replacement of blood loss should be performed.

MILD HAEMORRHAGE It is the sudden loss of blood of less than 10% of the total blood volume. The body compensatory

SURGERY - PRINCIPLES IN GENERAL

mechanisms keep the patient well-compensated haemodynamically. Active management accelerates 1,2,3 the recovery .

The most important factor is correct assessment of the amount of lost blood and its accurate replacement. Different method of measurement of blood loss are used such as : DIRECT MEASUREMENT OF LOST BLOOD MEASUREMENT OF CLOTS Clenched fist size clot is approximately 500 mls of blood.

SWAB WEIGHING Swabs soaked with blood are weighed. The difference of weight between soaked and dry swab is the amount of blood loss.

INDIRECT METHODS TO ASSESS THE BLOOD LOSS Repeated haemoglobin estimations.

Repeated observation of such patient.

Record keeping and repeated observation of the blood pressure, respiratory and pulse rate give good indication of concealed haemorrhage.

Swelling of the limbs due to fractures Closed fracture of tibia in adults equals 500-1500 mls loss of blood.

Shaft of femur fracture equals 500-2000 mls loss.

The closed fracture of pelvis equals loss about 2-3 liters in severe cases.

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Haematocrit (PCV) estimations .

Measurement of the central venous pressure (CVP) gives good indication of venous return (normal 5-15 cm of saline).

Pulmonary wedge pressure measurement is a better indication of cardiac output.

PATHYOPHYSIOLOGY EFFECTS OF BLOOD LOSS The effects of haemorrhage depend upon;

THE AMOUNT OF BLOOD LOSS Severe blood loss.

Moderate blood loss.

Mild blood loss.

SPEED OF BLOOD LOSS Acute.

Chronic.

The general post-haemorrhagic effects are slight when less then 20% blood volume is lost in adults as the compensation to maintain blood volume is adequate.

Death occurs after sudden loss of 33% blood volume. This is because the speed of blood loss is more. The compensatory mechanisms can not keep up pace with the losses.

A loss of 50% blood volume over a period of twenty four hours may not be fatal as the compensatory mechanisms to maintain blood volume are reasonably effective. However in such a huge loss, the effects of blood loss are always serious1.

NEUROGENIC SHOCK Loss of conscious level may be experienced even SURGERY - PRINCIPLES IN GENERAL

4

after smaller loss of blood when patient gets suddenly frightened at the sight of bleeding.

This is called neurogenic shock and it is due to emotional upsets1,2.

HAEMODYNAMIC STATE OF PATIENT The patients who are anaemic or who have been loosing blood over a prolonged period, have subnormal haemodynamic status. Their compensatory reserves are almost depleted.

These patients may show very poor response even after minor loss of blood. These patients experience early haemodynamic failure.

AGE OF THE PATIENT Small children or infants cannot withstand even smaller losses of blood as their absolute blood volume is smaller and post-haemorrhage consequences are serious.

FIRST FEW HOURS AFTER HAEMORRHAGE FAINTING ATTACK (Primary shock or immediate syncope) The patho-physiological changes are mainly due to nervous mechanism during the early period after bleeding.

The patient may have immediate fainting attack followed by redistribution of the remaining blood volume.

The fainting attack (immediate syncope) or primary shock is vaso-vagal attack and is seen only in human beings. It commences with yawning, sighing respiration, nausea and vomiting which is followed by loss of consciousness.

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The attack is associated with lowering of the blood pressure, slowing of the pulse and coldness of the extremities. This attack rarely lasts longer than a few minutes. The fainting attack after loss of blood is a compensatory mechanism.

As soon as an unconscious person falls horizontally or is laid down, the diversion of blood to brain is enhanced due to gravity. The cerebral circulation improves and the patient regains consciousness.

CIRCULATORY CHANGES The cardiac output remains normal in the beginning.

Later on the muscular vessels dilate and the pooling of blood occurs. The blood pressure lowers down and cerebral blood flow is diminished suddenly which leads to loss of consciousness.

5

There is increase in the activity of the vasomotor center which results in the increased peripheral resistance leading to rise in blood pressure.

The peripheral resistance does not affect the cerebral vessels but causes dilatation of coronary vessels. There is increase in heart rate which is due to drop in the vagal activity due to reduction in inhibitory impulses from the cardiac center in response to reduction of the stimulatory impulses from the aortic and carotid sinuses.

The amount of blood shifted to the vessels due to contraction of spleen is non significant in human beings1,2,3.

VENOUS CONSTRICTION AND ITS EFFECTS 60-70% of blood is in the veins in human beings. The constriction of these vessels is very important to increase the venous return.

The emotional stress leads to muscular vessel dilatation. Same changes are seen after smaller blood loss in sensitive and nervous individuals due to larger part played by psychological factors such as fear and anxiety. Pain also plays a larger role in such changes.

This leads to reduction in the size of venous reservoir and improvement of effective intravascular volume.

Circulatory system can recover as long as the degree of haemorrhage is less than the critical level. Blood loss of even few milliliters more than this critical level is fatal due to progressive shock like condition.

In fact after 10% loss of blood volume, the compensation can be achieved by venous constriction without bringing any changes in the blood pressure and cardiac output.

BARO-RECEPTORS AND VASOMOTOR CENTRE If significant amount of the venous return to heart is diminished due to haemorrhage, the right atrial pressure falls.

Blood loss more than 10% causes decrease in cardiac output and lowering of the blood pressure.

The cardiac output falls and blood pressure tends to lower down. These changes lead to reduction of tonic inhibitory impulses arising from the aortic and carotid sinuses.

SURGERY - PRINCIPLES IN GENERAL

Both blood pressure and cardiac output become zero after a sudden loss of 35-45% loss of blood volume.

If sympathetic system is absent or cut off, these changes are experienced after only 15% loss of 103

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blood volume as the natural compensatory mechanisms are not in use.

ARTERIOLAR CONSTRICTION AND ITS EFFECTS The arteriolar constriction is selective and helps in redistribution of the remaining blood volume. The constriction of the arterioles of the skin, salivary glands, intestinal tract and kidneys helps to improve the blood distribution to the brain, heart, diaphragm and intercostal muscles.

These changes are observed by cold, clammy and pale skin. There is dryness of mouth, feeling of thirst and impaired digestion.

This selective arteriolar constriction is due to autonomic stimulation and due to increased secretion of the catecholamines from adrenal medulla and also from increased renin production from the kidneys due to decrease in the blood flow and hypoxia1.

BLOOD PRESSURE CHANGES AND ITS EFFECTS The blood pressure may remain unchanged even after 30% slow loss of blood due to all the above mentioned compensatory mechanisms.

Thus the measurement of blood pressure is not a very specific method for assessment of amount of blood loss. When these mechanisms fail, the blood pressure falls and haemorrhagic shock results.

After blood loss when blood pressure falls below 50 mm of Hg, cerebral hypoxia results. It leads to extreme stimulation of sympathetic nervous system.

REGIONAL BLOOD FLOW CHANGES AND ITS EFFECTS The cerebral and coronary circulation is maintained by various compensatory mechanisms until the fall in SURGERY - PRINCIPLES IN GENERAL

blood pressure is below 70 mm of Hg. The pulmonary blood flow is reduced with the reduction in cardiac output. This causes increase in physiological dead space. This leads to increase in the respiratory rate (hyperpnoea).

The major factor causing air hunger is metabolic acidosis. When there is decrease in the cerebral blood flow, the PO2 of brain tissue (Oxygen pressure) falls and leads to rise in PCO2 (Carbon dioxide pressure). These cause cerebral vascular dilatation and increase in cerebral blood flow.

If the cerebral blood flow remains depressed below the critical level for sometime, the neuronal damage occurs due to hypoxia.

The coronary blood flow is related to the systemic blood pressure and duration of the ventricular diastole. Increased heart rate and decreased blood pressure may cause myocardial infarction.

The renal blood flow is depressed in acute blood loss.

This may lead to oliguria and even anuria.

Prolonged hypoxia may lead to acute tubular necrosis and renal failure. Oliguria is also caused by increased production of anti-diuretic hormone in such patients.

HAEMATOLOGICAL CHANGES The haemoglobin percentage and cell count per 100 mls of blood is unchanged soon after the haemorrhage. In fact there could be some degree of haemoconcentration immediately after blood loss asplasma is lost more than the cells.

The haemoglobin estimation can not be trusted 104

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blindly for estimation of the amount of blood loss during this early period.

These investigations are performed as a baseline data to compare with the future changes and observations.

The platelets rise after haemorrhage rapidly. Clotting time is decreased within few minutes after haemorrhage and fibrinolytic system is activated.

Aggregation of red cells (sludging) occurs within few hours of injury and it reduces the microcirculation.

These changes last for 2-3 days.

normochromic.

The active red cell production starts within a week and is almost complete by six weeks regardless of the severity of the initial haemorrhage.

This process can be accelerated by control of bleeding and blood transfusion to cover the lost amount.

There is rise in the sedimentation rate which falls to normal levels soon. White cell count rises within 2-5 hours.

The fluid is withdrawn from the tissue into the circulation soon after the haemorrhage and vascular volume is brought to normal as soon as possible.

FEW HOURS TO FEW DAYS AFTER HAEMORRHAGE The lost plasma proteins are replaced within 2-3 days. As soon as the blood volume is normalized, vasospasm disappears and capillary pressure is restored.

The compensatory changes lead to haemodilution which is complete by about two days after the haemorrhage. The haemoglobin and haematocrit estimation is valuable at this stage. Its comparison with initial haemoglobin level gives good indication of amount of the blood loss.

White cell count returns to normal within 2-3 days.

FOUR TO SEVEN DAYS AFTER HAEMORRHAGE During this period the anaemia is normocytic SURGERY - PRINCIPLES IN GENERAL

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8

REFERENCES 1. Arthur C. Guyton. Circulatory shock and physiology of its treatment. Text Book of medical physiology, 8th edition W. B Saunders company London. 1991; 263271.

2

Walter JB. Israel MS. The general reaction to trauma: Haemorrhage and shock. General pathology 6th edition Churchill Livingstone London. 1987; 441454.

3

Cotran. Kumar. Robbins. Pathologic basis of disease 5th edition. W.B Saunders Company London. 1994; 98-99.

4. Ganz R. Krushell RJ. Jakob RP. Kuffer J. The Antishock pelvic clamp. Clinical orthopaedics and related research. [JC:dfy]. 1991; (2670): 71-8.

6. Kram HB. Shoemaker WC. Clark SR et al. Spraying of aerosolized fibirin glue in the treatment of non suturable haemorrhage. American surgeon.

[JC:43e]. June 1991; 57(6) : 381-4.

5. Voyels CR. Vogel SB. Hepatic resection using stapling devices to control the hepatic veins. American journal of surgery. [JC:3z4]. Nov 1989; 158(5): 459-60.

7. Kram HB. Nathan RC. Stafford FJ. Fleming AW. Shoemake WC. Fibirin glue achieves haemostasis in patients with coagulation disorders. Archives of surgery. [JC:8ia]. March 1989; 124(3):385-7.

8. Lau WY. Arnold N. Guo SK. Li AK. Microwave tissue coagulator in liver resection for cirrhotic patients.

Australian and New Zealand journal of surgery.

[JC:9ic]. July 1992; 62(7):567-81.

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HAEMORRHAGE Haemorrhage (Site) Arterial Venous Capillary

! ! !

Haemorrhage (Etiology) Primary Reactionary Secondary

! ! !

Haemorrhage (Presentation) Revealed (external) Conceal (internal)

! !

Haemorrhage (Speed) Acute Chronic

! !

Haemorrhage (Amount) Severe Moderate Mild

! ! !

Measurement of blood loss Effects of haemorrhage

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BLOOD TRANSFUSION

TMA - 03d

BLOOD TRANSFUSION; INDICATIONS & COMPLICATIONS Shuja Tahir, FRCS, FCPS

Blood transfusion is the transfusion of blood intravenously.

donation6.

The blood transfusion could be ;

It could be transfusion of ; ! !

Whole blood.

Blood component transfusion.

Whole blood transfusion is transfusion of the complete blood without separating its components. It may be transfused after storage or immediately after donation (fresh blood transfusion).

BLOOD COMPONENT TRANSFUSION It is the transfusion of blood component for specific deficiency without overloading the patient’s vascular system to prevent unwanted reactions.

It is done to improve oxygen delivery, preserve intravascular volume, decrease the risk of infection, correct coagulopathies, reduce fatigue and improve growth and homeostasis. It should be done after assessment of risk/benefit ratio of transfusion for patient’s disease.

The blood components which can be prepared are; ! ! !

RBCs. Plasma.

Platelets.

The separation of components is done soon after

SURGERY - PRINCIPLES IN GENERAL

1. Autologous blood transfusion 2. Homologous blood transfusion 3. Heterologous blood transfusion AUTOLOGOUS BLOOD TRANSFUSION It is the transfusion of one's own blood intravenously.

It involves collection of one's own blood, its storage for some period ( commonly less than two weeks) and its transfusion during or after elective surgery.

Autologous blood transfusion has reduced the need for homologous blood transfusion by more than 80%.

This is the best and most safe method of blood transfusion but it requires satisfactory planning and correct understanding of the whole procedure by the patient and blood transfusion service officials.

It has its own limitations as well ; It is not available during emergencies.

It is available in only limited quantities even for elective surgery. Two to three pints of blood can be collected and stored a week or so before the elective

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surgery.

It is not so often used because of these limitations.

Under utilization of autologous blood transfusion is widespread.

Pre-operative autologous blood donations have following mild to moderate side effects1 ; ! ! ! !

! ! !

Decrease in cardio-circulatory volume due to donation of several units within few weeks.

Decreased oxygen transport capacity.

Fibrinogen degradation products may be immuno-suppressive.

Some patients show insufficient erythropoietic recovery after a pre-deposit autologous transfusion2.

Bacterial contamination due to storage.

Fat droplets increase the risk of fat embolism.

Activation of coagulation and fibrinolysis3.

HOMOLOGOUS BLOOD TRANSFUSION It is the transfusion of the blood intravenously which has been collected from the same species i.e. the transfusion of human blood to human beings.

It is available in almost unlimited quantities.

Satisfactory grouping and cross matching can be conducted and unwanted reactions can be avoided.

It is reasonably safe but not as safe as autologous blood transfusion and minor reactions may be encountered even after meticulous testing.

This is the most commonly used method of blood transfusion used in human beings.

HETEROLOGOUS BLOOD TRANSFUSION It is the transfusion of blood donated by other

SURGERY - PRINCIPLES IN GENERAL

2

animals and species. It is not used at all as it is unsafe and immediate rejection is most common.

INDICATIONS OF BLOOD TRANSFUSION Blood transfusion always carries some risk despite rigorous screening tests. Its indications should always be assessed independently for every patient.

Whenever the balance is in favour of transfusion, it should be given.

Common indications of blood transfusion are as follows : SUDDEN REDUCTION OF BLOOD VOLUME Reduction in blood volume occurs when any amount of blood is lost but significant reduction in blood volume occurs due to sudden loss of 10% or more of blood volume.

If the body compensatory mechanisms are adequate and blood losses are small, blood transfusion may not be always required for early and uneventful recovery.

This may occur in certain diseases leading to sudden blood loss such as bleeding from peptic ulcer, oesophageal varices and ruptured aortic aneurysm.

Sudden blood loss can occur in accidents, during major operations and in post partum or postoperative periods. Whole blood transfusion is indicated and ideally the lost amount should be replaced.

INADEQUATE CONCENTRATION OF CIRCULATING HAEMOGLOBIN Severe anaemia cannot be improved immediately by 110

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specific therapy. (Vitamin B12 or iron or bone marrow transplant).

Definitive treatment of anaemias must be given to the patient as blood transfusion is not the definitive treatment for anaemias.

Effective oxygen carrying capacity can be improved within a short period with suitable blood transfusion.

Such patients require blood transfusion during or after the surgery and parturition.

Severe anaemias require packed red cell transfusion as an emergency measure. (whole blood is not given to avoid the circulatory overload).

Blood transfusions are also useful and required in patients suffering from leukemia and chronic renal failure, besides the specific treatment of the condition.

SEVERE BURNS There is extensive loss of plasma and severe damage to the red cells in patients with severe burns.

These losses should be replaced. Whole blood transfusion is indicated in these patients. Fluid and electrolyte replacement is also required according to the losses.

BLOOD COMPONENT THERAPY In certain conditions, whole blood is not required but some component of the blood is required such as ; Platelet transfusions are useful in patient with thrombocytopenia. Failure of platelet production is the main pathology in these patients so these are to be replaced.

Granulocyte transfusions are useful in the patients SURGERY - PRINCIPLES IN GENERAL

who are neutropenic and are prone to frequent attacks of bacterial infections. It is seen in patients who are on cytotoxic drugs.

Fresh frozen plasma is useful for the treatment of Christmas disease due to factor IX deficiency.

Cryoprecipitated antihaemophilic factor is helpful in the treatment of haemophilia, due to factor VIII deficiency.

Albumen is useful in patients with severe burns, acute pancreatitis, cirrhosis of liver with ascites, bacteraemic shock and hypoalbumenemia.

Fibrinogen is useful in the treatment of congenital hypofibrinogenaemia. Gamma globulins are helpful in prophylaxis of some viral disease and treatment of hypo-gamma-globulinaemia.

Rh (D) immunoglobulin is used in the prevention of Rh sensitization of Rh negative women after the delivery of Rh positive baby or after miscarriage of foetus of unknown Rh group. (Dose 200-300 m gm of anti D intramuscularly) within 24-48 hrs of delivery or abortion.

COMPLICATIONS The common complications are ; 1. Immediate.

2. Delayed.

IMMEDIATE SIMPLE FEBRILE REACTION Febrile reactions occur during or shortly after the blood transfusion. These are due to; i. White cell antibodies. ii. Presence of gram-negative endotoxins.

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Proper use of aseptic technique for blood transfusion at collection, storage and donation will minimize this complication.

Anti-pyretic drugs (oral or parenteral) usually relieve the febrile episode.

Cold sponging may be required in case the pyrexia does not settle.

ALLERGIC REACTIONS Urticarial reactions are usually due to sensitizing antibodies. These reactions are more common in patients who suffer from atopic diseases such as asthma and hay fever. Oral or parenteral antihistaminic drugs usually relieve the symptoms.

Occasionally severe anaphylaxis can occur and may prove fatal.

One should be very careful in transfusing the patients with history of different allergic reactions.

The blood should always be transfused in a hospital equipped with facilities to treat severe anaphylactic reaction. A doctor should monitor the transfusion.

In the beginning, the transfusion should be started at a slower rate, if patient's condition remains satisfactory, the speed of transfusion can be increased.

HAEMOLYTIC TRANSFUSION REACTIONS Following reactions are seen due to mismatched blood leading to intravascular haemolysis ; Rigors.

Nasal bleeding.

Hypotension.

SURGERY - PRINCIPLES IN GENERAL

Hypoglycemia.

Bronchospasm.

Urticaria.

Anaemia.

Vasovagal reactions4.

These are usually due to rapid destruction of the donated cells due to antibodies in recipient's plasma.

It is commonly due to A, B and O group incompatibility.

This usually happens due to errors in identification of the blood and the recipient.

Soon after the transfusion, the patient complains of sensation of heat and pain along the transfused vein followed by facial flushing, rigors, tachycardia, fever and severe pain in loins and feeling of constriction in the chest.

After incompatible blood transfusion there is leukopenia, thrombocytopenia and raised bilirubin level in the blood.

The red cell breakdown leads to release of the clotting factors into the circulation and disseminated intravascular coagulation and generalized bleeding tendencies.

Oliguria and acute renal failure may occur. Jaundice appears late (in case the patient survives).

In severe cases there is significant intra-vascular haemolysis of red cells. It is associated with haemoglobinaemia, haemoglobinuria, lowering of the haptoglobin level and appearance of methaemalbumin in the plasma.

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Hypotension, shock and even death may occur.

The major incompatible blood transfusion can be very difficult to diagnose in an anaesthetized patient.

Bleeding tendencies, hypotension and hypoxia without any other reason may be due to major ABO incompatibility.

The blood transfusion should be immediately disconnected and patient should be resuscitated.

Intra-muscular injections should be avoided to prevent haematomas5.

Diagnosis of the mismatched blood can be confirmed by re-testing the blood. Plasma remains pink on centrifugation.

5

disease, should be transfused very carefully to avoid volume overload, congestive heart failure and arrhythmias.

These patients should be continuously monitored during transfusion.

If the signs of circulatory overload are seen, transfusion should be stopped and forced diuresis should be carried out to counter the circulatory overload.

The cardiac toxicity of blood transfusion is also experienced following transfusion. It should be carefully monitored and treated in time.

Prevention of such incompatible reaction is of paramount importance.

The anaemic patient have satisfactory effective intravascular fluid volume and transfusion raises the intravascular fluid volume over a shorter period which may lead to cardiac pump failure.

If such reaction occurs, transfusion should be stopped immediately and patient should be treated symptomatically.

Congestive cardiac failure may be precipitated and pulmonary edema may occur in patients after blood transfusion due to circulatory overload.

The treatment of acute renal failure should be carried out very intensively and immediately.

Packed red cells should be transfused to avoid circulatory over load in these patients.

Double check system should be employed for blood transfusion at collection, storage and donation.

Checking should be done by a senior member of the medical and nursing staff independently.

Transfusion should be given slowly and transfusions are repeated over a period of few days. Massive and quick transfusions are avoided.

Blood transfusion should always be monitored by a doctor who should be present near the patient during transfusion.

CARDIOVASCULAR COMPLICATIONS The patients who are anaemic or suffer from heart SURGERY - PRINCIPLES IN GENERAL

Thrombocytopenia and coagulation factor deficiencies occur due to lack of viable platelets and clotting factors V & VIII in stored RBCs. BACTERIAL CONTAMINATION OF BLOOD This can happen accidently during collection, storage or transfusion.

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Gram-negative bacilli such as coliform and pseudomonal organisms may contaminate and lead to septicaemic reactions. The patient suffers from fever, abdominal pain and severe shock and may die within hours.

Strict asepsis should be observed during collection, storage and donation of blood. The blood should be refrigerated properly.

As a rule, a unit of blood should be transfused in less than four hours because longer periods at the room temperature favour bacterial growth.

Pre-sterilized blood bags filled with measured amount of anti-coagulants are available commercially. These are used now-a-days and unwanted complications are prevented. These have replaced all other kinds of bags or bottles for the collection of blood. These are safe and satisfactory.

BIOCHEMICAL UPSETS Metabolic risk to neonates are hypoglycemia and hypocalcemia. These should be carefully monitored and treated in time.

BIOCHEMICAL UPSETS FOLLOWING MASSIVE TRANSFUSIONS During storage of the blood there is increased amount of potassium in the plasma due to degradation of the red cells.

In massive transfusions, severe hyperkalaemia may lead to sudden death. This can be avoided by packed red cell transfusions thus avoiding high concentration of potassium present in plasma.

Fresh blood transfusion should be preferred when massive amount of blood transfusion is required.

SURGERY - PRINCIPLES IN GENERAL

6

Citrate intoxication is another hazard in massive transfusions.

Stored blood has higher concentration of ammonia which is dangerous in patients with compromised liver function.

Concentration of 2, 3 DPG is increased thus the delivery of oxygen is reduced due to the shift of oxygen dissociation curve to the left.

One should be careful under such circumstances and avoid stored blood transfusion.

GENERALIZED BLEEDING TENDENCY This may be observed after massive transfusion due to dilution of clotting factors. It leads to serious haemorrhagic states.

Fresh blood should be transfused if massive transfusions are required to avoid such serious complications.

AIR EMBOLISM This used to be common in the past when glass bottles were used for collection of blood. This danger has been virtually eliminated with the use of collapsible pre-sterilized plastic bags.

No air gets collected in the bags. The air should be removed from drip set to avoid this serious problem.

TRANSFUSION RELATED ACUTE LUNG INJURY Lung injury following massive transfusions is experienced in patients who have suffered hemorrhagic shock following acute hemorrhage.

Special filtered sets for blood transfusion are used to avoid or minimize such injury.

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DELAYED COMPLICATIONS SENSITIZATION Minor blood group incompatibility and presence of undetected antigens in the donor blood may cause sensitization after transfusion of blood.

This sensitization complicates future transfusions and pregnancies.

Cross matching should be done for every transfusion independently to avoid adverse effects.

Preferably same blood group should be transfused.

Only in severe emergencies universal donor blood may be used.

DELAYED HAEMOLYTIC REACTIONS Usually some irregular undetected antibody is the cause for this problem.

These reactions occur late and are usually diagnosed from the appearance of jaundice or if the level of haemoglobin fails to rise to expected level after transfusion.

INFECTION INTRODUCED FROM DONOR Syphilis, malaria, brucellosis, trypanosomiasis, HIV, may be transmitted by transfusion from donor to recipient.

Most dangerous and impor tant hazard is transmission of Australian antigen "B" leading to serum hepatitis "B" and transmission of HCV causing hepatitis ‘C’.

Cytomegalovirus can also be transmitted.

Special care should be taken to avoid the collection of blood from donors suffering from these diseases.

SURGERY - PRINCIPLES IN GENERAL

7

Contaminated blood should not be used in patients.

The donor should very carefully be selected for the blood collection.

MULTIPLE MICRO-EMBOLISMS Certain particulate matter may be present in blood transfusion fluids such as rubber, plastic pieces, cellulose fibers, glass par ticles, debris of aggregated white cells and platelets.

These may lead to pulmonary embolism and may make the patient very seriously ill.

Careful blood collection can avoid this complication.

Use of micro-filter set for transfusion also avoids such complications. Blood is always transfused through specified microfilter transfusion sets to avoid micro-emboli.

TOXIC SUBSTANCES (PLASTIC) These may be present in plastic bags used for blood transfusion and may cause adverse effects on a patient. The bags for collection of blood should be chosen very carefully.

TRANSFUSION HEMOSIDEROSIS This is a hazard of repeated blood transfusions, the iron gets deposited into the tissues and organs. It is commonly seen in regular and chronic blood recipients.

THROMBOPHLEBITIS This is encountered due to the use of needle or cannula damaging the venous wall specially when the venepuncture has been carried out without proper aseptic precautions.

This may lead to septic thrombophlebitis and even 115

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septicaemia.

6. Laura A Basile; William M Southgate. Transfusion therapy. NBN 2004; 4(4): 223-230.

Proper aseptic technique should be used and bigger vein should be selected. As soon as the signs of phlebitis appear, the cannula should be removed and some other site for transfusion should be selected.

GRAFT VERSUS-HOST REACTION This reaction is seen in patients receiving viable white cells when they are immunologically deficient.

It occurs due to histocompatible difference between donor blood and immuncompromised recipient. The symptoms occur within 100 days of transfusion and include dermititis, wasting diarrhoea, hepatitis, bone marrow suppression. It is a rare complication.

REFERENCES 1. Singleartl G. Schleinzer W. The concept of autologous blood transfusion. Beitrage & zur infusious therapic.

[JC:b21]. 1991; 28: 283-6.

2. Weisbach V. Zerlor T. Zingsem J. et al. Risk of autologous blood transfusion. Beitrage zur infusious therapic [JC:b21]. 1991; 310-2.

3. Blanhut B. Risks and side effects of autologous transfusions. Beitrage & zur infusious therapic.

[JC:b21]. 1991; 28: 287-99.

4. Schmidt S. Mullar N. Preoperative autologous blood donation, analysis of side effects and complications.

Beitrage & zur infusious therapic [JC:b21]. 1991; 28: 307-9.

5. Marochkov AV. Doronin VA. Kravtsov NN. Complications in ultravioletn irradiations of blood.

Anaestezrologiia I Reanimatologiria [JC:4st]. Jul-Aug 1990; (4): 55-6.

SURGERY - PRINCIPLES IN GENERAL

SUMMARY Blood Transfusion Blood component transfusion Autologus Homologus Hetrologus

! ! ! !

Indications Sudden reduction of blood volume Inadequate concentration of haemoglobin Severe burns Blood component therapy

! ! ! !

Complications Immediate ! Febrile reactions ! Allergic reactions ! Haemolytic reactions ! Cardiovascular complications ! Infection ! Biochemical upsets ! Bleeding tendencies ! Air embolism ! Acute lung injury Delayed ! Sensitization ! Haemolytic reactions ! Infections ! Micro embolisms ! Haemosiderosis ! Thrombophlebitis ! Graft-versus-host reaction

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PS-014 b

HAEMORAGE SHOCK Shuja Tahir, FRCS, FCPS

The shock is a condition of generalized inadequate blood flow, inadequate tissue perfusion, and inadequate removal of cellular waste products. It can be defined in many ways.

The shock is a clinical condition characterized by cardio vascular collapse, inadequate peripheral circulation, tissue perfusion and oxygenation. It occurs whenever the cardiac output fails to maintain adequate circulation.

The shock is a condition in which patient has tachycardia and is pale, ashen in color and is sweating. It may also be characterized by hypotension, peripheral cyanosis, hyper-ventilation, clouding of conscious level and oliguria.

Tissue damage occurs due to hypoxia and lack of nutrients. Multiple organ function deterioration or failure occurs due to the disturbance of cellular function. All these changes lead to progressive shock and death of the patient.

ETIOLOGY AND TYPES OF SHOCK The basic patho-physiologic derangement in shock is the imbalance between the supply and requirement of the oxygen at the cellular level.

This imbalance leads to anoxic changes in the cellular metabolism due to insufficient tissue perfusion.

The anaerobic glycolysis leads to accumulation of; ! ! !

These changes lead to cellular and generalized metabolic acidosis.

Multiple and variable factors may affect individually or in combination and lead to following abnormalities and shock: FAILURE OF PUMP It is the basic cause of shock in following clinical conditions of inadequate cardiac output; ! ! ! !

Myocardial infarction.

Toxic states of heart.

Severe valvular dysfunction.

Arrhythmias.

85% of the patients suffering from this problem usually have a fatal ending.

FAILURE OF VOLUME Inadequate effective vascular volume is the basis of this type of shock. It is seen in following clinical conditions ; !

SURGERY - PRINCIPLES IN GENERAL

Excess lactic acid.

Inadequate carbon dioxide removal.

Accumulation of carbonic acid.

Diminished blood flow (haemorrhage).

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!

Decreased resistance to blood flow.

FAILURE OF RESISTANCE The shock due to this reason is seen in the following conditions; ! !

Failure or decrease in the vascular tone.

Septicaemia etc.

etiological factors are as following: HEMORRHAGIC SHOCK (ACUTE LOSS OF BLOOD) This is the type of shock which occurs following sudden and significant loss of blood.

Sudden loss of 35% to 45% of blood brings the cardiac output and blood pressure to zero.

Various types of shock depending upon the pathogenesis and course of shock are;

Sudden loss of 33% of blood volume may cause death.

COMPENSATED OR NON PROGRESSIVE SHOCK It is the type of shock when normal compensatory mechanisms reverse the shock and patient achieves full recovery without any exogenous help.

Smaller percentage of loss of blood volume and reduction in the cardiac output tends to lower the blood pressure and increase the heart rate.

Following factors play a significant role in managing the shock by body's own compensatory mechanisms; ! ! ! ! ! !

Baro-receptor reflex.

CNS ischemic stimulus.

Reverse stress relaxation of circulatory system.

Formation of angiotensin.

Formation of ADH or vaso-pressin.

Mechanisms such as absorption of fluid and electrolytes and maintenance of urinary output.

PROGRESSIVE SHOCK It is the type, when the shock becomes worse and eventually results in death. There is decrease in coronary blood flow and decrease in cardiac output.

IRREVERSIBLE SHOCK It is the end stage of progressive shock (shock of shocks).

Different types of shock depending upon primary

Haemorrhagic shock encephalopathy is highly fatal and it is common in infants. It presents with following features ; Convulsions, progressive coma, hyperpyrexia, shock, generalized bleeding tendency.

Abnormal hepatic and renal functions and metabolic acidosis.

Autopsy shows, cerebral edema, petechial haemorrhages of gut, lungs and kidneys.

It also shows generalized depletion of lymphocytes in lymphoid tissues1,2.

Significant unfavourable signs of haemorrhagic shock are ; ! ! ! !

SURGERY - PRINCIPLES IN GENERAL

Increase in pulmonary resistance.

Decreased pulmonary blood flow.

Ventilation, perfusion disturbances preceding onset of circulatory decompensation.

Congestive process in lungs.

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! ! !

Reduction of microvascular bed3.

Shock inhibits markedly the myelopoietic response4.

Severe and prolonged haemorrhagic shock leads to lack of microvascular blood flow.

Laser Doppler flowmetery (LDF) is a useful technique for repeated assessment of microvascular blood flow.

Resuscitation with Ringer's lactate does not restore microvascular blood flow although central venous pressure may be double the normal value.

Decreased microvascular blood flow is the basis of multi-organ failure in prolonged shock5.

Antishock clamp (External fixator) provides direct reduction and compression of pelvic fracture diastases about the sacroiliac joint.

It rapidly stablizes the posterior pelvic ring in hypotensive and shocked patients. It is new way of control of haemorrhage in specific conditions6.

similar to the haemorrhagic shock in the early period.

Early clinical picture is very much misleading as patients with severe burns may not be desperately ill one hour after the burn accident. But 8-10 hours later they may be in irreversible shock due to massive loss of fluids.

It is true that severity of the shock is proportional to the percentage of area burnt.

In children, if the burnt area is more than 10%, intravenous fluid therapy should be provided and the patient should be hospitalized.

In adults same should be done if the burns are more than 15% of the total body surface area.

The fluid loss is about the volume of whole plasma in the patient with 50% burnt area. This leads to severe reduction in circulatory volume and hypovolemic shock if treated inadequately.

Later on (a week after burn accident) wounds may get infected and patient is likely to develop septicaemic shock.

SEPTICAEMIC SHOCK (OVERWHELMING INFECTION) TOXIC SHOCK SYNDROME (TSS).

This occurs due to overwhelming infections. Gas gangrene also causes shock like condition due to powerful exotoxin. Staphylococcal toxins can also cause shock.

HYPOVOLEMIC SHOCK (LOSS OF FLUID AND ELECTROLYTES) This may be the result of excessive loss of fluids and inadequate replacement as in ;

Endotoxin, specially of coliform bacilli leads to generalized Schwartzman reaction leading to shock.

It is also known as endotoxic shock.

! ! !

BURN SHOCK (LOSS OF PLASMA) This is produced in extensive burns and is very

Infants are more vulnerable to this problem as they are unable to produce more concentrated urine.

SURGERY - PRINCIPLES IN GENERAL

Excessive sweating.

Vomiting.

Diarrhoea.

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!They cannot save more fluids. They have smaller fluid compartment. Their compensatory mechanisms are poor and under developed.

CARDIOGENIC SHOCK (MYOCARDIAL INFARCTION) Myocardial infarction produces shock similar to the hypovolemic shock. The cardiac output is reduced due to pump failure. It leads to reduction in tissue perfusion.

Cellular hypoxia leads to metabolic acidosis which causes peripheral vaso-dilatation and pooling of the blood. This makes shock even worse.

Failing heart further deteriorates this situation because failure of the pump action deteriorates progressively.

PSYCHOGENIC SHOCK (SUDDEN FRIGHT AND PAIN) This is the type of shock which follows sudden fright or severe pain. The patient may remain in shock and unconscious for few moments. Even death may occur in worst cases.

NEUROGENIC SHOCK This type of shock occurs in patients with sudden loss of vaso-motor tone. It leads to massive dilatation of veins. It leads to pooling of the blood into veins thus reducing the peripheral resistance, effective circulatory volume and adequate venous return.

The mean systemic filling pressure is reduced and patient suffers from neurogenic shock.

collapse.

Brain trauma or cerebral hypoxia also leads to vasomotor center depression and thus dilatation of peripheral veins which in turn result in neurogenic shock.

VASO -VAGAL SHOCK (EMOTIONAL FAINTING) This condition is seen in emotional states when there is vascular dilatation due to sympathetic signals and strong activation of parasympathetics causing bradycardia.

Both these features lead to decreased cardiac output, decreased venous return and decreased blood pressure.

This leads to the sudden pooling of blood into the limb muscle vessels and dilation of the splanchnic bed. There is loss of effective circulatory volume. It leads to hypotension and unconsciousness.

ANAPHYLACTIC SHOCK (ANTIGEN ANTIBODY REACTION) Many drugs and substances may cause this type of shock. Penicillin is notorious for causing anaphylaxis.

This is caused by the combination of antigen with the immunoglobulin E (IgE) leading to release of large amount of histamine, histamine-like-substances and slow-release-substance-anaphylaxis (S.R.S.A).

These lead to bronchospasm, laryngeal oedema, respiratory depression, hypotension and shock.

It is seen in patients after deep general anaesthesia when there is collapse of vaso-motor center.

These substances also cause sudden;

Spinal injuries and spinal anaesthesia may block the sympathetic outflow and thus cause vaso-motor

! !

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Generalized venous dilatation.

Dilatation of arterioles.

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Increased capillary permeability.

These changes decrease the venous return drastically and suddenly. It leads to severe shock and death may occur very quickly.

STATE OF SHOCK It is similar to end stage of irreversible shock. This condition frequently precedes death after different conditions regardless of the cause as electrocution, drowning and massive total body irradiation.

In this condition, there is depletion of high energy phosphates from the cells. ATP changes to ADP and AMP and then to adenosine which leaves the cell and is converted into uric acid.

Once depleted, these stores can never be replenished. It leads to death of cells, organs and the persons.

PATHOLOGY OF SHOCK Most of the changes are due to inadequate perfusion and inadequate removal of cellular waste products of the tissues.

Various compensatory mechanisms modify these changes.

The initial changes are at the cellular level.

Inadequate perfusion and hypoxia causing mitochondrial swelling or damage. This damage is seen maximally in the tissue at venous end of the capillaries.

These changes tend to depress almost all the cellular functions. The cellular anoxia is made worse by depressed circulation. There is anaerobic glycolysis.

There is accumulation of lactic acid.

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5

There is inadequate removal of carbon dioxide.

There is excessive production of carbonic acid. It causes cellular acidosis and then acidemia.

All these changes depress cell metabolism and lower the body temperature. The damaged cells release enzymes which are toxic on their own or activate other blood constituents which are harmful to the body such as conversion of fibrinogen which causes disseminated-intravascular- coagulopathy (D.I.C).

The other substances increase capillary permeability and thus cause loss of fluids. This leads to reduction in effective vascular volume. It causes lowering of blood pressure.

The capillaries have no muscles in their walls and are controlled by pre and post-capillary sphincters.

The normal transit time of red cells through capillaries is about one second. Low circulatory volume increases this period and causes stagnation and anoxia.

Adequate flow through capillaries is extremely important while treating the shock. The venous constriction while arterioles are relaxed leads to the pooling of blood in the capillaries. This is seen in shock due to myocardial infarction and septicaemia.

There is diminished carbohydrate metabolism and reduced energy production during shock. This leads to metabolic acidosis due to under perfusion of cells.

In shock, the problem is not only reduced circulatory volume but reduced flow of the blood as well.

This is also due to clumping and aggregation of the red cells. It is called "SLUDGING" and this process can 121

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!be reversed by infusing low molecular weight dextran and albumin.

with severe injuries or when patients have severe infection.

REVERSIBLE SHOCK This is the type of shock described according to the clinical presentation. This may be encountered in any kind of shock.

CLINICAL FEATURES PALLOR The patient looks pale, ashen gray, lethargic and ill.

The luster or shining look is lost.

In patients with impending shock, the heart rate increases and tries to improve the cardiac output.

Release of catecholamines and steroids in response to stress of injury or infection increases peripheral resistance leading to improvement in blood pressure.

SWEATING There is sweating but it is different than the sweating during hot weather because patient is cold and ashen in colour and has earthy gray looks.

Auto regulation mechanism shifts the blood to brain and heart from less vital organs like skin and muscles.

Blood pressure improves, pulse rate becomes normal and tissue perfusion shows improvement.

This process is called reversible shock.

IRREVERSIBLE OR NON PROGRESSIVE SHOCK It is the end stage of progressive shock. The body compensatory mechanisms fail or are inadequate and patient suffers from state of shock. It occurs when the blood pressure continues to lower down despite treatment. Once the critical level is reached, the shock becomes progressive (shock causes more shock and a vicious circle starts) until death. All methods of known therapy fail to reverse the shock.

The patient's condition deteriorates and death occurs. This occurs due to continuous underperfusion of vital organs leading to irreparable damage. This is usually due to inefficient treatment or

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PALPITATION This is an early sign when the heart rate is fast and patient is anxious. One should diagnose and treat shock adequately and actively at this stage and should not wait for other manifestations of shock to appear.

RESTLESSNESS The patient complains of being unwell and is restless and irritable.

AIR HUNGER The patient has hyperapnoea and air hunger. This is due to increased physiological dead space due to reduction in the alveolar perfusion and metabolic acidosis.

THIRST The patient usually complains of severe thirst and continue asking for drinks. Patient has dry mouth and depressed salivary secretion.

This is due to hypovolaemia and reduced blood supply of the salivary glands leading to compensatory diversion of blood to the brain.

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CONFUSION The conscious level deteriorates in patients with shock. They are confused, disorientated and fail to concentrate.

All these changes of depressed cerebral functions are due to cerebral hypoxia.

HYPOTENSION Hypotension develops later when body compensatory mechanisms have failed either temporarily or permanently. This is due to reduction in effective circulatory volume.

OTHER SYMPTOMS ! Rigors. ! Vomiting. ! Nausea. ! Diarrhoea. ! Fever.

adequate treatment of shock.

TREATMENT OF SHOCK The basic objective is restoration of adequate tissue perfusion as early as possible.

The treatment should be started on anticipation of shock before its features are even manifested.

Unless the shock is treated actively and efficiently, patients may go into irreversible shock and may die.

RESTORATION OF BLOOD VOLUME This is of primary importance because only after restoration of blood volume, the cardiac output, peripheral vaso-constriction and compensatory diversion of blood to brain and heart will reverse to normal.

These symptoms are seen in septic and other types of shock.

Although these compensatory mechanisms keep the blood pressure as near to normal as possible, their prolonged presence leads to damage to many vital organs like kidneys.

CYANOSIS This is one of the later manifestations of the shock when there is stagnation and pooling of blood and marked reduction in oxygenation.

Blood transfusion or other appropriate fluids should be given as fast as possible to replace the lost amount of blood volume which should be normalized quickly.

OLIGURIA OR ANURIA The urinary output is depressed. This is due to the compensatory diversion of blood from the kidneys to the brain and the heart.

FLUID AND ELECTROLYTES When the blood is not available or patient has lost more fluids and electrolytes, these should be replaced at fast speed. The central venous pressure monitoring should be done to avoid the sudden circulatory overload.

Later on, it may be due to continuous anoxia of the kidneys leading to acute cortical necrosis and acute renal failure.

Improvement in urinary output is a good indication of SURGERY - PRINCIPLES IN GENERAL

The estimation of left atrial pressure or pulmonary wedge pressure is thought to be better indicator of left heart function than central venous pressure 123

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which is a reasonable indicator of right heart function.

otherwise their is delay in the absorption and desired effects are not achieved.

MAINTENANCE OF RENAL FUNCTION Renal function improves after adequate replacement of the fluids. If there has been delay in the treatment of shock, irreversible renal damage may lead to death of the patient.

On the other hand repeated administration of the drugs and delayed absorption leads to undesirable accumulative toxic effects at the later stage.

Renal dialysis may help in reversing the acute tubular necrosis.

REVERSAL OF SLUDGING Adequate fluids, low molecular weight dextran (Rheomacrodex) and albumin lead to reversal of aggregation of the red cells.

This helps in the improvement of capillary blood flow and improvement of tissue perfusion.

CORRECTION OF METABOLIC ACIDOSIS The metabolic acidosis is reversed on adequate perfusion of the tissues and adequate oxygenation at cellular level.

Sodium bicarbonate is given intravenously for its correction.

CORRECTION OF PULMONARY VENTILATION Improvement in the vascular volume and clearance of the airways helps in the improvement of pulmonary ventilation.

Inhalation of 30% oxygen is also helpful for better diffusion of gases.

DRUGS In shocked patient, the drugs should be given by intravenous route and through larger veins SURGERY - PRINCIPLES IN GENERAL

Vaso-active drugs can be given to raise the blood pressure for a limited period and should be monitored very carefully.

Steroids have got very important role in the management of endotoxic shock. Larger bolus doses given intravenously are of great help. These should not be used repeatedly because their repeated use may mask the actual picture of the shock.

The vaso-dilator drugs can be used to reduce vaso constriction, (phenoxybenzamine 1 mg/kg intravenously over 24-48 hours) if the adequate fluid replacement fails to improve the tissue perfusion.

These should be used with great care and continuous monitoring of the central venous pressure is essential as vaso-dilatation may lead to further reduction of the blood pressure in already shocked patient.

DIGITALIZATION It is required in patients in whom central venous pressure rises above 10-12 cm of water without restoration of blood pressure after adequate fluid replacement.

GLUCOSE INSULIN INFUSION Intravenous infusion of glucose insulin drip helps in re-entry of potassium into the cells and improvement of the cellular perfusion.

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TEMPERATURE The patient should not be warmed when in shock.

Room temperature should be comfortable (18-21) degrees centigrade) and the fluid to be infused should be of the same temperature.

Higher temperature will lead to vaso-dilatation and reduction in effective vascular volume.

ANTIBIOTICS The antibiotics should be used to cover all the infecting organisms. If the culture and sensitivity of the infecting organism is available, proper antibiotics should be started immediately, otherwise after collecting the specimen for culture, a combination of antibiotics covering all types of organism should be given.

Usually triple regimen of antibiotics is used to cover all possible bacteria both aerobes and anaerobes.

One should be careful in using antagonizing each others actions.

antibiotics

TREATMENT OF THE CAUSE OF THE SHOCK The injuries causing haemorrhagic shock or infected focus causing septicaemic shock should be properly treated.

If any complication has occurred due to injuries or infection, this should be treated as well.

REFERENCES 1. Tam AV. Ng IO. Chang PT. Tang Ts. LiCH Haemorrhage shock encephalopathy. Acta Paediatrica Scandinavica [LC:11v]. May 1989; 78(3): 458-62.

2. Chin NC. Shen EY. Lee Hc. Haemorrhage shock and encephalopathy syndrome. Acta Paediatrica Sinia

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[JC:1m6]. Apr-Mar 1989; 30(2): 118-22.

3. Kirsanova AK. Noroderzhkincs IS. Kozhina VL. Berezina TL. Dvonetiskii SV. Early prognotic signs of disorders of the regional pulmonary circulation in the dynamics of haemorrhage shock and in the post resuscitation period. Anesteziologiia Reanimatologiia. [JC:4st]. Sep-Dec 1992; (5-6): 33-6.

4. Livingstone DH. Gentile PS. Malangoni MA. Bone marrow failure after Haemorrahgic Shock.

Circulatory Shock [JC:cay]. Mar 1990; 30(3): 25563.

5. Wang P. Hauptman JG. Choudry IH. Haemorrhage produces depression in microvascular blood flow which persists despite fluid resuscitation. Circulatory shock. [JC:cay]. Dec 1990; 32(4) :307-18.

6. Ganz R. Krushell RJ. Jakob RP. Kuffer J. The Antishock pelvic clamp. Clinical orthopaedics and related research. [JC:dfy]. 1991; (2670): 71-8, 1991.

SUMMARY Etiology ! Failure of pump ! Failure of volume ! Failure of resistance Types Non progressive Progressive Irreversible Haemorrhagic Septicaemic Burn Hypovolemic Cardiogenic Psychogenic Neurogenic Vaso-vagal Anaphylactic

! ! ! ! ! ! ! ! ! ! ! !

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PS-017

SEPSIS SYNDROME (SS) Shuja Tahir, FRCS, FCPS

SEPTIC SHOCK SYNDROME BACTERAEMIC SHOCK SEPTIC SHOCK ENDOTOXIC SHOCK TOXIC SHOCK SYNDROME (TSS) TOXIC SHOCK LIKE SYNDROME (TSLS) All the above named conditions mean the same syndrome. Septic shock or Sepsis syndrome (S.S) is the type of shock which occurs in patients with overwhelming infections.

Sepsis syndrome (S.S) is characterized by low cellular perfusion, subnormal supply of nutrients and oxygen and lack of removal of cellular waste products. It results as a host response to microorganisms and endotoxemia.

Septic shock is the intersection between infection, and severe organ dysfunction1.

Sepsis accounts for more than 210,000 deaths per year. The mal-distribution of blood flow may cause imbalance between oxygen delivery and demand leading to global tissue hypoxia, shock and death10.

The incidence of sepsis syndrome (S.S) has been rising progressively during past many years. It is characterized by: ! ! !

Low peripheral resistance.

Increased cardiac output.

Low venous filling pressure2.

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!

Cardiomyopathy.

Some times increased cardiac output may not be present, these patients have very poor prognosis.

The sepsis syndrome (SS) can also be defined as a condition of shock with evidence of infectious process, fever or hypothermia, tachypnoea and tachycardia, impaired organ perfusion, altered mentation, hypoxaemia, raised plasma lactate level and oliguria or anuria.

Sepsis syndrome (SS) is a serious clinical problem. It causes severe vasomotor collapse, neurogenic shock, massive intravascular hemolysis and anaemia. The positive blood cultures are seen in 45% of the patients. Adult respiratory distress syndrome (ARDS) is seen in at least 25% of the above patients 3 , 7 . All these pathological abnormalities lead to nephrotoxicity, acute tubular necrosis and acute renal failure.

This syndrome further complicates the serious underlying disease. It may cause toxic myocardial injury. It has got mortality rate of over 30% despite all the modern treatment. The rise in the incidence and poor outcome of the treatment is possibly due to; !

Widespread and inadequate use of antibiotics leading to a large reservoir of resistant strain

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and virulent organisms.

Larger number of patients with established infection due to organisms of high virulence and low host resistance. ! Increased incidence of trauma and critically ill patients. ! Increased use of steroids and other immunosupressive drugs. ! Availability of surgery for elderly and poor risk patients. !

Most of the symptoms may be due to the endotoxins.

This is why it is also called endotoxic shock. The toxins of bacteria cause shock as a result of vascular damage leading to generalized increase in the capillary permeability or disseminated arteriolar and capillary thrombosis. (Disseminated intra-vascular coagulopathy).

ETIOLOGY The Gram positive and Gram negative organisms usually cause sepsis syndrome. Even viraemia can cause this type of shock. It is not possible to distinguish clinically between Gram positive and Gram negative septicaemia.

Following clinical conditions predispose the development of sepsis syndrome.

GASTRO INTESTINAL TRACT Acute inflammatory bowel disease.

Ulcerative colitis.

Crohn's disease.

Typhoid fever.

Diverticulitis.

Gastro intestinal perforation.

Abscess formation.

Obstruction (Intestinal).

Carcinoma (Colon).

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BILIARY TRACT Cholecystitis.

Cholelithiasis and choledocholithiasis.

Cholangitis.

Obstructive Jaundice.

Biliary strictures.

Biliary malignancy.

RESPIRATORY TRACT Pneumonia.

Empyema thoracis.

Tracheostomy.

Bronchogenic carcinoma.

Foreign body.

URINARY TRACT Infection.

Obstruction.

Stone disease4.

Instrumentation.

Renal carcinoma.

Transitional cell carcinoma.

Prostatic malignancy.

REPRODUCTIVE SYSTEM Abortion.

Salpingitis, tubo-ovarian abscess.

Operations performed through vaginal route such as dilatation and curretage (D & C) and tubal ligation through vaginal route (Vaginal tubectomies) etc.

Post partum sepsis.

VASCULAR SYSTEM Venesection.

Vascular surgery.

Indwelling vascular catheter.

Pace maker.

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Shunt apparatus for dialysis.

GENERAL Immuno-suppression.

Agranulocytosis.

Leukaemia.

Carcinoma.

Severe skin sepsis.

Burns.

Road traffic accidents.

Use of contaminated infusion fluids.

Peritoneal dialysis.

Many conditions cause reduction of body defence mechanisms and lead to sepsis syndrome (S.S) even with relatively less virulent infections.

These conditions include; Male sex3.

Old age3 (more than 75 years of age).

Malignancy.

Collagen diseases.

Myeloma.

Aplastic anaemia.

Agranulocytosis.

Diabetes Mellitus.

Renal failure.

Cirrhosis and Liver failure.

Steroid therapy.

Radiotherapy.

Recent major surgery (such as splenectomy).

PATHOPHYSIOLOGY The basic defect of sepsis syndrome is severe infection leading to failure of adequate perfusion, oxygenation of the tissue and removal of cellular waste products.

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3

Gram positive organisms cause hypovolemic shock marked by vasodilatation and increased permeability of the capillaries leading to the extravasation of protein rich fluid. This is especially seen in the haemolytic streptococcal cellulitis or Erysiplas.

Endotoxemia develops as a result of disintegration of the Gram negative organisms. It may also occur in trauma and burn patients. Entry of the endotoxin and organisms occur into the portal circulation from the large colonic reservoir. Endotoxin induces a whole body inflammatory response which in turn mediates organ damage leading to multi-organ failure.

The first organ in which failure usually, is apparent is the lung with the appearance of non-cardiogenic pulmonary edema and adult respiratory distress syndrome. The cells involved in lung injury are neutrophils and macrophages which release mediators such as elastase, oxygen radicals and cytokines5,7.

In septic shock syndrome (S.S), the endotoxins lead to loss of vascular tone. There is pooling of blood in the venous system causing a reduction in effective venous return to heart leading to the circulatory failure.

Human patients are sensitive to endotoxins and develop Schwartzman type reaction (Hypersensitivity) in response to bacteraemia. Gram negative organisms lead to reduction in peripheral resistance due to release of kinins and other similar substances.

In patients with sepsis, abnormalities in coagulation and fibrinolysis are frequently observed including activation of complement and coagulation system.

These patients may develop disseminated intra

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vascular coagulation (DIC). Deposition of fibrin in microvasculature is associated with multi organ dysfunction syndrome (MODS). It is associated with very poor prognosis and mortality rates above 40%6.

It is certain that coagulation cascade is activated in sepsis leading to consumption of clotting factors, increase in anticoagulant mechanisms and a biphasic response in fibrinolysis first activation and then suppression11.

The circulating organisms and endotoxins trigger an immunological and inflammatory cascade with complement activation and release of a number of host derived mediators including Tumour Necrosis Factor (TNF), interleukines-1 and 2 and myocardial depressant factor. Release of platelet activating factor, vasodilator, prostaglandin and up regulation of adhesion molecules on polymorphonuclear leukocytes and endothelial cells2. These mediators are probably responsible for systemic vasodilation, hypotension and multi-organ failure3. Interferon gamma (INF-gamma) as well as other cytokines enhance macrophage antimicrobial function8.

Upper gastrointestinal (stomach and small gut) colonization with gram negative organisms is a major source of endogenous sepsis in critically ill patients9.

In ARDS following sepsis syndrome, it is the increased capillary permeability which is due to production of large amounts of inflammatory mediators and cytokines such as TNF, interleukine-I, complement, prostaglandins, leukotriens, histane, kinins and oxygen radicle. The increased capillary permeability leads to interstitial edema (pulmonary edema in case of lungs)7.

SURGERY - PRINCIPLES IN GENERAL

Oxygen consumption by the tissue is depressed in sepsis syndrome and it leads to metabolic acidosis.

Following abnormalities are seen in the earlier phases of the septic shock syndrome (SS). ! ! ! ! ! ! ! !

Sudden hypotension.

Oliguria and decreased renal function.

Warm extremities.

High central venous pressure.

Low peripheral resistance.

Disseminated Intravascular Coagulopathy (DIC).

Respiratory alkalosis (compensatory).

Elevated blood PH.

When patient's resistance is good, there is only bacteraemia with shock (presence of bacteria in the blood).

When the body resistance is low and general condition of the patient is poor, the condition deteriorates and patient develops shock. It can still be reversed with efficient and active treatment.

The patient develops irreversible shock leading to death if adequate treatment is not given or is delayed.

CLINICAL FEATURES The sepsis syndrome (SS) is characterized by the features of actual disease, signs and symptoms of infection, shock and multiple organ dysfunction.

GENERAL FEATURES ! Fever more than 38째C or hypothermia with core temperature less than 36.6째C. ! Nausea, Chills, Rigors, Diarrhoea. ! Jaundice (10% of the patients). ! Hypotension with blood pressure less than 90 130

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! !

mm of Hg or a fall of more than 40 mm of Hg in blood pressure even after adequate fluid replacement.

Localized focus of infection.

Features of sepsis and organ failure7.

CIRCULATORY SYSTEM Hypotension, cold and clammy skin with mottled cyanosis is seen in most of the patients. 10-15% of the patients may have warm extremities and flushed face.

Rarely some patients also present with peripheral gangrene (toes and fingers) in association with other symptoms of septicaemia.

Tachycardia more than 90/min or bradycardia with heart rate less than 50/min.

Hypotension with Blood Pressure less than 50 mm of Hg. Ventricular fibrillation .

Metabolic acidosis (pH less than 7.3 or a base deficit of more than 5).

Increased plasma lactate level.

RESPIRATORY SYSTEM ! Tachypnoea more than 20/min or patient on assisted ventilation. ! Respiratory rate less than 5/min or more than 40/min. ! Hypoxia (PO2 arterial less than 10kPa).

RENAL SYSTEM ! Polyuria followed by oliguria less than 150 ml/8 hours or hourly output less than 0.5 ml/kg/hour. ! Creatinine more than 150 mmol/L. HAEMATOLOGICAL ! Leukopenia with count less than 1000/cmm.

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! ! ! !

Coagulation defects with prothrombin time 1.5 times of the control.

Thrombocytopenia with platelet count less than 100,000 or more than 50% fall in count in 24 hours.

Anaemia.

Disseminated Intravascular Coagulopathy (DIC).

GASTROINTESTINAL ! Ileus. ! Gastroparesis. ! Haemorrhage.

NEUROLOGIC ! Cerebral ischaemia and altered cerebration (Confusion, disorientation, various levels of conscious level). ! Glasgow coma score < 6. ! Lethargy. ! Impaired mental functions. ! Irritable state. ! Seizures.

DIAGNOSIS The patients are usually admitted in the hospital suffering from some of the diseases causing septicaemia.

The patients are usually in their middle or old age.

Although young patients with extensive injuries, peritonitis and extensive burns may also suffer from severe septicaemia.

Septicaemia due to gynaecological reasons is common in younger females. The onset of shock is rapid and bacteraemia is characterized by other general feature.

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and diagnosed very early. Adequate treatment should be started immediately.

RISK FACTORS FOR SEPSIS SYNDROME3 ! Male sex. ! Age above 75 years. ! Creatinine level greater than 20 mg/l. ! Prothrombin time less than 60%. ! Presence of interstitial pattern on chest x-ray chest involving more than half of both lung field.

INVESTIGATIONS BLOOD EXAMINATION Blood examination reveals leukopenia, thrombocytopenia in early stages. Prolonged bleeding time (Disseminated intravascular coagulopathy) may also be present at a later stage.

Polymorpho-leucocytosis is common in later stages.

Blood culture should be performed to find out the causative organisms and their sensitivity to the antibiotics. Blood culture is positive in about 45% of these patients.

Other investigations required to diagnose the predisposing disease should be performed as soon as patient's condition permits.

Protein C levels should be obtained. Lower levels or depletion of protein is associated with critical illness sepsis and poor outcome in these illnesses.

Protein C deficiency is present in more than 85% of the patients with severe sepsis.

It correlates with the negative clinical outcome in severe sepsis, septic shock, DIC and MODS.

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6

It is not simply a marker of sepsis and severe sepsis.

Its levels and deficiencies parallel the course of illness.

Replacement therapy with activated protein C may improve the outcome in these patients11.

Increased level of transaminases, alkaline phosphatase and increased bilirubin level is seen.

Metabolic acidosis pH less than 0.3 or base deficit more than 5.

PaO2 less than 10 kPa Increased plasma lactate level Coagulation defects Prothrombin time 1.5 times more than control Thrombocytopenia less than 100.000 or more than 50% fall in 24 hours.

ELECTROCARDIOGRAPHY E.C.G. changes are seen due to toxic myocardial injury and increased heart load.

TREATMENT The treatment of septic shock remains a major problem in surgical practice. Current understanding of its pathogenesis suggests that future treatment of septic shock syndrome might involve inhibiting the body's inflammatory response to endotoxins5.

PREVENTION The patient with infection should be treated actively with appropriate antibiotics. Definitive treatment of the source of infection should be performed at the earliest. The patient should not be allowed to reach the stage of septic shock, only then the mortality can be reduced.

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The shock can be treated reasonably well at earlier stages but once the generalized tissue anoxia and metabolic acidosis are developed, the fatal results are almost inevitable.

Selective decontamination of digestive tract can minimize this risk. It can be done with oral use of polymyxin, amphotericin with a systemic beta lectam.

Vaccination against typhoid should be performed in endemic areas.

RESUSCITATION Objectives of early resuscitation in patients with sepsis include; ! ! !

Restoration of tissue perfusion.

Reversal of oxygen supply dependency.

Normalization of cellular metabolism10.

If the patient is already suffering from sepsis syndrome, active treatment should be started immediately.

The patient should be shifted to intensive care area.

It is essential to improve the general condition of the patient to make him/her fit for definitive treatment (recognition and elimination of the source of infection).

INTRAVENOUS FLUID THERAPY Intravenous fluid infusion should start immediately and should be given at a faster rate. Plasma and blood transfusions are required to improve the vascular volume.

Glucose and electrolyte solution can be infused to improve the effective vascular volume1.

7

CENTRAL VENOUS PRESSURE AND PULMONARY WEDGE PRESSURE MONITORING Large quantities of fluid are required to be infused over a shorter period. The risk of sudden circulatory overload is always present. This may have harmful and even fatal effect.

Central venous pressure gives reliable estimation of the right heart function and helps to maintain the rate of infusion within safe limits.

Pulmonary wedge pressure helps to monitor the left heart function. After adequate fluid replacement, most of the patients respond favourably and their extremities become warm.

The blood pressure normalizes. The heart rate decreases to normal limits. The urinary output improves. Improvement of sensorium and definite improvement of general condition results.

ANTIBIOTICS The selection of antibiotics is one of the most important factor in the treatment of sepsis syndrome. Blood culture should be performed as soon as possible. But it is not advisable to wait for the results of culture to come through.

Antibiotics which cover full range of possible organisms should be started immediately.

The antibiotics should be given via intravenous route because intramuscular and subcutaneous injections are not absorbed so quickly and their action is delayed. Oral use of drugs is of no use at all due to unnecessary delay in absorption and toxic accumulative effects at a late stage.

Antibiotics against anaerobes should be given where

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source of infection is related to gastro-intestinal tract. Bacteroides are the most common anaerobes in such infections. Intravenous metronidazole is quite effective against these organisms4.

IMMUNO-THERAPY Antibodies against Lipopolysaccharide component of the endotoxin in patients with gram negative sepsis should be used. The cytokines may have a positive role in sepsis syndrome (SS). Treatment with Anti IFN-Gamma offers protection against Lipopolysaccharide lethality8.

STEROIDS Steroids are supposed to be very helpful in the treatment of septic shock. These are used as adjuvant to rest of the treatment of septic shock.

These are recommended to be used in larger and bolus dose only once or twice (15-30 mg/kg body weight of methyl prednisolone or Decadron 20).

Repeated use of smaller doses is not helpful but is harmful in the treatment of sepsis syndrome (SS)11.

DIGITALIZATION Digitalization may be required in certain cases to improve the function of the heart (patients who fail to show improvement in blood pressure even after adequate replacement of fluids and show features of congestive cardiac failure). It is not helpful when inotropic drugs have been used.

Future therapies are aimed at restoring microcirculation through interaction with the coagulation system by redistributing blood flow or by activation of the efferent vagal system10.

Vasoactive therapy and vasodilating agents help in restoration of tissue perfusion and normalizing

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8

oxygen consumption. These have improved the outcome in patients with persistent shock despite crystalloid infusion.

INOTROPIC DRUGS These drugs (Dopamine and Dobutamin) help due to their inotropic effect on heart. These drugs are required as heart is unable to meet the increased circulatory needs during sepsis syndrome.

These drugs, when used in low doses, increase the myocardial contractility. Dopamine can dilate the renal vessels selectively. Thus it increases the renal blood flow and urinary output. It also increases the heart rate while Dobutamin does not show these effects.

Dopamine (less than 5 micro grams per Kg body weight per minute) have alpha-adrenergic effects. In shock, it may cause excessive vaso-constriction and severe peripheral ischemia leading to the gangrene of the toes. The aim of using these drugs is to increase cardiac index in these patients slightly. (5 Liters per minute per sq. meter in young patients) and (3.5 Liters per minute per sq. meter in old patients).

All these drugs have temporary effect and unless the sepsis is eliminated, patient will go into irreversible shock.

VASO-ACTIVE DRUGS These drugs help when enough fluids have been infused and excessive pooling has occurred. These drugs cause vaso constriction and make the vascular compartment smaller and improve the flow of blood and raise the blood pressure towards normality by improving the effective circulatory volume.

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Metaraminol and levophid (nor adrenaline) are used.

The patient has to be monitored during the medication and dose is adjusted according to the blood pressure and pulse rate.

INSULIN, GLUCOSE, POTASSIUM INFUSION Intravenous infusion of insulin, glucose and potassium helps in intracellular transfer of the potassium ions. It normalizes the electrolyte and blood glucose level of the patient. The response of the patient to rest of the treatment of bacteraemic shock is better after this infusion.

SODIUM BICARBONATE Persistent hypotension leads to tissue anoxia and metabolic acidosis. The response to treatment in such patient is not satisfactory due to acidosis.

Injection sodium bicarbonate should be given intravenously (20-30 mls) or the dose can be calculated depending upon the intensity of acidosis.

The patients respond better to the treatment of shock following treatment of acidosis. Any way the prognosis is very poor in patients who have developed metabolic acidosis following sepsis shock syndrome.

DEFINITIVE TREATMENT Treatment of the source of infection is performed by the drainage of pus or excision of the infective focus or repair of the leak in gastro-intestinal-tract or relieving the obstruction in gastro-intestinal-tract, urinary or biliary tract. If the septicaemia follows abortion, delivery or gynaecological manipulations, the infection may be localized to the pelvis in the form of pelvic abscess.

It should be drained through posterior colpotomy or supra-pubic extraperitoneal drainage of the abscess. The septic focus should be removed.

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9

Dilatation and curretage for the infected products of conception, pelvic peritoneal toilet and adequate antibiotic cover should be given.

When the infection is not localized in the pelvis and is present in general peritoneal cavity causing generalized peritonitis, laparotomy is mandatory.

Removal of the pus, focus of infection and necrotic tissue is performed. Extensive surgery should be avoided in these poor risk patients.

Ultrasound guided drainage of pelvic abscess or subphrenic collection is micro-invasive and achieves satisfactory results with minimum operative trauma to already unfit patient.

When sepsis follows sub-phrenic abscess, it should be drained through a wider incision and pus should be freely drained.

PREVENTION AND TREATMENT OF THE COMPLICATIONS RENAL FAILURE This is one of the major causes of death in sepsis syndrome due to any cause. Prolonged hypotension, toxicity of septicaemia and derangement of fluid and electrolyte balance leads to acute renal failure and death of the patient. Early and adequate treatment of shock cures renal failure.

Dialysis becomes necessary in severe cases of renal failure.

Exchange transfusion helps in renal failure due to clostridial septicaemia.

PULMONARY EDEMA This occurs during the treatment of sepsis syndrome. It is usually due to quick replacement of 135

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the vascular volume and inability of the left heart to cope with the increased demand. It is also due to the traumatic effects of prolonged anoxia of the lungs due to septicaemic shock.

Early and adequate treatment of the shock relieves this problem. Proper monitoring of central venous pressure, pulmonary wedge pressure and replacement of fluids accordingly is required to prevent and treat this complication. Diuretics and Digitalization or use of the inotropic drugs may be required in some cases.

STRESS ULCERS This is a common and a serious problem. Stress ulceration of the gastric mucosa secondary to septicaemia presents with haematemesis and melaena.

This may lead to acute blood loss in already ill patient and may be fatal. It should be prevented. Cimetidine or Rinatidine or other similar drugs should be given.

(H2 receptor antagonist or proton pump inhibitors intravenously 300 mg) POST SEPTICAEMIC PERIPHERAL GANGRENE Rarely the patient develops gangrene of the toes and fingers. It should be treated as peripheral gangrene due to any other cause.

SHOCK LUNG SYNDROME (ARDS) ADULT RESPIRATORY DISTRESS SYNDROME This is the syndrome of acute respiratory insufficiency following sepsis syndrome, major trauma and surgery. It presents as severe pulmonary insufficiency, hypoxia, tachypnoea and distress. This happens after satisfactory resuscitation from a stage of low tissue perfusion due to septicaemia or major trauma7.

SURGERY - PRINCIPLES IN GENERAL

The condition usually deteriorates to terminal hypoxia, hypercarbia and cardiac arrest. Increased pulmonary capillary permeability is probably the cause of this serious problem.

The etiology and treatment of this complication is still not very clear. Artificial ventilation and steroids may be helpful.

CARDIAC ARREST (DEATH) This is the terminal event in the course of septicaemia. Its incidence is very high and the challenge to all people treating sepsis syndrome.

REFERENCES 1. Annaue D, Prgerter P, Jars Guincestre MC, Guidet B. Current epidermology of septic shock. American journal of respiratory and critical care medicine 2003; 168(2):165-172.

2. Dal Nogare AR. Septic shock. American Journal of Medical Sciences. [JC:312]. Jul 1991; 302(1): 5065.

3. Aube H. Milan C. Blettery B. Risk factors for septic shock in the early management of bacteremia.

American Journal of Medicine. [JC:3ju]. Sep 1992; 93(3): 283-8.

4. Dragan P. Micleaf et al. Anuria due to lithiasis associated with septic shock. Acta Urologica Belgica.

[JC:26y]. 1992; 60(1):33-5.

5. Welbourn CR. Young Y. Endotoxin, septic shock acute lung injury: neutrophils, macrophages and inflammatory mediators. British Journal of surgery.

[JC:p34]. Oct 1992; 79(10): 998-1003.

6. Gorden R, Bernard. The pathophysiology and treatment of sepsis. A review of current information.

CME Activities med scope com Oct 2001.

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7. Balk RA. Bone RC. The septic syndrome definition and clinical implications. Critical Care Clinics. [JC:ccc].

Jan 1989; 5(1): 1-8.

8. Redmonel HP. Chavin KD. Browberg JS. Daly Jm. Inhibition of macrophage activating cytokines is beneficial in acute septic response. Annal's of surgery. [JC:67s]. Oct 1991; 214(4): 502-8: discussion 508-9.

9. Christopher S. Garrard. Critical care of the surgical patient. In. Peter J. Moris and Renold A. Malt. Oxford text book of Surgery Vol-I, Oxford University Press Oxford, 1994; 107-114.

10. Michael L, Stanchina, Mitchell M, Levy. Vaso active drug use in septic shock. Semin Respir Crit care med 2004; 25(6): 673-681.

11. Sjolin J. High dose Corticosteroid therapy in human septic shock has the jury reached the correct verdict.

Circulatory shock [JC:cay]. Nov 1991; 35(3): 13951.

SURGERY - PRINCIPLES IN GENERAL

SUMMARY Sepsis syndrome Etiology ! Gastrointestinal tract ! Billiary tract ! Respiratory tract ! Urinary tract ! Reproductive system ! Vascular system ! General causes Effects on various systems Risk factors Prevention Complications ! Renal failure ! Pulmonary edema ! Stress ulcer ! Peripheral gangrene ! ARDS

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PS-018

FLUID AND ELECTROLYTES -1 FLUID COMPARTMENTS Shuja Tahir, FRCS, FCPS Abid Bashir, FCPS TOTAL BODY WATER It is the amount of water content present in the body.

Females 50%

It is 75% of total body weight in a new born infant.

It is 55% of total body weight in adult males.

It is 50% of total body weight in adult females.

50%

The difference in the percentage of body water is due to excess amount of fat present in the females.

Total Body Water

Solids

Average

Infants

60% - 42 litres

75%

25%

Total Body Water

40%

Solids

Males

Total Body Water

Solids

Fluid Compartments

55% 66%

Extra cellular fluid Interstitial fluid 11.2 liters (15%)

45%

Total Body Water

34%

Solids

SURGERY - PRINCIPLES IN GENERAL

Intracellular fluid

Intra vascular fluid 2.8 liters (5%) Transcellular fluid 0.5 liter (3 %)

Extra cellular fluid 139

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The amount of total body water content (60% of total body weight or 42 liters in 70 Kg patient) is an accepted average in adults for clinical calculations.

rapidly equilibrating or functional compartment as well as several more slowly equilibrating or relatively non functioning components. These non functioning components comprise connective tissue water as well as transcellular water including;

INTRACELLULAR FLUID (ICF) Two third (66%) of total body water (40% of total body weight) is present in the intracellular compartment. Largest proportion of this water is present in skeletal muscle mass. Because of the smaller muscle mass in female, the percentage of intra cellular water is lower than in males.

! ! ! ! !

The principle cations of intra cellular compartments are potassium and magnesium and principle anions are phosphates and proteins.

This non functioning component normally represents only 10% of the interstitial fluid volume (1-3% of body weight).

EXTRACELLULAR FLUID (ECF) One third (33%) of the total body water (20% of body weight) is present in the extracellular compartment. It is further subdivided into intra vascular and interstitial fluid compartments.

MOVEMENT OF WATER The fluids keep on shifting between all these compartments to keep the electrical and osmolar equilibrium. Main factor controlling this fluid shift are pressure gradients (hydrostatic and osmotic pressure) and permeability of the membranes separating these compartments. (Cell membrane between the ICF and ECF and capillary membrane between intravascular and interstitial compartment).

In the ECF, sodium is the principle cation and chloride and bicarbonate are the principle anions.

INTRAVASCULAR FLUID It is the part of extra cellular fluid present in intravascular compartment. It is 5% of body weight or 1/4 of ECF (2.8 liters in 70 kg adult).

Intra-vascular fluid is present in the blood which is composed of cells (red cells, white cells, platelets) and plasma (fluids with dissolved protein).

INTERSTITIAL FLUID It is the part of the extracellular fluid present in the interstitial space (15% of body weight or 3/4 of ECF).

The interstitial fluid is further complicated by having a SURGERY - PRINCIPLES IN GENERAL

Cerebrospinal fluid.

Peritoneal fluid.

Joint fluids.

Secretions of the gastrointestinal tract.

Fluid in renal tubules.

Osmosis is the movement of solvent particle from an area of lower solute concentration to higher solute concentration when both are separated by a semi permeable membrane which allows the passage of solvent molecule but not the solute molecule.

The physiological and chemical activity of electrolytes depends upon number of particles present per unit volume (osmoles per litre) and number of electrical charges per unit volume (equivalents per litre).

It is important to note that number of particles and 140

FLUID AND ELECTROLYTES - 1

It is important to note that number of particles and not the amount or weight of solute is important in maintaining osmolality and osmotic pressure.

Plasma osmolality is calculated according to the following formula.

POsm (mosm/kg) = 2[Na+(mmol/L+ K+ (mmol/L)] + [BUN(mg/dl)/2.8] +[Glucose(mg/dl)/18] Putting average values in the equation we get; Posm = 2 [140+4] + 20/2.8 + 90/18 = 300 Normal plasma osmolarity is 280-310 mosm/L. Sodium is the main ion responsible for extracellular osmolarity as it is clear from the equation that 280 out of 300 mOsmol of plasma osmolality are contributed by sodium alone.

Although the concentration of different solute is different in various compartments, the membranes are freely permeable to water. Therefore osmolality of these compartments is same. Similarly electrical equilbirium is also maintained between all these compartments.

TONICITY Tonicity can be defined as osmolality due to effective solute.

Tonicity = total osmolality - ineffective osmolality There are two types of solutes.

Effective solutes are those solutes which can not permeate the cell membrane and, therefore, are restricted to ICF or ECF. These are mainly responsible

SURGERY - PRINCIPLES IN GENERAL

3

for water transport across the cell membrane.

Ineffective solutes can freely cross the cell membrane and are unable to effect the shift of water across the membrane. Therefore, these solutes contribute to total body osmolality but not to tonicity.

NORMAL CONTROL OF FLUIDS Kidneys play a major role in maintaining fluid, electrolyte and acid base balance.

In the glomerulus, almost every thing is filtered out of plasma. Glomerular filtration rate (GFR) is mainly dependent upon the hydrostatic pressure in the glomerular capillaries and capillary flow rate which is dependent upon the renal blood flow. In hypovolaemia, renal blood flow decreases, decreasing the GFR. In the proximal convoluted tabules, sodium is actively re-absorbed. Chloride passively follows the sodium to maintain the electrical equilibrium leading to water re-absorption by osmosis. The net result is decrease in volume of the filtrate but osmolality remains the same.

In the loop of henle, complex counter current mechanism is responsible for further re-absorption of water and salts. In the descending limb, the volume is further decreased by water re-absorption leading to increased osmolality. In ascending limb, further salts and water are re-absorbed. The fluid entering the distal convoluted tubules is hypo-osmolar.

In distal convoluted tubules, further re-absoption of water and sodium takes place but it is hormone dependent.

Aldosterone is the most important hormone which is secreted from the renal medulla in response to renin 141

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angiotensin system. It acts on the distal convoluted tubules to stimulate water and sodium re-absorption.

It increases the ECF volume.

Anti diuretic hormone (ADH) is secreted by the posterior pituitary gland. It increases the permeability of collecting ducts to water leading to water re-absorption and increase in the ECF volume.

Atrial natriuretic hormone (ANH) is secreted from atria in response to increase ECF volume. It is responsible for increased GFR and decreased sodium re-absorption. The net result is increased excretion of water and sodium and decreased ECF volume.

CLASSIFICATION OF FLUID AND ELECTROLYTE CHANGE VOLUME CHANGES Addition or subtraction of isotonic fluids from body would lead to significant change in ECF volume but little or no change is noticed in ICF. CONCENTRATION CHANGES Addition or subtraction of water or sodium alone would lead to changes in volume as well as tonicity of the ECF. It will lead to significant shift of water across the cell membrane i.e addition of water or subtraction of sodium would lead to hypotonicity of ECF and water will move into the cell to balance the osmolarity and vice versa.

COMPOSITION CHANGES Changes in concentration of ions other than sodium would not lead to volume or concentration change but can have significant changes in the composition + +2 +2 + of the ECF. These ions includes K , Ca , Mg , Cl , H and OH-.

SURGERY - PRINCIPLES IN GENERAL

DISTRIBUTIONAL CHANGES The volume is redistributed to third space (tissues in trauma and burn, GIT in intestinal obstruction) leading to distributional hypovolemia. Total water may be normal or even more but effective intravascular volume significantly falls.

REFERENCES 1.

Shires III, GT, Borber AB, Shires GT. Fluid & Electrolyte management of the surgical patient, In Shwortze I, Shires GT, Spencer FC, Doly JM, Fisher JE, Galloway AC. (Ed).

Principles of surgery 7th Ed. 1999. Mc Grath Hills New York PP 53-76.

2.

Shires GT, Canizoro PC. Fluid, Electrolyte management of surgical patient. In sabiston DC (Ed). The text book of surgery. The biological bases of modern surgical practice 14th Ed. 1991. W.B Sanden Co. Philadelphia PP 57-76.

3.

Doly JM, Barie PS, Dudnch SI. Preparation of the patient. In Nylium (Lm), Baker RJ, Fischer JE. (Ed) Mastery of surgery 3rd Ed. 1997, Little Drown, Co. Boston. PP. 22-49.

4.

Franklin EW, Buchman TA. Fluid, Electrolyte, Acid base disorders. In Doherty GM, Meko JB, Olson JA, Peplinshi GR, Worral NK. (Ed) Washington Manual of surgery 3rd Ed. 2003. Lippincott Williams & Wilkins, Philadelphia. PP 3859.

5.

Steele RJC, Patients with metabolic disorders. In Cuschieni A, Steelw RJC, Moosa AR (Ed). Essential surgical practice 4th Ed. 2000. Butterworth Heinmann Oxford PP. 205-14.

SUMMARY Fluid and Electrolytes Body fluid compartments ! Intracellular fluid compartments ! Extracellular fluid compartments Movement of water across compartments Tonicity Normal control of fluids Classification of fluid & electrolyte changes 142

1

FLUID AND ELECTROLYTES - 2 (FLUID BALANCE)

PS-019

FLUID AND ELECTROLYTES -2 FLUID BALANCE Shuja Tahir, FRCS, FCPS Abid Bashir, FCPS NORMAL DAILY INTAKE (70 Kg person) Water from drinks Water from food (solids) Water from oxidation Total intake

1200 ml 1000 ml 300 ml 2500 ml

Patient's intake also includes;

1500ml 0.5ml/kg/hour 1 ml/kg/hour 900 ml 100 ml 2500 ml

Patient's output also includes excessive losses due to;

I/V fluids infusion I/V blood transfusion Absorption from enema fluid Absorption from irrigation fluids All these are counted in total daily intake between specified period (24 hours).

NORMAL DAILY OUTPUT (70 Kg person) Normal daily output includes urine, water in faeces and insensible loss from respiratory tract and skin.

Urine output is 1-7 litres depending upon the weather, fluid intake and diuretics like coffee, tea and drugs. Minimum amount of urine to get rid of solid wastes is 0.5 ml/kg/hour. 1 ml/kg/hour of urine output is considered adequate. Insensible loss is usually 500-900 ml/day but it may exceed 5 litres/day in hot and humid weather or in febrile and hyperventilating patients.

Urine

Average Minimum Adequate Insensible loss faeces Total output

1-7 litres

SURGERY - PRINCIPLES IN GENERAL

Vomiting.

Diarrhoea.

Fever.

Sweating.

Fistulae.

Nasogastric aspiration.

Drains.

NORMAL VALUES OF GASTRO-INTESTINAL-TRACT FLUIDS (70 KG ADULT) Saliva Gastric juice Bile Pancreatic juice Succus entericus Total

1500 mls/24 hours 2500 mls/24 hours 500 mls/24 hours 700 mls/24 hours 3000 mls/24 hours 8200 mls/24 hours

CHILDREN Children may have more demand of fluids because

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they have; ! Large surface area in relation to body. ! More metabolic activity. ! Poor concentrating ability of the immature kidneys.

SURGICAL PATIENTS In surgical patients, fluid loss may occur from a number of sites depending upon the disease and type of surgery such as;

! ! ! ! !

Evaporation during laparotomy.

Burns.

Fluid loss in nasogastric aspiration.

Fistulae.

Sequestration into bowel lumen.

VOLUME STATUS ASSESSMENT Following investigations may be performed to assess the volume status of a person;

! ! ! ! ! ! !

Direct (only academic).

ECF volume by isotope tracing.

Indirect.

BUN. Creatinine.

Haematocrit.

Urinary osmolality, sodium concentration.

Specific gravity.

MONITORING Following clinical parameters help in assessment and monitoring of fluid status of the patient.

! ! ! !

Pulse.

Blood pressure.

Urine output.

CVP. SURGERY - PRINCIPLES IN GENERAL

VOLUME DEFICIT It is the most common fluid disorder in surgical patients. Lost fluid has almost same composition as that of extra cellular fluid (Isotonic).

CAUSES Gastrointestinal tract Diarrhoea Vomiting Nasogastric aspiration Fistulae Sequestration Soft tissue injuries Burns Infections (peritonitis etc) Intra-abdominal or retroperitoneal inflammations Intestinal obstruction CLINICAL FEATURES MODERATE DEFICIT Central Nervous System Sleepiness Apathy Slow responses Anorexia Cessation of normal activity Gastrointestinal Tract Progressive decrease in food consumption (Anorexia) Cardiovascular System Orthostatic Hypotention Tachycardia Collapsed veins Collapsing pulse Tissues Dry tongue, wrinkling of skin Mild decrease in temperature

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SEVERE DEFICIT Central Nervous System Decreased tendon reflexes.

Anesthesia of distal extremities.

Stupor.

Coma.

Gastrointestinal Tract Nausea, vomiting, Refusal to eat.

Silent ileus and distension.

Cardiovascular System Cutaneous lividity.

Hypotension.

Distant heart sounds.

Absent peripheral pulses, cold extremeties.

Miscellaneous Atonic muscles, sunken eyes.

Marked decreased temperature.

TREATMENT The general principles regarding fluid replacement are as follows; Fluid deficit should be corrected with isotonic solutions. Ringer lactate is the most commonly used solution as it contains electrolytes in almost similar ratio as that of plasma.

5% dextrose water is an isotonic solution but it behaves as hypotonic as the glucose is taken up by the cells and utilized. Water also moves into the ICF .

Amount of fluid to be infused can be calculated on the basis of utilization of body water, or output. Minimum amount of urine to get rid of solid wastes is 0.5 ml/kg/hr. Insensible loss is variable but for simple calculation we may consider 500 ml.

So daily fluid requirement would be;

SURGERY - PRINCIPLES IN GENERAL

Calculated 24 hourly urine output + Insensible loss + output (fistula, nasogastric tube, drain etc) = (body weight x 0.5x 24) + 500 + drainage fluid.

Another method of calculating daily fluid requirement is according to body weight. It is specially important in children. According to this formula; 100 ml/kg is given for upto 10 kg.

50 ml/kg is given for next 10 kg.

20 ml/kg is given for 21 kg onward. e.g., for a person of 35 kg, 24 hourly fluid requirement would be; (100x10) + (50x10)+ (20x15) = 1800 ml.

This fluid is added to calculate 24 hourly output other than urine (fistula, drain, naso-gastric tube etc).

VOLUME EXCESS CAUSES Iatrogenic Renal insufficiencies Cirrhosis of liver Congestive Cardiac Failure CLINICAL FEATURES MODERATE EXCESS (During surgery, edema of stomach, colon, omenta, mesentery).

Elevated Jugular Venous Pressure.

Distended Veins.

Increased cardiac output.

Loud heart sounds.

Gallop rhythm.

Functional murmurs.

Increased Pulmonary 2nd sound.

High pulse pressure.

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Bounding pulse.

Subcutaneous pitting edema.

Crepitations at lung basis.

SEVERE Vomiting.

Diarrhoea.

Anasarca.

Moist rales in lungs.

Pulmonary edema.

TREATMENT The main stay of treatment is to get rid of extra water.

Diuretics are given to increase water excretion. It is important to prevent electrolyte imbalance at the same time. In acute emergency and in renal failure dialysis may have to be performed.

WATER BALANCE Water intake is normally by mouth and absorption is from all parts of gastro-intestinal tract. Its output is through urine, faeces, sweating and insensible losses. Its intake is controlled by thirst which is stimulated by loss of water without loss of electrolytes. Clinically it can be monitored by measurement of urinary output (normal 60ml/hour).

1 This is controlled by antidiuretic hormone secretion .

The patients on intravenous fluids may be overloaded when the speed of infusion is more than the excretion of excess water because the patients are less able to deal with water load through antidiuretic hormone control.

DEHYDRATION WATER DEPLETION It is a condition of decrease in total body water without proportionate loss of sodium. Water

SURGERY - PRINCIPLES IN GENERAL

depletion may either be due to increased losses or due to low intake of water alone.

CAUSES OF DEHYDRATION Low intake is common cause which is due to ; Weakness Nausea Painful lesions of mouth and throat Urinary retention when patient avoids drinking Old age Carcinoma oesophagus Voluntarily Increased losses of water are due to; Vomiting Hyperventilation Diabetes insipidus Severe diarrhoea Chronic nephritis Burns Profuse sweating When there is deficiency of 1.5 liters of water in an adult, thirst is noticed, urinary output falls and urinary osmolarity is increased. This is due to the stimulation of the secretion of antidiuretic hormone which stops the water loss through the kidneys.

When the water loss is more than 04 liters, blood volume is diminished, blood pressure falls, pulse rate increase and patient develops a shock like condition.

Normal body compensatory mechanisms come into action, water loss through kidneys is stopped by antidiuretic hormone secretion. Fluid is withdrawn from the tissues into the vessels to raise the vascular volume.

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There is auto diversion of blood towards brain from other organs.

dextrose. Water intoxication leads to intracellular swelling.

There is loss of skin elasticity and lowering of the intraocular pressure. If the condition is not treated or further loss of water continues to occur, shock becomes irreversible, confusion and coma occurs and patient dies. The effect of loss of water is mainly on the intracellular compartment.

Weakness, lethargy and apathy are the first symptoms to appear. The face become puffy, generalized edema appears and slight increase in blood pressure may be detectable.

When blood volume decreases, or aldosterone secretion is stimulated, there is retention of salt and water, which brings the vascular volume to normal.

Haematological changes are late. After significant loss of water these are; Raised plasma sodium.

Increased haematocrit.

Raised serum urea and protein levels.

Water depletion is treated by oral water intake or 5% dextrose intravenously till thirst disappears and urinary output becomes normal1.

Patient's weight is increased. There is fall in the haematocrit and plasma sodium levels. Confusion and convulsions may appear later on.

The intravenous fluids are immediately stopped if these are being infused and this condition should be treated by 100 mls of 5% saline hourly until convulsions stop.

Diuretics are used and electrolytes estimation is frequently performed to prevent over treatment.

Isotonic solution of saline is of very little help in these cases and should not be used.

REFERENCES 1.

Shires III, GT, Borber AB, Shires GT. Fluid & Electrolyte management of the surgical patient, In Shwortze I, Shires GT, Spencer FC, Doly JM, Fisher JE, Galloway AC. (Ed).

Principles of surgery 7th Ed. 1999. Mc Grath Hills New York PP 53-76.

2.

Shires GT, Canizoro PC. Fluid, Electrolyte management of surgical patient. In sabiston DC (Ed). The text book of surgery. The biological bases of modern surgical practice 14th Ed. 1991. W.B Sanden Co. Philadelphia PP 57-76.

3.

Doly JM, Barie PS, Dudnch SI. Preparation of the patient. In Nylium (Lm), Baker RJ, Fischer JE. (Ed) Mastery of surgery 3rd Ed. 1997, Little Drown, Co. Boston. PP. 22-49.

4.

Franklin EW, Buchman TA. Fluid, Electrolyte, Acid base disorders. In Doherty GM, Meko JB, Olson JA, Peplinshi GR, Worral NK. (Ed) Washington Manual of surgery 3rd Ed. 2003. Lippincott Williams & Wilkins, Philadelphia. PP 38-

WATER INTOXICATION It is increase in total body water without a comparable (proportionate) rise in sodium content.

This is overloading with water alone. It is rare without renal insufficiency.

Normally it is controlled by increased urinary output.

Only indiscriminate use of intravenous fluids may cause this problem. Use of irrigation fluids after traunsuretheral resection may lead to water toxicity.

It also occurs when gastro-intestinal secretions losses rich in electrolytes are replaced with 5% SURGERY - PRINCIPLES IN GENERAL

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-59.

5.

Steele RJC, Patients with metabolic disorders. In Cuschieni A, Steelw RJC, Moosa AR (Ed). Essential surgical practice 4th Ed. 2000. Butterworth Heinmann Oxford PP. 205-14.

SUMMARY Fluid Balance ! Normal daily intake ! Normal daily output Volume status ! Assessment ! Monitoring Volume deficit ! Causes ! Clinical features ! Treatment Volume excess Causes ! Clinical features ! Treatment Water balance ! Water depletion (dehydration) ! Water intoxication

SURGERY - PRINCIPLES IN GENERAL

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FLUID AND ELECTROLYTES - 3 (SODIUM BALANCE)

PS-020

FLUID AND ELECTROLYTES -3 SODIUM BALANCE Shuja Tahir, FRCS, FCPS Abid Bashir, FCPS The main function of sodium is the control of distribution of water throughout body by its effects on osmolality. Basal daily requirement of sodium is about 40 mEq /day. Average daily intake is about 75 mEq or 4.5 grams.

Output is highly variable. Most of the sodium is lost in urine. Average daily urinary sodium loss is 10-80 mEq. It may be less than 1mEq/d in salt restricted patients and may exceed 200mEq/L urine in salt wasting kidneys. Upto 20 mEq are lost in stools. This loss may be increased in fistulae, vomiting and diarrhea.

Another source of sodium loss is from the skin in the form of sweating. This loss may increase to 300 mEq/day in very hot weather. It is important to note that the sweat is hypotonic in acclametized persons (15 mEq of sodium/L) but hyper tonic in unacclemetized (upto 60 mEq/L).

Normal serum levels of sodium is 135-150 mEq/L HYPONATRAEMIA Hyponatraemia is defined as serum sodium level of less than 130 mEq/L. CLASSIFICATION There are many classifications of hyponatraemia.

Simplest one is as under;

SURGERY - PRINCIPLES IN GENERAL

Primary hyponatraemia (due to loss of sodium).

Secondary hyponatraemia (dilutional hyponatraemia due to water intoxication).

Another classification is; Hypotonic hyponatraemia.

Isovolaemic.

Hypovolaemic. hypervolaemic.

Hypertonic hyponatraemia.

Isotonic hyponatraemia.

HYPOTONIC HYPONATRAEMIA Decrease in serum levels of sodium is expected to result in decreased osmolality and tonicity.

It may be primary (due to loss of sodium) or secondary (due to excessive accumulation of water).

The primary hyponatraemia is accompanied by loss of water as well but proportionate loss of sodium is more. Therefore, it may be termed as hypovolemic hyponatraemia. On the other hand, cause of secondary hyponatraemia is excessive accumulation of water which results in hyper volaemic hyponatraemia.

ETIOLOGY Primary (hypovolaemic hyponatraemia) There is acute loss of Sodium and water from the body. The total body sodium is usually deficient. The causes are;

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Vomiting Diarrhoea Fistulae Diuretics Adrenal insufficiency Secondary ( hypervolaemic hyponatraemia) It is due to accumulation of excess water. It is seen in following conditions; Congestive Cardiac Failure (CCF) Cirrhosis of Liver Chronic Renal Failure (CRF ) Stress There are distributional changes leading to inadequate circulating volume which result in sodium and water retention. The total body sodium is usually in excess.

2

Normal plasma osmolality is 290 mOsmol/L. It is reset to a lower level in chronic diseases like tuberculosis or chronic liver disease. These patients respond normally to water loads.

In syndrome of inappropriate ADH, the excessive secretion of antidiuretic hormone (ADH) results in water reabsorption from the kidneys. Due to excessive water reabsorption, plasma osmolality is decreased and urinary osmolality is increased to more than 100-150 m Osmol/L. Urinary sodium contents are also more than 20mOsmol/L. ISOTONIC HYPONATRAEMIA The increase in other solutes results in isotonic expansion of plasma volume leading to dilutional hyponatraemia. The solutes may be lipids, proteins or glucose etc.

Isovolaemic hyponatraemia (Total body sodium may be normal).

Hyperlipidaemias In case of hyperlipidaemias, the reduction of serum sodium level is plasma lipids (in gm/dl) x 0.002

The volume of body fluids is normal but there is dilutional hyponatraemia. It is also known as water intoxication.

Hyperproteinaemia The reduction in serum sodium level is rise in serum protein level above 8gm/dl x 0.25.

The causes are;

It is important to note that isotonic infusions of dextrose water , mannitol etc. may also result in transient hyponatraemia.

! ! ! ! ! !

Polydypsia with impaired renal functions.

Infusion of hypotonic solutions in comatosed patients.

Replacement of isotonic losses with hypotonic solutions.

TURP syndrome if irrigation is done with dextrose water. (It is rare now because normal saline or glycine are used for irrigation).

Syndrome of inappropriate ADH (SIADH).

Reset Osmolality.

SURGERY - PRINCIPLES IN GENERAL

HYPERTONIC HYPONATRAEMIA It is factitious or spurious hyponatraemia as total body sodium may be in excess. Hyperglyecaemia results in transient fluid shift from ICF to ECF resulting in volume expansion and dilutional hyponatraemia. It also interferes with laboratory procedures to measure serum sodium levels. For every 100 mg% increase in plasma glucose levels, serum sodium 150

3

FLUID AND ELECTROLYTES - 3 (SODIUM BALANCE)

decreases by 3 mmol/L or 1.6 mEq/L. Therefore, hyperglycaemia should be ruled out as a cause before starting treatment of Hyponatraemia. For example with plasma glucose levels of 1100 gm/dl, measured serum sodium is 127 mEq/L but actually it is 157 mEq/L In hyperglycaemic coma, volume deficit is due to osmotic diuresis and is treated with normal saline.

! ! !

Increased blood pressure Bounding pulse Raised JVP

It is important to note that in closed head injury, mild hyponatraemia may be fatal. With severe hyponatraemia, oliguric renal failure may ensue.

CLINICAL FEATURES The clinical features of hyponatraemia depend upon severity and rate of fall in serum sodium levels. With rapid fall in serum sodium, symptoms appear at serum sodium levels of 130 mEq/L. With gradual decrease, symptoms may not appear till serum sodium level falls to 120mEq/L.

TREATMENT Principles of treatment include; determination and treatment of the underlying cause, restriction and correction of intravenous fluids, and if the patient is symptomatic, correction of deficit. The deficit is corrected with hypertonic saline (3%) till serum sodium levels reaches 120mEq/L or improvement of symptoms followed by isotonic saline. 1L of 3% NaCl provides about 1283mEq Na.

Clinical features of primary hyponatraemia are different from those of secondary hyponatraemia.

Clinical features of primary hyponatraemia are similar to those of hypovolaemia. They are;

Replacement of sodium should be slow as rapid correction may lead to pontine demyelination. It should be done at a rate of less than 0.5 mmol/hr or less than 12mmol/day.

! ! ! ! !

Dry tongue.

Decreased skin turgor.

Oliguria.

Tachycardia.

Hypotension.

The clinical features of secondary hyponatraemia are due to hypotonia leading to increase in intracellular fluid volume. They are;

! ! ! ! ! !

Symptoms of cerebral oedema Increased deep tendon reflexes Drowsiness Convulsions Increased intracranial pressure Symptoms of volume overload SURGERY - PRINCIPLES IN GENERAL

Treatment of Primary Hyponatraemia is with salt and water repletion. Total sodium deficit is calculated as under; Fall in level of serum sodium x body water (0.6 x body weight), for example at serum sodium level of 115 mEq/L in a 70 kg, the sodium deficiency would be; (140-115)x(0.6x70)= 25 x 42 = 1050 mEq. Half of this deficit is corrected by slow infusion of 3% NaCl. Remaining deficit and maintenance dose is give as isotonic saline over next 48hrs.

Treatment of secondary hyponatraemia is salt and water restriction. These patients should not receive 151

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sodium containing crystalloid solutions as it would further increase ascites and tissue edema without raising serum sodium concentration. The main problem is to get rid of extra water and sodium. Loop diuretics can be administered to get rid of extra water along with hypertonic saline to cover sodium loss. An important point is to replace 25% of the hourly urine output.

These patients may be hypoproteinemic. 25% salt poor albumin may be given if albumin is below 2 gm/dl.

HYPERNATRAEMIA Hypernatraemia is defined as serum sodium level of more than 150 mEq/L. The main cause is the administration of sodium containing fluids to replace hypotonic water loss.

CLASSIFICATION ! Hypovolaemic hypernatraemia ! Hypervolaemic hypernatraemia ! Isovolaemic hypernatraemia CAUSES Hypovolaemic Hypernatraemia. ! Loss of sodium and water. > Renal. ! Diuretics. > Glycosuria/Ureamic diuresis. ! Acute Renal Failure ! Chronic Renal Failure ! Gastrointestinal Tract > Diarrhoea ! Skin > Burns > Sweating ! Lungs (treacheostomy) ! Adrenal insufficiency SURGERY - PRINCIPLES IN GENERAL

Hypervolaemic Hypernatraemia. ! Salt and water intake. > Iatrogenic. ! NaHCO3. ! Parenteral nutrition. ! Saline solutions. > Mineralocorticoids excess.

Isovolaemic Hypernatraemia ! Loss of water. ! Diabetes insipidus (Large volumes of hypotonic urine (<200 mOsmol/L are passed due to decreased or ineffective ADH). ! Central Diabetes insipidus (decreased ADH) > SOL (Space occupying lesion). > Head injury. > Hypophysectomy. > Infections. > Hypoxia. > Medications(clonidine, phenclocyclin). ! Nephrogenic DI (renal insensitivity to circulating ADH) > Familial. > Drugs (Lithium, methoxyflurane etc). > Hypokalaemia. > Hypercalcaemia. > Intrinsic renal disease. ! Reset osmostat. ! Iatrogenic (replacement of hypotonic losses with isotonic saline).

CLINICAL FEATURES Clinical features are those of volume depletion and dehydration. They are;

! CNS. > Moderate (restlessness, weakness). > Severe (delirium, fasciculations, seizures,

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! ! ! ! ! ! !

coma may lead to irreversible brain damage).

Dry, sticky mucous membranes (characteristic).

Red swollen tongue.

Flushed skin.

Oliguria.

Tachycardia/ Hypotension.

Thirst.

Hyperthermia (may be fatal).

TREATMENT Hypernatraemia is treated with hypotonic saline along with monitoring of sodium levels. Replacement should be slow as rapid correction may lead to cerebral edema. If total body water is deficient, free water infusions are given. The body water deficit is calculated by the formula Current body water = Normal Na/Measured Na x Total body water (0.6 x body weight) Deficit = Total body water-Current body water Half deficit is corrected in 24 hours. Rest is given over 2-3 days with adequate monitoring. Water may be given orally or as intravenous infusions of dextrose water, ½ saline or ½ D/saline In cases of hypervolaemia, sodium is restricted and if this is not possible oral free water or hypotonic solutions are infused along with diuresis.

Underlying cause has to be treated. Treatment of diabetes inspidus is as under For central diabetes inspidus, Desmopressin acetate 0.1-0.4 ml (10-40 ug) is given intranasally or 0.5-1 ml (2-4ug) is given by subcutaneous or intravenous injections.

SURGERY - PRINCIPLES IN GENERAL

For nephrogenic diabetes inspidus, drugs should be discontinued, electrolyte abnormalities should be corrected and sodium is restricted along with thiazide diuretics (50-100mg/d).

REFERENCES 1.

Shires III, GT, Borber AB, Shires GT. Fluid & Electrolyte management of the surgical patient, In Shwortze I, Shires GT, Spencer FC, Doly JM, Fisher JE, Galloway AC. (Ed).

Principles of surgery 7th Ed. 1999. Mc Grath Hills New York PP 53-76.

2.

Shires GT, Canizoro PC. Fluid, Electrolyte management of surgical patient. In sabiston DC (Ed). The text book of surgery. The biological bases of modern surgical practice 14th Ed. 1991. W.B Sanden Co. Philadelphia PP 57-76.

3.

Doly JM, Barie PS, Dudnch SI. Preparation of the patient. In Nylium (Lm), Baker RJ, Fischer JE. (Ed) Mastery of surgery 3rd Ed. 1997, Little Drown, Co. Boston. PP. 22-49.

4.

Franklin EW, Buchman TA. Fluid, Electrolyte, Acid base disorders. In Doherty GM, Meko JB, Olson JA, Peplinshi GR, Worral NK. (Ed) Washington Manual of surgery 3rd Ed. 2003. Lippincott Williams & Wilkins, Philadelphia. PP 3859.

Steele RJC, Patients with metabolic disorders. In Cuschieni A, Steelw RJC, Moosa AR (Ed). Essential surgical practice 4th Ed. 2000. Butterworth Heinmann Oxford PP. 205-14.

5.

SUMMARY Sodium Balance Hyponatraemia ! Classification & etiology ! Hypotonic hyponatraemia ! Isotonic hyponatraemia ! Hypertonic hyponatraemia ! Clinical features ! Treatment Hypernatraemia ! Classification ! Causes ! Clinical features ! Treatment

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1 PS-021

FLUID AND ELECTROLYTES -4 POTASSIUM BALANCE Shuja Tahir, FRCS, FCPS Abid Bashir, FCPS PHYSIOLOGY Potassium is the main intracellular cation. Only 2% of total body potassium in present in the ECF. Normal serum levels of potassium ranges from 3.3 - 4.5 mEq/L. Total ECF Potassium is only 63 mEq.(4.5 x 14L in 70 kg adult) but this little amount is critical for cardiac and neuromuscular functions.

Normal daily requirement of potassium is 1 mEq/kg.

Normal dietary intake is 50 - 100 mEq/day. Most of this intake (99%) is lost in urine. In patients with renal failure, the main problem is to get rid of potassium.

1% potassium is lost in stools. This loss may be increased in diarrhoea or mucous producing tumors of the colon.

In the kidneys H+ & K+ compete for exchange with Na+. In alkalosis, potassium is lost to conserve H+.

Similarly potassium also shifts to intracellular fluid compartment in exchange for H+ to compensate alkalosis. In acidosis exactly opposite happen.

Renal tubular excetion of potassium is increased when large quantity of sodium in the filtrate is available for reabsorption. Therefore, for isotonic fluids replacements for hypovolemia, potassium should also be replaced to cover increased losses.

SURGERY - PRINCIPLES IN GENERAL

HYPOKALEMIA Hypokalemia is defined as serum level of potassium below 3 mEq/L. CAUSES Hypokalemia is unusual because of large body stores and ample amount of potassium in diet. Main causes of hypokalemia are increased excretion through kidneys or prolonged deprivation.

The main causes can be summarized as follow: Increased Losses Increased renal excretion Diuretics Loss from GIT Diarrhoea Nasogastric aspiration Vomiting Entero-cutaneous fistulae Loss from skin Burns Decreased Intake Prolonged starvation Anorexia Continuous parenteral fluids without potassium for prolonged periods (in presence of obligatory urinary losses (20 mEq / day) Re-feeding syndrome (total parenteral nutrition without potassium as potassium is incorporated

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in rapidly dividing cells).

Intracellular Shift (Total potassium is same but ECF level falls because of shift to intra cellular compartment).

! ! !

2

To correct the deficit To treat the cause of hypokalemia To prevent further hypokalemia by replacing daily requirement and loss of potassium.

Metabolic alkalosis.

Increased insulin infusion.

Myocardial infarction.

Hypothermia.

Theophyllin.

Total Parenteral Nutrition without potassium.

CORRECTION OF DEFICIT Although potassium is main intracellular cation, still in the absence of redistribution factors, decrease in serum potassium gives some clue to the total body.

Potassium deficit: On an average decrease in serum level of 1 mmol/L (mEq/L) shows a total deficiency of 200-400 mEq. If serum level falls below 2 mEq/L, the deficit is about 1000 mEq.

CLINICAL FEATURES Mild hypokalemia is asymptomatic. Clinical features of hypokalemia are because of failure of normal muscular contractility.

This deficit is corrected with KCl at a rate of 20-40 mEq/hr.

They are ; Decreased tendon reflexes.

Generalized weakness leading to flaccid paralysis.

Paralytic ileus.

Following important precautions must be observed in replacing potassium ;

! ! !

Renal function of the patient must be adequate.

Use of CVP line if replacement has to be done at a rate of more than 10 mEq/h.

Proper cardiac monitoring should be done during the replacement.

Never replace more than 40 mEq/hour Never add more than 40 mEq of potassium to a litre of solution.

These features may be masked when the patient is dehydrated. Rehydration may further aggravate hypokalemia.

! !

ECG CHANGES Ectopics T - wave depression Prominent U wave Depressed ST segment Increased PR interval QRS Widening

TREATMENT OF CAUSE The cause of hypokalemia has to be treated e.g; diuretics should be stopped or changed. Similarly alkalosis if present, has to be corrected.

TREATMENT Principles of treatment are ; SURGERY - PRINCIPLES IN GENERAL

REPLACEMENT /PREVENTION Potassium may have to be replaced for prevention of hypokalemia in the presence of continuous losses.

The best way of replacement is oral. 40-100 mEq potassium may be replaced depending upon the 156

FLUID AND ELECTROLYTES - 4 (POTASSIUM BALANCE)

deficiency and daily loss.

In case of oral intolerance, severe depletion or symptomatic patient, potassium may be replaced parenterally taking all the above mentioned precautions.

It is safe to replace the upper limit of daily GIT losses provided the renal function is adequate. Potassium replacement without indication has to be avoided in oliguric patients and for up to 12-24 days postoperatively.

HYPERKALAMIA Hyperkalaemia is defined as serum potassium level of 6 or more than 6 meq/L. CAUSES

3

Shift of Intracellular Potassium To ECF Acidosis Insulin deficiency Tissue necrosis Severe injury, trauma, surgical stress Catabolic states Revascularization of severely ischemic limb Intravenous haemolysis Sepsis Cell lysis after chemotherapy Rhabdomyolysis as in crush syndrome Spurious Serum potassium levels are normal, but if the blood sample is taken from a strangulated limb (as if tourniquet is applied for a long time before taking blood sample), falsely high potassium levels are observed (because of potassium release from platelets and WBCs).

Renal Failure It is the most important and most common cause of hyperkalaemia. Kidneys play a major role (99%) in getting rid of extra potassium.

CLINICAL FEATURES Clinical features are because of hyper excitability of tissues.

Iatrogenic Administration of potassium in patients with impaired renal functions. Massive blood transfusions as stored blood has high serum potassium because of hemolysis.

Gastrointestinal Tract Nausea Vomiting Cramps Diarrhoea

Excessive GIT Bleeding Absorption of potassium from hemolysed blood in the gut.

Cardiovascular System ECG changes Elevated T wave Widening of QRS complex Decreased voltage of P wave Sinusoidal ECG pattern Heart blocks

Drugs Digitalis Succinyl choline

Cardiac arrest may occur in diastole.

SURGERY - PRINCIPLES IN GENERAL

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4

TREATMENT FOR MILD HYPERKALAEMIA Administration of exogenous potassium should be with held.

NaHCO3 50-100 ml 8.4% NaHCO3 (1 mmol/kg) is given I/V over 3-5 minutes. It may be repeated after 10-15 minutes.

Drugs which may interfere with the potassium metabolism should be discontinued. they include: Beta blockers.

NSAIDs. ACE inhibitor.

Potassium sparing diuretics.

CALCIUM GLUCONATE Calcium gluconate.has no effect or serum potassium levels but stabilizes the neuromuscular membrane minimizing the risk of fatal arrhythmias.

Dose is 5-10 ml of 10% Ca gluconate I/Vover 2-3 minutes.

Diuresis should be enforced using loop diuretics.

SEVERE HYPERKALAEMIA (Serum potassium > 6.5 meq/L). It is an acute emergency. Treatment of severe hyperkalaemia can be divided into two phases.

Emergency measures can temporarily shift the potassium into the cells, lowering serum potassium levels. It provides sufficient time for therapeutic measures.

TEMPORIZING MEASURES GLUCOSE + INSULIN One of the physiological effects of insulin is to take the potassium inside cells. Therefore insulin can be used as a temporary measure to deal with hyperkalaemia. To avoid hypoglycaemia, glucose has to be infused is at the same time.

The regimens are ; 1. 5% dextrose water (0.5 g/kg) + insulin (0.3 units/gm of glucose) as infusion.

2. 25 gm Dextrose water with 6-10 unit of insulin as a bolus.

3. 10% dextrose water (100 ml) + 20 units of insulin + 45 m Eq NaHCO3 SURGERY - PRINCIPLES IN GENERAL

It should not be given to patient on digitalis as heart block may occur.

INHALED b -AGONISTS Beta agonists may decrease serum potassium temporally for upto 2 hours, but may increase heart rate and blood pressure 2-4 ml of 0.5% solution (10-20 mg) of albuterol SO4 is given via nebulizer THERAPEUTIC MEASURES include: ADEQUATE HYDRATION WITH STRONG DIURESIS Normal saline is given with loop diuretics (frusemide) SODIUM/POTASSIUM EXCHANGE RESINS Na poly sterene sulfonate (Kayexalate) is used to exchange potassium for sodium. Sodium is retained and potassium is excreted as Potassium polysterene sulfonate. It takes upto 24 hours after administration to lower the serum potassium.

It may be given; 158

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Orally as 20-50 gm resin in 100-200 ml of 20% sorbitol every 4 hours.

Retention enema (20 gm in 50 ml 70% sorbitol added to 100-200 ml of water. It has to be repeated every 1-2 hours initially. As the patient stabilizes. The frequency may be reduced to 6 hourly.

DIALYSIS It helps to maintain the electrolyte balance. It may be the last option to get rid of extra potassium when other measures fail.

REFERENCES 1.

Shires III, GT, Borber AB, Shires GT. Fluid & Electrolyte management of the surgical patient, In Shwortze I, Shires GT, Spencer FC, Doly JM, Fisher JE, Galloway AC. (Ed).

Principles of surgery 7th Ed. 1999. Mc Grath Hills New York PP 53-76.

2.

Shires GT, Canizoro PC. Fluid, Electrolyte management of surgical patient. In sabiston DC (Ed). The text book of surgery. The biological bases of modern surgical practice 14th Ed. 1991. W.B Sanden Co. Philadelphia PP 57-76.

3.

Doly JM, Barie PS, Dudnch SI. Preparation of the patient. In Nylium (Lm), Baker RJ, Fischer JE. (Ed) Mastery of surgery 3rd Ed. 1997, Little Drown, Co. Boston. PP. 22-49.

4.

Franklin EW, Buchman TA. Fluid, Electrolyte, Acid base disorders. In Doherty GM, Meko JB, Olson JA, Peplinshi GR, Worral NK. (Ed) Washington Manual of surgery 3rd Ed. 2003. Lippincott Williams & Wilkins, Philadelphia. PP 3859.

5.

Steele RJC, Patients with metabolic disorders. In Cuschieni A, Steelw RJC, Moosa AR (Ed). Essential surgical practice 4th Ed. 2000. Butterworth Heinmann Oxford PP. 205-14.

SURGERY - PRINCIPLES IN GENERAL

SUMMARY Potassium balance Hypokalaemia ! Causes ! Increase losses ! Decreased intake ! Intracellular shift ! Clinical features ! Treatment ! Correction of deficit ! Treatment of cause ! Replacement and prevention Hyperkalaemia ! Causes ! Renal failure ! Iatrogenic ! GIT bleeding ! Drugs ! Intracellular to extracellular shift ! Spurious ! Clinical features ! Treatment ! Temporizing measures ! Therapeutic measures

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PS-022

FLUID AND ELECTROLYTES - 5 CALCIUM BALANCE Shuja Tahir, FRCS, FCPS Abid Bashir, FCPS Most of calcium in the body is present in the bones.

Plasma calcium is present in three forms; 1. Bound to albumin(40%).

2. Free unionized form (complexed to freely diffusible compounds (15%).

3. Free ionized form(45%). This unbound ionized form is physiologically active.

Calcium plays major role in neuro-muscular transmission, muscle contraction and coagulation.

Daily Ca intake is 500-1000 mg.

Serum calcium levels are 8.9 10.3 mg% (2.23-2.57 mmol/L).

Ionized calcium is 4.6-5.1mg% (1.15-1.27mmol/L).

The calcium metabolism is controlled by hormones (parathormone and calcitonin) and vitamin D. The unionized and ionized calcium are in equilibrium.

Alkalosis leads to ionized to unionized shift resulting in decreased serum levels of ionized calcium.

Ionization and solubility decreases in alkaline urine leading to stone formation. Acidosis has exactly opposite effect.

HYPOCALCAEMIA Hyopcalcaemia is defined as serum calcium levels less than 8mg/dl.

SURGERY - PRINCIPLES IN GENERAL

CAUSES ! Malnutrition. ! Vitamin D deficiency. ! Hypoparathyroidism.

- Surgery (parathyroid, thyroid).

Even after subtotal thyroidectomy transient hypocalcaemia may occur for 48-72 hrs which improves in next 2-3 days.

- Hypomagnesaemia (Impairs PTH secretion & functions) ! High GIT losses - Short gut syndrome, vomiting, diarrhoea ! Sequestration - Pancreatitis - Rhabdomyolysis (crush syndrome) - Massive blood transfusions (EDTA binds Ca) - Hypohosphataemia ! Ionized to unionized shift - Acute alkalosis Hyperventilation Vomiting.

NaHCO3 CLINICAL FEATURES Neurological Circumoral numbness Tetany Carpopedal spasm (Trousseu's sign) Facial twitching on taping Facial Nerve (Chevostek's sign) Laryngeal spasm

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Seizures (in extreme cases) ECG Prolonged QT interval Ventricullar Arrythmias TREATMENT Depends upon severity of symptoms and degree of hypocalcemia.

Severe symptomatic patients ! Parenteral Bolus 200 mg of elemental Ca (10-20 ml Ca gluconate 10% in 10 minutes is given to abort tetany Maintenance is done on 1-2 mg/kg/hr elemental Ca as infusion After improvement of symptoms/serum levels dose may be reduced to 0.3-0.5 mg/kg/hr Once normal, switch to oral therapy Serum levels of K, Mg & P should also be checked and corrected.

Asymptomatic or chronic hypocalcaemia For asymptomatic patient and mild hypocalcemia (serum calcium > 7.6 mg/dL) oral calcium can be replaced in doses of 1-2 g/day.

For severe asymptomatic hypocalcemia serum calcium < 7.6 mg/dL Vitamin D has to be added in following doses.

50,000 i.u Calciferol or 0.4mg dihydrocalciferol or 0.25-0.5 m g 1,25,dihydroxy vit D3 HYPERCALCAEMIA Hypercalcaemia is defined as serum calcium levels of more than 10.5mg/dl.

CAUSES

SURGERY - PRINCIPLES IN GENERAL

! ! ! ! ! ! !

! !

Milk alkali syndrome.

Vitamin D intoxication.

Total Parenteral Nutrition.

Thiazide Diuretics.

Hyperthyroidism.

Granulomatous disease.

Demineralization of bone.

- Hyperparathyroidism.

- Malignancies.

Primary.

Secondaries (metastasis).

Multiple myeloma.

Prolonged Immobilization.

Sarcoidosis.

If levels of serum Ca and PTH both are raised, hyperparathyroidism is the most likely diagnosis and if PTH level is low or normal, other causes should be considered.

CLINICAL FEATURES Bones (bone Pains).

Stones .

Groans (abdominal cramps).

Mental Moans (psychiatric problems).

Weight loss / anorexia.

Dehydration.

Increased thirst.

Adynamic ileus.

Nausea, vomiting, constipation CNS Altered mental status Somnambulance leading to stupor leading to coma Diffuse weakness leading to fatigue and lethargy Depression ECG QT shortening Arrythmias 162

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TREATMENT Treatment should be accompanied by strict monitoring. The principles of treatment include restriction of exogenous Ca intake, treatment of underlying cause and correction of volume deficit.

Thiazide diuretics should be stopped. Aggressive measures are required in severe cases. Critical level is 15mg/dl which may be lethal. This is usually encountered in cancer patients and patients on cytotoxic therapy.

SALINE + LOOP DIURETICS 250-500ml normal saline is infused per hour along with 20mg lasix I/V every 6 hours. The rate of infusion and dose of diuretic is adjusted and monitored accordingly. The aim is to maintain output at 200-300 ml/ hr. KCl 20mEq and MgSO4 8-16mEq (1-2g) may be added to each liter of normal saline to prevent magnesium and potassium deficiency.

Regimen may promote a loss of 2gm Ca in 24hrs SALMON THYROCALCITONIN It is mainly used in hypercalcaemia due to malignancy or hyperparathyroidism. After a test dose of 1 IU subcutaneously, 4 IU are given subcutaneous or intramuscular every 12 hours. It usually takes 6 to 10 hours to lower the serum calcium. The dose may be doubled after 48 hours if desired results are not achieved to a maximum dose of 8 IU 6 hourly.

Adequate hydration must be ensured to avoid renal failure.

PALMIDRONATE DISODIUM It is also used in malignancy induced Hypercalcaemia. Adequate hydration should be ensured. For mild to moderate hypercalcaemia (12-13.5 mg%), 60 mg is give in one liter of ½ saline, saline or dextrose water over 24 hours. For severe hypercalcaemia, the dose is 90 mg. The dose SURGERY - PRINCIPLES IN GENERAL

can be repeated after 7 days if required.

PLICAMYCIN The dose is 25 ug / kg / day. It is also given in 1 Liter of Normal saline or dextrose water over 4-6 hour once daily for 3-4 days. It takes 1-2 days to lower serum calcium which remains low for up to 1 week GALLIUM NITRATE The dose is 200mg/m2 body surface area. The dose is diluted in a liter of normal saline or dextrose water and infused over 24 hrs.

SODIUM SULPHATES MITHRAMYCIN (CYTOTOXIC) DRUG Its direct effect is on the bone to stop demineralization. Calcium levels remain normal for 12 weeks.

STEROIDS Prednisolone 40-80mg is given per day. It decreases calcium absorption from the gastrointestinal tract as well reabsorption from the bones.

HAEMODIALYSIS The haemodialysis may be required in case of emergency as most of the above mentioned measures take some time to lower the serum calcium.

PARATHYROIDECTOMY Emergency parathyroidectomy has to be performed if medical measures fail.

INORGANIC PHOSPHATE Inorganic phosphates decrease bone re-absorption and form CaPO4 salts. These may be used in emergency to lower the serum calcium. These are used very cautiously as rapid infusion may lead to 163

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tetany, acute renal failure or hypotension. Slow infusion over 12 hrs for no more than 2-3 days REFERENCES 1.

Shires III, GT, Borber AB, Shires GT. Fluid & Electrolyte management of the surgical patient, In Shwortze I, Shires GT, Spencer FC, Doly JM, Fisher JE, Galloway AC. (Ed).

Principles of surgery 7th Ed. 1999. Mc Grath Hills New York PP 53-76.

2.

Shires GT, Canizoro PC. Fluid, Electrolyte management of surgical patient. In sabiston DC (Ed). The text book of surgery. The biological bases of modern surgical practice 14th Ed. 1991. W.B Sanden Co. Philadelphia PP 57-76.

3.

Doly JM, Barie PS, Dudnch SI. Preparation of the patient. In Nylium (Lm), Baker RJ, Fischer JE. (Ed) Mastery of surgery 3rd Ed. 1997, Little Drown, Co. Boston. PP. 22-49.

4.

Franklin EW, Buchman TA. Fluid, Electrolyte, Acid base disorders. In Doherty GM, Meko JB, Olson JA, Peplinshi GR, Worral NK. (Ed) Washington Manual of surgery 3rd Ed. 2003. Lippincott Williams & Wilkins, Philadelphia. PP 3859.

5.

Steele RJC, Patients with metabolic disorders. In Cuschieni A, Steelw RJC, Moosa AR (Ed). Essential surgical practice 4th Ed. 2000. Butterworth Heinmann Oxford PP. 205-14.

SURGERY - PRINCIPLES IN GENERAL

SUMMARY Calcium Balance Hypocalcaemia ! Causes ! Clinical features ! Treatment Hypercalcaemia ! Causes ! Clinical features ! Treatment

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PS-023

FLUID AND ELECTROLYTES - 6 MAGNESIUM BALANCE Shuja Tahir, FRCS, FCPS Abid Bashir, FCPS Magnesium is mainly an intracellular cation. It shares some properties of potassium and some of calcium.

There is no direct hormonal regulation of Mg metabolism. Excretion is through the kidneys.

Normal serum levels are 1.3 - 2.2 meq / L (0.65 - 1.1 mmol / L) HYPOMAGNESEMIA CAUSES Excessive Losses From GIT Diarrhoea Vomiting Malabsorpotion Biliary fistula From kidneys Marked diuresis Hyperaldosteronism Renal tubular acidosis Chronic Alcoholism Drugs Loop diureties Cyclosporine Cisplastin Aminoglycosides Shift into ICF compartment Acute MI Alcohol withdrawal Glucose containing solutions Redeposition into bone

SURGERY - PRINCIPLES IN GENERAL

Trauma Patients After parathyroidectomy CLINICAL FEATURES Hypomagnesemia is usually accompanied by hypokalaemia and hypo- phosphatemia. Main problem is hyperexcitability of neurological tissues.

The symptoms are: Tremors Exaggerated reflexes Tetany Altered mental status in severe deficiency ECG changes are similar to that of hypokalaemia.

They are ; Depression of T wave.

QRS Complex Widening.

Increased PR and QT intervals.

Ventricular arrythmias may occur in patients on digitalis.

TREATMENT Mg can be given orally or parenterally depending upon the severity of the situation. In acute emergency (serum Mg < 1.0 meq/L or if the patient is symptomatic)1-2 gm of MgSO4 (equivalent to 816m eq/L) is given an as I/V bolus over five minutes, followed by infusion of 1-2 gm hourly. Once the

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patient in stabilized the dose can be reduced to a maintenance dose of 0.5 - 1g /hour.

!

For asymptomatic patients, the dose of parenteral MgSO4 is 50 - 100 mEq / day (6-12gm) for 3-5 days till the stores are replenished.

!

It is important to note that I/V MgSO4 is treatment of choice for patients of torsades de pointes as well es eclampsia and pre-eclampsia. For maintenance, magnesium can be given orally.

In life threatening conditions, as for cardiac conduction abnormalities or respiratory depression, 10-20ml of 10% Ca-gluconate can be administered I/V over 5-10 minutes.

In case of renal failure, haemodialysis has to be done to get rid of extra Mg.

In life threatening conditions as for cardiac conduction abnormalities or respiratory depression 10-20 ml of 10% calcium gluconate can be administered I/V over 5-10 minutes. In case of renal failure, dialysis has to be done to get rid of extra Mg.

Oral magnesium is available in three forms ; REFERENCES

! ! !

MgO2 available as 400mg tab, equivalent to 241mg elemental magnesium (20m eq).

Magnesium gluconate (500mg tab.) Eq. to 27mg or 2.3m eq, magnesium.

Mg chloride

HYPERMAGNESEMIA ! Hypermagnesemia is highly infrequent ! In severe hypermagnesemia clinical features are due to (over-stable) / latent neuromuscular membranes They are ;

! ! ! ! !

Depressed tendon reflexes.

Paralysis of voluntary muscles.

Hypotension.

Sinus brady cardia.

Prolonged PR, QT interval.

TREATMENT Stop any exogenous Mg administration. Hydration and diuresis (in presence of normal renal functions, normal saline is administrate a rate of 250-500 mg/ml along with 20mg frusenide I/V every 6 hourly.

SURGERY - PRINCIPLES IN GENERAL

1.

Shires III, GT, Borber AB, Shires GT. Fluid & Electrolyte management of the surgical patient, In Shwortze I, Shires GT, Spencer FC, Doly JM, Fisher JE, Galloway AC. (Ed).

Principles of surgery 7th Ed. 1999. Mc Grath Hills New York PP 53-76.

2.

Shires GT, Canizoro PC. Fluid, Electrolyte management of surgical patient. In sabiston DC (Ed). The text book of surgery. The biological bases of modern surgical practice 14th Ed. 1991. W.B Sanden Co. Philadelphia PP 57-76.

3.

Doly JM, Barie PS, Dudnch SI. Preparation of the patient. In Nylium (Lm), Baker RJ, Fischer JE. (Ed) Mastery of surgery 3rd Ed. 1997, Little Drown, Co. Boston. PP. 22-49.

4.

Franklin EW, Buchman TA. Fluid, Electrolyte, Acid base disorders. In Doherty GM, Meko JB, Olson JA, Peplinshi GR, Worral NK. (Ed) Washington Manual of surgery 3rd Ed. 2003. Lippincott Williams & Wilkins, Philadelphia. PP 3859.

5.

Steele RJC, Patients with metabolic disorders. In Cuschieni A, Steelw RJC, Moosa AR (Ed). Essential surgical practice 4th Ed. 2000. Butterworth Heinmann Oxford PP. 205-14.

SUMMARY

Magnesium Balance Hypomagnesemia Hypermagnesemia

! !

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Burns

BURNS

1 PS-024

BURNS Shuja Tahir, FRCS, FCPS M. Y Shah, FRCS Burn is destruction of skin or body tissues due to thermal, physical, chemical or electrical trauma.

Spontaneous healing occurs with good cosmetic results within 3-6 days.

The burn is a wound in which there is coagulation necrosis of the tissue.

The burns can be classified on basis of ;

! ! ! ! ! !

Degree of burns.

Depth of burns.

Zones of burnt area.

Extent of burns.

Nature of burns.

Site of burns.

DEGREE OF BURNS ! First degree. ! Second degree. ! Third degree. ! Fourth degree.

FIRST DEGREE BURNS Only superficial layers of epidermis are destroyed in these burns. The usual cause is exposure to sun light1,2.

These present with erythema, are quite painful and sensitive to touch. The surface clearly and widely blanches to pressure. These may be dry or have small to moderate size blisters.

SURGERY - PRINCIPLES IN GENERAL

SECOND DEGREE BURNS All layers of epidermis and some part of dermis is destroyed in these burns. Usual cause is limited exposure to heat, flames or chemicals1,2.

These present with erythema and whitish fibrinous exudate and blisters. The skin colour is pink or mottled red. The burnt area is painful. There is coagulation necrosis and fluid collection (blister formation). There is coagulation and congestion of the subdermal plexus. The wound is sensitive to touch. The surface may blanch to pressure.

Sometimes deep second degree burns may be insensitive to pin prick but have intact pressure sensations. Superficial layers of skin can be removed easily.

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The healing occurs over a period of 2-3 weeks or more. Usually skin grafting may not be required in these burns. If the area gets infected, these change into full thickness burns.

Hair can be easily pulled out of the follicles. These are insensitive to touch, pin prick or pressure.

These burns don't heal without skin grafting.

FOURTH DEGREE BURNS These are the burns when deeper tissue such as fascia, muscles, bones and tendons are also involved1,2.

DEPTH OF BURNS ! Superficial burns. ! Partial thickness burns. ! Deep or full thickness burns.

THIRD DEGREE BURNS Whole of the skin is destroyed and patient presents with dry, hard, inelastic burnt area. The skin may look pale and be mistaken for normal. The skin looks white, black charred and leathery1,2. Black thrombosed veins may also be visible.

SUPERFICIAL BURNS These are the type of burns when only epidermis or part of epidermis has been destroyed. These show blisters on examination and are pink in colour.

Sensations are also present. If treated adequately, these heal within 2-3 weeks requiring no skin cover and do not cause contractures or deformities.

Good cosmetic results are achieved without much residual losses and there is minimal scarring. These are similar to first degree burns.

PARTIAL THICKNESS BURNS These are the burns in which whole of the epidermis and part of dermis is lost. As some areas of dermis are not destroyed, healing may occur spontaneously provided the infection is prevented and patient is treated adequately.

It may be bright red due to fixation of haemoglobin in sub-dermis. It is anaesthetic or hypoaesthetic. No blisters are seen. Subdermal vessels don't blanch.

SURGERY - PRINCIPLES IN GENERAL

The cosmetic results are not as good as in superficial burns and some residual damage is left. These burns become full thickness in the presence of infection.

These are similar to second degree burns.

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FULL THICKNESS OR DEEP BURNS These are the burns in which whole of the epidermis and dermis is burnt. Sensations are absent on examination. These can be diagnosed from charred colour, loss of sensations and inspection of the burnt area.

These require skin grafting otherwise chronic ulceration, keloid formation, contracture formation and deformities are seen.

treatment. Unfortunately the cells die within 24-48 hours if not treated properly. iii). ZONE OF HYPERAEMIA It is the area which is minimally injured and it eventually heals within seven days. It is the most peripheral part of the burnt area.

EXTENT OF BURNS The extent of burns is measured in the percentage area of the total body surface.

These are similar to third degree burns.

ZONES OF BURN Three zones are seen at and around the burnt area.

Skin surface Zone of Hyperaemia Zone of stasis

Zone of Coagulation

The extent of each zone is proportional to the intensity and duration of exposure of the tissue to the causative agent. i). ZONE OF COAGULATION It is the burnt area which is dead due to thermal trauma.

This can be measured by the Wallace's Rule of nine.

The percentage of various areas of the body is given below ; Head and Neck Right upper limb Left upper limb Right lower limb Right lower limb Left lower limb Left lower limb Chest Chest Abdomen Abdomen Perineum

(front) (back) (front) (back) (front) (back) (front) (back)

9% 9% 9% 9% 9% 9% 9% 9% 9% 9% 9% 1%

The percentage area of burns can also be measured by comparing it with the size of the out-stretched hand of the patient.

Out stretched hand of the patient = 1% The burns can be classified as below ;

ii). ZONE OF STASIS It is the area just out side the zone of coagulation. It may survive in ideal conditions with adequate SURGERY - PRINCIPLES IN GENERAL

! !

Minor burns.

Moderate burns.

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! ! ! !

Major burns.

Massive burns.

Simple burns.

Complicated burns.

25% body surface area in adults15.

Full thickness burns with 2-10% body surface area involvement.

No primary area is involved.

No inhalation injury is present.

No associated injury is present.

The patient is usually low risk.

These patients require resuscitation and respond to treatment satisfactorily. These patients must be hospitalized3.

MAJOR BURNS These are first and second degree burns with greater than 20% body surface area involvement in children and more than 25% body surface area in adults.

Full thickness burns involving more than 10% body surface area.

MINOR BURNS These are the first or second degree burns with less than 10% body surface burns in children and less than 15% body surface burns in adults3,15.

Full thickness burns involving less than 2% body surface area are also minor burns.

No primary area is involved.

No inhalation injury.

No associated injury is present.

These do not require resuscitation and hospitalization. These can be treated as out patients3.

MODERATE BURNS These are first or second degree burns with 10-20% body surface area involvement in children and 10SURGERY - PRINCIPLES IN GENERAL

All burns involving hands, face, ears, eyes, feet and perineum (Primary areas).

All inhalation injuries, electrical and complicated burns.

Co-morbid factors are present.

The patient is poor risk.

These patients must be hospitalized and require special burn unit management.

CRITERIA FOR REFERRAL TO BURN UNIT ! More than 10% surface area burn in children. ! More than 15% surface area burns in adults. ! Inhalation injury. ! Burns involving airway. ! Electrical burns. ! Chemical burns. ! Involvement of primary areas.

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MASSIVE BURNS (EXTENSIVE BURNS) These are major burns with more than 70% body surface area involvement.

! ! ! !

Electric burns.

Sun burns.

Irradiation burns.

Friction burns.

The prognosis is extremely poor in these patients15.

SIMPLE BURNS These are the minor burns when there is no associated problem (complication) present.

COMPLICATED BURNS These are the burns with associated problems such as inhalation of smoke.

Associated injuries are also present.

Septicaemia, renal failure and shock is present.

Respiratory embarrassment and anoxia complicates the burns.

The outcome is poorer in such cases.

DRY BURNS OR BURNS DUE TO DRY HEAT These are the burns received directly from fire and flames.

FAT BURNS Cooking fat or oil has a much higher temperature (1800C) than boiling water and hot fat moves slowly on the skin surface. Therefore fat spills cause deep burn.

INHALATION INJURY The inhalation of poisonous gases is the single most lethal component of a burn and should always be looked for at the initial assessment.

Mechanism of Burn Injury Type of Burn

Tissue Injury

Scalds

Partial thickness deep burn

Fat burns

Usually full thickness burn

Flame burns Electrical burns Cold injury Friction injury

Patches of partial and full thickness Full thickness with deep extension Ice formation, tissue freezing, vasospasm Heat injury & abrasions

NATURE OF BURNS ! Dry burns. ! Burns due to moist heat or scalding. ! Fat burn. ! Caustic burns. ! Acid burns.

SURGERY - PRINCIPLES IN GENERAL

Apart from the history of the accident having occurred in an enclosed space, examination may show burnt skin around the mouth and nostrils with carbon inside the nose and oedema of the oral, nasal and pharyngeal mucosa.

Inhaled hot air damages the upper respiratory tract and in particular, produces oedema of the larynx.

This is usually diagnosed early. It is compounded by hypoxia.

The inhalation of carbon mono-oxide and particularly in a domestic setting, very toxic gases such as hydrogen cyanide, are released from the combustion of synthetic modern upholstery.

The damage produced by these chemicals tends to become apparent later and affect the lower respiratory tract leading to atelectasis and 173

6

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pneumonia.

ACID BURNS These are caused by coming into contact with acids.

Investigations include baseline chest radiography, monitoring of blood gases, serum carbon monoxide concentrations, examination of the upper respiratory tract by laryngoscopy and fibreoptic bronchoscopy.

Treatment rests on the inhalation of humidified air, correction of pulmonary oedema and the administration of prophylactic antibiotics. Treatment with a short course of high dose steroids may be helpful.

More severe injuries require oxygen treatment and if the blood gases deteriorate, positive pressure ventilation may be required. Tracheostomy is generally best avoided.

MOIST BURNS OR SCALDS These occur due to steam, tea, hot water or hot milk.

These cause early blistering and are very painful.

CHEMICAL BURNS When strong alkalies are accidentally brought into contact with skin, it is burnt.

Specific problems and remedies for chemical burns Agent Acids Alkali

Penetrate slowly & deeply

Corrosive deeply Hydrochloric acid Penetrates Hypo-calcaemia Aryhthmias Cement

Alkali burn Symptoms develop later

Chemical burns are often deeper than these initially appear to be and may progress with time. Initial treatment is dilution of the chemical, which is usually best achieved by prolonged submersion in continuous running water.

In general, neutralizing agents are contraindicated as they may cause exothermic reactions and increase tissue damage. Damage to the eye should be managed by initial copious irrigation with saline or water and an ophthalmic opinion should be obtained.

ELECTRIC BURNS AND ELECTRICAL INJURY These are the burns which occur due to passage of electric current through the body. These are associated with electric shock.

These are usually full thickness burns and involve deeper tissue as well. The damage is much more than it appears. These are usually complicated by vascular thrombosis and general problems of electrical shock.

Remedy

Problems Very painful

The severity of a chemical burn depends on the agent encountered, its concentration, quantity, and the length of time the tissues are in contact with it.

Irrigation Sodium bicarbonate Prolonged irrigation > 1 hr Excision Irrigation Calcium gluconate 10% injections Early excision Prolonged irrigation

SURGERY - PRINCIPLES IN GENERAL

Resistance to the flow of electrical current results in the production of heat. Bone has the highest resistance, followed by in descending order, fat, muscle, skin, blood vessels and least of all, nerves.

Skin epidermis is non vascular and offers a high resistance when dry, but this resistance is proportional to the thickness of the skin, its temperature, and the amount of moisture it contains.

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Skin can be damaged by either the flow of electricity through it, an arcing injury or by the ignition of clothing causing flame burns.

Deeper damage depends on the path of the electric current. Passage along bone produces the greatest heat and will result in adjacent deep muscle damage.

The indication for a fasciotomy (releasing of the deep fascia) may not initially be evident. Delay in treatment results in even more muscle necrosis from ischaemia caused by the unrelieved oedema.

The passage of the current along blood vessels can produce intimal damage with vessel thrombosis. This will in turn produce tissue death, which may become apparent only at later stage. Both these factors account for many electrical burns being far more extensive than apparent at the initial examination.

Lowest voltage burns (<1000 v) such as from a domestic supply (240 V), 950 1&2) causes significant contact wounds and may induce cardiac arrest but no tissue damage.

High voltage burns (>1000 v) cause damage by flash and current transmission.

The flash forms an arc which may cause cutaneous burns and ignite the clothing but it will not result in deep damage. Electric current transmission will result in cutaneous entrance and exit wounds and deep tissue damage.

IMPORTANT FACTORS IN ELECTRICAL INJURY ! Type of current. ! Voltage of current. ! Amperage of current. ! Resistance offered by body. ! Pathway of current through body. ! Duration of contact.

COMPLICATIONS OF ELECTRICAL INJURY ! Cardiac arrest. ! Renal failure. ! Renal calculus. ! Spinal cord damage. ! Cataract formation.

COLD INJURY Tissue damage from cold occurs in industrial accidents due to spills of liquid Nitrogen or similar substances.

The injuries cause acute cellular damage with the possibility of partial or full thickness burn severe cooling can freeze tissues and produce in ice formation causing cellular disruption.

Frost bite is due to prolonged exposure to cold climate. There is often ischaemic damage due to vasospasm.

Lighting stroke cause very high voltage, very short voltage discharge and direct strike has a high mortality.

SUN BURNS These occur when skin is exposed to excessive sun heat in patients not used to exposure to sun such as white skin people. These burns are usually superficial burns and heal spontaneously. These can be associated with sun stroke in hot weather. The outcome may be serious in these cases.

A side stroke may cause superficial burns to the skin and deep exit burns to the feet.

IRRADIATION BURNS These are due to x-ray or radio-active irradiation.

SURGERY - PRINCIPLES IN GENERAL

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General effects of irradiation are far worse than the skin damage. These are often associated with hyperpigmentation.

SITE OF BURNS Following areas are called primary burn areas. The burns of these areas are considered as major burns because of special problems faced for adequate treatment.

Face.

Neck.

Hands.

Feet.

Perineum.

MANAGEMENT PLAN AND PROGNOSIS OF EXTENSIVE BURNS The idea about prognosis of the burns is helpful in making the decision about treatment of these patients.

The chances of survival become poorer with;

! !

FIRST AID ! Stop the burning process. ! Try to remove the victim from site of burn. ! Remove the clothes and jewelry and cool the burnt area with water. ! Remove the dry chemical by wiping off as much as possible, then wash the area. ! Check the cardiopulmonary function and clear the airway5.

RESUSCITATION The active resuscitative measures are used according to the standard trauma management plan such as;

Increase in percentage burnt area over 60% body area4.

The chance of survival become poor with age after forty years.

The objectives of management of extensive burns are ;

! First aid. ! Resuscitation.4 ! Diagnosis and assessment. ! Early period managements. > a. Maintenance of hemodynamic status of the patient.

100

PROGNOSIS IN A BURNT PATIENT 80

PERCENTAGE AREA BURNT

! ! ! ! !

> Wound management.4 > Prevention of infection. > Patient's comfort. ! Provision of skin cover. ! Rehabilitation6,7 ! Physiotherapy. ! Reconstruction. ! Treatment of complications. ! Psychotherapy.

No chance of recovery

Little chance of recovery 60

40

Good chance of recovery after adequate treatment

20

0 0 years

20 years

40 years

60 years

80 years

AGE IN YEARS

SURGERY - PRINCIPLES IN GENERAL

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A. AIR WAY Adequate airway should be secured. The debris and blood from the oral and tracheo-bronchial passages should be mechanically removed or sucked with the help of an electric sucker.

The airway should be maintained and breathing of patient should be assessed and maintained.

Endotracheal intubation or tracheostomy will ensure clear airway if required.

Assisted ventilatory support should be offered if required.

B. BREATHING Breathing problems are seen due to decreased respiratory drive and unstable chest wall. These are commonly seen in patients with inhalation injuries.

The breathing problems are worst in burnt patients who already suffer from respiratory diseases. It can be managed with assisted ventilation.

The common causes of ineffective ventilation after clear and patent airway are ;

! ! !

Malposition of endotracheal tube.

Haemothorax.

Pneumothorax.

These can be properly managed after correct diagnosis.

C. CIRCULATORY VOLUME The fluid losses are proportionate to the %age body surface area of burns. These should be replaced actively and urgently to prevent hypo-volemic shock and renal failure.

Loss of blood may also occur from associated injuries or due to the thermal necrosis of the vessel wall. It should be stopped as quickly as possible.

Bleeding from superficial wounds can be controlled by compression dressing, ligation or stitching of the wound. Internal bleeding requires surgery and control.

The lost amount of blood is replaced with blood or other intravenous fluids to keep the circulatory volume as normal as possible.

Regular and careful monitoring of the circulatory volume is performed by measurement of pulse and blood pressure record, skin perfusion and calculating urinary output.

D. DISABILITY The patients with associated brain trauma have various degree of neurological disability.

Glasgow coma score should be accurately documented mentioning clearly whether the patient is paralysed or intubated endotrachealy.

E. EXPOSURE Proper exposure is most important for accurate and complete examination. The patient should be completely exposed after adequate resuscitation for re-examination.

It is advisable to perform structured examination so that nothing is missed and it should be ticked on the examination check list.

Accurate calculation of %age body surface area; Depth of the burnt area and on the diagram.

SURGERY - PRINCIPLES IN GENERAL

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Associated injuries should be documented and treated according to the priority.

Continuous monitoring and repeated examination is very important in these patients.

EARLY PERIOD MANAGEMENT The burn wound should be cleaned adequately and patient should be put on clean bed with a cradle and clean sheets over it.

The room temperature should be acceptable and comfortable to the patient. Overheating is not helpful to these patients as it increases fluid loss and discomfort to the patient.

The number of attendants should be kept to minimum possible to avoid hospital (nosocomial) infection which is quite common and serious in burn victims.

Sedation and analgesia is essential in early post burn period.

FLUID REPLACEMENT Assessment of fluid replacement is identified from;

! ! !

Time of burn injury.

Weight of patient. %age burnt area.

The amount of fluid requirement for early period;

!

10

Careful observations and active management should be started soon after the burns. The fluid and electrolyte balance should be maintained.

All fluids and medicines are given intravenously for proper absorption and early action.

Intravenous line is secured to a large size vein with a large bore cannula so that adequate amount of fluid can be infused in the calculated time to compensate the losses.

The patient with burns are infused Ringers solution 4 ml per kg body weight per % of burnt area during first twenty four hours (Parkland formula).

Colloid solution (plasma) is also infused in addition to the electrolyte solution during subsequent period.

Replacement of fluids and electrolytes must be started immediately.

Extensive knowledge of pathophysiology of burns is very helpful in adequate management of burns.

In children with more than 10% burnt area and adults with more than 20% burnt area, intravenous fluid therapy is mandatory. The amount and speed of fluid replacement is calculated according to the following formula ; mls of fluid to be given over four hours = weight of the patient in kgs x %age burnt area / 2.

Weight (Kgs) x % burnt area x 2

This calculated amount of fluid is infused as below; Every 4 hours for first 12 hours.

Every 6 hours for next 12 hours.

Every 12 hours for next 12 hours.

SURGERY - PRINCIPLES IN GENERAL

The amount of fluid thus calculated should be given at first in four hourly rations then six hourly and then in twelve hourly rations depending upon the state of hydration which can be assessed by monitoring following parameters regularly; 178

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1.

2.

3.

4.

5.

Urinary output.

Blood pressure estimation.

Pulse rate.

Body temperature estimation.

Haematocrit estimation.

The plasma or similar fluid should be used for the replacement.

Daily requirement of fluids 2.5 liters should also be replaced by 5% dextrose and 0.9% saline intravenously.

The urinary output of the patient is measured very carefully. This is a very simple and effective guide for assessment of renal function and hydration of the patient.

Urinary output of 30 - 50 mls per hour in an adult or 1.2 mls / kg / per hour in a child is satisfactory indication of adequate renal function.

Examination of the urine for presence of red cells or haemoglobin is helpful prognostic index.

Haemoglobinuria is a bad prognostic sign.

Serial haematocrit or haemoglobin estimations are helpful in assessing the amount of loss of blood.

Estimations of electrolytes and urea level are performed for the adequate maintenance of fluid and electrolyte balance and assessment of renal function.

Parenteral or adequate oral feeding should be offered to keep the calories in balance.

Following factors are critical in achieving positive outcome in all burnt patients specially the paediatric SURGERY - PRINCIPLES IN GENERAL

patients;

! ! ! ! ! ! !

Burn size (%age).

Depth of burn.

Appropriate fluids and electrolytes replacement.

Respiratory management.

Nutritional support.

Wound care.

Psycho social needs of patient as the recovery time is lengthy16.

DIAGNOSIS AND ASSESSMENT Proper history and adequate examination help to reach a correct diagnosis and accurate assessment.

One should try to make following observations ;

! ! ! ! ! !

General condition of the patient.

Area involved in burns.

Extent of burns.

Depth of burns.

Type of burns.

Associated problems (Co-morbid factors).

GENERAL CONDITION The condition of the patient usually deteriorates four to six hours after the burns due to loss of fluids and proteins.

These changes and losses are so dramatic that the patient may look absolutely well half an hour after the burns but may be in irreversible shock six hours later.

One should assess the general condition of patient and document all the vital observations which are to be compared with future changes.

LOCATION OF BURNS The importance of burnt area location cannot be minimized as the effects of burns will depend upon 179

BURNS

the areas involved.

Face burns lead to cosmetically unacceptable situations. The inhalation of smoke may lead to respiratory embarrassment and death if not managed adequately.

The burns over flexor areas of the joints lead to contracture formation, restricted joint movement and deformities.

The hand burns may lead to serious effects due to contractures, deformities and stiffness.

The burns over the anterior part of the chest may lead to hypertrophic scar and keloid formation.

The treatment of burns at different areas varies depending upon the functional needs of that area.

The involvement of primary areas changes the extent of burns to major burns. These should be clearly noted.

EXTENT OF BURNS The extent of burns can be assessed using rule of nine to calculate percent area burnt. The outcome of management will depend upon the extent of burns.

12

chronic ulceration and deformities. These take longer time to heal and require active surgical management.

TYPE OF BURNS Burns due to chemicals such as acid or caustics and electric burns are usually full thickness burns and there may be involvement of the deeper tissue including muscles and bones.

The chances of delayed healing, keloids, deformities and contracture formation are more. These require skin grafting to avoid complications.

The electric shock causes added problems due to passage of electric current through the vessels and thus causing severe intimal damage and anoxic changes due to impaired circulation.

ASSOCIATED PROBLEMS OR CO-MORBID FACTORS The associated problems with the burns are due to the effects of burns. In the early post burn period shock and acute renal failure are common problems.

Respiratory failure may also be present in patients with the history of smoke inhalation.

DEPTH OF BURNS Superficial burns are relatively easy to treat as these do not require skin grafting if treated adequately.

These do not cause deformities. Satisfactory cosmetic results are achieved without much residual losses. These burns heal early.

The involvement of eyes in burns will require its treatment.

The myocardial insufficiency of the burned patients is due to the changes of preload-afterload, disturbances of myocardial compliance and desynchronisation of the left and right ventricular function. Fluid therapy also affects the myocardial function.

Partial thickness and deep or full thickness burns are the ones which may require skin grafting. If not treated properly may lead to contracture formation,

Calcium channel blockers and 창 adrenergic blockers are useful to improve the myocardial function in these patients.

SURGERY - PRINCIPLES IN GENERAL

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Associated injuries during burn accident alter the outcome of the burnt patient. Previous illnesses also increase the morbidity of the burn victim.

TREATMENT OF BURNT AREA (WOUND CARE) The treatment of burnt area is star ted simultaneously as soon as the patient is resuscitated.

The patient should be isolated under strict aseptic conditions.

The burnt area can be treated by exposure method or by dressing method depending upon the choice of the surgeon and needs of the patient.

! ! !

DRESSING METHOD Sterile and oily gauze dressing is used, dry gauze dressing leads to removal of the granulation tissue.

! ! !

Meticulous hand washing and use of sterile gloves while wound handling improves the outcome tremendously.

Topical antibacterial agents should be used over the wound. Vigorous surgical debridement on regular basis must be performed.

Wound biopsy for histological examination and quantitative culture is highly recommended in severely ill patient with unclear etiology or site of skin infection.

Blood culture and wound biopsy culture should be performed and appropriate systemic antibiotics should be given10.

The advantages and disadvantages of exposure and dressing method are as follows: TREATMENT OF BURNS EXPOSURE METHOD ! The burnt wound dries quickly.

SURGERY - PRINCIPLES IN GENERAL

There are less chances of infection in dry wound. Nursing care is easy.

All areas can be treated.

Private or isolated aseptic room is required as the patient cannot be nursed without clothes in the middle of ward.

All areas cannot be dressed easily This is a good method for minor burns in out patient cases, in burns over fingers and joint areas.

In both cases the patient should be kept in a separate clean room at temperature which should be comfortable for the patient.

If patient feels cold and shivers, infra red lamp should be used for providing warmth and stimulating wound healing.

PREVENTION OF INFECTION Dead tissue and debris should be removed to minimize toxaemia. Antiseptic warm bath of the burnt area is helpful in keeping the infection away. Early skin grafting can be helpful but failures are more due to the poor general condition of the patient.

BURN WASH The patient is encouraged to clean and wash the burnt area on regular basis. It helps to get rid of dead and burnt tissue.

PROVISION OF SKIN COVER The skin cover can be achieved by; Split skin graft.

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Meshed skin grafts (useful in extensive burns).

The skin cover should be provided as early as possible. It prevents wound infection and achieves acceptable cosmetic results.

REHABILITATION Early mobilization of the patient and physiotherapy helps in rehabilitation of the patient. The patient should be able to look after himself independently at home and at work.

The patient should be able to involve in his leisure occupation independently12.

PHYSIOTHERAPY The burn victim must have physiotherapy in the bath or room after the bath. It prevents the joint stiffness and contracture formation.

Analgesia and warm water hydrotherapy helps in better compliance.

RECONSTRUCTION Reconstruction of the burnt areas is an important aspect of treatment of burn victims.

TREATMENT OF COMPLICATIONS EARLY COMPLICATIONS PULMONARY COMPLICATIONS Chest infection and pneumonia are common problems which follow inhalation injuries in burn cases.

Adult respiratory distress syndrome (ARDS) is one of the worst pulmonary complications in burnt patients.

Pulmonary edema follows inhalation injuries or fluid over-load in burnt patients. The early appearance of SURGERY - PRINCIPLES IN GENERAL

pulmonary edema in a burnt patient is a bad prognostic sign.

Collapse of lung and aspiration pneumonia may be seen in patients with burns.

Pulmonary embolism is relatively rare in burnt patients.

The treatment is symptomatic.

STRESS ULCERATION (CURLING'S ULCERS) It is the generalized ulceration of the gastric mucosa in a severely burnt patient. The patient presents with haemetemesis and melaena. It should be prevented.

The burn victim should be given intravenous doses of H2 blockers on regular basis during initial treatment.

ACUTE GASTRIC DILATATION This is one of the less common problems in burnt patients15. The patient presents with sudden deterioration in general condition and vomiting.

Ultrasonography or barium meals studies help in diagnosing this condition.

PARALYTIC ILEUS This is another common gastro-intestinal complication in burnt patients. It occurs as a result of sepsis, fluid overload and electrolyte imbalances15.

ACUTE ACALCULOUS CHOLECYSTITS This is a less common complication in a burnt patient15. It is probably due to sepsis following burns.

PERFORATING CHOLECYSTITIS It is a very rare complication. The outcome is usually fatal. Surgical treatment at an earlier stage is the only

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Hope for survival8.

RENAL FAILURE Acute renal failure is quite common complication in severely burnt patients. It is secondary to hypoperfusion and hypoxia of the kidney15.

SEPSIS SYNDROME This is the most serious problem faced by the burn victims. Adequate and timely treatment can offer satisfactory results.

MISCARRIAGE IN PREGNANT BURN VICTIM The maternal and perinatal outcome is poor in burn patients. In severe burns, stillbirth occur within less than 48 hrs.

LATE COMPLICATIONS CONTRACTURES Contractures are treated by release incisions and skin grafting or by a variety of plastic surgical operations.

HYPERTROPHIC SCAR AND KELOIDS These are treated conservatively with intracutaneous steroid injections locally.

SQUAMOUS CELL CARCINOMA (MARJOLIN'S ULCER) Squamous cell carcinoma is seen in post burn wound.

Rarely basal cell carcinomatous change is also seen11. Plastic repairs may be required for cosmetic reasons.

GROWTH DELAY Growth is delayed in post burn paediatric patients.

The cause is unknown. This is seen despite normal nutritional support13.

PSYCHOTHERAPY Psychotherapy and reassurance is also very SURGERY - PRINCIPLES IN GENERAL

important part of the treatment during rehabilitation.

Depression, phobias, insomnia, sexual problems, high divorce rates, Juvenile delinquency, impaired employment or academic status is seen in post burn patients. There are many other psychosocial problems14.

REFERENCES 1.

Basil.A., Pruitt JR., Cleon. W, Goodwin JR., Scott. K., Burns; text book of surgery sabiston; W.B saunders Company Philadelphia 14th ed. 1991; 178-209.

2.

Ronald.G, Tompkins. Burns; oxford text book of surgery; Peter. J., Morris and Ronald. A, Malt; oxford medical publications 1994; 2711-2719.

3.

Martin C. Robson. Treatment of burn victim essential surgical practice: A. Cuschieri-G-R-Giles. A.R-Moosa; 2nd edition Wright London 1988; 312-327.

4.

Faldma L. Kravitz M. Management of acute burns and burn shock resuscitation. Aacn clinical issues in critical care nursing. [JC:atw]. May 1993; 4(2): 351-66.

5.

Gurdak G. Thermal injuries in the workplace. Aaghn journal. [JC:aao]. Oct 1990; 38(10): 492-6.

6.

Casa B. Calaffi E. Bocchi a et al. Rehabilitation of burned patients II. Therapeutic exercise Acta Biomedica De L Anteneo Parmasses. [JC:oe7]. 1990; 61(1-2): 67-71.

7.

Casa B. Calaffi E. Bocchi a et al. Rehabilitation of burned patients I. General aspects Acta Biomedica De L Anteneo Parmasses. [JC:oe7]. 1989; 60(5-6): 213-6.

8.

Polacek V. Broz L. Kripper J et al. Unexpected gastrointestinal complications in severely burned children Acta Chirurgiae plasticae. [JC:ojo]. 1991; 33(2): 98-109.

9.

Sabo K. Cardiac support in burned patients with heart disease. Acta chirurgiae plasticae [JC:ojo]. 1989; 31(1): 22-34.

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10. Dodd D. Stutman HR. Current issues in burn wound infections. Advantages in paediatric infections diseases.

1989; 17-24.

13. Rutan R.L. Herndon D.N. Growth delay in post burn paediatric patients. Archives of surgery. [JC:8i a]. Mar 1990; 125(3): 392-5.

14. Wallace E. Nursing a teenager with burns. British journal of nursing. [JC:big]. Mar 1993; 2(5): 278-81.

15. Ronald G. Tompkins. Burns. Oxford text book of surgery: Peter J. Morris. Ronald A Malt. Oxford university press London. 1994; 2711-2719.

16. Merz J, Schrand C, Mertens D, Foote C, Porter K, Regnold L. Wound care of pediatric burn patient AACN clin issues.

Nov 2003; 14(4): 429-41.

SURGERY - PRINCIPLES IN GENERAL

SUMMARY Burns Degrees of burns ! First degree ! Second degree ! Third degree ! Forth degree Depth of burns ! Superficial burns ! Partial thickness ! Full thickness Zones of burnt area ! Zone of coagulation ! Zone of stasis ! Zone of hyperemia Nature of burns ! Dry burns ! Scalds ! Fat burns ! Caustic burns ! Acid burns ! Electric burns ! Sun burns ! Cold burns ! Irradiation burns ! Friction burns Site of burns (primary areas) ! Face ! Neck ! Hands ! Feet ! Perineum Extent of burns ! Minor burns ! Moderate burns ! Major burns ! Massive burns ! Simple burns ! Complicated burns Criteria for referral to burn unit Management ! Resuscitation ! Early period management ! Definitive treatment ! Treatment of complications

184

SPLIT SKIN GRAFT

1 PS-025

SPLIT SKIN GRAFT Shuja Tahir, FRCS, FCPS M Y Shah, FRCS

It is partial thickness graft. It is also called Thiersch graft. It is cut to such a thickness that islands of epithelium in the deep layers of epidermis, sebaceous glands, sweat glands and hair follicles are left intact.

Partial thickness (Thiersch's) grafts1,2 are harvested as large sheets from either the arm, leg or buttocks using a drum dermatome, a power dermatome or a free-hand knife.

These are precise instruments whereby a given thickness of the skin is obtained.

As epidermal remnants are left behind, the skin heals within 10 to 14 days. If a large area of skin loss needs grafting, the split skin graft can be meshed using a machine that permits an expansion as much as 2-9 times the graft giving it a string vest appearance1,3.

It also permits drainage of any exudate and allows better conformability to the wound.

The advantage of these grafts is that donor area heals with epithelialization on its own.

The split skin graft can survive by gaining nutrition through diffusion from the recipient area until new blood vessels grow into the graft. This is possible due to the thinness of the graft.

SURGERY - PRINCIPLES IN GENERAL

Split skin graft is indicated where skin and mucosal defects are too large to be closed directly and have a base (graft bed) which has a reasonably good vascular supply to support the graft.

Commonly this is used for the areas not to be kept exposed as the cosmetic results are not so good.

These grafts are delicate and cannot be used at areas subjected to more wear and tear. These are also not suitable for weight bearing areas.

These grafts may be used as skin cover in emergency situations and can be replaced by full thickness grafts later on.

These grafts are cut very thin and epithelialization of donor area occurs within few days and it becomes ready for another donation if so required.

The skin graft is immobilized and must be in close contact with the recipient bed (achieved by dressings) so that a plasmatic circulation (serum imbibition) can support the graft until revascularization (inoculation) of the graft can occur.

These processes are called the "taking of the graft".

The "take" of the graft is also determined by the type and the amount of bacterial contamination.

Pseudomonas and streptococcus are particularly detrimental to graft take. Tissue containing less than

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105 organisms per gram of tissue by quantitative culture usually allow a graft to take.

CONTRAINDICATIONS These grafts are contra indicated in ;

a. More liable to contraction (approximately 30%) b. Unpredictable changes of colour (hyper-or hypo-pigmentation).

REFERENCES

1. Where the graft bed is avascular as in ; a. Exposed cortical bone devoid of its periosteum (Medullary bone readily accepts split skin graft). b. Exposed car tilage devoid of its perichondrium c. Exposed tendon devoid of its peritenon or sheath d. Exposed joints e. Prosthesis

1. M.Y. Shah. Skin cover. "The Professional" medical journal.4(1):3-13, 1997 Mar. 2. Thiersch K. Epidermis transplantation lectreffend. zentbl. chir 24: 17, 1986.

3. Lanz O. Die Transplantation lectreffend zbl. Chir 35: 3, 1908.

2. Exposed major arteries, veins and nerves 3. Tissue treated with deep x-ray therapy.

ADVANTAGES The advantages of split skin graft are ; a. It is quick and simple to cut.

B. The graft is of uniform thickness and the cut surface is smooth. c. It is also successful in a contaminated recipient bed. d. Size is unlimited. e. Can be stored in a domestic fridge if kept moist and can be used upto three weeks later. f. Donor site heals quickly and spontaneously with minimal scar. g. Donor site can be reused after 1-2 months.

DISADVANTAGES The disadvantages are ;

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186

Benign Tumors

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EPIDERMAL INCLUSION CYST (SEBACEOUS CYST)

PS-026

EPIDERMAL INCLUSION CYST (SEBACEOUS CYST) Shuja Tahir, FRCS, FCPS

This benign cystic tumor is present in the skin. It has a membranous capsule which is filled with white cheesy sebaceous material.

It is the most common cyst of skin. It is actually an epidermal inclusion cyst. It is wrongly named as sebaceous cyst.

These may occur in childhood but are more common in early adulthood. The most common sites are scalp, face and back.

The cysts may be solitary or multiple . These are compressible intradermal masses. The punctum or dilated follicular orifice may connect the cyst to the skin surface.

overlying skin is of normal colour and temperature unless the cyst is infected. The punctum of the obstructed duct of the cyst is usually visible over the maximum convexity of the swelling. This is one of the confirmatory features of the sebaceous cyst.

PALPATION It is a rounded swelling of variable size. It is firm or elastic in consistency. The edges are ill defined. The cyst is mobile but skin is not movable over the cyst as the cyst is present in the skin.

Thick yellowish white cheesy material may be expressed out from the duct of the cyst on application of pressure.

The cyst is usually not painful unless it is infected.

It is formed due to the obstruction of the duct of the gland. This obstruction leads to accumulation of the sebaceous secretions of the gland.

The cyst wall is composed of fully differentiated epithelium. Desquamated keratinocytes are shed into the center of the cyst forming white cheesy material.

PHYSICAL SIGNS INSPECTION Epidermal inclusion cyst (sebaceous cyst) looks like a rounded swelling. It is usually present in the hairy areas of the body. The size of the cyst is variable. The

SURGERY - PRINCIPLES IN GENERAL

Sebaceous cysts scrotum (Courtesy: Dr. Abid Bashir, FCPS)

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COMPLICATIONS Epidermal inclusion cysts (sebaceous cysts) are innocent tumors. These may be cosmetically unacceptable or may cause following problems if not treated adequately and in time.

INFECTION AND ABSCESS FORMATION The cyst may get infected and re-infected. Typical signs of inflammation are present. Abscess formation can also occur.

The infected cyst may burst and pus is discharged.

On re-infection similar symptoms are seen again.

Infection of the epidermal inclusion cyst leads to fibrosis of the surrounding dermis.

SINUS FORMATION AND ULCERATION Repeated infection leads to necrosis of the skin overlying the cyst. Ulceration of the cyst occurs and infected material is discharged leading to sinus formation.

Infected cysts are difficult to remove. Enmass excision is the treatment of choice to avoid recurrence in these cases.

Cosmetic incisions should be used while removing these cysts from face or other exposed areas.

REFERENCES 1. Arthur J SOBER. Benign pigmented lesions of skin oxford text book of surgery. Oxford medical prblications. Peter J. Morris. Ronald. A malt. 1994; 1512-1515.

2. George F. Murphy Martin C. MIHM. The skin. Robbins.

Pathologic basis of disease. 5th edition. Cobran, Kumar, Robbins W.B. Saunders company London.

1994; 1173-1181.

This condition looks very similar to chronic osteomyelitis or epithelioma.

Repeated ulceration of sebaceous cysts of the scalp and face occurs due to trauma while brushing the hair or shaving.

HORN FORMATION Occasionally a horn is formed in the cyst. The horn may remain small or attain larger size which could be unacceptable cosmetically.

TREATMENT Conservative treatment does not help.

Complete excision of the cyst should be performed surgically.

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LIPOMA

PS-027

LIPOMA Shuja Tahir, FRCS, FCPS It is the most common soft tissue tumor (STT). It is a benign tumor commonly present in the subcutaneous tissue.

It is a slowly growing tumor of the fat cells of adult type. It may be encapsulated or diffuse swelling.

Lipomas may be single or multiple.

It has a typical thin capsule. The lipoma is aggregation of mature adipocytes.

Common age is mid adult life. These are soft mobile and painless lesions except angio-lipomas.

Encapsulated lipomas are one of the most common tumors.

Characteristic features are presence of definite edge and lobulation. A sense of fluctuation may be felt on palpation. Lipoma may be present anywhere in the body where fat is present.

Mostly these are painless but may cause aching symptoms.

Multiple and mixed lipomas are not uncommon.

If there is more fibrous tissue in lipoma, it is called fibro-lipoma.

The lipomas may have other types of tissue and may

SURGERY - PRINCIPLES IN GENERAL

be mixed types of Lipomas such as ;

! ! ! ! !

Fibro-lipoma.

Angio-lipoma.

Spindle cell lipoma.

Myelolipoma.

Pleomorphic lipoma.

Neuro-lipomatosis, Dercum's disease (adiposis dolorosa) is characterized by tender deposits of fat specially on trunk.

Retroperitoneal lipoma, or lipomas of the thigh may occasionally undergo sarcomatous change.

Myxomatous change, saponification and calcification may also occur in lipomas of longer duration.

Lipomas can be present at different sites and are classified according to their site such as ;

! ! ! ! ! ! ! ! !

Sub-cutaneous.

Sub fascial.

Sub synovial.

Intermuscular.

Periosteal.

Sub serous.

Sub mucous.

Extradural.

Intra-glandular.

Lipoma could be present in gastrointestinal tract commonly in colon, ileum and jejunum. These are 191

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2

rarely responsible for any symptoms. Most of these lipomas are present in submucous part of stomach.

These are found in patients in their fifth or sixth decade of life. These present as solitary , smooth, discrete and soft mass2.

Rare sites of lipoma are trachea, spinal cord and colon. These may be symptomatic and have to be treated surgically.

TREATMENT If symptomatic, surgical excision should be performed. If asymptomatic, no treatment is required.

Large retroperitoneal and lipomas should be removed as sarcomatous changes may occur.

REFERENCES 1. Andrew E. Rosenberg. Skeletal system and soft tissue tumors. Robbin's pathologic basis of disease.

Cotran, Kumar, Robbin. 5th edition W.B. Saunders company London. 1994; 1261-121.

2. John Robinson saltzman, David L-cau-Locke; Scott Andreco joint lipoma case report medscape General medicine 2005; 7(1).

SURGERY - PRINCIPLES IN GENERAL

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DERMOID CYST

PS-028

DERMOID CYST Shuja Tahir, FRCS, FCPS Sohail Amer, FCPS Dermoid cyst is a benign cystic tumour which is lined by squamous epithelium or endothelium and is filled with collection of fluid.

It is lined with granulation tissue when infected. It is present deeper in the skin in various parts of the body.

Many varieties of dermoid cysts present in the body are : TERATOMATOUS DERMOID CYSTS These are congenital abnormalities. These contain all types of embryonic tissue such as bone, cartilage, muscles, teeth, skin etc. Teratomatous dermoids are present in the :

! ! ! ! !

Ovaries.

Retroperitoneal area.

Pre-sacral areas.

Testes.

Superior mediastinum.

These are benign tumors but malignant changes may occur and carcinomas or sarcomas may develop.

These are diagnosed due to special features on ultrasonography.

SEQUESTRATION DERMOID CYSTS These are also congenital type of dermoid cysts.

These are present where lines of developing skin join

SURGERY - PRINCIPLES IN GENERAL

and some epithelial cellular inclusion occurs. The common sites of presentation are ;

! ! ! !

Forehead.

Root of nose.

External angular process.

Neck.

Branchial cyst is also a type of dermoid cyst. It is situated along the anterior border of the sternocleidomastoid muscle. It arises from vestigeal remnants of second branchial cleft. Its contents may look like tooth-paste or may be clear.

Its content contains cholesterol crystals on chemical analysis.

Tubulo-embryonic dermoids are also congenital dermoid cysts such as ; 1. Thyroglossal cyst.

2. Post anal dermoid.

3. Ependymal cysts.

IMPLANTATION DERMOID CYSTS It is an acquired type of dermoid cyst.

It follows punctured wounds usually at fingers and sole of foot due to needle puncture.

It is commonly seen in tailors and other people

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working with needles.

It presents as a slowly growing firm to hard rounded swelling at the site of puncture. It is a freely mobile cyst unless it is infected, then it becomes adherent and immobile.

RARE DERMOID CYSTS The dermoid cysts are seen at various sites. Some of these sites are given below ;

! ! ! ! ! ! ! ! ! !

Paravaginal dermoid cyst1 Intraspinal dermoid cyst 2 Subglial dermoid cyst4 Auricular dermoid cyst5 Congenital dermoid cyst of base of tongue6 Dermoid cyst of pancreas7 Sublingual dermoid cysts Supratentorial dermoid cysts Inguinal dermoid cyst8 Dermoid cyst in undescended testis9

TREATMENT Surgical excision is the only treatment option.

4. Stannard MW. Currarino G. Subgaleal dermoid cyst of anterior fontenelle: diagnosis with sonography. Ajnramerican journal of neuro-radiology. [JC:3ag].

1990; 11(2):349-52.

5

Ikeda M. Muto J. Omachi S. Dermoid cyst of auricle: report of two cases. Auris, Nasus, larynx. [Jc9fz].

1990; 16(4):193-7.

6. Tokimoto T. Yoshizaki T. Tanaka S. Congenital dermoid cyst at the base of tongue. Auris, Nasus, Larynx.

[JC:9fz]. 1990; 17(4) :217-9.

7. Vermeulen RJ. Widgren S. Gur V. et al. Dermoid cyst of pancreas. Case report and review of literature.

Gastroenterologie Clinique Et Bioloique. [JC:fgx].

1990; 14(2):1023-5.

8. Leaming R. Olsen M. Ponsky JL. Inguinal dermoid cyst presenting as an incarcirated inguinl hernia. Journal of paediatric surgery. [JC:jmj]. Jan 1992; 27(1):117-8.

9. Broggi G. Appetito C. Di Leone L. et al. Dermoid cyst in undescended testis in a 9-year-old boy. Urologia Internationalis. [JC:wri]. 1991; 47(2):110-2.

REFERENCES 1. Hirose R. Imai A. Kondo ID. Itod K. Tamaya T. A Dermoid cyst of para-vaginal space. Archives of gynaecology and obstetrics. [JC:6ys]. 1991; 249(1):39-41.

2. Buchwald C. Borgesen SE. Intra-spinal thoracolumbar dermoid: a case report. Acta Neurochirurgics [JC:19c]. 1989; 101(3-4):163-4.

3. Owre A. Pedersen JF. Characteristic fat fluid level at ultrasonography of ovarian dermoid cyst. Acta radiologica. [JC:ata]. Jul 1993; 32(4):317-9.

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194

FIBROMA

1 PS-029

FIBROMA Shuja Tahir, FRCS, FCPS This is a benign tumor of fibrous tissue. The dermato-fibromas are common cutaneous tumors.

spots). It may also be associated with pheochromocytoma and acoustic neuroma.

Fibromas are small tumors. These are well encapsulated. These are hard or firm in consistency.

These are encapsulated. These are pearly gray in color. These are tumors of aggregation of fibroblasts. Mitosis is rare1.

A special variety of neurofibroma is plexiform neurofibroma in which there is diffuse involvement of the nerve sheath causing enlargement of the part supplied by that nerve

Fibromas are common in the subcutaneous tissue of the face and appear as soft brown swellings.

Unusual types of fibroma are desmoid tumor of the abdominal wall and keloids.

True fibromas are very rare.

Multiple fibromas are common tumors.

Mixed fibromas are benign tumors of fibrous and other mesodermal tissues such as; NEUROFIBROMA It is relatively common tumor. There is collection of nerve sheath tissue and fibrous connective tissue. It moves at right angle to the nerve but not along the long axis of the nerve on examination.

Multiple neurofibromas may occur in autosomal dominant condition called Von-Recklinghausen's disease (generalized neurofibromatosis). It is characterized by multiple neurofibromas, dark chocolate-coloured spots on the body (cafe'au'lait

SURGERY - PRINCIPLES IN GENERAL

The lesions are present all over the body. It is a premalignant condition.

FIBRO-MYOMA It contains abnormal collection of fibrous tissue and muscle tissue. It is a rare type of fibroma.

FIBRO-LIPOMA It is the tumor having collection of fibrous tissue and fat. It is also a rare type of fibroma.

The consistency of fibroma may be hard when the fibrous tissue is more.

The consistency is soft when the fibrous tissue is less and other cellular tissue is more.

TREATMENT If symptomatic and causing pain or disfigurement, the surgery is indicated.

The surgical excision of dermato-fibroma is usually unsatisfactory as the recurrence is quite common.

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Radio-therapy may be used in some cases.

REFERENCES 1. Andrew E. Rosenberg. Skeletal system and soft tissue tumours. Robbin's pathologic basis of disease. COTRAN, KUMAR, ROBBINS. 5th edition WB. Saunders company London. 1994; 1261-71.

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196

1

JUNCTIONAL NAEVUS

PS-030

JUNCTIONAL NAEVUS

Shuja Tahir, FRCS, FCPS This is a simple benign melanocytic tumor. The melanocytes appear in increased number as localized aggregations projecting into the dermis.

These may arise anywhere in the skin. The melanocytes are present at the dermo-epidermal junction or in the epidermis in clumps with some clear spaces between and around the individual cells.

These have sharp border. Fine pigmentary stippling is noted specially on magnification1,2.

Usually these lesions are smaller and flatter than other types of pigmented naevi.

In pre-pubertal age group, almost all pigmented naevi are of junctional type regardless of their location or flat or raised margins. In adults most of the naevi are not junctional1.

transform into neoplastic melanoma. The risk is quite low and it decreases with increase in age.

Photography and mole mapping is performed in high risk patients.

The pigmented naevi on the distal portions of the extremities and on the genital region in all age groups are usually junctional in nature.

TREATMENT No treatment is required unless the lesion is cosmetically unacceptable or is at a site where recurrent injury is inflicted upon.

Cryosurgery is less invasive and offers good cosmetic results in case the naevus is to be removed.

Surgical excision and biopsy is another choice of treatment.

REFERENCES

It is formed from the aggregation of melanocytes which are round or oval and grow to form nests along the dermo-epidermal junction. The nuclei are uniform and rounded in shape and have inconspicuous nucleoli. There is little or no mitotic activity.

This is an early developmental stage of naevus.

Eventually it changes into compound naevus2.

There is minimum chances of these naevi to

SURGERY - PRINCIPLES IN GENERAL

1. Arthur J Sober. Benign pigmented lesions of skin oxford text book of surgery. Oxford medical publications. Peter J. Morris. Ronald. A malt. 1994; 1512-1515.

2. George F. Murphy martin.C. MIHM. The skin. Robbins.

Pathologic basis of disease. Cotran, Kumar, Robbins. W.B. Saunders company London. 5th ed.

1994; 1173-1181.

3. George J Hruza. Transformation of moles into melanoma. Journal watch. 2003 2(4).

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Malignant Tumors

1

MALIGNANT TUMORS

PS-031

MALIGNANT TUMORS

Shuja Tahir, FRCS, FCPS

Malignant tumor is a mass of cells, tissue or organs arranged atypically which always invades the surrounding tissue

Malignant tumors show a lot of mitotic activity and synthesis of D.N.A. prior to division. This results in nuclear enlargement and hyperchromatism.

These malignant tumors eventually invade the blood vessels, tissue planes and are carried to the distant parts of the body where they set up secondary growths.

The nuclei are disproportionately large for the cell.

The nuclear cytoplasmic ratio may approach 1 : 1 instead of normal 1 : 4 or 1 : 62.

The malignant tumors of the epithelial origin are called carcinomas and those of connective tissue are called sarcomas.

FEATURES OF MALIGNANCY Following features are typical of malignancy : INVASIVENESS The characteristic feature of malignancy is invasiveness, infiltration and destruction of surrounding tissue, that is why the name cancer (crab) has been given to such tumours2,3.

The malignant tumors are not well capsulated. They grow rapidly but due to death of the patient at earlier stage, do not achieve enormous size.

MITOSIS The rate of growth of the malignant tumors is erratic.

It may be slow or rapid. Mitotic figures are numerous and abnormal. It generally correlates with the level of differentiation of the tumor.

SURGERY - PRINCIPLES IN GENERAL

PLEOMORPHISM The nuclear enlargement and polyploid cells account for irregular shapes, size and staining qualities of the malignant cells. Malignant cells and their nuclei both show variation in size and shape. It is called pleomorphism2.

The cells contain abnormal number of chromosomes.

Tri-radiate mitosis leading to three daughter cells formation is typical of malignancy.

Different sorts of giant cells are seen in the malignant tumors such as ; Disease

Giant cell type

Osteoclastoma

Giant cell tumor of bone

Hodgkinâ&#x20AC;&#x2122;s disease

Reed-Sternberg cells (RS cells)

Choriocarcinoma

Giant cells of chorionic origin

Giant cells occur as a feature of anaplasia in malignant tumor of the thyroid and lung.

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Giant cells are also seen in tumors growing into a bronchus. Foreign body giant cells may form by engulfing the necrotic tissue.

without keeping the boundary of original tissue.

ANAPLASIA Anaplasia is deviation of malignant cells from normal to embryonic pattern. This term is also used to describe the structural and functional abnormalities of the malignant cells.

STAGING The staging of any malignancy is the assessment of the extent of the malignancy. It is evaluated clinically, per-operatively, histo-pathologically and with various investigations or operative procedures to detect distant metastasis. It involves following criteria for staging assessment.

Orientation of anaplastic cells is markedly disturbed.

Sheets or large masses of tumor cells grow in disorganized fashion2.

T.... TUMOUR N.... LYMPH GLANDS M... METASTASIS

DYSPLASIA Dysplasia is the loss of uniformity of individual cells as well as loss of orientation of cellular architecture.

The following TNM staging for carcinoma breast is given for example.

The dysplastic cells show pleomorphism and hyperchromatism.

The mitotic figures are abundant and appear in abnormal locations.

When dysplastic changes involve entire thickness of the epithelium, the lesion is pre-invasive and is called as carcinoma -in-situ. The basement membrane is not invaded and is intact in these lesions METASTASIS Metastasis is the quality of malignancy without any doubt. All malignant tumors metastasize2,3.

Metastasis is the growth and progress of tumors with lack of recognition of parenchymal boundaries. The tumor grows into adjacent tissues, organs and viscera locally.

T-1 Tumor size 2 cm or less No fixity No nipple retraction T-2 Tumor size 2 - 5 cm Less than 2 cm with skin involvement Nipple retraction T-3 Tumor size 5 - 10 cm Less than 5 cm with infiltration or ulceration of the skin not exceeding the tumor margins.

Peau-de-orange Tumor fixed to underlying muscles T-4 Tumor size more than 10 cm.

Any size with infiltration or ulceration of the skin morethan the tumor mass.

It also spreads to distant tissues, organs and viscera SURGERY - PRINCIPLES IN GENERAL

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Tumor fixed to the chest wall.

Peau-de-orange more than the tumor.

N-0 No palpable axillary lymph glands.

N-1 Palpable but mobile axillary lymph glands N-2 Fixed axillary lymph glands N-3 Palpable supraclavicular lymph glands, mobile or fixed.

Edema of the arm.

M-0 M-0 No metastasis.

M-1 Distant metastasis including skin involvement outside the breast.

Opposite breast involvement.

Involvement of the lymph nodes of the opposite axilla and supra clavicular lymph glands.

Other distant metastasis GRADING Grading is the assessment of the tumor biology (nature). The grading helps in the assessment of course and prognosis of the tumor.

The malignant tumors have been graded according to the degree of differentiation. It is always performed histo-pathologically2,3.

Differentiation of tumor cells is the extent of

SURGERY - PRINCIPLES IN GENERAL

resemblance to the normal parenchymal cells both morphologically and functionally. Most of the malignant tumors range from well differentiated to undifferentiated2.

GRADE-I When more than 75% of malignant cells are very well differentiated.

These are also called well differentiated tumors.

GRADE-II When 50%-75% cells are well differentiated.

These are also called moderately differentiated tumors.

GRADE-III When 25%-50% cells are well differentiated.

These are also called poorly differentiated tumors.

GRADE-IV When less than 25% of cells are differentiated (This is also called anaplastic tumor).

These are also called undifferentiated tumors.

TUMOR SPREAD The spread of malignant tumors is called metastasis.

The reduction in cell adhesiveness (a quality of the malignant cells) increases the chance of spread of malignancy.

DIRECT SPREAD Infiltration into the surrounding tissue is a characteristic feature of malignancy. Local expansion of the tumor is by local invasion. The tumor has usually spread to the area in excess of the macroscopic lesion. The tumor spreads through the natural planes quickly and may be contained by fascial sheaths for some time.

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The spread through tissue septa gives characteristic (peau-de-orange) appearance in carcinoma of the breast.

Epidermal invasion is a prominent feature in malignant melanoma and Paget's disease of the nipple.

LYMPHATIC SPREAD Carcinomas spread quite early via lymphatics and sarcomas spread so occasionally. The spread occurs by permeation and embolization.

treatment against malignancy.

The spread is by permeation when tumor cells grow like a cord through smaller vessels and then on to the bigger vessels.

The distal cord separates due to necrosis of the tumor cells and is taken away by the circulating blood (embolization) thus spreading the tumor to a distant place away from the primary tumor.

Sarcomas spread via blood vessels early and carcinomas spread through blood vessels as well.

Tumor cells grow into the lumen of lymphatic vessels as a cord (permeation). The distal cells of the cord separate and are carried away to the draining lymph glands (embolization).

The most common sites of haematogenous spread are lungs and liver due to anatomical reasons.

Further growth of these cells blocks the lymphatic channels and causes edema of the area and spread of the tumor in a retrograde fashion.

Bones and other organs are also sites of secondary spread. It is not only the anatomical site of liver, lungs and bones making them more prone for secondaries but the nature of these organs and some unclear factors.

Extensive involvement of the pulmonary lymphatics is known as lymphangitis carcinomatosa. This is usually seen in patients with carcinoma of the breast.

Retrograde spread from the carcinoma of breast shows involvement of the left supra-clavicular lymph nodes (Virchow's node) which is probably due to the blockage of thoracic duct near its entry into the subclavian vein.

Carcinoma of the tongue spreads to local lymph glands quickly due to the movement of the tongue.

HAEMATOGENOUS SPREAD Haematogenous spread or spread via blood vessels is the notorious cause of death due to malignancy.

This also limits the surgical and radiotherapeutic SURGERY - PRINCIPLES IN GENERAL

Bone is the 3rd most common site for metastasis through the blood stream specially in carcinomas of the breast, kidney, prostate, lung and thyroid.

Bone metastasis is either osteoblastic or osteolytic.

Brain is usually secondary site of tumor spread from lungs. Carcinoma of the breast and malignant melanoma also spread to the brain.

Adrenal medulla and ovaries get secondary deposits via blood spread.

PERINEURAL INVASION AND SPREAD Many types of the tumors specially prostatic, pancreatic and cholangio-carcinomas spread via 204

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perineural spaces.

TRANS-COELOMIC SPREAD Spread of the malignant cells also occurs in the body cavities leading to the spread to other organs.

Commonly gastric, colonic and ovarian carcinomas spread into greater omentum and also into the pouch of Douglas.

Krukenberg's tumor is the name given to metastatic tumor of the ovaries.

! ! ! ! ! !

Cryosurgery.

Laser Ablation.

Chemo therapy.

Hormone therapy.

Immuno therapy.

Various combinations of above modes.

SURGERY Surgical excision of the malignant tumors is still the most popular and most effective method of local tumor control.

The primary malignant tumor with some surrounding healthy tissue is removed.

TREATMENT OBJECTIVE OF TREATMENT OF MALIGNANT TUMORS ! Removal of primary tumor completely or as much as possible. ! Removal of distant metastasis as much as possible. ! Prevention of local recurrence. ! Prevention of distant metastasis.

Surgical excision of the local recurrence also helps in treatment of the recurrence.

The diagnosis is confirmed with as much certainty as possible before starting the treatment.

The trends have changed from more radical surgery to more conservative methods.

Minimally invasive methods are available for correct and confirmatory diagnosis such as FNAC, Tru-cut needle biopsy. If these are not helpful, excision biopsy can be performed.

RADIOTHERAPY It is used in very advanced malignancies as a primary source of treatment or when the tumor is inoperable or as an adjuvant therapy to surgery.

Staging of the malignancy is done before planning the treatment.

Its disadvantages make it less popular than surgery but in many diseases it has much better results than surgery such as lymphomas and carcinoma of cervix.Recent advances in radiotherapeutic equipment and techniques have made it more popular than before.

MODES OF TREATMENT Following methods of treatment are mostly used for the local and systemic treatment of malignancy ; ! !

Surgery.

Radiotherapy.

SURGERY - PRINCIPLES IN GENERAL

This also helps in the confirmation of the diagnosis histologically, grading of the tumor and staging of the disease.

CRYOSURGERY It is freezing of the malignant tumor and causing cell 205

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death by this mechanism. This is not as good as surgery but certain advantages make it worthwhile.

effects and maximizes the killing power of tumor cells.

It may prove an alternative to conventional surgery in the treatment of superficial malignant tumors such as lentigo maligna.

Chemotherapy can be used for hyperthermic isolated limb perfusion for the malignant melanoma of limbs and it achieves very satisfactory results (90% survival for stage II & III)5.

Repeated use of cryosurgery helps in the progressive ablation of tumor cells and to increase the immune response of the host which is not possible in any other type of treatment for the malignant tumors. It can be performed without anaesthesia.

LASER SURGERY Laser ablation provides simple and effective method of treating superficial malignancies. Laser ablation provides simple and effective alternative to isolated limb perfusion in the treatment of malignant melanoma of the limbs. This method can be used for the ablation of many malignancies such as carcinoma of prostate, sub-epithelial malignancy of oesophagus and cutaneous malignancies.

The chemotherapy as an adjuvant to other types of cancer therapy is very helpful mode of treatment. It is very much under research at present time.

HORMONE THERAPY The relationship of hormones in suppression of many malignant tumors is being used successfully in treatment of various malignancies, such as antioestrogens in cancer of the breast.

Stilboestrol is used in carcinoma of the prostate.

This is also very helpful as an adjuvant therapy.

Laser probe is used for this mode of treatment. It has been found to be a good method of treatment.

IMMUNO-THERAPY Improvement in the personal resistance of the patient helps the regression of malignancies. This is used successfully in many cases. But it has not been developed to more practical use yet.

Carbon dioxide laser is used to treat the small recurrences1.

It is used successfully as an adjuvant therapy in malignant melanoma.

CHEMOTHERAPY Different antimitotic drugs are used to kill the tumor cells selectively during different phases of regeneration.

Three to four weeks after regional lymphadenectomy, the patient is given a single intradermal injection of BCG (Bacillus Calmette Guerin). Three weeks later, immunization with allogenic melanoma cells obtained from live donors with distant metastasis is performed.

These also have toxic effects on many body tissues, specially the rapid growing ones.

Combination of many drugs minimizes the side SURGERY - PRINCIPLES IN GENERAL

Three vaccinations are given. Each vaccine is obtained from a separate donor to avoid 206

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development of HLA response. Each vaccine consists of mitomycin-C treated tumour cells mixed with purified protein derivative of tuberculin given intradermally every month6.

Recombinant alpha 2a-interferon 3-15 Mu / M2 is given subcutaneously for three days followed by intravenous use of anticancer chemo-therapeutic agents (Cisplastin 25-60mg /M2.) every three weeks.

REFERENCES 1. Hunter DC. Thomas IM. Controversies in the management of malignant melanoma. British Journal of Hospital medicine [JC:b 35]. Feb 1993; 49(3):174. 178-180, 183, 3-16.

2. Robines Cotran, Kumar, Robbines. Neoplasia, Robbines pathologic basis of disease 5th edition W.B saunders company London 1994; 241-303.

3. Walter JB Israel MS. General pathology 6th edition Churchill hiringstone London. 1987; 342-369.

4. Bahler Somumereggar K. Schuller petrorics.

Neumann R. Muller E. Cryosurgery of lentigo maligna Plastic and Reconstruction surgery [JC:p99]. Sep 1992; 90(3):436-40:441-4.

SUMMARY Malignant Tumors Features of malignancy ! Invasiveness ! Mitosis ! Pleomorphism ! Anaplasia ! Dysplasia ! Metastasis Staging (TNM) Tumor spread ! Direct spread ! Lymphatic spread ! Haematogenous ! Perineural spread ! Trans-coelomis Treatment

! Objectives of treatment ! Modes of treatment > Surgery > Radiotherapy > Cryo surgery > Laser ablation > Chemotherapy > Hormone therapy > Immunotherapy > Different Combinations

5. Omlor G. Bahmer F. Messen S. et al. Technique and results of hyperthermic perfusion of the extremity in melamana patients. Langenberks archiv fur. chirurgic [JC: 11m]. 1993; 378(1):21-5.

6. Elias EG. Tomazic VJ. Buda BS. Adjuvant immuntherapy in melanoma: a new approach.

Journal of surgical oncology [JC: K79]. Jul 1992; 50(3):144-8.

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PS-032

NON MELANOMA SKIN CANCER-1 SQUMOUS CELL CARCINOMA (EPITHELIOMA) Shuja Tahir, FRCS, FCPS

It is a malignant tumor of the squamous epithelium. It is also called squamous cell carcinoma1.

! ! ! ! ! ! ! ! ! ! ! ! !

It is very common tumor of the epidermis.

It arises from the sites of body exposed to sun.

It is more common in males than females.

The incidence is higher in immuno-suppressed individuals.

Its prevalence in USA is alarming.

It accounts for over a third of all cancers in USA. Almost 100,000 new cases are reported every year.

Its incidence has been increasing at the rate of 4% - 8% per year2.

Squamous cell carcinoma of penis accounts for 0.3% malignancies of men.

Nodal involvement is a poor prognostic indicator.

It is less common than basal cell carcinoma.

It is more rapidly growing and more malignant than rodent ulcer (basal cell carcinoma).

Usually it occurs in the presence of some preexisting lesion as a result of previous irradiation.

It can occur in the skin of old people without any preexisting lesion. It also occurs in the presence of following pre-malignant conditions;

! ! ! !

Bowen's disease.

Leukoplakia.

Solar keratosis (Actinic Keratosis).

Radio-dermatitis.

SURGERY - PRINCIPLES IN GENERAL

! ! ! ! ! ! ! ! ! !

Chronic scars (Marjolin ulcer).

Basal cell carcinoma.

Ingestion of arsenicals.

Chronic ulcers.

Chronic discharging osteomyelitis.

Chronic venous ulcers.

Chronic lupus vulgaris.

Prolonged irradiation of the skin.

Chemicals such as dyes, soot and tar.

Polycyclic aromatic hydrocarbons (PAHS)3.

Common exogenous cause is exposure to ultraviolet light which causes DNA damage and its mutation to malignancy.

Sunlight also causes local skin immuno-suppression in addition to DNA damage .

Typical ulcer is irregular in outline. Its edges are raised and everted. Its base is indurated and is usually attached to deeper structures.

Blood stained discharge is present which is increased in the presence of secondary infection.

Regional lymph nodes are involved and deposits may undergo mucoid degeneration or may get infected secondarily.

Actinic keratosis is the earliest manifestation of squamous cell carcinoma. Clinically, histologically and

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molecularly, all of its characteristics are those of squamous cell carcinoma2.

! !

Highly anaplastic round cells may be seen with areas of necrosis.

Invasive squamous cell carcinoma is easily diagnosed at early stage4.

SQUAMOUS CELL CARCINOMA IN SITU ! Highly atypical cells at all levels of epidermis are seen. ! The basement membrane is intact and not invaded4.

INVASIVE SQUAMOUS CELL CARCINOMA ! The cells break through the basement membrane. ! Cells of variable differentiation are seen. ! Polygonal cells may be arranged in orderly lobules.

! ! !

!

Large zones of keratinization are seen.

SURGERY - PRINCIPLES IN GENERAL

Less than 5% of squamous cell carcinoma metastasize to regional lymph glands.

In transit metastasises from squamous cell carcinoma is also seen in some patients.

Satellite lesions or in transit metastatic lesion appear either with the primary or recurrent lesion. Its presence is poor prognostic feature and represents management challenge. These are managed with wide excision and adjuvant 210

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radiotherapy5.

disease, surgery is indicated.

MOHS MICROGRAPHIC SURGERY It is the removal of entire tumor with smallest possible margin of normal skin.

It is highly effective technique for removal of some skin cancers. It is based on idea of excision of tumor with minimal margins and immediate histologic examination of horizontal frozen section of specimen. Subsequent excisions are done in the same sitting if residual tumor is present histologicaly.

It offers the highest cure rates. It should be considered in lesions with high risk attributes such as larger diameter, high risk location recurrent lesion, aggressive histology and scar carcinoma5,6.

WIDE EXCISION Wide excision of the lesion is performed. About 6mm of healthy skin surrounding the tumor is excised in higher risk patients. Margin biopsies from excised specimen are assessed for tumor infiltration5.

Skin grafting is performed if required otherwise wound is closed.

SENTINEL LYMPH NODE BIOPSY It is performed in squamous cell carcinoma at higher risk of regional and distant metastasis.

DIAGNOSIS It is mainly clinical but edge-biopsy is confirmatory.

Bipedal lymphangio-graphy may be required for the epitheliomas of the lower limb to assess the extent of disease.

TREATMENT Immediately after histological confirmation of the

SURGERY - PRINCIPLES IN GENERAL

BLOCK DISSECTION Block dissection of the palpable and mobile regional lymph glands is performed.

RADIOTHERAPY It can be used both as primary treatment or adjuvant therapy after surgery.

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illumination and targets abnormal cells selectively 7 and preserves the normal surrounding tissue .

The basic principle of photodynamic therapy is preferred uptake of a photosensitizer by the malignant cells.

It may be helpful or may be the only possible treatment depending upon the site of the lesion and stage of the epithelioma.

Radiotherapy to the regional glands may be required if the glands are inoperable. Radiotherapy can cause some regression of the fixed and inoperable lymph glands.

Following less radical procedures can be used under different circumstances such as ; Topical chemotherapy (5-fluoro-uracil) is effective in flat lesions.

DESTRUCTION Electrodescication and curettage are best reserved for superficial lesions not located on high risk areas.

The photosensitizer is activated by a light of specific wavelength in the presence of oxygen. It leads to creation of singlet oxygen which is toxic to malignant cells.

It has many advantages and many disadvantages or limitations.

LIMITATIONS ! Limited depth of penetration. ! Time delay in optimal uptake of photosensitizer by cancer cells. ! Rate of metabolism of photosensitizer. ! Avoidance of sunlight till clearance of drug and skin is no longer sensitive.

ADVANTAGES ! Short duration of treatment. ! In expensive equipments. ! No expensive back up requirement.

CRYO SURGERY It is best reserved for the treatment of actinic keratosis patients5.

LASER ABLATION N.D Yag laser is used for tumor ablation.

PHOTODYNAMIC THERAPY (PDT) Topical photodynamic therapy is used in the treatment and diagnosis of venous cutaneous malignancies. It uses intrinsic cellular haem biosynthesis pathway and principles of photoSURGERY - PRINCIPLES IN GENERAL

Drug Application & Conversion

Light Exposure

Cell Injury or Destruction

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REFERENCES

SUMMARY

1. Thmas G Cropley. Pre malignant and malignant tumours of the skin oxford text Book of surgery peter J Morris. Ronald Amalt. Oxford University Press London. 1994; 1515-1520.

! !

2

Bryan andrew lober, chfford warren lober. Actinic keratosis is squamous cell carcinoma south med J. 2000; 93(7): 650-655.

3. Chris Carlsten. Steplren carl Hunt Joal D Kawforman Squamous cell carcinoma of the skin and coal tar creasote exposure in a railroad worker. ENVIRON Health prospect. 2005; 113(1) :96-97.

Squamous Cell Carcinoma (Epithelioma) Squamous cell carcinoma in situ Invasive squamous cell carcinoma

Treatment ! MOHâ&#x20AC;&#x2122;s micrographic surgery ! Wide excision ! Sentinel lymph node biopsy ! Radiotherapy ! Destruction ! Cryo surgery ! Laser ablation ! Photo-dynamic therapy (PDT)

4. George F. Murphy. Martin. C MIHM. The skin Robbins pathologic lesion of disease W.B samders company London. 5th edition. Cetran KUMAR ROBBINS. 1994; 1173-1185-1185.

5

J A Carucci. Squamous cell carcinoma in organ transplant recepients. Approach to management.

Skin therapy dept. 2004; 9(4): 5-7.

6

Keyvan Nouri; Maria Patricia Rivas. A Primer of Mohs micrographic surgery: Common indications. Skin Med 2004; 3(4):191-196.

7

T Kormeili; P. S Yamauchi; N. J. Lowe. Topical photodynamic therapy in clinical dermatology. Br. J. Dermatol. 2004; 150(6): 1061-1069.

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PS-033

NON MELANOMA SKIN CANCER-2 BASAL CELL CARCINOMA (RODENT ULCER) Shuja Tahir, FRCS, FCPS

Basal cell carcinoma usually begins in the basal cell layer of epidermis. It accounts for about 75% - 80% of non melanoma skin cancers.

1. Multiple basal cell carcinomas in childhood 2. Abnormalities of nervous system, eyes, reproductive organs and the bones.

This is also called basal cell carcinoma of the skin.

90% of these lesions are present on the face.

Advanced lesions involve bone and facial sinuses due to excessive local invasion. These lesions may ulcerate.

It usually presents as a firm pearly nodule covered with thin layer of epidermis in which there are often dilated capillaries.

It may ulcerate at a later stage. The epidermis over the tumor breaks down and reforms many times before frank ulceration.

The usual site is the area of face above the line drawn from lobe of the ear to the corner of the mouth.

Rarely it can occur any where on the body. The lesion is slow growing and only locally malignant. It rarely metastasize.

It commonly occurs on the exposed areas of body due to effects of sunlight. It is common in lightly pigmented people1.

It is more common in immuno-suppressed people.

It is associated with xeroderma pigmentosum.

Dominantly inherited basal cell naevus syndrome is a rare condition which is associated with ;

SURGERY - PRINCIPLES IN GENERAL

TYPES OF RODENT ULCER The common presenting types are ;

! ! ! !

Nodular Ulcerative Cystic Field fire rodent ulcer or multifocal rodent ulcer

NODULAR BASAL CELL CARCINOMA2 79% of all basal cell carcinomas It is the most common type. Its usual size is 1-3 mm in the beginning but it may enlarge to many centimeters in size.

It develops in area chronically exposed to sun light (head, neck, face). If left untreated, it may spread to bones and other tissue beneath the skin3.

ULCERATING LESION The ulcerated type has raised, rolled edges like a tyre with central ulceration.

Microscopically it shows masses of darkly staining

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cells with characteristic arrangement. There is an outer palisade layer of columnar cells surrounding a central mass of polyhedral cells.

Multiple cystic spaces may also be seen.

2

Nodular basal cell carcinoma presents as a reddish brown or pearly, translucent papule with telangiectasia. The lesion has rolled borders and a central depression. It may bleed spontaneously or develop into an open ulcer3.

It presents as a single expansible nodule made up of tumor cells and part of dermis.

The tumor is rounded or dome shaped, shiny and translucent.

There is no color change from the surrounding skin.

Certain lesions may be grossly pigmented as well.

Large tumors ulcerate due to ischaemic necrosis.

SURGERY - PRINCIPLES IN GENERAL

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The basal cell carcinoma of nasal tip, alar groove, medial canthus, pre-auricular, post auricular and external auditory canal are more invasive.

2

SUPERFICIAL BASAL CELL CARCINOMA 15% of all basal cell carcinomas. It is less common than nodular variety but more common than other types.

Superficial basal cell carcinoma usually appears on trunk and limbs as slow growing shiny pink or red slightly scaly plaques which bleed easily3.

It primarily occurs on the trunk and extremities.

It presents as thin scaly pink plaque having irregular margins.

A thin rim may be seen at the periphery of the spreading lesion The tumor spreads radially.

When the plaque becomes larger (few cms in size), its ulceration occurs as well.

Surgical excision may lead to cosmetically poor results in these lesion. It should be chosen carefully.

Sclerosing basal cell carcinoma appears as a skincolored waxy thickened scar3.

It is the third most common type.

Common site of involvement is head and neck like nodular basal cell carcinoma.

Microscopically it has narrow cords of tumor cells looking similar to dense scar-like fibrosis.

The tumor lacks shiny gelatinous appearance of basal cell carcinoma.

The lesions are firm, indurated and fixed to adjoining tissue.

The tumor is light in color than surrounding skin.

This type is more aggressive and deeper invasion to bone and other tissues is more common.

TREATMENT ! Surgery (wide excision) with or without skin grafting. ! Radio therapy. ! Cryosurgery (very popular now-a-days). ! Fulguration after curettage can be done.

Treatment of choice in these cases is :

! ! !

Cryosurgery.

Electro fulguration and curettage.

Topical chemotherapy (5-fluorouracil).

Regular follow up for keeping careful observation for any recurrence should be performed and recurrence should be treated immediately.

REFERENCES

Treatment for recurrent tumor: Mohs micrographic surgery or excision with frozen section histological control.

1. George F. Murphy. Martin. C MIHM. The skin Robbins pathologic lesion of disease. COTRAN, KUMAR, ROBBINS. W.B samders company London. 5th edition. 1994; 1173-1185-1185.

SCLEROSING BASAL CELL CARCINOMA2 6% of all basal cell carcinomas.

2. Thomas G Cropley, Peter J Morris, Ronald AMALT. Pre malignant and malignant tumors of the skin. Oxford text Book of surgery. Oxford University Press

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London. 1515-1520.

3. Mark Naylor. The epidemic of non-melanoma skin cancer: Prevention, diagnosis and treatment CME. Royal College of Physicians & Surgeons. Canada.

2004; 1-21.

SUMMARY Basal Cell Carcinoma (Rodent Ulcer) Types ! Nodular ! Ulcerative ! Cystic ! Field fire (multi-focal) Superficial basal cell carcinoma Sclerosing basal cell carcinoma

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PS-034

MALIGNANT MELANOMA Shuja Tahir, FRCS, FCPS It is a malignant tumor of melanocytes. Commonly the primary tumor is present in the skin but it may be present in the eye, meninges, muco-cutaneous junction of anus and mouth, urinary bladder, esophagus, subungual area, sole of the foot, palm of the hand, urethra, vulva, vagina, rectum and penis.

!

! !

It is an uncommon tumor in Pakistan but is getting very common in Europe, Australia and North America.

!

It has very unpredictable behavior which varies from spontaneous regression to rapid progress and death1.

! !

"Malignant melanoma writes its message in the skin with its own ink.... Some see but do not comprehend" INCIDENCE ! It is rising more than any other malignancy in caucasians specially those living near the equator other than bronchogenic carcinoma. ! Its incidence has doubled every 10 years. ! Its incidence has risen four times in Australia. ! At the present rate of rise in incidence, it will be more common than carcinoma of the breast in next few years. ! Its risk is greater in light pigmented people. ! It is present more on upper back in males and on the lower back and legs in females. ! About 30-40% of the malignant melanomas

SURGERY - PRINCIPLES IN GENERAL

arise from long standing naevi.

Pregnancy has no significant effect on the progression or regression of the malignant melanoma2.

Survival rate is significantly lower in males and blacks3.

It accounts for almost all deaths due to skin cancers.

The prognosis has improved over years due to better understanding and improved treatment3.

Five years survival in 1945 was 40%.

Five years survival in 1983 was 83%.

ETIOLOGY Exact cause of appearance of malignant melanoma is not known. Following possible explanations and predisposing factors are known to cause malignant melanoma4: EXPOSURE TO SUN LIGHT Exposure to sunlight is a very strong predisposing factor specially during first fifteen years of life.

Intermittent recreational sun exposure and sun burns are strong risk factors5.

PRE-EXISTING NAEVUS (DYSPLASTIC NAEVUS) Malignant melanoma is common in these patients.

EXPOSURE TO CARCINOGENS Although no specific agent has been isolated to

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cause malignant melanoma yet the incidence of this malignancy rises with exposure to certain non specific carcinogens.

HEREDITARY FACTORS Epidemiological studies confirm the role of hereditary factors in appearance of malignant melanoma.

SOLAR IRRADIATION & DECREASED OZONE LAYER OF OUTER SPACE The association of malignant melanoma with these factors is of great significance and leads to higher risk for appearance of malignant melanoma6.

causing malignancy are not clearly understood.

The discovery of oncogenes and suppressor genes is an important step forward in the understanding of development of malignancy.

The evolution of the new growth can be predicted due to ;

! ! !

ETHNIC ORIGIN, CLIMATE & SOCIO-ECONOMIC STATUS Caucasians living near equator, light pigmented people, poor economical conditions are strong risk factors for appearance of malignant melanoma.

!

LIFE STYLE AND CLOTHING HABITS OF PATIENTS Casual life style, enjoying the sun bath with leaving some areas of the body uncovered and unprotected by sun bath creams and lotions, run a great risk of malignant melanoma.

!

SKIN DISEASES Such as albinism and xeroderma pigmentosum lead to higher risk of malignant melanoma. Solar lentigo is the most common precursor of the malignant melanoma in patients with xeroderma pigmentosum7.

GENETIC MUTATION The understanding of molecular genetics explains the appearance of malignant melanoma.

!

Consistent and progressive loss of tumor suppressive genes.

Gene amplification, resulting in over expression of proteins which aid tumor progression.

Gene mutation which alters the orderly biochemistry of normal cells.

Genes (proteolytic enzymes, enzyme inhibitors, integrins, metastatic genes, chemotactic factors) that allow the cells like melanocytes to escape the confining nature of epidermis and to invade the dermis, blood vessels, lymphatics and distant organs.

Tumor growth factor (TGF-창-2) which confuses host defence mechanisms.

S.O.S type genes which cause more damage than good.

The extraordinary plasticity and instability of melanoma genome suggests genetic flux and its etiological relevance8.

PATHOLOGY The predominant cell type in the infiltrating melanoma is the melanoma macrophage9.

Malignant melanoma shows a characteristic growth pattern. The growth occurs in two dimensions and has special features10.

The human genome is remarkably stable. The molecular basis responsible for genetic instability SURGERY - PRINCIPLES IN GENERAL

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GROWTH PATTERN The malignant melanomas usually show following growth pattern ;

this stage the melanoma cells have not metastasized yet.

Radial growth.

Vertical growth.

Clinically it presents as a flat lesion.

(Carcinoma in situ or stage IV of Clark's model).

Melanoma in situ is a distinct entity which can be effectively treated surgically with 0.5 cm healthy surrounding skin clearance11.

VERTICAL GROWTH After a while, the vertical growth also starts and melanoma grows into deeper dermal layers as an expansile mass lacking cellular maturation.

Clinically it presents as a nodule in the relatively flat radial growth phase. It co-relates with the emergence of a clone of cells with true metastatic potential. (stage V of Clark's model).

RADIAL GROWTH It is the centrifugal spread of the tumor in a flat pigmented lesion. It is seen in all types of malignant melanoma except nodular melanoma. Radial growth indicates the tendency of melanoma to grow horizontally within the epidermal and superficial dermal layers for a prolonged period of time. During SURGERY - PRINCIPLES IN GENERAL

The metastatic prediction can be done by measuring the depth of invasion in vertical direction below the granular layer of over-lying epidermis with the help of Vernier's scale.

The nature and extent of vertical growth phase determines the biological behavior of the malignant 221

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melanoma.

heart and breast.

The melanoma cells in vertical type of growth possess distinctive abnormalities ;

Secondaries are typically black but may have little or no melanin. Extensive tumor spread may even lead to melanuria.

a. antigenic b. cytogenic c. biosynthetic Immune response is very important in the prevention or emergence of tumor progression.

Lack of immune response due to local exposure to ultra violet light creates permissive environment for the tumor growth.

PROGNOSTIC INDICATORS Tumor thickness or the depth of the tumor spread is the most significant prognostic indicator.

100

80

Percent survival - 7 years

HISTOLOGICAL FEATURES ! Individual melanoma cells are larger than naevus cells. ! Nucleus is large with irregular contours. ! Chromatin is clumped at the periphery of the nuclear membrane. ! Prominent nucleoli (red colored) are seen. ! Cells grow in poorly formed nests or as single cells at all levels of epidermis and in the dermis as expensile balloon like nodules.

Survival Rates as per depth of tumor

60

S. # 40

20

< 1.69

1.70 - 3.99

% of 7 year survival

1.

Less than 1.69 mm

90%

2.

Between 1.7-3.99mm More than 4 mm

60% 30%

3.

0

Depth of Tumor

> 4.00

Tumor thickness in millimeters

Tumor spreads via local extension, lymphatics and blood vessels. Tumor cells spread by permeability and embolization and may produce local satellite lesions or transit deposits.

Regional spread occurs as secondary lymph adenopathy in the area. Distant metastasis is usually present in lungs, liver, brain, skin and bones.

Occasionally spread is also seen in small intestine, SURGERY - PRINCIPLES IN GENERAL

Tumor ulceration, primary site of the tumor, regional lymph node involvement and distant metastasis are the other important prognostic indicators for malignant melanoma12,13.

Prognostic features include ;

! ! ! ! !

Gender.

High risk anatomic site such as scalp.

Race (black).

Microscopic satellites.

Tumor volume.

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! ! ! ! !

Indices of tumor proliferation.

Tumor cell motility.

Volume weighted mean nuclear volume.

DNA ploidy.

Nuclear organisation regions14.

CLINICAL FEATURES Malignant melanoma is almost unknown before puberty. Although it has been seen in children very rarely.

Usually it is asymptomatic.

Common sites for primary melanoma are skin, scalp, oral, anal and genital mucous membrane, nail beds and conjunctiva. Less common sites are esophagus, leptomeninges, bladder, penis, urethra, vulva, vagina and rectum etc.

Malignancy should be suspected if following changes are seen in a pre-existing mole;

! ! ! ! ! ! ! !

Itching.

Tingling.

Change in color, size, shape, outline and elevation.

Changes in surface characteristics and surrounding tissue of the mole.

Shades of black, brown, red, dark blue, and grey color pigmentation are seen.

Occasionally a halo of white or flesh color hypopigmentation is seen.

Bleeding Rough, irregular, uneven and notched borders are present.

VARIETIES OF MALIGNANT MELANOMA Following clinical varieties are seen;

SURGERY - PRINCIPLES IN GENERAL

! ! ! ! !

Superficial spreading melanoma.

Lentigo malignant melanoma.

Acral lentiginous melanoma.

Nodular melanoma.

Amelanotic melanoma.

SUPERFICIAL SPREADING MELANOMAS It is the most common type. 64% of malignant melanomas are of this type.

It may present at any part of the body. The size is usually larger than 0.5 mm in diameter. It is seen in middle aged patients. It has irregular edge and color variation is commonly seen.

LENTIGO MALIGNA MELANOMA (HUTCHINSON'S MELANOTIC FRECKLE) It is the least common type. 7-15% of malignant melanomas are of this type.

It is the least malignant. It occurs in old people above 60 years of age. It is usually present on face. It appears as irregularly pigmented flat brown macular lesion . It grows slowly over 10-15 years changing its shape.

Malignant change becomes obvious due to thickening and appearance of nodules which may grow upto 5 cm in size.

Early surgical excision is the treatment of choice15,16.

NODULAR MELANOMA It is the most malignant type. It is seen in about 1225% of patients.

It is seen in younger age group. It is convex and irregular in shape. It may present at any part of the body. Its color is uniformly blue, grey or black. It 223

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shows sharp demarcation from the surrounding skin.

It has smooth surface and irregular margins.

Ulceration, discharge and bleeding may also be seen in these lesions.

STAGE-III Primary tumor.

Regional lymph gland enlargement.

Distant metastasis.

ACRAL LENTIGINOUS MELANOMA These are seen on palm of hands or sole of the feet and under the nails.

This type is most common in Japan.

Its prognosis is poor17.

INVESTIGATIONS Following investigations help in the general assessment of the condition of the patient.

AMELANOTIC MELANOMA The lesions are lightly pigmented. These may be pink but some pigmentation is always present at the base of the lesion.

These have very poor prognosis and usually present with regional lymph node metastasis.

STAGING It is used to determine the extent of disease. It helps in planning of the best mode of treatment.

STAGE-I Primary tumor only.

URINE EXAMINATION BLOOD EXAMINATION UREA AND ELECTROLYTES ESTIMATION These investigations help in the assessment of the general condition of the patient. These also help for general screening of the patient and diagnosis of associated diseases.

X-RAY CHEST AND SKULL These simple investigations help to see any obvious secondary deposits.

ULTRASOUND SCAN It also helps to find out distant metastasis specially in liver if present.

STAGE-II (a) Primary tumor.

Presence of satellite lesions.

CT SCAN It is less extensively used as it is not helpful to find out occult metastasis and to follow up malignant melanoma patients18.

STAGE-II (b) Primary tumor.

Enlarged regional lymph nodes.

LABELLED MONOCLONAL ANTIBODIES These are used to detect the metastatic deposits.

HMB-45 monoclonal antibodies uptake is tested.

STAGE-II(a&b) Primary tumor.

Satellite lesions.

Regional lymph gland enlargement.

Simple use and the staining of HMB-45 monoclonal antibody is of great interest to assess the depth of 19 primary and secondary cutaneous melanoma .

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SURFACE MICROSCOPY (DERMOSCOPY) OR (DERMATOSCOPY) It is an extremely reliable investigation for the initial assessment of malignant melanoma. It is used for screening for melanoma. The pigmented lesion is covered with immersion oil and a glass slide.

The dermoscopy is followed by an improvement of the malignant/benign ratio in excised lesions suggesting a more appropriate selection of pigmented lesions. It helps to bring down the cost of large scale screening programme28.

The lesion is seen with the help of a dermatoscope (A magnifying lens of 10 times magnification). The usual criteria for diagnosis with surface microscopy is;

! ! !

Presence of pigment network.

Black dots or irregular extensions.

Amplified surface microscopy can also be used but it is a tedious process20.

LYMPHANGIOGRAPHY It has been used extensively to assess the deep seated lymphatics and lymph glands during treatment and for follow up of the patients with malignant melanoma.

The number of false positive and false negative results is significantly high. It is not so often used now.

EXCISION BIOPSY & HISTOPATHOLOGY This is the only confirmatory investigation. It should be done with care. The depth of the spread should always be measured and noted with the help of Vernier's scale.

SURGERY - PRINCIPLES IN GENERAL

DIFFERENTIAL DIAGNOSIS Following conditions look like malignant melanoma clinically. These should be clearly differentiated from malignant melanoma20;

! ! ! ! ! !

Seborrhoeic wart.

Pigmented basal cell carcinoma.

Pigmented granuloma.

Telangiectatic lesion.

Thrombosed angioma.

Hemangioma.

TREATMENT PREVENTION No cautery, curettage or shaving of the suspected lesions should be done. It will only mask the diagnosis and the disease will present at a later stage with distant metastasis.

Repeated self examination for any relevant changes in the already present naevi is a very helpful screening test.

Early diagnosis and appropriate treatment should be the aim. Screening of all suspected lesions should be performed very carefully.

Education and knowledge of the predisposing factors is helpful in avoiding the malignancy and decreasing morbidity and mortality11.

Primary and secondary prevention are both possible with appropriate action21.

Patients with early melanoma are at a lower risk of relapse but are at a high risk for development of subsequent melanoma and should be followed up carefully.

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8

Family members are at an increased risk and should be followed up.

malignant melanoma. Elective lymph gland clearance is not recommended in early melanoma14,22,23,24.

PLAN OF TREATMENT Different modalities are used to eradicate the disease.

Sentinal lymph node biopsy identifies patients with early stage malignant melanoma having nodal metastasis. These patients do not get benefitted from radical lymph adenectomy. It has been seen that sentinal lymph node biopsy does nothing to alter the course of metastasized melanoma. It can only cause lymph edema following dissection of lymph glands29.

Various methods of treatment of malignant melanoma can be used for various stages.

The plan of treatment depends upon correct diagnosis which is made by clinical assessment and is confirmed by histological examination.

The pathologist should confirm the exact depth and type of the malignant melanoma so that accurate treatment may be planned.

SURGERY The correct and effective treatment for malignant melanoma begins with early recognition and paranoid suspicion of any ulcerated, nodular, pigmented or irregular dermal lesion.

It is surgical excision of the lesion with clear margins and wound closure or skin grafting of the defect.

Histopathological confirmation of the disease is done and definitive surgical wide excision is done if so required.

Tumors less than 0.76 mm depth are excised with one (1) cm healthy margin clearance and tumors with deeper spread are excised with three (3) cm healthy margin clearance.

These have 90% long term survival rate.

Prophylactic lymph gland sampling of the draining lymph glands is a better method of management of SURGERY - PRINCIPLES IN GENERAL

CHEMOTHERAPY Different chemotherapeutic agents such as Cisplastin, Decarbazine, Carmustine and Tomoxifen appear to be most effective.

ISOLATED HYPERTHERMIC LIMB PERFUSION The diseased limb is perfused in isolation with a single chemotherapeutic agent usually melphalan at a temperature more than 40 degrees centigrade25.

RADIOTHERAPY The response of radiotherapy is dependent upon the tumor volume.

It is most effective against microscopic or subclinical disease26.

IMMUNOTHERAPY Irradiated allogenic melanoma cells are given parenterally. These are the cells which express high levels of HLA-1 and HLA-2. These secrete IL-2 after 5,27 transfection with interleukin-2 gene .

These are used successfully as an adjuvant therapy in malignant melanoma.

Three to four weeks after regional lymph-

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adenectomy, the patient is given a single intradermal injection of BCG (Bacillus Calmette Guerin). Three weeks later, immunization with allogenic melanoma cells obtained from live donors with distant metastasis is performed.

Three vaccinations are given. Each vaccine is obtained from a separate donor to avoid development of HLA response. Each vaccine consists of mitomycin-C treated tumor cells mixed with purified protein derivative of tuberculin given 5 intra-dermally every month .

Recombinant alpha 2a-interferon 3-15 Mu / M2 is given subcutaneously for three days followed by intravenous use of anticancer chemo-therapeutic agents (Cisplastin 25-60mg /M2.) every three weeks5.

CRYOSURGERY It is performed with the help of cryoprobe. It freezes the lesion and kills the tumor cells.

LASER SURGERY Laser ablation provides simple and effective alternative to isolated limb perfusion.

cm healthy surrounding skin must be excised.

STAGE-II(a) Surgery (wide excision).

Cryosurgery.

Laser surgery.

Superficial electron radiotherapy.

Isolated hyperthermic limb perfusion.

STAGE-II (b) Surgery (wide excision).

Cryosurgery.

Laser surgery.

Regional lymph gland sampling in head and neck.

Superficial partial parotidectomy and lymph gland excision in head and neck STAGE-III CHEMOTHERAPY Following chemo-therapeutic and immunotherapeutic agents may be used.

Vindesine. interferon.

Interleukin.

REFERENCES

Laser probe is used for this mode of treatment. It has been found to be a good method of treatment.

Carbon dioxide laser is used to treat the small recurrences22.

STAGE WISE TREATMENT STAGE-I EXCISION BIOPSY The depth of the lesion must be measured. In thin lesions it is enough, otherwise wide excision with 2-3

1. Reacle G. Haot J. et al., Primary melanosarcoma of rectum. Acta chirurgica Belgica [Jc:oh8]. Mar-Apr 1993; 93(2):63-6.

2. Slingluff CL Jr. Sergler HF. Malignant melanoma and pregnancy. Annals of plastic surgery. (JC: 5VP). Jan 1992; 28(1): 95-9.

3. Osterlind A. Kiem E. Survival of Danish cancer patients 1943-1987, Malignant melanoma of skin.

APMIS. Supplimentum [jc:adz]. 1993; 33:149-55.

4. Sanchez JA. Robinson WA. Malignant melanoma.

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10

Annal review of medicine [JC: 6 dr]. 1993; 44:33542.

malignant melanoma. Anticancer research.[JC:591].

Sep-Oct 1992; 12(5);1507-11.

5. Elias EG. Tomazic VJ. Buda BS. Adjuvant immunotherapy in melanoma: a new approach.

Journal of surgical oncology [JC:k79]. July 1992; 50(3): 144-8.

14. Hundahl S. Surgical treatment of melanoma, Hawali medical journal. [JC:gld]. May 1993; 52(5):130-2.

6. Lee JA. Etiology, risk factors, epidemiology and public health issues in melanoma and other cutaneous neoplasms current opinion in oncology. [JC:alv]. Apr 1992; 4(2):347-50.

7. Stern JB. Peck GL. et al., Malignant melanoma in xerodermia pigmentosum: Search for a precursor lesion. Journal of american Academy of Dermatology. [JC:hvg]. Apr 1993; 28(4):591-4.

8. Albine AP. Fountain JW. Molecular genetics of human malignant melanoma. Cancer Treatment and Research [JC:ava]. 1993; 65:201-55.

9. Bammhill RL. Pathology and prognostic factors current opinion in oncology [JC;alv]. Mar 1993; 5(2):364-76.

10. Gerrge F. Murphy, Martin.C. Milm Jr. The skin, Robbins pathologic basis of disease, W.B Saunders Philadelplia Cortan, Kumar. Rubbins 4th edition 1989.

11. Anonymous. Diagnosis and treatment of early melanoma N.I.H consensus development conference Jan 27-29 1992. Consensus statement. [JC:93 q].

Jan 1992; 10(1):1-25.

15. Kelly JW. Following lentigo maligna may not prevent the development of life threatening melanoma.

Archiaes of Dermatology [ JC:6 WU]. May 1992; 128(5);657-60.

16. ROSIN RD. Skin, Burns, Bailey and love's, short practice of surgery, charles V. Maron and R.C.G Russell. ELBS with chapman and hall London. 21st ed 1991.

17. Sutherland CM. Mather FJ. et al. Acral lentiginous melanoma. American Journal of surgery. [Jc:3z4]. Jul 1993; 166(1):64-7.

18. Buzaid AC. Sadler AB. et al., Role of computed tomography in the staging of primary melanoma.

Journal of clinical oncology. [JC:1co]. Apr 1993; 11(4): 638-43.

19. Lampert A. Thomine E. Lauret P. Hemat J. Comparative study of HMB-45 monoclonal antibody uptake on various benign and malignant melamoytic lesions.[french] Annals De pathologic. [JC: aaz].

1993; 13(2):100-7.

20. Soyer HP. Kerl H. Surface microscopy of pigmented cutaneous tumors. Annal De Dermatologie Et De Venereologie [Jc:5rc]. 1993; 120(1):15-20.

12. Reintgen DS. Cox. C et al., Recurrent malignant melanoma, the identification and prognostic factors to predict survival.[Jc:5v12]. Jan 1992; 28(1):45-9.

21. Greene MH. The prevention of cutaneous malignant melanoma. High risk groups. Chemotherapy, education and screening. Cancer Treatment and Research [JC:ava]. 1993; 65:103-40.

13. Karlalainen J. Eskelinen M. et al. Clinical, histological and quantitative prognostic factors in cutaneous

22. Hunter DC. Thomas JM. Controversies in the management of malignant melanoma British Journal

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of Hospital medicine [JC:b 35]. Feb 1993; 49(3):174-178.

23. Cruse CW. Wells KE et al. Treatment of the primary in malignant melanoma of skin. Annals of plastic surgery (JC: 5 Vb). Jan 1992; 28(1): 22-5.

24. Cuuse CW. Reintgoen D. Treatment of the primary malignant melanoma. a review. Seminars in surgical oncology. [JC:sso] May-June 1993; 9(3):215-8.

25. Reintgen DS. Cruse CW et al. Isolated limb perfusion for Recurrent melanoma of extremity Annals of plastic surgery. (JC; 5 Yb) Jan 1992; 28(1):50-4.

26. Trotti A. Peters LJ. The role of radiotherapy in the primary management of cutaneous melanoma.

Annals of plastic surgery. [JC:Svb] Jan 1992; 28(1): 39-44.

27. Schuchter LM. Wohlganger J. et al, Sequential chemotherapy and immunotherapy for the treatment of metastatic melanoma. Journal of immunotherapy.

[JC:azo]. Nov 1992; 12(4):272-6.

28. P. Carls. V; De Giorji; E Crocetti; F Mamone; D. Mossi; A. Chiarugi; B. Giannotti. Br j Dermatol. 2004; 150(4): 687-692.

29. N Medalie; A.B. Ackerman; Sentinal node biopsy has no benefit for patients who primary cutaneousmelanoma has metastatized to a lymph node. Br. J. Dermatol. 2004; 151(2): 298-307.

SUMMARY Malignant Melanoma Incidence Etiology ! Exposure to sun light

SURGERY - PRINCIPLES IN GENERAL

Pre existing naevus (dysplastic naevus) Exposure to carcinogens Hereditary factors Solar irradiation Decrease ozone layer of outer space Ethnic origin Climate Socio-economic status Life style and clothing habits Skin diseases Genetic mutation Pathology ! Radial growth ! Vertical growth Varieties ! Superficial spreading melanoma ! Lentigo malignant melanoma ! Acral lentiginous melanoma ! Nodular melanoma ! Amelonotic melanoma Staging Investigations ! Imaging studies ! Labeled monocolonal antibodies ! Dermoscopy ! Lymphangiography ! Excision biopsy Differential diagnosis ! Seborrhoeic wart ! Pigmented basal cell carcinoma ! Pigmented granuloma ! Telangiectatic lesion ! Thrombosed angioma ! Haemangioma Treatment ! Surgery ! Chemotherapy ! Isolated hyperthermic limb perfusion ! Radiotherapy ! Immunotherapy ! Cryo surgery ! Laser surgery

! ! ! ! ! ! ! ! ! ! !

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PS-035

SUPRA CLAVICULAR LYMPH GLAND ENLARGEMENT Shuja Tahir, FRCS, FCPS

The right supra-clavicular lymph gland enlargement may occur due to disease process in its drainage area.

DIAGNOSIS Clinical history and examination features are suggestive of the correct diagnosis.

The lymph glands may enlarge due to generalized lymphoid disease or due to disease processes from distant draining areas.

Following features are noted :

The common causes of enlarged supra-clavicular glands are ; INFLAMMATORY These could be ; (i) Acute. (ii) Chronic. (a) Specific (tuberculous)1 (b) Non specific VIRAL German measles.

Infectious mono-neucleosis etc.

NEOPLASTIC 1. Primary.

2. Secondaries from intra and extra-thoracic tumors such as carcinoma of oesophagus and carcinoma of breast and metastasis from GIT malignancy.

SWELLING Detailed history of duration of appearance of the mass in the supra clavicular region is noted.

Its mode of onset, its size and recent change in its size is noted.

The character of the swelling is noted whether it is mobile or fixed. Its consistency is noted. Its relationship with adjacent glands, underlying structures and overlying skin is noted.

If the swelling is fluctuant, it may have progressed from inflammed gland to abscess formation.

PAIN The swelling may be painful or painless. The painful swellings are usually inflammatory.

FEVER The duration of fever, its character and its intensity should be noted as it will help in finding the cause of lymphadenitis.

It is associated with both inflammatory and

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neoplastic enlargements.

COUGH If the primary cause of enlargement of supraclavicular gland is intra-thoracic and related to respiratory passages, cough may be the presenting symptom.

HAEMOPTYSIS It is coughing of the blood from lungs and tracheobronchial tree. It is noticed in various lesions of the respiratory system in association with enlargement of lymph glands, such as tuberculosis and tracheobronchial malignancies.

DYSPNOEA Difficulty in breathing is also a common feature of cardio-thoracic lesions. It may be associated with the enlargement of supra clavicular lymph glands in both benign and malignant lesions.

DYSPHAGIA (DIFFICULTY OF SWALLOWING) Difficulty of swallowing is a presentation of oesophageal lesions (both primary and secondary).

The enlarged supra clavicular glands and dysphagia both help to diagnose the primary lesion.

WEIGHT LOSS Neoplastic and tuberculous lesions are often associated with progressive loss of weight.

neoplastic lesions. It leads to weakness, malaise and loss of weight.

WEAKNESS, APATHY AND LETHARGY These are all the features of generalized diseases both inflammatory and neoplastic.

History of injury, occupation, living and working conditions must be available.

Smoking habits with exact duration and quantity must be noted.

EXAMINATION Complete examination is extremely important to establish proper diagnosis.

All groups of lymph glands should be palpated.

Abdominal examination may reveal any abdominal mass or a retroperitoneal mass which may be the primary site of the disease.

The breast must always be palpated for primary disease specially in females and testes should be palpated in males. The scalp, ear, nose, neck and thorax should be examined very carefully for the presence of primary lesion.

INVESTIGATIONS Following investigations must be performed to confirm the diagnosis and treat the patient.

Many times the primary lesion is not even noticed and weight loss is the presenting symptom. Clinical examination and investigations may help to find the primary lesion or it may remain occult for quite late.

URINE EXAMINATION It is very simple and economical but most valuable investigation for general assessment of the patients.

ANOREXIA It is a common symptom for inflammatory and

BLOOD EXAMINATION Haemoglobin percentage.

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Total leucocyte count.

Differential leucocyte count.

Erythrocyte sedimentation rate.

Peripheral blood film.

Polymerase chain reaction (PCR)2.

TREATMENT ACUTE INFLAMMATORY LYMPH GLAND ENLARGEMENT (PYOGENIC) Broad spectrum antibiotics should be used for about a week for the treatment of acute phase.

RADIOLOGICAL EXAMINATION (X-RAY OF THE CHEST) It should always be performed as a primary investigation.

Bacteriological examination of the pus helps to find out the correct antibiotics. It should be performed before starting any antibiotics.

It helps to diagnose the thoracic lesions like tuberculosis and malignancy responsible for supraclavicular lymphadenopathy.

If there is abscess formation, the incision and drainage is performed. The pus is cultured and sensitivity to the antibiotics is found out before prescribing antibiotics.

F.N.A.C Fine needle aspiration cytology is a minimally invasive and simple investigation.

Analgesics are required to relieve the pain.

It helps in the diagnosis immediately. It has minimized the number of excision biopsies and anaesthetic risks3,4,5,6.

TUBERCULOUS LYMPH ADENOPATHY Antituberculous drugs are used for adequate period.

Following drugs are commonly used for an adult patient ;

C.T. SCAN M.R.I. SCAN These are very useful to find out the primary disease and also in staging of the disease.

Isoniazid Pyrazinamide Ethambutol Rifampicin

The only problem is that these are not available everywhere and are too expensive to be cost effective always.

These drugs are used in different combinations and treatment is continued for six to nine months in pulmonary tuberculosis and 1 year in abdominal tuberculosis.

BIOPSY Biopsy of the lymph glands is confirmatory of the diagnosis. It is used when simple methods fail to offer satisfactory diagnosis.

Its place is limited but it is the only confirmatory investigation in difficult cases.

300 mg daily 1-1.5 G daily 1-1.5 G daily 450-750 mg daily

NEOPLASTIC LYMPH ADENOPATHY If the lymph glands enlargement is due to malignancy (primary or secondary), excision of lymph glands and treatment of the primary lesion must be done depending upon the stage of the disease.

All modalities of treatment of malignancy may be

SURGERY - PRINCIPLES IN GENERAL

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LYMPH GLAND ENLARGEMENT

required to control the disease such as ; 1.

2.

3.

4.

Surgery.

Radiotherapy.

Chemotherapy.

Immunotherapy.

4

6. Lau SK. Wei WI. Hsu C. Engzell UC. Efficacy of fine needle aspiration cytology in the diagnosis of tuberculous cervical lymphadenopathy. Journal of laryngology and otology. [JC: iwn]. Jan 1990; 104(1): 24-7.

FOLLOW UP All patients with supra-clavicular lymph adenopathy should be followed up till the disease is completely eradicated or patient dies whether it is infective or neoplastic in nature.

REFERENCES 1. Fongrac I. Roglic M. Kotanski Z. Tuberculosis of the peripheral lymph nodes. Fluene bolesti [JC:p94].

Jan-Jun 1990; 42(1-2): 71-3.

2. BUH. Etiology diagnosis of tuberculous lymphadenitis by polymerase chain reaction. Chung Hua ping li Nseuh Tsa Chib-Chinese journal of pathology.

[JC:czq). Dec 1991; 20(4): 260-2.

3. Lau SK. Wei WI. Kwan S. Yew WW. Combined use of fine needle aspiration cytologic examination and tuberculi skin test in the diagnosis of cervical tuberculosis lymphadenitis. Archives of otolaryngology head and neck surgery.[JC:aLq]. Jan 1991; 117(1) : 87-90.

4. Finfer M. Perchick A. Bursteub DE. Fine needle aspiration biopsy diagnosis of tuberculous lymphadenitis in patients with or without the acquired immune deficiency syndrome. Acta cytologica.

[JC:ol1]. May-Jun 1991; 35(3): 325-32.

5. Singh JP. Chaturvedi NK. Das A. Role of fine needle aspiration cytology in the diagnosis of tubercular lymphadenitis. Indian journal of pathology and microbiology. [JC:gkK). 1989; 32(2): 100-4.

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ENLARGEMENT OF LYMPH GLANDS

PS-036

ENLARGEMENT OF LYMPH GLANDS

Shuja Tahir, FRCS, FCPS

The enlargement of the lymph glands could be due to many reasons such as ; INFLAMMATORY Acute.

Chronic.

The infection could be; Specific.

Non specific.

VIRAL Glandular fever (infective mononucleosis).

Toxoplasmosis.

Cat scratch fever.

NEOPLASTIC Lymphomas.

Hodgkin's disease.

Reticulo-sarcomas.

Leukaemias.

Myelomatosis.

Fibrosarcomas.

ACUTE INFLAMMATORY LYMPHADENITIS Acute inflammation of any area leads to enlargement of the lymph glands draining that area.

The cervical lymph glands are enlarged in the ear, nose and throat infections. Scalp infections also give

SURGERY - PRINCIPLES IN GENERAL

rise to enlarged cervical glands.

Inguinal lymph glands are usually enlarged in the farmers and laborers working bare footed.

Enlarged glands are painful and tender on palpation.

If the organism is of high virulence or the patient is mal-nourished or immuno-suppressed, abscess formation may also occur.

CHRONIC (INFLAMMATORY) NON SPECIFIC LYMPHADENITIS Recurrent episodes of acute infection of the lymph glands leads to chronic infection and enlargement of the lymph glands.

Chronic cervical lymphadenopathy is seen in patients with recurrent attacks of acute tonsillitis and scalp infection.

CHRONIC (INFLAMMATORY) SPECIFIC LYMPHADENITIS Tuberculous lymphadenitis is one of the most common (nearly 91%) cause of cer vical lymphadenopathy.

It is common in children and young adults. Primary site is tonsil which may be associated with pulmonary tuberculosis.

Syphilis (acquired) can also cause lymph adenopathy.

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MANAGEMENT OF TUBER-CULOUS LYMPH- ADENITIS Correct and early diagnosis is very essential for proper management.

performed very accurately. Size and site of lumps, their mobility or fixity and tenderness, erythema, warmth, fluctuance and consistency is assessed. consistency should be examined.

CLINICAL ASSESSMENT Detailed history helps in the diagnosis of tuberculous lymphadenitis. History of;

Chest is examined throughly as these patients may have open pulmonary tuberculosis.

Cough.

Fever.

Anorexia.

Loss of weight.

Weakness.

Malaise.

Lethargy and nights sweats is usually available.

The family history of tuberculous infection is taken.

Details of living conditions and social back ground is asked.

INVESTIGATIONS Following investigations are performed to diagnose the cause of lymphadenopathy.

COMPLETE URINE EXAMINATION Physical, biochemical and microbiological examination is performed. Sugar and albumin are specially looked for.

Macroscopic and microscopic examination is performed carefully. Urine culture is performed. It is negative in renal tuberculosis.

History of occupation and details of working conditions should be found out.

BLOOD EXAMINATION Haemoglobin % Estimation : The patient is usually anaemic.

History of any other debilitating disease like diabetes mellitus and malignancy should be asked.

Total & Differential Leucocyte Count Lymphocytosis is a common feature.

Malnutrition or poor growth suggests chronic diseases such as tuberculosis7.

Sedimentation Rate Sedimentation rate is raised. Although it is a non specific test, yet it helps to monitor the progress or regression of the disease. (most important)

General and systemic examination of the patient is performed very carefully.

All groups of lymph glands is inspected and palpated.

Drainage areas of these glands are seen and examined for any inflammatory or neoplastic focus.

Examination of the enlarged lymph glands is SURGERY - PRINCIPLES IN GENERAL

It is performed to differentiate from other causes of lymphadenitis.

MONTOUX TEST This is an intradermal test which is performed by giving an injection of 1:1000 tuberculin.

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Positive test is highly suggestive of tuberculosis (nearly 100%).

The excised lymph glands are examined histologically and microbiologically for tubercle bacilli.

POLYMERASE CHAIN REACTION (PCR) TEST The tuberculous lymphadenopathy can be diagnosed by using polymerase chain reaction (PCR) in amplifying a referative DNA sequence specific for mycobacterium tuberculosis.

The lymph glands in tuberculosis are usually matted together and there is great deal of induration of the surrounding area (peri-lymph-adenitis).

It is a more powerful and sensitive test in the diagnosis of tuberculous lymphadenitis3.

X-RAY CHEST This should always be done as it proves or excludes the evidence of pulmonary tuberculosis.

There may be tuberculous abscess formation. There could be single or multiple sinuses present.

TREATMENT GENERAL Improvement of general health is done by better food and well ventilated living conditions.

Patient should be advised to rest as well.

Any other calcified glands may be seen. Many times bronchial carcinoma is diagnosed on x-ray chest.

FINE NEEDLE ASPIRATION CYTOLOGY (FNAC ) This is an excellent method of quick diagnosis of tuberculosis lymphadenitis. It is minimally invasive and very sensitive and highly specific test.

Its sensitivity is more than 75%4,5,6. It has almost replaced cervical lymph glands excisional biopsy for the diagnostic purposes.

Treatment of other disease like diabetes mellitus should be performed.

Anaemia should be treated if present.

MEDICAL TREATMENT Antituberculous drugs should be given for adequate period.

Following drugs are used in different combinations.

BIOPSY OF THE LYMPH GLANDS This is required for the histo-pathological confirmation of the diagnosis and for treating the T.B lymphadenitis. The bulk of the diseased and infected glands are removed so that the adequate drug treatment can be offered.

1. Inj Streptomycin 1 G intra muscularly daily (It is less often used because of its toxic effect).

2. Isoniazid tab:300 mg daily (5-8 mg/kg).

3. Ethambutol 1 g daily (15 mg/kg).

4. Rifampicin 450-600 mg daily.

5 Para amino salicylate (PAS) 10-15 G daily.

6. Tabrazid 300 mg daily.

Excision of enlarged lymph glands (cervical) should be performed under general anaesthesia and under proper aseptic conditions in an operation theatre.

These combination therapies are used for six months or more depending upon the disease process.

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ENLARGEMENT OF LYMPH GLANDS

The combination therapy prevents drug resistance formation.

The patient is monitored very carefully against the ill effects of these drugs and drugs causing toxicity are withheld immediately.

Vitamin supplements are also given to the patient to avoid ill effects of antituberculous drugs.

SURGERY (ASPIRATION) This is performed in case the enlarged infected lymph gland has changed into an abscess.

Repeated aspirations may be required in addition to anti tuberculous therapy.

1991; 117(1) : 87-90.

3. BUH. Etiology diagnosis of tuberculous lymphadenitis by polymerase chain reaction. Chung Hua ping li Nseuh Tsa Chib-Chinese journal of pathology. [JC:czq]. Dec 1991; 20(4):260-2.

4. Finfer M. Perchick A. Bursteub DE. Fine needle aspiration biopsy diagnosis of tuberculous lymphadenitis in ptients with or without the acquired immune deficiency syndrome. Acta cytologica.

[JC:ol1]. May-Jun 1991; 35(3):325-32.

5. Singh JP. Chaturvedi NK. Das A. Role of fine needle aspiration cytology in the diagnosis of tubercular lymphadenitis. Indian journal of pathology and microbiology. [JC:gkK]. 1989; 32(2):100-4.

EXCISION Excision of diseased lymph glands is performed to confirm the diagnosis and to treat the disease.

6. Lau SK. Wei WI. Hsu C. Engzell UC. Efficacy of fine needle aspiration cytology in the diagnosis of tuberculous cervical lymphadenopathy. Journal of laryngology and otology. [JC: iwn]. Jan 1990; 104(1): 24-7.

This is very essential in many cases as badly diseased tissue doesn't receive proper concentration of the drugs and remains a continuous source of infection.

7. Alexander KC Leung; W Lave M. Roleson. Childhood cervical lymphodenopathy. J Pediatr Health Care.

2004; 18(1): 3-7.

This is also required in patients resistant to adequate medical treatment.

REFERENCES 1. Fongrac I. Roglic M. Kotanski Z. Tuberculosis of the peripheral lymph nodes. Fluene bolesti [JC:p94].

Jan-Jun 1990; 42(1-2):71-3.

2. Lau SK. Wei WI. Kwan S. Yew WW. Combined use of fine needle aspiration cytologic examination and tuberculi skin test in the diagnosis of cervical tuberculosis lymphadenitis. Archir es of otolaryngology head and neck surgery. [JC:aLq]. Jan

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1

HODGKINâ&#x20AC;&#x2122;S DISEASE

PS-037

HODGKIN'S DISEASE

Shuja Tahir, FRCS, FCPS

It is the most common type of malignant lymphomas.

It was originally described by Thomas Hodgkin in 1832. It is a type of malignant lymphoma in which Reed-Sternberg cells are present in a characteristic background of reactive inflammatory cells of various types accompanied by fibrosis of variable degree1.

It is more common in Europe than in India and Pakistan.

It can present anywhere in the body where the lymphoid tissue is present. But commonly it presents as cervical lymph gland enlargement.

EBV (Ebstein Bar Virus) has possible role as an infectious cause, as supported by EBV genome in biopsy material.

PATHOLOGY Macroscopically the lymph glands are pink gray in colour, rubbery in consistency and discrete without any peri-lymph-adenitis1.

At first when the spleen is involved, it doesn't have same homogenous appearance but later on it becomes diffusely infiltrated2.

Microscopic picture varies with the stage and grade of the tumor.

Young males are usual victims of this disease but any age and sex can be involved. Average age at the time of diagnosis is 32 years2.

Microscopically typical features of Hodgkin's disease are ;

It is a potentially curable malignancy in most of the patients.

! !

Clinically there is generalized enlargement of the lymph glands, which may be the only symptom.

!

The glands are rubbery in consistency and are freely mobile. Bony metastasis occurs in the vertebral column and pelvis. Rarely disease may be confined to one organ only, commonly known as single-organdisease (Isolated-organ-disease).

SURGERY - PRINCIPLES IN GENERAL

!

Cellular pleomorphism.

Replacement of the normal lymph gland architecture by lymphocytes, reticular cells or eosinophilic cellular infiltration.

Fibrous tissue infiltration may also be prominent.

Typical giant cells known as Reed- Sternberg cells (R-S Cells) are present2.

REED-STERNBERG CELL (R-S CELL) It is a large cell about 15-45 micrometers in size having two mirror-image pale nuclei. Its identification

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is essential for the histological diagnosis of any form of Hodgkin's disease.

corresponds to follicular Hodgkin lymphoma3.

It can have single multi-lobate and polypoid nucleus or multiple nuclei. The nucleus is enclosed within abundant amphophilic cytoplasm.

FOLLICULAR HODGKIN LYMPHOMA (FHL) Follicular Hodgkin lymphoma (FHL) shows prominant follicular architecture. Follicles are seen with expanded mantle zones occasionally with small well defined, often eccentric, germinal centers. Scattered R-S cells are seen3.

The nucleus contains large inclusion bodies and has "owl eyed" appearance i.e., nucleoli are surrounded by a clear halo.

Follicular Hodgkin lymphoma is a variant of Hodgkin lymphoma similar to nodular lymphocyte predominant Hodgkin lymphoma (LPHL).

The nucleoli are acidophilic or amphophilic. One variant is called lacunar cell and is seen in nodular sclerosis type of Hodgkin's disease.

LYMPHOCYTIC PREDOMINANCE It is seen in 6% of all the patients of Hodgkin's disease. It is an uncommon type.

The R-S cells have been found in following other conditions as well ;

Commonly found cells have a delicate multi-lobed puffy nucleus which is also called "popcorn cell".

Most of the R-S cells are bi-lobed or bi-nucleate.

Infectious mononucleosis.

Solid tissue cancers.

Mycosis fungoides.

Lymphomas (Non Hodgkin's).

! ! ! !

GRADING (HISTOLOGICAL) Hodgkin's disease is classified according to histological features (Rye classification); 1.

2.

3.

4.

Lymphocytic predominance.

Nodular sclerosis.

Mixed cellularity.

Lymphocytic depletion.

Eosinophils, neutrophils and plasma cells are either scanty or absent. There is hardly any evidence of necrosis or fibrosis.

This is the type where lymphocytic infiltration is very prominent. Reed Sternberg (RS) cells are difficult to find.

The prognosis is best in this variant of Hodgkin's disease ; Prognosis of Lymphocytic predominance type % Survival

WHO CLASSIFICATION Lymphocyte rich classic Hodgkin lymphoma is new subtype of Hodgkin lymphoma instead of lymphocytic predominance variant. It includes both nodular and diffuse variants. Nodular variant SURGERY - PRINCIPLES IN GENERAL

2 years

5 years

99%

55%

NODULAR SCLEROSIS It is the most common type of Hodgkin's disease.This variant has more fibrous reaction and relatively less marked lymphocytic infiltration. The number of 242

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typical Reed Sternberg cells (RS cells) is more than the lymphocytic predominant type.

Its prognosis is worse than both of the previous two variants ; Prognosis in mixed cellularity type

The lacunar cell which is a variant of R-S cell is seen.

This cell is large and has a single hyper-lobated nucleus with multiple small nucleoli and an abundant pale staining cytoplasm with well defined borders.

The collagen bands divide the lymphoid tissue into nodules. Fibrosis is scanty or more. Lymphocytes, eosinophils and lacunar cell are present.

Classical RS cells are less in number.

It is more common in females.

The prognosis is relatively bad than lymphocytic predominance type ; Prognosis in nodular sclerosis type % Survival

2 years

5 years

73%

47%

MIXED CELLULARITY It is the second most common type of Hodgkin's disease.

This is the variant of Hodgkin disease which is characterized by cellular infiltration with all types of cells such as lymphocytes, histiocytes and eosinophils.

These are present in lesser number than lymphocytic predominant type. Typical Reed Sternberg cells are present in large numbers.

% Survival

SURGERY - PRINCIPLES IN GENERAL

5 years

41%

03%

This type is more common in older age group.

LYMPHOCYTIC DEPLETION It is the least common type of Hodgkin's disease.

This is the variant of Hodgkin disease with worst prognosis. It has minimal lymphocytic infiltration. It has lots and lots of Reed Sternberg cells (RS cells).

It is present in two distinct types ; ! !

Diffuse fibrosis type.

Reticular variant.

In diffuse fibrosis type whole lymph gland is replaced by proteinaceous fibrillar material which contains few lymphocytes, few typical and atypical R-S cells and pleomorphic histiocytes.

In reticular variant the anaplastic cells are in large number. Only few typical RS cells are seen. It is a widespread type of disease with systemic manifestations.

It has worst prognosis than all other variants of Hodgkin's disease.

Prognosis % Survival

Small areas of necrosis and fibrosis are also present.

These patients present with widespread disease and have systemic manifestations as well.

2 years

2 years

5 years

18%

00%

CLINICAL FEATURES Hodgkin disease presents with progressive

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enlargement of the lymph glands which are painless and are usually present in the cervical or supraclavicular region.

Additional presentations include mass, ascites, inferior vena cava obstruction, intussussception jaundice, obstructive uropathy, nephrotic syndrome and hepatosplenomegaly.

Its clinical features are ; SWELLING The most common presentation is painless swelling of the cervical or supra-clavicular lymph glands.

These are discrete, non tender and rubbery in consistency. These can be very easily clinically differentiated from tuberculous lymph glands which are matted together and are fixed due to periadenitis.

WEAKNESS AND MALAISE Unexplained weakness is one of the presenting symptoms.

ANOREXIA Loss of appetite is common feature of most of the malignancies. This is also seen in patients suffering from Hodgkin's disease.

LOSS OF WEIGHT Weight loss without any obvious reason should be investigated properly as it may be because of Hodgkin's disease.

FEVER Typical Pel-Ebstein fever is not seen. In fact it is not characteristic of Hodgkin's disease. Irregular rise of temperature is seen in these patients.

INTERIOR MEDIASTINAL MASS It presents with cough, stridor, pneumonia, tracheo bronchial compression.

SURGERY - PRINCIPLES IN GENERAL

GENERAL FEATURES Pruritis is present.

Superior vena caval syndrome or mediastinal pressure due to effects of enlarged lymph glands may be seen.

Bone pain due to secondaries may be very troublesome in patients with advanced Hodgkin's disease.

Bone marrow infiltration presented with anaemia, neutropenia or thrombocytopenia.

Hepato-splenomegaly may be the presenting feature in certain cases.

Anaemia, jaundice and skin lesions due to secondaries may also be present.

Isolated optic-neuropathy is associated with Hodgkin's disease4.

STAGING (CLINICAL) ANN ARBOR STAGING OF HODGKIN DISEASE This is important as treatment and prognosis depends upon the clinical stage of the disease.

Staging has been done according to the anatomical involvement of the disease.

A. Absence of systemic symptoms.

B. Presence of fever and weight loss.

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STAGE-I A- Symptomatic B- Asymptomatic Single group of the lymph glands is involved in the disease process.

5 years survival more than 90%, even total cure is possible.

STAGE-II A- Symptomatic B- Asymptomatic All diseased lymph glands are present on the same side of the diaphragm.

STAGE-III A- Symptomatic B- Asymptomatic The involvement of the lymph glands is present above and below the diaphragm. Spleen may also be involved.

STAGE-IV A-Symptomatic B- Asymptomatic Wide spread involvement of the organs such as liver, lungs, bones and lymph-glands is present.

5 year survival is about 60-70%.

INVESTIGATIONS Following investigations are performed to stage the disease accurately : Complete blood count.

Peripheral film evidence of bone marrow involvement.

SURGERY - PRINCIPLES IN GENERAL

ESR, Serum Copper, Serum Protein levels are of some prognostic significance and, if abnormal at diagnosis, serve baseline to evaluate effects of treatment12.

FINE NEEDLE ASPIRATION CYTOLOGY (FNAC) It is a simple and almost non invasive procedure.

Aspiration cytology of the solid mass shows diagnostic Reed-Sternberg cells and characteristic polymorphic elements5,6.

LYMPH NODE BIOPSY This procedure confirms the diagnosis. It provides accurate grading of the disease. It cures the symptoms as well. The lymph gland is not crushed during surgery. It is excised very gently so that the microscopic examination of the lymph gland architecture is accurate and not altered due to crushing by forceps during surgery.

BONE MARROW ASPIRATION BIOPSY It is performed to confirm its involvement in the disease process but bone marrow infiltration does not influence the treatment or its outcome7.

X-RAY CHEST AND TOMOGRAPHY These radiological investigations help to detect the enlarged mediastinal lymph glands and other chest lesions.

ULTRASONOGRAPHY Ultrasonography of liver and spleen helps to diagnose presence of focal masses (secondaries). It also helps to assess the enlargement of para-aortic glands.

C.T SCANNING This helps to show the involvement of liver, spleen

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and other organs in the disease process. It also helps in staging the disease.

It still remains the most important tool in choosing appropriate therapy in Hodgkin's disease9.

MRI SCANNING It is expensive and not available at all centers. It is extremely helpful in many patients where CT scan is not conclusive. It picks up the chest wall and pleural sites of disease and offer positive help in planning correct and timely treatment8.

It also appears to be a valuable procedure in patients with positive and doubtful clinical findings at reevaluation after radical therapy10.

GALIUM SCAN It is particularly helpful in identifying areas of increased uptake, especially in patients with mediastinal masses that do not resolve completely on chest radiograph or CT Scan13.

INTRAVENOUS UROGRAPHY It shows the position of ureters. It shows the displacement of the ureters if the enlarged para aortic lymph glands have displaced them.

Splenectomy, liver biopsy and para-aortic lymph gland biopsy is performed at laparotomy.

Splenectomy is performed for both diagnostic and therapeutic reasons.

In young female patients both ovaries are fixed in the midline (oophoropexy). Metallic clips are applied at the areas of para aortic lymph glands. These procedures are helpful while radiotherapy is given.

The ovaries in the midline can be shielded when the radiotherapy is applied post operatively to the iliac and para aortic lymph glands. As the clips are metallic and radio opaque, these help in provision of well focused radiotherapy under x-ray control.

BIPEDAL LYMPHANGIOGRAPHY It is a procedure which outlines the lymphatics and lymph glands. This procedure alters the architecture of the lymph glands and may cause diagnostic problems at histological examination of the lymph glands and may lead to incorrect diagnosis.

TREATMENT Two modalities are commonly used for the treatment of Hodgkin's disease after the staging has been done.

It has very high sensitivity 80% in detecting retroperitoneal lymph glands9.

Both methods have ill effects such as bone marrow suppression.

The biopsy of the lymph glands is performed before lymphangiography is carried out.

Regular blood examination is essential during the treatment.

LAPAROTOMY Laparotomy is essential for the accurate staging of the disease and planning of adequate treatment of the disease.

These two modalities are ;

SURGERY - PRINCIPLES IN GENERAL

! !

Radiotherapy.

Chemotherapy.

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!RADIOTHERAPY It is the treatment of choice for stage-I Hodgkin's disease. Rest of stages are treated with combination therapy It may be commonly used for the stage-I, II and III. 3500 to 4000 rads are given for few weeks

therapy when used early. It is used as an adjunct to chemotherapy11.

REFERENCES 1. Juan Rosai; Malignant lymph, Rosai & Surgical Pathology. 9th Edition Mosby 1917-1930.

Normal tissue is protected with the help of shields and mega-voltage radiotherapy.

2. Robbins. Disease of white cells, lymph nodes and spleen. Robbins pathologic basis of disease 5th edition. Cotran Kumar Robbins WB Saunders company London. 1994; 629-648.

CHEMOTHERAPY Various combinations of the drugs are used and repeated at regular intervals for the treatment of stage III & IV disease.

3. Rina Kansal; Timothy P. Singleton; Charles W. Ross; William G Fim, Ruth F. Padmore; Betram Schnitzer: Follicular Hodgkin lymphoma. Am J. Clin Pathol. 2002; 117(1): 29-35.

Following drugs and their combinations are used; MOPP ! Mustine ! Oncovincristine ! Procarbazine ! Prednisone ABVD ! Adriamycin ! Bleomycin ! Vinblastine ! Dacarbazine CEM ! Carmustine ! Etoposide ! Methyl-GAG BONE MARROW TRANSPLANT Autologous bone marrow transplant for patients with relapsed Hodgkin's disease is a very effective SURGERY - PRINCIPLES IN GENERAL

4. Siatkowski RM, Lam BL. Schatz NJ et al. Optic neuropathy in Hodgkin's disease. American journal of ophthalmology. [JC : 3oq]. Nov-15, 1992; 114(5) : 625-9.

5. Corrigan C. Sewell C. Martin A. Recurrent Hodgkin's disease in breast. Diagnosis of a case by FNAC and immunocyto chemistry. Acta cytological. [JC: Oli].

Sep-Oct 1990; 34(5): 669-72.

6. Das DK. Gupta SK. FNAC of Hodgkin's disease and its subtypes. II Subtyping by differential cell counts Acta cytological. [JC: Oli]. May-Jun 1990; 34(3): 337-41.

7. Abrahamen AF. Jakobsen E. Longboln R. Abrahamsen JF. Kvaloys. None O. Bone Marrow examination in Hodgkin's disease. Acta oncologica.

[JC: aon]. 1992; 31(1): 41-2.

8. Carlsen SE. Bergin CJ. Hoppe RT. MR Imaging to detect chest wall and pleural involvement in patients with lymphna: Effect on radiation therapy planning.

Ajr- American journal of Roentgenology. [JC : 3ae].

Jun 1993; 160(6) : 1191-5.

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9. Baker LL. Parker BR. Donaldson SS. Castellino RR. Staging of Hodgkin's disease in children: Comparison of CT and lymphography with laparotomy. Ajr American journal of Roentgenology.

[JC : 3ae]. Jun 1990; 154(6) : 1251-5.

10. Blagini C. Enrici RM. Anselmo AP et al. The role of restaging laparotomy in Hodgkin's disease. Acta oncologica. [JC: aon]. 1989; 28(5): 659-62.

11. Armitage JD, Blerman PJ Vose JM et al. Autologous bone marrow transplantation for 2 patients with relapsed Hodgkin's disease. American journal of medicine. [JC: 3ju]. Dec 1991; 91(6) 605-11.

12. Hudson MM, Donaldson SS: Hodgkin’s disease.

Pediatr Clin North 1997, An 44: 891.

13. Scwartz RS: Hodgkin’s disease - time for a change. N Engl J Med. 1997; 337: 495.

SUMMARY Hodgkin’s Disease Grading ! Lymphocytic predominance ! Nodular sclerosis ! Mixed cellularity ! Lymphocytic depletion Diagnosis History Clinical examination Blood examination FNAC Lymph gland biopsy Bone marrow biopsy X-ray chest Ultrasonography CT scanning MRI scanning Galium scanning Urography Lymphangiography Laparotomy

! ! ! ! ! ! ! ! ! ! ! ! ! !

Treatment ! Radiotherapy ! Chemotherapy ! Bone marrow transplant

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248

Arterial System

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PERIPHERAL ISCHAEMIA

PS-038

PERIPHERAL ISCHAEMIA Shuja Tahir, FRCS, FCPS Faisal Bilal Lodhi, FCPS

VASCULAR SYSTEM The vascular system is made up of arteries, veins and micro-vessels.

The arteries have a luminal lining of single layer of endothelium. The major arterial system has primary transport function (Elastic arteries) and distributing function (muscular arteries). The muscular arteries branch many times to become arterioles of (0.1 mm) diameter size.

Capillaries arise from arterioles directly. Flow is regulated through directly communicating vessels between arterioles and venules. Capillary flow is regulated through pre capillary sphincters. Met arterioles act as arterio venous shunts when capillaries are closed. Capillaries have a diameter of 8-10 m m.

The venous system has capacitance function.

Venules collect blood from capillaries. These are of 8-100Âľm size diameter. Venules join and become veins of various sizes.

The blood flow in most of vessels is of laminar nature.

The blood moves with higher velocity in center of the vessels.

The blood velocity is increased sufficiently in stenotic vascular lesions to produce post stenotic turbulence of blood flow. It causes progressive intimal damage

SURGERY - PRINCIPLES IN GENERAL

of that area.

The turbulence of blood flow is heard in ascending aorta at peak of systole in healthy people.

PERIPHERAL VASCULAR ISCHAEMIA (PVI) PERIPHERAL VASCULAR DISEASE (PVD) PERIPHERAL ARTERIAL DISEASE (PAD) Limb ischemia is the result of Peripheral Vascular Occlusive Disease (PVOD) also known as Arteriosclerosis Obliterans. It is nearly a pandemic condition that has the potential to cause loss of limb, or even loss of life.

It manifests as insufficient tissue perfusion caused by existing atherosclerosis that may be acutely compounded by either emboli or thrombi1.

PATHOPHYSIOLOGY Atherosclerosis underlies most peripheral arterial disease. The atheroma consists of a core of cholesterol joined to proteins with a fibrous intravascular covering. The atherosclerotic process may gradually progress to complete occlusion of medium and large arteries resulting in critical limb ischemia2.

A common site for Peripheral Arterial Obstructive Disease (PAOD) is in the lower limb. The disease 251

2

PERIPHERAL ISCHAEMIA

ei

ci

!

df

A nonhealing wound or gangrene of the foot or toes, with similar hemodynamic measurements.

ii

CLI is more common in men than women.

Male to female ratio is 1.48 : 1. The peak incidence is at 70-79years of age. sf pop tib

ci = common iliac artery ei = external iliac artery ii = internal iliac artery df = deep femoral artery sf = superficial femoral artery pop = popliteal artery tib = tibial artery

The hemodynamic parameters of limb ischaemia may be less reliable in patients with diabetes because arterial wall calcification can impair compression by a blood pressure cuff and produce systolic pressure measurements that are greater than the actual levels4.

Vascular disease may manifest as chronic limb ischemia or acutely when thrombi, emboli, or acute trauma compromises limb perfusion.

Thromboses are often of an atheromatous nature and occur in the lower extremities more frequently than in the upper extremities.

typically is segmental, with significant variation from patient to patient.

Multiple factors predispose patients for thrombosis.

These factors include;

CRITICAL LIMB ISCHEMIA It is a stage of limb ishcaemia which will lead to limb loss (amputation) if not improved.

! ! ! ! ! ! !

Chronic critical limb ischemia(CLI) is defined not only by the clinical presentation but also by an objective measurement of impaired blood flow. Criteria for diagnosis include either one of the following; !

More than two weeks of recurrent foot pain at rest that requires regular use of analgesics and is associated with an ankle systolic pressure of 50 mm Hg or less, or a toe systolic pressure of 30 mm Hg or less.

SURGERY - PRINCIPLES IN GENERAL

Sepsis.

Hypotension.

Low cardiac output.

Aneurysms.

Aortic dissection.

Bypass grafts.

Underlying atherosclerotic narrowing of the arterial lumen.

The development of chronic critical limb ischemia usually requires multiple sites of arterial obstruction that severely reduce blood flow to the tissues.

Emboli, the most common cause of sudden ischemia, 252

3

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usually are of cardiac origin (80%); these can also originate from proximal atheroma, tumor, or foreign objects. Emboli tend to lodge at arterial bifurcations or in areas where vessels abruptly narrow.

Critical tissue ischemia is manifested clinically as rest pain, nonhealing wounds (because of the increased metabolic requirements of wound healing) or tissue necrosis (gangrene)6.

The femoral artery bifurcation is the most common site (43%), followed by the iliac arteries (18%), the aorta (15%), and the popliteal arteries (15%).

The site of occlusion, nature of the occlusion (thrombus or embolus), presence of collateral circulation and determine the severity of the acute manifestation.

Emboli tend to carry higher morbidity because the extremity has no time to develop collateral circulation. Whether caused by embolus or thrombus, occlusion results in both proximal and distal thrombus formation due to flow stagnation.

The poor peripheral circulation results as a complication of many diseases such as ; ! ! ! !

Diabetes mellitus.

Atherosclerosis.

Buerger's disease.

Raynaud's disease

RISK FACTORS Chronic critical limb ischemia is the end result of ar terial occlusive disease, most commonly atherosclerosis. Common causes of chronic critical limb ischemia include atherosclerosis, hypertension, hypercholesterolemia, cigarette smoking and SURGERY - PRINCIPLES IN GENERAL

diabetes. Buerger's disease, thromboangiitis obliterans, and some forms of arteritis4,5.

The peripheral circulation is compromised due to various reasons. Highest risk factors for atherosclerosis which leads to increased risk of peripheral arterial disease are; AGE Old age is associated with higher risk of peripheral ischaemia.

HYPERTENSION It leads to higher risk of peripheral ischaemia.

SMOKING It increases oxidation of fatty acids and atherogenicity of LDL cholesterol (related to decrease of antioxidants).

LIPIDS Abnormalities in lipoproteins, cholesterol and triglycerides, lead to increased risk of athrosclerosis and ischaemia.

Cholesterol level of > 7 mmol/L doubles the risk.

DIABETES It is associated with 15-70 times more chances of amputation due to ischaemia.

Diabetes Mellitus is a particularly important risk factor because it is frequently associated with severe peripheral ar terial disease. Atherosclerosis develops at a younger age in patients with diabetes and progresses rapidly.

Moreover, atherosclerosis affects more distal vessels in patients with diabetes; the profunda femoris, popliteal and tibial arteries are frequently affected, 253

4

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while the aorta and iliac arteries are minimally narrowed. These distal lesions are less amenable to revascularization.

Atherosclerosis in distal arteries in combination with diabetic neuropathy contributes to the higher rates of limb loss in diabetic patients compared with nondiabetic patients.

!

!

!

calcification1.

The aneurysmal dilatation of vessels occurs due to ischemia and weakening of the vessel wall.

The aneurysmal dilatation occurs due to interaction between congenital and acquired proteolytic enzymes and their inhibitors1.

Other problems that often coexist are coronary artery disease, myocardial infarction (MI), atrial fibrillation, transient ischemic attack, stroke, and renal disease.

Other etiologies for developing PVOD may include phlebitis, injury or surgery, and autoimmune disease, including vasculititis, arthritis, or coagulopathy.

PVOD rarely exhibits as an acute onset; it instead manifests a more chronic progression of symptoms.

Patients with acute emboli causing limb ischemia may have new or chronic atrial fibrillation, valvular disease, or recent MI, whereas a history of claudication, rest pain, or ulceration suggests thrombosis of existing PVOD7.

HEMATOLOGICAL FACTORS Increased haematocrit and increased viscosity leads to increased risk of limb ischaemia.

Other risk factors related to blood vessels are ; ! ! !

Intimal injury.

Deposition of lipids.

Interaction between inflammatory cells and growth factors. All these changes lead to progressive fibrosis of the vessel wall leading to complete obliteration of its lumen and its

SURGERY - PRINCIPLES IN GENERAL

CLINICAL FEATURES Following features are associated with peripheral vascular ischaemia. The severity of symptoms depends upon severity of occlusion.

A systematic examination of the peripheral vasculature is critical for proper evaluation. Physical signs of PVOD are the classic "5 P's"; ! ! ! ! !

Pulselessness.

Paralysis.

Paraesthesia.

Pain.

Pallor.

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ASYMPTOMATIC DISEASE The peripheral ischaemia is asymptomatic in its early stages. If it is diagnosed at early stage, deterioration can be prevented and complications may be avoided.

Following features help to assess the condition; ! ! !

ABPI ratio of ÂŁ 0.9 is good marker.

Resting ABPI of 0.9 is 95% sensitive and 100% specific in diagnosing healthy people.

Decreased ABPI is associated with increased risk of death from PAOD.

REST PAIN It is the pain felt all the time even while resting. The severity of pain depends upon the severity of vascular occlusion and resultant ischaemia. The pain gets worse on lying down and elevation of the limb . It is relieved by hanging the limb lower down from bed.

When it is persistent even after adequate analgesia the limb salvage becomes questionable.

Ischemic rest pain is classically described as a burning pain in the ball of the foot and toes that is worse at night when the patient is in bed. The pain is exacerbated by the recumbent position because of the loss of gravity-assisted flow to the foot. Ischemic rest pain is located in the foot, where tissue is farthest from the heart and distal to the arterial occlusions.

Patients with ischemic rest pain often need to dangle their legs over the side of the bed or sleep in a recliner to regain gravity-augmented blood flow and relieve the pain. Patients who keep their legs in a dependent position for comfort often present with considerable edema of the feet and ankles.

Ischemic rest pain is more worrisome; it refers to

SURGERY - PRINCIPLES IN GENERAL

pain in the extremity due to a combination of PVOD and inadequate perfusion.

Ischemic rest pain often is exacerbated by poor cardiac output.

The condition is often partially or fully relieved by placing the extremity in a dependent position, so that perfusion is enhanced by the effects of gravity.

INTERMITTENT CLAUDICATION8 It is cramp like pain in the limb muscles after walking some distance. It is relieved on resting. It is less common in upper limb. The distance covered which brings this pain is called claudication distance.

Change in this distance signifies the progress or deterioration of vascular occlusive disease. The special features of intermittent claudication are; ! ! !

It is not present in the beginning of walking.

It is brought on walking.

It is relieved by rest.

Intermittent claudication may be the sole manifestation of early symptomatic PVOD. The level of arterial compromise and the location of the claudication are closely related as follows: Aortoiliac disease manifests as pain in the thigh and buttock, whereas femoral-popliteal disease manifests as pain in the calf.

Symptoms are precipitated by walking a predictable distance and are relieved by rest.

Collateral circulation may develop, reducing the symptoms of intermittent claudication, but failure to control precipitant factors and risk factors often

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PERIPHERAL ISCHAEMIA

causes its reemergence.

Claudication also may present as the hip or leg â&#x20AC;&#x153;giving out" after a certain period of exertion and may not demonstrate the typical symptom of pain on exertion.

The pain of claudication usually does not occur with sitting or standing.

LERICHE SYNDROME Leriche syndrome is a clinical syndrome presenting with intermittent claudication, pain in thigh, buttock, impotence, and significantly decreased or absent femoral pulses.

This syndrome indicates chronic peripheral arterial insufficiency due to narrowing of the distal aorta.

6

blanched on elevation and purple on hanging or dependency.

LEVELS OF PALLOR A semiquantitative assessment of the degree of pallor may also be helpful. While supine, the degree of pallor is assessed.

Level 4 Pallor manifests when the extremity is at level.

Level 3 The extremity is raised 60°; If pallor occurs within 30 seconds.

Level 2 If pallor occurs in less than 60 seconds.

Level 1 If pallor occurs in 60 seconds.

Level 0 If no pallor within 60 seconds.

COLD NESS The temperature of limb is usually changed to atmospheric temperature due to ischaemia. It is cold in cold weather or warm with blanket as limb temperature can not be adequately maintained by ischaemic limb.

NUMBNESS It is experienced in moderate degrees of ischemia. It is essential to exclude neurological causes.

Numbness may improve on limb hanging in ischemic patients.

Paralysis and paraesthesia suggest limb-threatening ischemia and mandate prompt evaluation and consultation.

COLOUR CHANGES The colour changes are seen in limbs with peripheral vascular ischemia. The limb may be pale and SURGERY - PRINCIPLES IN GENERAL

ULCERATION It is seen with severe ischaemia commonly involved areas are terminal parts of toes, worst hit by ischemia. Even minor injury leads to ulceration of skin or superficial erosion. The ulcer fails to heal because of lack of adequate blood supply to the 256

PERIPHERAL ISCHAEMIA

7

area. The ulcers are seen on toes, dorsum of foot, around malleolus and skin9,10.

feature also exist. Expansile arterial pulsation with a mass may also be seen in case of arterial aneurysms.

Non healing wounds are usually found in areas of foot trauma caused by improperly fitting shoes or an injury. A wound is generally considered to be nonhealing if it fails to respond to a 04 to 12-week trial of conservative therapy such as regular dressing changes, avoidance of trauma, treatment of infection and debridement of necrotic tissue.

When the pulses are present, patient may be asked to exercise upto claudication point. A disappearing pulse at that time is indicative of arterial occlusion.

GANGRENE Gangrene is usually found on the toes. It develops when the blood supply is so low that spontaneous necrosis occurs in the most poorly perfused tissues.

The toes or any part of limb usually most peripheral becomes black and dry. The mummified skin and tissue are very obvious of dry gangrene. It is associated with other features of ischaemia as well.

DIMINISHED SENSATION The ischaemic limb presents with diminished sensations, it has to be differentiated from other neurological causes.

The patient's medication may provide a clue to the existence of PVOD. DIMINISHED MOVEMENTS The paralysis or loss of movements may be seen in acute ischaemia of the limb but it is not seen with chronic ischaemia. Hyperasthenia is seen with this type of ischaemia which signifies poor prognosis.

DIMINISHED OR ABSENT PULSES The arterial pulses below the occlusion are either diminished or absent . Development of collateral vessels keep the limb viable sometimes ischaemic SURGERY - PRINCIPLES IN GENERAL

The heart is assessed for murmurs or other abnormalities. All peripheral vessels, including carotid, abdominal, and femoral, for pulse quality and bruit are examined. The dorsalis pedis artery is absent in 5-8% of normal subjects, but the posterior tibial artery usually is present. Both pulses are absent in only about 0.5% of patients. Exercise may cause the obliteration of these pulses. The Allen test may provide information on the radial and ulnar arteries.

SKIN COLOR The skin may have an atrophic, shiny appearance and may demonstrate trophic changes, including alopecia; dry, scaly, or erythematous skin; chronic pigmentation changes and brittle nails.

Advanced PVOD may manifest as mottling in a â&#x20AC;&#x153;fishnet patternâ&#x20AC;? (livedo reticularis), pulselessness, numbness, or cyanosis. Paralysis may follow, and the extremity may become cold; gangrene eventually may be seen.

Poorly healing injuries or ulcers in the extremities help provide evidence of preexisting PVD. Using Doppler ultrasonography, the pressure at the brachial artery and at the posterior tibial artery is measured.

The ankle systolic pressure is divided by the brachial pressure, both measured in the supine position.

Normally, the ratio is more than 1. In severe disease, 257

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it is less than 0.5.

ARTERIAL THRILL AND BRUITS Arterial pulse in a stenosed vessel gives rise to turbulent flow of blood. It can be palpated as a thrill on the artery below the stenosis. The same palpable thrill when auscultated is heard as systolic bruit. The bruit is conducted distally. A continuous machinery murmur is heard in arteriovenous fistula.

DELAYED VENOUS FILLING The suspected ischaemic limb is elevated for 30 seconds and the blood is milked out of veins . When the limb is put on the bed, the veins fill immediately in normal limbs. Reduced venous filling or delayed venous filling is seen in ischaemic limbs.

speed of refilling of vein (Harveyâ&#x20AC;&#x2122;s) . It is slow in ischaemia and increased filling is seen in varicose veins and arterio venous fistulas.

DIFFERENTIAL DIAGNOSIS Ischemic rest pain may be confused with night cramps, arthritis or diabetic neuropathy. Night cramps occur in the calf muscles; these usually awaken the patient from sleep and are relieved by massaging the muscle, by walking or by using antispasmodic agents.

Patients with arthritis of the metatarsal bones may have pain in the foot. This pain is often experienced at night and may be relieved by standing.

The distinguishing characteristic of arthritic pain is that it usually occurs intermittently and at sporadic intervals, whereas ischemic rest pain consistently occurs after a specific interval of recumbency.

Diabetic neuropathy may also present with pain in the foot and is occasionally associated with diminished pulses and trophic skin changes.

This pain, however, is not steadfastly associated with recumbency. The other features of diabetic neuropathy, such as loss of light touch (i.e., the monofilament test) and decreased vibratory sense, can also serve as distinguishing characteristics.

Other conditions that must be included in the list of as differential diagnosis include:

Two index fingers are kept on a segment of empty vein. One towards heart and other distally. The release of distal finger from vein allow assessment of

SURGERY - PRINCIPLES IN GENERAL

! ! ! ! !

Soft-tissue Injures.

Back Pain.

Mechanical.

Deep Venous Thrombosis and Thrombophlebitis Lumbar (Intervertebral) Disk Disorders.

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(lipid profile, coagulation tests) are also evaluated.

An ECG is obtained to look for evidence of dysrhythmia, cardiac enlargement, or MI. IMAGING STUDIES Plain films are of little use in diagnosing of PVOD. Doppler ultrasound studies are useful as primary non-invasive studies to determine flow status. Upper extremities are evaluated over the axillary, brachial, ulnar, and radial arteries. Lower extremities are evaluated over the femoral, popliteal, dorsalis pedis, and posterior tibial arteries.

The presence of Doppler signal and the quality of the signal (ie, monophasic, biphasic, triphasic) is noted.

The presence of distal flow does not exclude emboli or thrombi because collateral circulation may provide these findings.

! ! !

Thrombophlebitis, Septic.

Thrombophlebitis, Superficial.

Trauma, Peripheral Vascular Injuries.

More accurate information with regard to the extent and location of arterial lesions is obtained from segmental blood pressures taken at the thigh, calf, and ankle, and segmental plethysmographic recordings of pulse waveforms before and after exercise.

Isolated aortoiliac disease can be distinguished from femoropopliteal disease, below-knee disease, or any combination of these by noting pressure gradients and abnormal waveforms.

INVESTIGATIONS LAB. STUDIES Blood tests generally are indicated in the evaluation of patients with suspected serious compromise of vascular flow to an extremity. CBC, BUN, creatinine, and electrolytes studies help evaluate factors that might lead to worsening of peripheral perfusion.

Arteriography provides details of the location and extent of occlusion. Complete angiography includes aortography and bilateral femoral arteriography, visualizing the arteries as far distally as the feet.

Risk factors for the development of vascular disease

Digital subtraction angiography allows visualization

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of the vascular system while "subtracting" other soft tissues.

Magnetic resonance angiography (MRA) is of clinical benefit due to its high visual detail. Plaques are imaged easily, as is the difference between vessel wall and flowing blood. MRA also has the benefits of to provide even higher detail, and can replace traditional arteriography. The utility of MRA is limited in the emergency setting, often due to location of the device and the technical skill required to interpret the highly detailed images.

OTHER TESTS The ankle-brachial index (ABI) is a useful test to compare pressures in the lower extremity to the upper extremity. Blood pressure normally is slightly higher in the lower extremities than in the upper extremities. Comparison to the contralateral side may suggest the degree of ischemia11,12.

macrovascular disruption. Its use is increasing, especially in the realm of wound care and patients with diabetes. Transcutaneous oximetry has not been studied extensively in emergent occlusion.

METHODS OF IMPROVING LIMB ISCHAEMIA The exact cause of decreased peripheral circulation and exact status of the circulation is established before the optimum method to improve the circulation is selected. Careful evaluation of riskbenefit ratio helps in correct decision making and choosing the mode of treatment11.

The circulation of the lower limbs can be improved by following methods ; ! !

Conservative.

Surgical.

CONSERVATIVE MEASURES15,16,17,18 Risk factor modification, including smoking cessation, blood pressure control, good glycemic control and reduction of lipid levels, should be instituted.

Antiplatelet therapy with aspirin has been shown to substantially decrease the risk of a myocardial infarction, stroke and death in patients with peripheral vascular disease and also reduces the rate of arterial reocclusion after angioplasty or bypass grafting.13

Transcutaneous oximetry affords assessment of impaired flow secondary to both microvascular and SURGERY - PRINCIPLES IN GENERAL

ISCHEMIC REST PAIN Patients with ischemic rest pain should be given pain medication as necessary, and any underlying systemic cause of inadequate blood flow, such as cardiac failure, should be corrected. If pain persists after four to eight weeks of conservative therapy with pain medication and interventions to optimize the 260

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patient's overall condition, the possibility of operative intervention should be explained to the patient, including the risks and benefits of the procedure.

Conservative therapy includes teaching the patient ways to avoid trauma to the wound site, including the wearing of properly fitting shoes. Dressings should be changed frequently; the patient should be seen weekly until the wound heals.

Further intervention may be required if conservative therapy does not lead to improvement, as indicated by increasing wound size, persistent or spreading infection or no evidence of healing after four to eight weeks.

Progressive gangrene, rapidly enlarging wounds and continuous ischemic rest pain unrelieved by dependency are each unstable conditions that can rapidly lead to limb loss and require urgent intervention. However, many patients with critical limb ischemia have a stable or slowly improving limb condition.

Smoking should be stopped immediately as it is the main cause of peripheral ischaemia in Buerger's disease and leads to worsening of atherosclerosis. It also interferes with the oxygenation of the blood.

Avoidance of smoke should be perfect and one should not be present where others are smoking (passive smoking).

Stopping of smoking helps in improvement of symptoms. It also minimizes the deterioration of the circulatory status.

NONHEALING WOUNDS Patients with nonhealing wounds or gangrene should be evaluated for the presence of infection. Infected wounds require antibiotic therapy, surgical debridement, or both.

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WEIGHT REDUCTION Obese patients should be motivated to lose weight.

The diet control and exercise should be used for weight reduction. It helps to ; ! !

Lower the blood lipids.

Slow the disease process.

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! !

Improve the peripheral circulation by opening up collateral vessels.

Decrease the needs of tissue at periphery due to less fat in the body.

It helps to improve the symptoms of peripheral ischaemia.

LOW FAT DIET This helps to reduce the weight, decrease serum lipid level and slow the generalized atherosclerotic disease process. Thus it helps the ischaemic limb by subjective improvement of symptoms.

EXERCISE Exercises are designed to encourage the collateral circulation to open up so that more blood is available to the limb.

Exercise helps the partially blocked vessels to dilate and carry more blood to the periphery.

Exercises are very helpful in the treatment of early disease and relief of symptoms.

ANTI-COAGULANTS These help to lower the viscosity of the blood. These decrease the fibrino-peptide-A (FP-A) level and minimize the risk of intravascular coagulation.

The anticoagulants help to improve the flow of blood through smaller vessels. It has been seen that results of treatment in patients with polycythemia are worse (viscous blood). The use of anticoagulants with bypass surgery is extremely helpful to achieve good results13.

VASO-DILATORS The efficiency of vasodilator drugs is still SURGERY - PRINCIPLES IN GENERAL

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questionable. But in early ischaemia of the lower limbs, these may be helpful to some degree. Intra arterial injection of different drugs such as paraxlene and guanethidine have been tried and variable results have been achieved.

CHEMICAL SYMPATHECTOMY Lumbar sympathetic chain and lumbar ganglion against 2nd, 3rd and 4th lumbar vertebrae are destroyed chemically with phenol injection under xray control. This helps to achieve vasodilatation and improvement of the blood supply of the lower limb of that side. This procedure is less traumatic than its surgical counterpart but results may be poorer and uncertain.

SURGICAL MEASURES PERCUTANEOUS TRANSLUMINAL BALLOON ANGIOPLASTY This minimally invasive procedure is performed to widen a narrowed portion of an artery. The physician guides a catheter to the narrowed artery.

A smaller balloon-tipped catheter is inserted by passing it through the guiding catheter to the obstructed area. The balloon is inflated to exert pressure on the narrowed area, thereby relieving the obstruction.

Antithrombolytic agents such as streptokinase may be used to dissolve an atherosclerotic obstruction.

Obstructions in the renal, iliac, vertebral, and femoropopliteal arteries may be successfully treated in this way.

SYMPATHECTOMY It is a more specific procedure than chemical sympathetic block. 2nd, 3rd and 4th lumbar sympathetic ganglia with their chain are excised. It is 262

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more invasive procedure. The sympathectomy is complete and vasodilatation is better14.

more often. These are available in various sizes and shapes.

There is sudden change in the temperature and color of the limb as soon as the operation is performed.

The saphenous vein is the most commonly harvested vessel for peripheral bypass procedures.

These days the lumbar sympathectomy is performed infrequently as its effectiveness is less clear. It may still be helpful in following conditions of compromised circulation;

ARTERIAL STENTING Intravascular stents are tubular implants that resemble wire cages. They are designed to restore normal blood flow in a vessel by maintaining an open lumen after angioplasty has been performed. The stent is first attached to the end of a catheter and then guided to the site of the narrowed vessel via an introducer through a peripheral vessel, such as the femoral artery. Stenting is usually performed in a catheterization lab by skilled person.

! ! ! !

Hypertensive patients with painful leg ulcer.

Toe and foot amputations where bypass grafting is not feasible.

Sympathetic dystrophy (post-traumatic causalgia).

With bypass grafting to improve the results14.

ENDOLUMINAL REPAIR OF ANEURYSMS Removal of thrombus and endoluminal repair of the aneurysm is performed to improve the luminal diameter and circulation.

ENDARTERECTOMY This is the method in which the diseased vessel is opened up (arteriotomy) and the blocking atheroma is excised and repair of vessel is performed. The chances of reformation of an atheroma are present.

Thrombus formation and blockage of the vessel may occur after some time1.

HETEROGRAFTS Heterografts are the grafts from the animals and these are also not used anymore.

BY-PASS GRAFTING When the vessels are diseased to a greater degree and larger areas of the vessels are blocked or aneurysms are formed and endarterectomy is not likely to be helpful, the diseased part is excised or bypassed and new circulatory channel is formed.

PROSTHESIS Dacron or teflon vascular grafts are used quite frequently as these are easily available in different sizes and shapes and cause very little immune response. These do not block early. These are strong and easy to anastomose with vessels.

Auto-grafts may be used as alternate arterial channels such as reversed vein graft (long saphenous vein) of the patient himself.

ANGIOSCOPIC-ASSISTED19,20,21,22,23 IN-SITU BYPASS MINIMALLY INVASIVE IN-SITU BYPASS The greater saphenous vein is the most commonly used arterial substitute for bypasses below the groin.

Older bypass techniques involve removal of the entire vein through a long incision inside the leg.

Artificial prosthesis for by-pass-grafts are also used

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Newer techniques leave the vein in place ("in-situ") and disrupt the valves and side-branches through a series of short incisions that heal more easily than a single long one.

The in-situ saphenous vein bypass has been the standard surgical treatment of lower extremity arterial occlusive disease for three decades. In this most recent procedural advancement, only two small leg incisions are used, one at the groin and one in the lower leg. Under angioscopic visualization, the saphenous vein is dissected and divided at the level of the proximal and distal anastomotic sites. A retrograde valvulotome is inserted distally, and an introducer catheter is inserted proximally. Working down the vein, first the valves are visualized and lysed with the valvulotome, then occlusion coils are advanced into the side branches. The proximal and distal anastomoses are constructed, and the results are confirmed with an intraoperative angiogram.

Branches that cannot be occluded by coils are ligated through very small extra incisions, if needed.

PRIMARY AMPUTATION Primary amputation may be indicated in certain patients, such as those with extensive tissue necrosis, life-threatening infection or lesions not amenable to revascularization. The decision to monitor the patient's condition with watchful waiting and conservative management or to perform revascularization or amputation depends on careful assessment of the attendant risks and benefits of surgery versus conservative management.

More importantly, it depends on the patient's interpretation of the invasiveness or appropriateness of the available options. Even patients unable to walk because of their condition may consider amputation inappropriate, and not all SURGERY - PRINCIPLES IN GENERAL

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patients are motivated to do the work necessary for rehabilitation after amputation. If the decision is made to amputate, the level of amputation should be one that has the greatest likelihood of healing while giving the patient the maximal chance for functional rehabilitation.

MERITS AND LIMITATIONS CONSERVATIVE MEASURES These are helpful only in early disease. These are helpful in chronic ischaemia of the lower limb. These take longer period for minor improvements.

The advantage of conservative measures is that no surgery is involved and it can be offered to people otherwise unfit for surgery.

SURGICAL MEASURES These are very helpful in ischaemic disease of the lower limb. The circulation improves dramatically.

There are chances of complications of surgery.

Morbidity is greater after surgery than with conservative methods.

The incidence of blockage of the vessels after endarterectomy is quite high.

Steal phenomenon may cause unacceptable morbidity.

BLOCKAGE As the diseases leading to peripheral ischaemia are generalized, the by-pass-grafts are also blocked after some years requiring active treatment again.

STEAL PHENOMENON More blood is diverted to the limbs suddenly after surgical bypass. Acute cardiac and cerebral 264

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ischaemia may precipitate (steal phenomenon) as a consequence.

FOLLOW-UP Patients with chronic critical limb ischemia require life long follow-up for a number of reasons. After amputation or revascularization, patients require rehabilitation to hasten their return to maximal independence. Careful attention to nutritional status will assist in wound healing and recovery. In addition, bypass graft patency should be assessed frequently after revascularization. Some authorities recommend periodic surveillance with duplex ultrasonography every three months to maximize the chance that re-stenosis is identified early, when it is more amenable to repair.6 Four-year survival rates as low as 40 percent are reported in patients with critical limb ischemia, with the vast majority of deaths caused by coronary artery disease and cerebrovascular disease.17 Close follow-up of coronary artery disease and cerebrovascular disease may help extend life expectancy in these high-risk patients.

REFERENCES

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4. Dormandy J, Verstraete M, Andreani D, et al. Second European consensus document on chronic critical leg ischemia. Circulation. 1991; 84(suppl 4):1-26.

5. Haimovici H. Patterns of arteriosclerotic lesions of the lower extremity. Arch Surg. 1967; 95:918-33.

6. Mavor GE. The pattern of occlusion in atheroma of the lower limb arteries. The correlation of clinical and arteriographic findings. Br J Surg. 1956;43:352-64.

7. Welch HJ. Chronic lower extremity ischemia. Compr Ther. 1997; 23:534-8.

8. Golledge J. Lower-limb arterial disease. Lancet.

1997; 350:1459-65.

9. Santilli JD, Rodnick JE, Santilli SM. Claudication: diagnosis and treatment. Am Fam Physician. 1996; 53:1245-53.

10. DeBakey ME, Crawford ES, Garrett E, et al. Occlusive disease of the lower extremities in patients 16 to 37 years of age. Ann Surg. 1964; 159:873-90.

11. Haid SP, Conn J Jr, Bergan JJ. Cystic adventitial disease of the popliteal artery. Arch Surg. 1970;101:76570.

1. Robert J Hye Peripheral vascular disease. Essential surgical practice A Cuschieri G. R.Giles. Introduction A.R Moosa 3rd edition. Butterworth Heimemann.

1994; 890-927.

12. Cutajar CL, Marston A, Newcombe JF. Value of cuff occlusion pressures in assessment of peripheral vascular disease. Br Med J. 1973; 2(863):392-5.

2. Gordon T, Kannel WB. Predisposition to atherosclerosis in the head, heart, and legs. The Framingham study. JAMA. 1972; (221):661-6.

13. Ouriel K, McDonnell AE, Metz CE, Zarins CK. Critical evaluation of stress testing in the diagnosis of peripheral vascular disease. Surgery. 1982; 91:68693.

3. Brown AL, Juergens JL. Arteriosclerosis and atherosclerosis. In: Allen EV, et al. Peripheral vascular disease. Philadelphia: Saunders, 1972; 5766.

14. Nydahl S. Swedenberg J. Egberg N. Pre-operative anticoagulation with antithrombin or heparin in Infra inguinal bypass surgery. European Journal of vascular surgery. [JC: eus]. Nov 1992; 6(6): 610-5.

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15. Boltax RS. Lumbar sympathectomy a place in clinical medicine. Connecticut medicine. [JC: dqf]. Dec 1989; 53(12): 716-7.

16. Eklund AE, Eriksson G, Olsson AG. A controlled study showing significant shor t term effect of prostaglandin E1 in healing of ischaemic ulcers of the lower limb in man. Prostaglandins Leukot Med. 1982; (8):265-71.

17. Schuler JJ, Flanigan DP, Holcroft JW, Ursprung JJ, Mohrland JS, Pyke J. Efficacy of prostaglandin E1 in the treatment of lower extremity ischemic ulcers secondary to peripheral vascular occlusive disease: results of a prospective randomized, double-blind, multicenter clinical trial. J Vasc Surg 1984; (1):16070.

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23. Bergamini TM, Towne JB, Bandyk DF, Seabrook GR, Schmitt DD. Experience with in situ saphenous vein bypasses during 1981 to 1989: determinant factors of long-term patency. J Vasc Surg. 1991; (13):13747.

24. Quinones-Baldrich WJ, Prego AA, Ucelay-Gomez R, Freischlag JA, Ahn SS, Baker JD. Long-term results of infrainguinal revascularization with polytetrafluoroethylene: a ten-year experience. J Vasc Surg.

1992; (16):209-17.

18. Cheshire NJ, Wolfe JH, Noone MA, Davies L, Drummond M. The economics of femorocrural reconstruction for critical leg ischemia with and without autologous vein. J Vasc Surg 1992; (15):167-74.

19. Albers M, Fratezi AC, De Luccia N. Assessment of quality of life of patients with severe ischemia as a result of infrainguinal arterial occlusive disease.

J Vasc Surg 1992; (16):54-9.

20. Taylor LM Jr, Porter JM. Current status of the reversed saphenous vein graft. In: Bergan JJ, Yao J, eds. Arterial surgery. New York: Grune and Stratton, 1987; 494-501.

21. Taylor LM Jr, Edwards JM, Porter JM. Present status of reversed vein bypass grafting: five-year results of a modern series. J Vasc Surg. 1990; 11:193-205.

22. Donaldson MC, Mannick JA, Whittemore AD. Femoraldistal bypass with in situ greater saphenous vein.

Long-term results using the Mills valvulotome. Ann Surg. 1991; (213):457-64.

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SUMMARY Peripheral vascular ischaemia (PVI) Peripheral vascular disease (PVD) Peripheral arterial disease (PAD) Critical limb ischaemia (CLI) Risk factors ! Age ! Hypertension ! Smoking ! Lipids ! Diabetes ! Haematological factors

> Excercise > Anti coagulants > Vaso-dilators > Chemical sympathectomy ! Surgical > balloon angioplasty > sympathectomy > Endarterectomy > Bypass grafting > Arterial stenting > Endoluminal repair > Heterografts > Prosthesis > Angioscopic-assisted in situ bypass > primary amputation

Clinical features Asymptomatic Rest pain Intermittent claudication Leriche syndrome Coldness Numbness Color changes Ulceration Gangrene Diminished sensations Diminished movements Diminished or absent pulses Investigations ! Lab studies ! Imaging studies ! Doppler sonography ! Arteriography ! Digital subtraction angiography ! Magnetic resonance angiography ! Ankle brachial index ! Transcutaneous oximetery

! ! ! ! ! ! ! ! ! ! ! !

Treatment

! Conservative > Weight reduction > Low fat diet

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PS-039

PERIPHERAL ARTERIAL ANEURYSMS Shuja Tahir, FRCS, FCPS Faisal Bilal Lodhi, FCPS The aneurysm is a segmental dilatation of an artery with an expansion of one and a half to double the 1 actual arterial diameter .

An aneurysm can also be defined as focal dilatation of an artery involving an increase in diameter of at least 50% compared with an adjacent normal segment.

It is a sac filled with the blood and in direct communication with the interior of the artery.

Popliteal aneurysms form the bulk of arterial aneurysms (approx 70% of all peripheral aneurysms). 80% of these have another associated aneurysm. Next common are femoral aneurysms.

Brachial and radial arterial aneurysms are less common.

INCIDENCE ! The incidence of arterial aneurysms is 1 in every 33 autopsies. ! Male to female ratio is 1.8 : 1 ! These are most common in 8th decade of life.

! ! ! !

Cerebro-vascular accident.

Obstructive airway disease.

Syphilis Connective tissue disease.

An aneurysm may be congenital or acquired.

ETIOLOGY Aneurysms are thought generally to result from localized weakening of the vessel wall. Specific causes include:

! ! ! ! ! !

Arteriosclerosis / atherosclerosis.

Cystic medial necrosis.

Infection ( Mycotic aneurysm).

Arteritis.

Trauma.

Syphilis.

There may be a familial tendency, particularly for some aortic aneurysms.

PATHOPHYSIOLOGY Most of the aneurysms have decreased elastic content with a compensatory increase in the collagen content within the arterial media.

The common associations are ;

! ! !

Peripheral vascular disease.

Ischaemic heart disease.

Diabetes mellitus2.

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Once formed the enlargement of aneurysm is governed by the 'Law of Laplace' according to whichT = PR where T is tangential stress, P is transmural pressure and R is radius. Thus, for a

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given transmural pressure, the wall tension is proportional to the radius. This explains increased incidence of rupture of large aneurysm and hypertension as an important risk factor for rupture.

Aneurysm may be focal (saccular) or extend along a certain length of artery (fusiform). Both forms of aneurysms may arise in preexisting ectatic vessels.

The aneurysms can be;

The turbulent blood flow within an aneurysm causes laying down of a laminated thrombus which lines the affected segment to a varying degree and may result in the lumen of the artery appearing normal or only slightly dilated on arteriography. The thrombotic material can embolize into the distal circulation and present as “trash foot” or in case of popliteal aneurysm as “an acute ischemic leg”.

CLASSIFICATION OF ANEURYSMS The aneurysms can be ; 1. True.

2. False.

3. Arterio venous fistulae.

True aneurysm contains all the layers of the arterial wall in the aneurysm sac.

False aneurysm has a single layer of fibrous tissue as the wall of the sac e.g. aneurysm following trauma e.g. femoral aneurysm in I/V drug addicts.

! !

Fusiform.

Saccular.

These can also be ; 1. Congenital.

2. Acquired.

FUSIFORM ANEURYSM It is the type of aneurysm in which the segmental dilatation of the vessel is symmetrical. The aneurysmal dilatation involves whole circumference of the vessel.

The vessel wall is weak due to the disease process (atherosclerosis, hypertension or end-arteritis of vasavasorum in syphilis). These aneurysms are degenerative. These commonly involve abdominal aorta.

False aneurysm is a dilated sac lined by cellular tissue communicating with the artery through an abnormal opening (commonly it occurs in a peri-arterial clot).

Arterio-venous fistula is an abnormal communication between artery and vein leading to dilatation and arterialization of the vein.

Mycotic aneurysm develops due to vessel wall weakness following infection of the segment of the vessel.

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These are five times more common in males and are seen in 4% of population above 65 years of age.

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rupture.

MYCOTIC ANEURYSM The aneurysmal dilatation occurs due to the weakness of the vessel wall following infection.

It is not due to fungal infection but is due to either a local abscess or an infected embolus being present at the site of aneurysm.

Mortality and morbidity is greater in this type of aneurysm. It could be true or false (Pseudo) aneurysm.

Mycotic pseudo aneurysm is a vascular lesion composed of laminated clot, fibrous tissue and containing bacterial micro-organisms. It can be secondary to atherosclerosis of the vessels4.

SACCULAR ANEURYSM The aneurysmal dilatation occurs on the weaker side of the vessel wall due to over-stretching. The segmental dilatation is not circumferential rather it is an out pouching of part of the vessel wall.

It is common in superficial vessels like radial artery. It usually occurs due to injury to the vessel wall.

Rupture of the aneurysm is the most dreadful complication which requires early diagnosis and treatment.

The aneurysms above 5 cm in diameter are more likely to rupture and those of smaller diameter, are less likely to rupture.

POPLITEAL ANEURYSMS The most common peripheral arterial aneurysms are those of the popliteal arteries. Most of these are of atherosclerotic or degenerative etiology. Popliteal aneurysms are bilateral in 50% of cases and are associated with AAAs (Abdominal Aortic Aneurysms) in 8-30% cases.

CLINICAL FEATURES All aneurysms can cause symptoms due to expansion, thrombosis, rupture or the release of emboli. The symptoms relate to the vessel affected, the site supplied or the tissues compressed by the lesion. Important features include;

! !

Expansile pulsation.

Compressible swelling filling again in two or three beats, compressibility may be absent in aneurysms containing a thrombus.

Length of the aneurysm has no significant effect on SURGERY - PRINCIPLES IN GENERAL

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! !

Palpable thrill.

Audible bruit.

Most common acute manifestation is distal ischemia due to embolic occlusion of the run-off vessels or following complete thrombosis of the aneurysm.

! ! !

Local discomfort by nerve compression.

Rupture is very rare.

Asymptomatic in majority of the cases.

An aneurysm may affect the neighboring or distal structures such as:

! ! !

Venous compression leading to distal oedema.

Nerve compression causing altered sensations.

Bones may get eroded causing local bone pain.

Tubular structures such as trachea and esophagus may manifest signs of compression (dysphagia lusoria). The aneurysms may be symptomless or these may present with following features : LUMP Most of the aneurysms are diagnosed accidently.

Small aneurysms are not physically palpable. Larger aneurysm may be palpable clinically in thin patients.

A pulsatile lump is present at the anatomical pathway of the limb vessels. Usually the lump is non-tender. Its size may be variable.

If pressure is applied to the lump proximal to the aneurysm, the pulsations of the lump are diminished (Branhamâ&#x20AC;&#x2122;s sign). When the pressure is released, the lump is refilled and it starts pulsating outwards from everywhere of its circumference.

Thrill may be palpable and bruit may be audible on SURGERY - PRINCIPLES IN GENERAL

auscultation.

WASTING Wasting of the limb muscles distal to the lump may be the presenting feature . These muscles are wasted due to chronic ischaemia.

ISCHAEMIA Ischaemia of the limb muscles distal to the lump or aneurysm could be the cause of presenting features such as ;

! ! ! ! ! ! ! ! !

Loss of hair.

Shining thin skin.

Rest pain.

Hyper-pigmentation of the skin.

Edema.

Coldness.

Paraesthesia.

Numbness.

Ulceration and even gangrene.

The peripheral pulses are usually absent distal to the aneurysm.

PRESSURE SYMPTOMS Pressure symptoms on the adjoining tissue may be the presenting feature in certain patients.

DIFFERENTIAL DIAGNOSIS Swelling under an artery may push it forward, e.g. subclavian artery by a cervical rib, making it moreprominent. Careful palpation and a radiograph is helpful.

Pulsation may be transmitted to an overlying swelling, e.g. a pancreatic pseudo cyst may exhibit pulsations from underlying aorta. These are typically non expansile and diminish when patient is examined 272

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in genopectoral position in which the cyst falls away from aorta.

Tumors having increased vascularity may present as pulsatile swelling resembling an aneurysm. Examples include bone sarcoma, osteoclastoma and metastasis especially from a hypernephroma.

An abscess especially in the supraclavicular fossa, axilla, groin and popliteal fossa must be carefully examined before subjecting it to incision and drainage because of possibility of an aneurysm in these areas of passage of major arteries.

A tortuous artery (serpentine) may sometimes resemble an aneurysm, e.g. innominate, carotid.

INVESTIGATIONS Popliteal aneurysms are usually detected on physical examination and confirmed by Ultrasonography or CT scan.

Sagittal MRI is often helpful in diagnosis and in revealing an intramural thrombus.

is no single accurate or comprehensive approach to evaluate aortic aneurysm. Multiple investigations are 5 required for proper assessment .

ANKLE PRESSURE MEASUREMENTS This is a good guide of circulation of the limb and helps to assess the extent of ischaemia of the limb.

Doppler apparatus may be required to take blood pressure at ankle if the pulses are not audible with the help of stethoscope.

URINE EXAMINATION Macroscopic.

Microscopic.

Chemical analysis.

BLOOD EXAMINATION Haemoglobin percentage.

Total leucocyte count.

Sedimentation rate.

Urea level.

Electrolytes level estimation.

Serum lipid profile.

ELECTROCARDIOGRAM (E. C. G ) This is performed to see the cardiac status and presence of any central cause of peripheral ischaemia.

X-RAY CHEST X-ray chest is performed to see any abnormality in the chest and size of the heart.

Ankle pressure estimation with doppler

Arteriography can also confirm the diagnosis and assess the circulation distal to the aneurysm. There SURGERY - PRINCIPLES IN GENERAL

X-RAY ABDOMEN X-ray plain abdomen is performed. Both anteroposterior and lateral views are performed to estimate the size of the aneurysm.

The aneurysm is seen only if there is calcification as a 273

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6

radiopaque shadow with typical (egg shell appearance).

arterial disease and cause chronic ischaemia of the limb distal to the aneurysm.

ULTRASOUND SCANNING This is a very helpful investigation to assess the exact size of the aneurysm and the size of lumen of the vessel. Its sensitivity and prediction value is about 100%. It is non invasive and inexpensive. It is available at most of the places5.

Symptoms vary with the severity and duration of the ischaemia. Claudication, coldness, numbness and pain in the limb is experienced. The limb is relatively wasted, pale, hairless and shiny due to chronic ischaemia.

COMPUTERIZED TOMOGRAPHY (C.T. SCANNING) It is an expensive investigation which is not available at all places. It provides accurate size and information about the aneurysm. It also gives better idea of the status of neighbouring structures. It is excellent in evaluation of pre-operative and postoperative aneurysms5.

GANGRENE When the ischaemia is severe and limbs are unable to get reasonable amount of oxygen and nutrients, gangrene develops.

Usually it is mummification or dry gangrene as the ischaemia is chronic.

Sometimes wet gangrene develops in the presence of infection.

MAGNETIC RESONANCE IMAGING (MRI) It is as good as C.T. scan but is more expensive and is less readily available. It is a very powerful tool to visualize and stage the aneurysms5.

The gangrene is precipitated by injury to toes or limbs. The injury may be trivial such as cutting the nails or pressure from ill fitting shoes.

ANGIOGRAPHY This investigation is less frequently used because of availability of ultra-sonography. It is an invasive investigation. It is only used in specific situations to see the patency of renal artery, inferior mesenteric artery and distal run off in case of aortic aneurysm.

CHRONIC ULCERS Chronic ulceration of the periphery of the limb is also present as the ulcers fail to heal when the blood supply of the area is less than a critical level. This may change into gangrene if not treated adequately and in time.

It is performed if surgery is to be undertaken depending upon the condition of the patient and of the limb5.

THROMBO EMBOLIC PHENOMENON The peripheral aneurysms are complicated by thrombus formation.

COMPLICATIONS PERIPHERAL ISCHAEMIA Peripheral aneurysms are part of the generalized

Embolization is relatively less common but sometimes it is the first manifestation of abdominal aortic aneurysm7.

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Emboli further deteriorate the already critical supply of the blood to the areas supplied by these vessels.

7

3. Gucrguis EM. Barber GG. The natural history of abdominal aortic aneurysms. American Journal of surgery. [JC: 3Z4]. Nov 1991; 162(5): 481-3.

These problems are usually acute and lead to gangrene of the limb. These should be preferably prevented and if develop, should be treated actively and surgically otherwise loss of limb will be inevitable.

4. Shroyer KR. Svedlow GS, Adcock DM. Mycotic pseudoaneurysms of the thoracic aorta with purulent pericarditis. American journal of cardiovascular pathology. [JC: amm]. 1990; 3(4): 347-52.

HAEMORRHAGE This is experienced either due to spontaneous rupture of the aneurysm or following injury to the aneurysm.

5. LaRoy LL. Cormier PJ. Matalon Ta et al. Imaging of abdominal aortic aneurysms. Ajr-America journal of Roentgenology. [JC:3ae] Apr 1989; 152(4): 78592.

Sometimes wrong diagnosis of abscess is made and incision in the aneurysm is given with obvious consequences.

6. Baxter BT. MCGEE GS. Flinn WR et al. Distal embolization as a presenting symptom of aortic aneurysms. American journal of surgery [JC: 3Z4].

Aug 1990; 160(2): 197-201.

PROGNOSIS Prognosis of peripheral aneurysms is variable and depends upon the condition of distal vasculature and associate disease such as diabetes mellitus.

7. Aburahma AF. Woodruff BA. Stuart SP et al. Early diagnosis and survival of ruptured aor tic aneurysms. American journal of emergency medicine. [JC: aa2] Mar 1991; 9(2): 118-21.

Overall mortality of ruptured aortic aneurysm is 62% and patients with intraperitoneal rupture have mortality upto 97% and with retroperitoneal rupture (25%)7.

REFERENCES 1. Robert J. Hye peripheral vascular disease. Essential surgical practice A Cuschieri G. R.Giles. Introduction A.R Moosa 3rd edition. Butterworth Heimemann.

1994; 890-927.

2. Lom AK. Chan AC. Aortic aneurysm at autopsy: A 5 years surgery in Hong Kong. American Journal of cardiovascular pathology. [JC: amm]. 1992; 4(1): 31-40.

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8

SUMMARY Peripheral Arterial Aneurysms Etiology ! Atherosclerosis ! Cystic medial necrosis ! Infection ! Arteritis ! Trauma ! Syphlis Classification ! True ! False ! Arterio venous fistulae

! !

Fusiform Saccular

! !

Congenital Acquired

Differential diagnosis Investigations Complications ! Peripheral ischaemia ! Gangrene ! Chronic ulcers ! Thromboembolic phernomina ! Haemorrhage Prognosis

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GANGRENE

PS-040

GANGRENE

Shuja Tahir, FRCS, FCPS

Gangrene is the death (massive necrosis) of macroscopic part of the tissue with super-imposed putrefaction.

ETIOLOGY It is caused by the tissue ischaemia secondary to following conditions : ARTERIAL OBSTRUCTION Acute or chronic obstruction to the flow of arterial blood leads to gangrene formation.

The arterial obstruction occurs due to ; ! ! ! ! ! ! ! ! ! ! !

Atherosclerosis.

Thrombosis.

Embolus (from atrial fibrillation).

Post diabetic neuropathic arteritis.

Constriction ring of strangulated loops of bowel in volvulus and strangulated hernias.

Buerger's disease (thrombo-angitis obliterans).

Raynaud's disease.

Cervical rib.

Ergot poisoning.

Tourniquets, tight plaster and bandages.

Intra arterial injection of thiopentone or sclerosing substances.

INFECTION The anaerobic infections may lead to various types of gangrene.

SURGERY - PRINCIPLES IN GENERAL

Following organisms commonly cause the infections leading to gangrene2; ! ! ! ! ! !

Clostridial infection.

Non clostridial anaerobic infection.

Staphylococcal infection.

Streptococcal infection.

Bacteroides infection.

Mixed infection.

TRAUMA The injured tissue leads to loss of blood supply and death of major part of distal tissue in following conditions ; ! ! !

Crush injuries.

Pressure sores.

Circumferential burns.

VENOUS OBSTRUCTION The common diseases causing venous obstruction and gangrene are ; ! ! !

Polycythemia.

Pancreatic neoplasms.

Trousseau's syndrome.

These may lead to peripheral venous thrombosis which leads to retrograde arterial obstruction and gangrene formation.

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TYPES OF GANGRENE Following clinical varieties of the gangrene are seen ; ! ! ! ! ! ! ! !

Dry gangrene.

Moist or wet gangrene.

Gas gangrene.

Infective gangrene.

Carbuncle.

Meleney's synergistic gangrene.

Fournier's gangrene.

Cancrum oris and noma vulvae.

2

WET (MOIST) GANGRENE There is massive tissue necrosis and plenty of moisture. The putrefactive organisms grow rapidly and are very active.

The gangrene spreads rapidly. The gangrenous area is black, swollen and smelly. The line of demarcation is not clear as the gangrene spreads rapidly. There is large area of cellulitis at the junction of gangrenous area and healthy area.

DRY GANGRENE This is not true gangrene and should be called mummification. There is massive necrosis but putrefaction is almost negligible. Although putrefactive organisms are present but their growth and activity is very much limited.

Toxaemia is very common in this type of gangrene.

Septic shock syndrome and death of the patient may occur if not treated adequately and in time.

This is usually secondary to sudden occlusion of the arterial supply and venous drainage. It also follows infection and is associated with diseases such as diabetes mellitus.

The typical odor of gangrene is minimal. This is due to slow and progressive occlusion of the arteries supplying the gangrenous area.

The gangrenous part is black, dry and of the original shape. It is just mummified. The line of demarcation is very clear and separates the gangrenous area from healthy area eventually leading to auto-amputation.

SURGERY - PRINCIPLES IN GENERAL

GAS GANGRENE It is a life threatening condition. This occurs due to infection with gas-forming organisms. The infection with gas forming clostridia causes myositis in the presence of dead or damaged muscles and foreign bodies. The local infection is associated with liquefaction and gas formation.

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The common causative organisms are ; ! ! !

Clostridium perfringens (cl. welchii).

Clostridium Novyi (cl. oedematiens).

Clostridium septicum.

3

The exotoxins produce cellulitis and progressive myonecrosis. These also ferment muscle carbohydrates and produce lactic acid and gas (H2CO2) leading to fishy odor and greenish black appearance.

Progressive putrefaction is caused by Cl. Sporogenies and Cl. histolyticum.

There is marked edema and enzymatic necrosis of muscles commonly 24-72 hours after trauma.

The clostridia causing it produce potent toxins such as ;

Extensive exudate lacking in inflammatory cells is present. The affected region is swollen and large bullous vesicles are present on the skin which rupture.

! ! ! ! !

Hyaluronidase.

Collagenase.

Haemolysins.

Lecithinase.

Other toxins.

It is a rare problem (0.1/100,000/annum)3.

It is an exogenous infection which follows accidents, gun shot and other injuries leading to severe tissue damage with contamination.

It could be endogenous infection from one's own intestinal tract.

There is gross necrosis, putrefaction and gas formation.

This is common after severe trauma, roadside accidents, high velocity missile injuries, perineal injuries and above knee amputations.

It is characterized by profound toxemia, extensive local edema, massive necrosis and variable degree of gas formation.

Inflammed muscles show massive myonecrosis. The muscles are soft, black, friable and semifluid due to action of proteolytic enzymes.

Gas bubbles are also present due to bacterial fermentation of the necrotic tissue.

Microscopically there is myonecrosis, extensive haemolysis and marked vascular injury with thrombosis.

There is widespread formation of gas bubbles. The neuropathologic changes are usually non specific1.

The mortality rate in treated patients varies between 25-40%. Untreated patients have almost always fatal end2.

Septic shock syndrome is also accompanied by haemolytic anaemia, renal failure and jaundice. End stage of gas gangrene may show foamy liver and presence of gas bubbles in other viscera as well.

Gas gangrene is diagnosed clinically. Dirty and

There is no fibrosis or leukocytic reaction.

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infected wound is present with lot of necrotic tissue and features of septicaemia.

On palpation there is crepitus at local area.

Plain x-ray of the area shows presence of gas in subcutaneous tissue in patients with gas gangrene SYNERGISTIC GANGRENE It is progressive gangrenous infection of the skin, fascia and areolar tissue2.

It is progressive bacterial gangrene. It commonly involves skin and superficial tissue. It is caused by the synergistic action of micro-aerophilic nonhaemolytic streptococci.

It occurs a week or two weeks after the infection. It spreads very quickly unless treated adequately.

Burrowing ulcers (Meleny's ulcers) are seen with gangrenous skin on the edges. There is gross necrosis of large areas of skin. The necrosis of sub cutaneous tissue extends far beyond the gangrenous skin.

Non clostridial gas gangrenous cellulitis is usually caused by B. melaninogenicus and anaerobic streptococci.

CANCRUM ORIS AND NOMA VULVAE These are types of infective gangrene of mucocutaneous junctions of mouth and vulva.

These are seen in mal-nourished children with infective lesions such as measles or chest infection There is slow necrosis of the tissue and death may occur due to inhalation pneumonia.

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4

FOURNIER'S GANGRENE It is a condition similar to synergistic gangrene. It is necrotizing fasciitis spreading rapidly along facial planes, muscles, subcutaneous tissue and skin.

There is subcutaneous edema. There is dermal gangrene and appearance of sero-sanguinous discharge.

It occurs probably due to thrombosis of perforating vessels. The area involved is usually scrotum, penis or both.

Systemic toxicity may lead to septic shock syndrome3.

It is often associated with high morbidity and mortality.

Surgical debridement, broad spectrum antibiotics and use of hyperbaric oxygen followed by plastic reconstructive procedures are used to improve the survival of patients4,5.

URAEMIC GANGRENE SYNDROME It is the cutaneous gangrene seen in patients with chronic renal failure and hyperparathyroidism. It is associated with vascular calcinosis and local ischaemia6.

PYODERMA GANGRENOSUM It is the infected cutaneous gangrene.

It is a rare, recurrent and chronic condition.

It presents as progressive papulo-pustular lesion or large necrotic sterile ulcers.

It follows systemic disorders such as inflammatory bowel disease, rheumatoid ar thritis, paraproteinemias, haemotologic malignancies and other

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malignant solid tumors.

Appropriate antibiotics are given intravenously.

There is rapid improvement after treatment of the cause7.

The gangrenous area is excised (amputation or resection) and repair and restoration of the remaining tissue is performed (anastomosis in case of intestine and stump formation in case of limbs).

TREATMENT OF IMPENDING GANGRENE The causes leading to gangrene are treated and blood supply of the area is improved as soon as possible.

Treatment of general diseases such as diabetes mellitus, hypertension, atrial fibrillation and peripheral ischaemia is performed.

Smoking should be stopped immediately.

The area at risk should be carefully protected form minor trauma as well. Slight pressure by ill fitting shoes can be detrimental and may lead to gangrene formation.

Vasodilator drugs may be used for the improvement of local blood supply.

Sympathectomy whether surgical or chemical is helpful in the treatment of peripheral ischaemia.

Anticoagulants can be used in gangrene secondary to thrombo-embolic causes.

TREATMENT OF ESTABLISHED GANGRENE Analgesics are required to relieve the pain.

Intra-venous fluids and blood transfusion is given if so required.

SURGERY - PRINCIPLES IN GENERAL

In cases of dry gangrene, one should try to keep it dry and nothing more should be done and one should wait for auto-amputation.

In cases of gas gangrene following management is performed ; ! ! ! ! !

Wound debridement.

Excision of necrotic tissue.

Wound toilet and appropriate antibiotics.

Anti-gas gangrene vaccination is given parenterally.

Hyperbaric oxygen may be of help in limiting the growth of causative anaerobic organisms.

REFERENCES 1. John Saunders Franz Von. Lichtenberg. Infectious disease. Robbins pathologic basic of disease.

Cotran, Kumar, Robbins 5th edition WB Saunders company London. 1994; 338-339.

2. RE. Condon. Dietmar H. Withmann. Surgical infection. Peter J. Moris and Ronall A. Malt . Oxford text book of surgery. Oxford medical publication.

1994; 34-35.

3. A Cuschieri.H. Gilles. Specific infections of surgical importance. In essential surgical practice. A. cuschieri GR. Giles AR. Moosa. Butterworth Heinam.

Third edition. 1995; 262-267.

4. Van Brien P. Mallelaer J. Ballist I. Fournier's gangrene. Report of three cases and review of the

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literature. Acta urologica Balgica. [JC: 26y]. 1990; 58(2):161-70.

5. Lucca M. Unger AD. Deveuny AM. Treatment of fournier's gangrene with adjunctive hyperbaric oxygen. American journal of emergency medicine.

[JC:aa2]. Sep 1990; 8(5):385-7.

6. Tork L. Kozepessy L. Uraemic gangrene syndrome.

Acta dermato-venercologica. [JC:Omg]. 1991; 71(5):455-7.

7. Cole HG. Neloon RL. Peters MS. Pyoderma gangrenosum and adrenocortical carcinoma cutis.

[JC: dxb]. Sep 1989; 44(3):205-8.

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SUMMARY Gangrene Etiology ! Arterial obstruction ! Infection ! Trauma ! Venous obstruction Types Dry gangrene Moist or wet gangrene Gas gangrene Infective gangrene Carbunci gangrene Meleney’s synergistic gangrene Fournier’s gangrene Cancrum oris and noma vulvae

! ! ! ! ! ! ! !

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GANGRENE OF THE BIG TOE

PS-041

GANGRENE OF THE BIG TOE

Shuja Tahir, FRCS, FCPS

The gangrene of the big toe in 50 years old man could be dry or wet. The big toe may be the only gangrenous tissue or other toes may also be involved in the gangrenous process.

vessels.

Diabetic neuropathy and vasculopathy both lead to gangrene of the big toe and rest of the lower limb but causing chronic peripheral arterial insufficiency

One or more of the following factors may be responsible for the causation of the gangrene of the big toe.

Diabetes mellitus still remain a very common cause of the gangrene of the big toe.

CAUSES PERIPHERAL ISCHAEMIA SECONDARY TO ARTERIAL OBSTRUCTION Various diseases of Aorta or limb vessels lead to compromised peripheral circulation such as ; ATHEROSCLEROSIS It is a generalized disease of vessels, which leads to decrease in the expansibility of vessels. It decreases the diameter of the vessels. It causes thickening of the intima and decreases peripheral circulation.

THROMBOSIS AND EMBOLISM Thrombosis and embolism of the limb vessels may lead to acute ischaemic episodes and resultant gangrene of the big toe or even whole of the limb.

DIABETES MELLITUS Diabetic vasculopathy leads to narrowing of the small

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THROMBO ANGITIS OBLITERANS It is a vaso-occulsive disease common in smokers. It involves peripheral small and medium size vessels leads to gangrene of the big toe and other toes.

RAYNAUD'S DISEASE It also leads to gangrene of the big toe.

VASCULAR INJURIES Vascular injuries necessitating ligation of vessels or causing stenosis of vessels may lead to acute ischaemia and gangrene.

ERGOT POISONING It leads to contraction of the vessels leading to acute ischaemia and gangrene.

TOURNIQUET, TIGHT BANDAGE AND PLASTER INJURIES When lower limb vessels are obstructed from external pressure of tourniquets, plaster, tight bandages, gangrene of the peripheral part and big toe may occur unless the external pressure is released and fasciotomy is performed in time.

LOCAL DAMAGE Crush injuries lead to soft tissue injuries and vascular injuries. The local damage minimizes or completely stops blood supply to distal areas leading to gangrene formation.

FROST BITE When the weather is too cold, it leads to contraction of peripheral vessels and thus stops blood supply to the most distal areas like big toe which gets gangrenous.

CARBOLIC ACID APPLICATIONS Carbolic acid local applications if used as potent SURGERY - PRINCIPLES IN GENERAL

2

antiseptic or for chemical ablation of unwanted lesions, may lead to local damage to the tissue and gangrene.

ELECTRIC BURNS These are deep burns with involvement of peripheral vessels leading to vasculitis and intimal damage and thrombosis (obliteration of the vessels). It leads to stoppage of blood supply to the peripheral areas and leads to gangrene formation.

AIDS (ACQUIRED IMMUNODEFICIENCY SYNDROME) Digital gangrene has also been seen in patients suffering from AIDS. It is a serious condition but responds well to treatment with high doses of steroids. There is vasculitis of digital arteries and gangrene of the toe.

Skin biopsy and angiography confirm the vasculitis of digital arteries1.

CEREBRAL MALARIA Children suffering from cerebral malaria may develop gangrene of toes and feet.

It may occur due to dehydration, sluggish peripheral circulation, platelet activation and subclinical intravascular coagulation. These are combined with strain-specific parasite factors, tissue sequestration of mature forms and rosette formation. It may predispose to peripheral vascular occlusion and infarction of the tissue. It may lead to peripheral gangrene2.

MANAGEMENT The cause of the gangrene and the type of gangrene has to be found out for the proper management of the patient with gangrenous toe.

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History of smoking, occupation, medication, other relevant disease such as angina, diabetes mellitus and migraine is essential. History of injury and effects of cold should also be looked for.

Complete examination of the patient with special attention to the vessel wall palpation, palpation of all limb pulses and observation of ischaemic changes of the limbs should be performed.

Assessment of the general condition of the patient is also essential.

[Normal range of (ABI) is 1.1-1.5].

INVESTIGATIONS Following investigations are performed to confirm the diagnosis and assess the general condition of the patient before planning the best line of treatment URINE EXAMINATION Complete urine examination should be done.

Presence of sugar and albumen should also be noted.

Blood pressure measurement at ankle is a good indicator of the blood supply of the limb.

Ankle brachial pressure index measurements should always be performed.

SURGERY - PRINCIPLES IN GENERAL

BLOOD EXAMINATION ! Haemoglobin estimation. ! Sedimentation rate. ! Leucocyte count. ! Urea and electrolyte estimation. ! Lipid profile and sugar estimation.

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RADIOLOGY (X-RAY OF THE CHEST) X-ray chest should be performed to check the size of the heart and condition of the lungs.

X-RAY OF THE ABDOMEN Antero-posterior and lateral views should be performed to see the presence of aortic aneurysms.

X-ray of the foot specially of toe should be done to see the bony involvement (AP and lateral views).

TREATMENT GENERAL The treatment of the gangrenous toe depends upon the cause, extent and the type of the gangrene. it also involves the treatment of the general disease.

If the patient is diabetic, diabetes is controlled by insulin injections. The dose is calculated according to the sliding scale.

Anaemia is treated.

ELECTROCARDIOGRAM (E.C.G.) It should be performed to check up the cardiac status.

SCANNING ! Doppler studies provide physiological function of limb, vessels, pressure, flow and obstruction. ! C.T. scanning. ! MRI scanning.

These help to diagnose aneurysmal lesions if present.

DOPPLER WAVEFORMS STRESS TEST DUPLEX IMAGING These tests are performed to assess the status of peripheral circulation.

ANGIOGRAPHY It is the contrast medium visualization of the interior of the vessels (large and medium size). It is usually not required for isolated big toe gangrene.

It is performed if one plans to under take surgery in obstructive vascular disease of the limbs.

SURGERY - PRINCIPLES IN GENERAL

Atrial-fibrillation and other heart problems are treated.

Super-imposed infection is controlled by appropriate antibiotics.

If the gangrene of the big toe is of wet type, one should try to convert it into dry type.

If the gangrene is dry, one should avoid doing any thing actively and more conservative approach should be followed for keeping the gangrene dry.

The gangrene is kept dry by using methylated spirit or ether washings and sprays.

CONSERVATIVE Smoking is strictly prohibited.

Injury to the toe should be avoided. Soft shoes linedwith sheepskin should be used to avoid any pressure.

The gangrenous toe should be cleaned with ether, alcohol or spirit and should be kept dry. One should wait till auto-amputation of the toe occurs which takes few weeks.

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The spontaneous wound healing is good at the line of demarcation as the circulation develops through the collaterals.

MEASURES TO IMPROVE PERIPHERAL CIRCULATION The gangrenous toe or any adjacent gangrenous part is removed either by surgery or by autoamputation.

The causes of gangrene are to be treated to avoid further damage or gangrene formation.

Following measures are also taken to improve the circulation of the limb ; !

! !

Lumbar sympathetic block or surgical lumbar sympathectomy on the side of gangrenous toe is performed to improve the circulation if other conservative methods for improving the circulation have failed. As gangrene of only one toe is due to occlusion of digital vessels. It is very much possible to salvage the foot and the limb with such measures.

Bypass grafting of occluded vessels helps to improve the peripheral circulation.

If the gangrene of the toe is wet, active surgical treatment (Rayâ&#x20AC;&#x2122;s amputation) is required in addition to conservative measures. Measures to improve the peripheral circulation are adopted to prevent future ischaemic complications.

2. Chittichal P. Chierakul N, Devis TM. Peripheral gangrene in non fetal paediatric cerebral malaria: a report of two cases. Southeast Asian journal of tropical medicine and public health. [JC:uvn]. Jun 1991; 22(2): 190-4.

SUMMARY Gangrene of the big toe Causes ! Peripheral ischaemia ! Athrosclerosis ! Thromboembolism ! Dibetes mellitus ! Thromboangitis obliterans ! Raynaudâ&#x20AC;&#x2122;s disease ! Vascular injuries ! Ergot poisoning ! Tourniquets ! Tight bandages ! Tight plaster ! Local damage (crush injuries) ! Frost bite ! Carbolic acid applications ! Electric burns ! Aids ! Cereberal malaria Treatment General Conservative Surgical

! ! !

Measures to improve peripheral circulation

REFERENCES 1. Enelow RS, Hussein M, Grant K et al. Vasculitis with eosinophilia and digital gangrene in a patient with acquired immunodeficiency syndrome journal of Rheumatology. [JC: jwx]. Nov 1992; 19(11): 18136.

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LEG ULCER

PS-042

LEG ULCER

Shuja Tahir, FRCS, FCPS

An ulcer is a macroscopic discontinuation of the skin or mucous membrane with underlying pathology. It is ulceration of the skin in case of leg ulcers.

History of the ulcer is vital for the proper diagnosis and differential diagnosis of the ulcer. Duration of ulceration and the history of beginning of the ulcer helps in diagnosis.

Examination of edges, floor and base of the ulcer, the condition of neighbouring tissue and lymph glands should be noticed. Accurate description of site, size, shape of the ulcer should be noted.

Apar t from the local examination, general examination of the patient will uncover systemic diseases leading to ulceration of the legs.

Many times the diagnosis may not be clear clinically, then hematological, biochemical, radiological and specialized investigations for vascular problems may help in confirmation of the diagnosis.

Histological examination of the tissue from ulcer edge confirms the diagnosis.

Following types of ulcers may be present on the legs; ! ! !

Traumatic ulcers.

Post-burn ulcers.

Ischaemic ulcers.

SURGERY - PRINCIPLES IN GENERAL

! ! ! !

Perforating ulcers (Neuropathic ulcers).

Venous ulcers or Gravitational ulcers.

Inflammatory ulcers.

Miscellaneous ulcers.

TRAUMATIC ULCERS These ulcers have a clear history of trauma. These ulcers may be acute (of shorter duration) or chronic (of longer duration).

All traumatic ulcers are acute to start with. These heal adequately if there is no loss of skin, no infection and treated adequately.

Post-injection necrosis of the skin also causes ulceration of the limb.

Insect bites causing local necrosis of the skin of the leg also lead to leg ulceration.

Super-added infection may be visible on examination from the signs of inflammation which are ; 1.

2.

3.

4.

5.

Redness.

Pain.

Loss of function.

Increased temperature.

Swelling (edema).

Repeated trauma may lead to chronic ulceration.

Irradiation and exposure to chemicals may cause 289

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injury and ulceration of the legs.

The ulcer may lead to gangrene of the limb as well.

Chronic ulceration is usually due to excessive loss of skin, due to infection, due to continuous presence of underlying pathology or when the loss of skin is over the bone where epithelialization does not occur.

History and examination usually confirm the diagnosis as history of rest pain and intermittent claudication may be present.

Many times chronic osteomyelitis leads to chronic discharging sinus and chronic ulceration. This is common over compound fractures of the tibia and fibula.

These can be treated by removal of dead and degenerate tissue, control of infection and skin grafting.

POST BURN ULCERS These are the unhealed areas of burnt skin or breakdown of healed burn scar.

History is clear and there is little problem in diagnosing these ulcers. These are common after full thickness burns. These can be treated by control of infection with appropriate antibiotics and skin grafting.

The neoplastic change can occur in these ulcers leading to Marjolin's ulcer.

ISCHEMIC ULCERS It is a common type of leg ulcer. It is usually seen in older age group.

Atherosclerosis is the probable cause of peripheral ischaemia.

These occur in chronic ischaemia of the legs. The ulcer is usually dry.

SURGERY - PRINCIPLES IN GENERAL

History of smoking and effects of weather may be present in cases of Buerger's disease and Raynaud's disease.

On examination, the skin is usually pale, shiny and hairless. The nails are brittle, rigid or deformed.

The limb is cold to touch and shows delay in skin perfusion. Venous filling is also delayed in these limbs.

The arterial pulses are absent or feebly palpable in such limbs. The ulceration is usually at a pressure point or where trauma can occur easily (toes etc.)

Many specialized investigations are required to confirm and assess the disease process. These are ; ! ! ! ! ! !

Ankle pressure measurement.

Arm Ankle index measurement (Ankle brachial pressure index) (AB ratio).

Doppler Flowmetry.

Plethysmography.

Phlebography.

Ultrasonography.

A systolic digital pressure below 60 mm of Hg indicates arterial occlusive disease as a cause of leg ulcers1.

These ulcer should be treated by treating the cause of ischaemia conservatively with vaso-dilator drugs or by surgery (bypass grafting or sympathectomy).

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Circumferential leg ulcer

Marjolin ulcer over left leg

Healing leg ulcer

Chronic leg ulcer

Ischaemic leg ulcer

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3

PERFORATING ULCERS (NEUROPATHIC ULCERS) These occur in cases where the loss of sensations of limb have occurred due to some general disease such as diabetes mellitus, hemiplegia, quadriplegia, tabes dorsalis or major nerve injuries of the limb.

rheumatoid arthritis and venous ulceration impairs the venous muscle pump action and increases mean venous pressure of the lower leg. The venous distension leads to cutaneous hypoxia and leads to further ulceration3.

Minor injuries of the limb followed by infection may lead to chronic ulceration of the legs in such cases.

These may be seen in diseases like;

There is collection of pericapillary fibrin cuff in the vicinity of the ulcer which delays healing of the ulcer.

! !

Spina bifida.

Leprosy.

The site is very typical, usually on the dorsum of the foot near the ankle or along the medial or lateral malleolus extending upwards upto lower leg.

These ulcers are to be prevented most carefully and infection should be avoided or treated actively.

Occasionally the ulcers of medial and lateral sides merge to become circumferential ulcers.

VENOUS ULCERS These ulcers are secondary to chronic venous stasis due to varicose veins of the long or short saphenous system of leg veins.

There is venous hypertension at the dependent part of the limb which leads to capillary exudation and formation of fibrin barrier along the capillaries.

These ulcers occur due to chronic progressive venous insufficiency. These ulcers cause lot of disability and socio-economic problems.

In Western countries 90% of leg ulcers are venous in origin.

These are commonly seen in patients with ambulatory venous hypertension. Arterial supply is good and ischaemia is not the cause.

The ulcerated extremities have greater venous volume. There is deterioration of venous valvular competence and calf muscle-pump function. These are more common in females than males. The ulcer is usually wet2.

Reduced ankle mobility due to any type of arthralgia, SURGERY - PRINCIPLES IN GENERAL

There is decreased blood supply to the local tissue.

There is also white cell trapping which occurs due to endothelial anoxia.

There is further destruction due to decreased capillary flow and thrombus formation.

Superadded infection is usually present in these cases.

In chronic cases, the base of ulcer is tough. The fibrous avascular scar tissue is present which is unstable and is likely to break down again and again even with minor trauma such as removal of dressing.

These should be treated by avoidance of venous stasis which can be achieved by using elastic bandage on legs or by surgical treatment of the varicose veins and perforators leading to decreased

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Venous leg ulcer

Perforating (neuropathic) ulcer

Traumatic leg ulcer

Venous leg ulcer

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Tropical leg ulcer

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venous pressure at ulcer site and improved venous circulation.

Ulcer may have to be excised and treated by skin grafting with the treatment of varicose veins.

The venous ulcers can also be treated by low-energy laser therapy which stimulates wound healing4.

INFLAMMATORY ULCERS These ulcers may occur due to specific or non specific infection. These are acute or chronic ulcers depending upon the type of the infection.

Usually history and examination makes the diagnosis obvious. Occasionally radiological and histological examination may be required to confirm the diagnosis.

Chronic ulcers include tuberculous ulcer, madura foot, actinomycosis and many dermatological lesions. All these can be treated according to their causes.

SYPHILITIC ULCERS Syphilitic ulcers are very rare these days.

TUBERCULOUS ULCERS Tuberculous ulcer may be seen on the leg rarely as a part of generalized disease.

MISCELLANEOUS ULCERS Acquired immune deficiency syndrome (AIDS) may lead to local ulceration of the leg.

Blood dyscrasias cause leg ulcers. Severe anaemia, sickle cell anaemia, thalassemia, leukaemia, uraemia and hereditary spherocytosis can cause local leg ulceration5,6.

SURGERY - PRINCIPLES IN GENERAL

Nutritional and metabolic disorders, vitamins and nutritional deficiencies may cause or aggravate already existing ulcers on the leg.

Systemic vascular obstructive and microvascular diseases also cause limb ulceration.

Systemic lupus erythematous and polyarteritis nodosa cause eczematous lesions on the legs which cause ulceration.

Rheumatoid arthritis patients may develop ulcer on the leg due to vasculitis.

NEOPLASTIC ULCERS These are the ulcers occurring in benign or malignant lesions. Benign ulcers are uncommon and when present are usually due to super-added infection.

Malignant ulcers are due to ulceration of malignant melanoma and epithelioma. The epithelioma or squamous cell carcinoma is a common malignant tumor of the lower limb.

Rarely the rodent ulcer may be present on the leg.

Malignant change in a long standing venous ulcer or burnt area is commonly known as Marjolin's ulcer7.

These patients should be followed up by bipedal lymph-angiography and radiotherapy.

TROPICAL ULCERS These are also present in the leg. These may occur in patients living in endemic areas. These may be due to cutaneous leishmaniasis or fungal infections.

These should be treated after biopsy and histological examination with wide excision.

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SUMMARY

REFERENCES 1. Sindrup JH. Danielsen L. Karlsmark T. et al.

Prognostic significance of digital blood pressure in leg ulcer patients. Acta Dermato-Venereologica.

[JC:Omg]. 1990; 70(3):259-61.

2. Welkie JF. Comerota AJ. Kerr RP. et al. The Haemodynamics of venous ulceration. Annals of vascular surgery. [JC:avs]. Jan 1992; 6(1) : 1-4.

3. Gaylard PM. Dodd HJ. Sarkany I. Venous ulcers and arthropathy. British Journal of Rheumatology.

[JC:bit]. Apr 1990; 29(2) : 142-4.

Leg ulcer Traumatic Post burn Ichaemic Perforating (neuropathic) Venous Inflammatory Miscellaneous Neoplastic Tropical

! ! ! ! ! ! ! ! !

4. Lundeberg T. Malm M. Low power HeNe laser treatment of venous leg ulcers. Annals of plastic surgery. [JC:5vb]. Dec 1991; 27(6) : 537-9.

5. Durosinmi MA. Gevao SM. Esan GJ. Chronic leg ulcers in sickle cell disease: Experience in a ibadan, Nigeria.

African Journal of medicine and medical sciences.

[JC:29g]. Mar 1991; 20(1) : 11-4.

6. Torok I. Kozepessy L. Uraemic gangrene syndrome.

Acta dermato-venereologica. [JC:omg]. 1991; 71(5):455-7.

7. Fishman JR. Parker MG. Malignancy and chronic wounds: Marjolin's ulcer. Journal of Burn care and Rehabilitation. [JC:hik]. May-June 1991; 2(3) : 21823.

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VARICOSE VEINS

PS-043

VARICOSE VEINS; ETIOLOGY, COMPLICATIONS & TREATMENT Shuja Tahir, FRCS, FCPS

The varicose veins are the superficial veins of lower limb which are dilated, tortuous and thickened in a standing patient due to valvular incompetence resulting in venous hypertension.

EPIDEMIOLOGY The prevalence varies from 2% - 60% in different areas.

The venous blood flows from lower limb veins to veins of the trunk and heart. 90% of blood flows through deep veins of limbs.

10% of blood flows through superficial venous system of the lower limbs (long and short saphenous veins).

Both superficial and deep venous systems are connected with each other through perforating veins which act as check valves.

The venous blood flows from toes towards right heart due to; 1. The pumping action of the heart.

2. Pumping action of the lower limb muscles.

3. Negative intra thoracic pressure during inspiration.

PATHOPHYSIOLOGY The causes of varicose vein formation are multifactorial: The competent venous valves prevent retrograde reflux of venous blood. This also helps to maintain normal venous flow in association with calf muscle pump.

This flow of blood is helped by the valves of the veins.

Valves are present in superficial and deep venous systems. These prevent the flow of blood towards periphery but allow the flow towards heart.

SURGERY - PRINCIPLES IN GENERAL

These valves when normal can withstand pressure upto 300 mm of Hg. Failure of valvular function leads to appearance of varicose veins. It may be due to;

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!

Hydrostatic pressure.

2

pump action and let the veins dilate into varicosities.

Which is raised persistantly in long periods of standing, obesity, pregnancy and any other condition leading to raised intra abdominal pressure.

Their wasting also makes the varicose veins more prominent. Prolonged inactivity of muscles seen in paralysed limb also affects the venous flow.

In animals, the varicose veins are not seen. The adoption of erect posture by human beings puts more pressure on lower limb veins and may possibly cause varicosities. These are more common in people who have to stand for longer hours.

Diseases inhibiting limb movements lead to subnormal or absent muscle pump action. The blood flow through these muscles is reduced and the venous pressure is much raised.

HEREDITARY FACTORS There is a definite relationship between heredity and development of varicose veins. A dominant type of inheritance is present.

There are 85% chances of having varicose veins in children of varicose vein suffering parents1.

These children are twice as likely to have varicose veins. The inherited alteration in vein wall collagen and/or elastin might be a major aetiological precursor in these patients. They may have few or diseased valves.

AGING The prevalence of varicose veins increases with age.

It is due to degenerative changes in venous valves in elderly. This is not a very significant cause of varicose vein formation.

CONGENITAL PAUCITY OF VALVES It is thought that venous valves may be absent or less effective in some people. It leads to stasis and retrograde down flow into the superficial veins leading to varicosities formation and venous stasis.

MUSCLE WEAKNESS AND WASTING Muscular wasting could lead to defective muscle SURGERY - PRINCIPLES IN GENERAL

DEEP FASCIAL STRETCHING This may lead to varicose veins formation by decreasing the efficiency of muscle pump action.

INCOMPETENT PERFORATING VEINS There are nearly 60-100 perforating veins which are communicating between the superficial and deep veins of the lower limbs.

These have valves which prevent blood flow from deep to superficial veins. If these valves become incompetent, the retrograde flow of blood starts and varicose veins develop.

The perforators are often paired and some of these communicate with venous sinuses of the muscles.

Small perforators of 2 mm or lesser size are not valved and keep equalization of pressure among superficial and deep veins and lead to venous hypertension and stasis.

INCOMPETENT VALVES The superficial veins have multiple valves which prevent the flow of blood from proximal to distal part of the leg veins. If due to some reasons these valves become incompetent, the retrograde flow of blood leads to stasis and varicose vein formation.

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OBSTRUCTION TO VENOUS RETURN Intra-pelvic tumors and pregnancy may lead to pressure on inferior vena cava and this back pressure leads to dilatation of leg veins due to improper venous drainage and raised venous pressure.

DEEP VEIN THROMBOSIS When deep veins are blocked, the venous blood is diverted from deep to superficial veins and it leads to varicose vein formation. There is impairment of muscular venous pump and raised venous pressure in the superficial veins.

VENOUS PRESSURE CHANGES In a standing person, the venous pressure at ankle rises upto 100 mm of Hg depending upon height of the patient.

In a walking person this pressure drops to 20 mm of Hg because of emptying of the limb veins regularly due to calf muscle pump action.

The venous pressure in a normal standing person falls after exercise. It becomes normal within 20 seconds after cessation of exercise. If the valves are incompetent, the venous pressure is raised very quickly.

HORMONES Progesterone is likely to cause varicose veins due to weakening effect on smooth muscle.

This is also seen that during pregnancy when varicose veins get worse and if had already been treated, recurrence occurs.

The varicose veins are troublesome during premenstrual period in many patients due to altered SURGERY - PRINCIPLES IN GENERAL

hormonal levels.

PREGNANCY 70-80% of pregnant patients develop varicose veins during first trimester. It is mainly due to hormonal influence. During second and third trimester, there is obstruction to the flow of femoral venous blood leading to venous hypertension and stasis1.

ARTERIO-VENOUS FISTULA In these conditions, the pressure in the superficial veins is increased as a consequence of direct flow of high pressure arterial blood leading to dilatation, varicose vein formation and venous hypertension.

EXTENSIVE CAVERNOUS HAEMANGIOMAS This is a rare vascular anomaly which is also associated with varicose vein formation.

Clinical assessment is essential for diagnosis and management of varicose veins and associated complications. It should be performed in standing patient with adequate exposure.

Special interview of the patient regarding various symptoms related to venous system is noted. A photograph may be obtained for future reference2.

INVESTIGATIONS URINE EXAMINATION BLOOD EXAMINATION SPECIALIZED INVESTIGATIONS; CONTINUOUS WAVE DOPPLER EVALUATION The patient is examined while standing. The doppler probe is put on the vein and patient is examined during coughing, Valsalva-manoeuvre and local manual compression and sudden release. It is the most commonly used test for most of the patients 301

4

VARICOSE VEINS

with varicose veins. !

ULTRASONOGRAPHY The ultrasonography is performed by color flow duplex scanning. The details of venous abnormalities are displayed. It is specially important in evaluating the potency of deep veins.

DIRECTIONAL DOPPLER FLOWMETERY A directional doppler flowmeter is used to map the direction of venous blood flow. Normally it should be in the direction of valves towards the heart from periphery.

The flow in opposite direction indicates incompetent valves.

anatomy.

Duration and velocity of venous reflux.

Enhanced flow in normal direction is seen in blocked deep veins or arterio-venous fistulae. (pulsations are similar to those of arteries) PHOTO-PLETHYSMOGRAPHY It measures the number of red cells present is the capillaries which is closely related to local venous pressure.

It is used to demonstrate; The abnormally brief recovery time after exercise.

The suspected pathway of venous incompetence is selectively occluded by finger pressure.

PULSED BEAM ULTRASONOGRAPHY It gives the images of veins and their valves on the monitor screen.

It is important in assessing; ! Patency and competence of deep veins. ! Site and level of major incompetence. ! Accurate identification of popliteal fossa SURGERY - PRINCIPLES IN GENERAL

PHLEBOGRAPHY It is an invasive investigation. The radio-opaque dye 302

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is injected into the veins and x-ray picture is taken to see the anatomical abnormalities.

COMPLICATIONS OF VARICOSE VEINS THROMBO-PHLEBITIS Thrombus formation is often seen in these vessels due to stasis of venous blood. It is common with varicose veins as these are thin walled and more prone to damage.

The diseased vein becomes red, tender cord-like structure in the subcutaneous tissue.

Compression elastic bandage and exercises of lower limbs are helpful.

Analgesics are also used to relieve the pain. The thrombus from these veins does not dislodge usually and pulmonary embolism is less likely.

PIGMENTATION There is increased pigmentation of area around the ankle due to tissue anoxia, stasis, extravasation of blood and increased breakdown of red cells.

The accumulation of haemosiderin occurs due to raised venous pressure locally. It is the earliest change.

ECZEMA The skin over venous hypertensive area is prone to allergens and is very sensitive. Pigmented areas are most vulnerable.

Chronic dermatitis is common in these patients with varicose veins. It is present due to increased venous pressure, stasis and reduced oxygenation of the tissue.

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5

It may follow scratching or minor trauma. It may be due to allergic reaction of adhesive tapes used for treatment of varicose veins.

Conservative treatment is done with zinc oxide cream locally and compression bandages.

Definitive treatment of the varicose veins is required for permanent cure.

FAT NECROSIS Lipo-dermato-sclerosis or lipo-sclerosis with induration is seen in the vicinity of varicose veins.

CHRONIC VENOUS ULCERS These occur due to venous hypertension leading to varicose veins formation, thinning of overlying skin and lack of nutrition to the skin. There is progressive chronic venous insufficiency locally.

The ulcerated extremities have greater venous volumes, incompetent valves and defect in calf muscle pump function3.

The ulceration is usually surrounded by the pigmented skin.

Venous stasis occurs in patients with varicose veins thus leading to local tissue anoxia near the ankle.

This area ulcerates and doesn't respond to conservative treatment.

These ulcers are to be differentiated from ischaemic ulcers due to arteritis and syphilis.

These can be treated by treatment of varicose veins, excision of ulcer and skin grafting.

RECURRENT HAEMORRHAGE The skin overlying varicose veins is thin and weak.

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Slight trauma leads to injury to the delicate vessel wall and recurrent attacks of bleeding occur in these patients.

Treatment is compression bandage as emergency measure and definitive treatment of the varicose veins should be performed as early as possible.

DELAYED WOUND HEALING The wounds at and around the ankle in patients with varicose veins heal after a long time or even may not heal at all due to local tissue anoxia and stasis of blood around that area.

MALIGNANCY In patients with chronic venous ulcers, malignant change is sometimes noticed. It occurs in chronic scars of diverse causes. These may present as very large, fungating masses.

More commonly it is squamous cell carcinoma and is called Marjolin's ulcer.

Rarely basal cell carcinoma is also seen in association with venous ulcer. The ulcer and lesions tend to be multifocal and of sclerosing type. These extend into the reticular dermis but never extend deep to subcutaneous tissue4,5.

TREATMENT OF VARICOSE VEINS The objectives of management are; 1.

2.

3.

4.

To select the right patient for treatment To offer cosmetic management.

To prevent deterioration of disease.

To prevent complications.

CONSERVATIVE TREATMENT This is required in patients who are too ill to undergo SURGERY - PRINCIPLES IN GENERAL

surgery or are pregnant or refuse surgical treatment.

ELASTIC STOCKINGS Different size of tight fitting elastic stockings are available. These are cosmetically acceptable and are good for symptomatic relief.

CREPE BANDAGE OR ELASTIC BANDAGE Compression bandage of whole of the lower limbs with elastic or crepe bandage should be done. It avoids venous stasis and helps in symptomatic relief.

INJECTION SCLERO-THERAPY The varicose veins are emptied by elevating the limb.

The skin overlying varicose veins is cleaned with antiseptic solution.

1-2 ml sclerosing agent is injected into the empty varicose veins to obliterate the lumen. The compression bandage is applied for 7-10 days to ensure the permanent obliteration of the varicosities.

The commonly used sclerosing agents are ; 1. Ethanolamine oleate 5%.

2. Sodium tetra decyle sulphate (STD) 3%.

3. Polydocanol.

The patient is advised to avoid standing and is encouraged to walk during early post treatment period. Sclerosant â&#x20AC;&#x153;foamâ&#x20AC;? is also available now which sets on contact with blood.

SURGERY Surgery is indicated for all symptomatic patients.

It can be performed during pregnancy in obese patients.

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7

The patient must be informed about the operative risk and the cosmetic outcomes. The patients can be treated as a day care patient.

3. Walkie JF, Comerota AJ. Kerr RP et al. The hemodynamics of venous ulcerating Annal of vascular surgery. [JC: avs]. Jan1992; 6(1): 1-4.

The varicose veins are marked pre-operatively by the surgeon himself.

4. Fishmns. Pasker MG. Malignancy and chronic wounds, Marjolin's ulcer journal of Bwm care and Rehabilitation. [JC: hlk]. May-Jun 1991; 12(3): 21823.

Following procedures are used ; 1. Ligation at sapheno femoral junction (Trendlenberg's operation).

2. Ligation at incompetent perforators (Cocket's operation).

3. Stripping or avulsion of varicose veins totally or partially.

4. These procedures may be used in combination depending upon the cause and extent of varicose veins.

5. Gosain A. Samger JR Yousaf NJ. Matlonb HS. Basal cell carcinoma of the lower leg occurring in association with chronic venous stasis. Annals of plastic surgery.

[JC: 5vb]. Mar 1991; 26(3): 279-83.

The tourniquets are used during surgery to avoid excessive leakage of blood following phlebotomies.

POST OPERATIVE CARE ! Compression bandages are used for four to six weeks. ! Walking is encouraged. ! Standing is discouraged. ! Contraceptive pills are discontinued. ! Pregnancy is avoided.

REFERENCES 1. John J, Bergan venous and lymphatic surgery.

Essential surgical practice 3rd edition. A cuschieri, GR Gibs and AR Moosa Butterworth Great Britian 1995.

2. Shuja Tahir; Mahnaaz Roohi. Examination of Varicose Veins â&#x20AC;&#x153; Clinical examination systemâ&#x20AC;? 5th edition. UroObs Pvt Ltd. Pakistan. Jan 2005; 187-190.

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SUMMARY Varicose veins Etiology ! Hydrostatic pressure ! Hereditary factors ! Aging ! Congenital paucity of valves ! Muscle weakness and wasting ! Deep fascial stretching ! Incompetent perforating veins ! Obstruction to venous return ! Deep vein thrombosis ! Venous pressure changes ! Hormones ! Pregnancy ! Arterio venous fistula ! Extensive cavernous haemangiomas Investigations Complications ! Thrombophlebitis ! Pigmentation ! Eczema ! Fat necrosis ! Chronic ulcer ! Recurrent haemorrhage ! Delayed wound healing ! Malignancy Treatment

!Conservative ! Elastic stockings ! Crepe or elastic bandage ! Injection sclerotherapy Surgery ! Trendlenbergâ&#x20AC;&#x2122;s operation ! Cocketâ&#x20AC;&#x2122;s operation ! Partial or total avultion of varicosities ! Combination of these procedures

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1

DEEP VEIN THROMBOSIS

PS-044

DEEP VEIN THROMBOSIS

Shuja Tahir, FRCS, FCPS Deep vein thrombosis is the thrombus or clot formation in the deep veins of the calf leading to interruption of flow of blood through deep veins. It is a common cause of increased morbidity and mortality in surgical patients.

The risks of embolization to pulmonary artery and almost fatal consequences are very high. Fortunately it is less common in this part of the world (IndoPakistan).

INCIDENCE The incidence of DVT is increasing.

140,000 - 250,000 new cases are seen every year in USA. It leads to 50,000-200,000 deaths every year.

It causes 15% in hospital deaths every year.

PATHOLOGY & PATHOGENESIS Stasis of blood, injury to the vessel wall and increased coagulability are the common factors leading to thrombus formation in the calf veins.

Virchow's triad for thrombo embolism formation is primary mechanism for development of venous thrombosis; (Venous stasis)

! ! !

Reduced blood flow.

Injury to veins.

State of hypercoagulability.

SURGERY - PRINCIPLES IN GENERAL

The vascular injury leads to promotion of adherence of platelets to the endothelium.

Platelets also release mediators after activation which allow fibrinogen to stick to adjacent platelets.

Hemostatic plug is formed and strengthened.

Thrombolysis also begins after plug formation.

The formation, propagation and dissolution of venous thrombus represent a balance between thrombus formation and bodyâ&#x20AC;&#x2122;s protective mechanisms such as circulating inhibitory of coagulation and fibrinolytic systems1.

Age is important in thrombus formation and pulmonary embolism is more common in middle aged and elderly. It is more common with disorders such as ;

! ! ! ! ! ! ! ! ! ! !

Congestive cardiac failure.

Acute myocardial infarction.

Atrial fibrillation.

Metastatic malignancy.

Carcinoma of pancreas.

Carcinoma of prostate.

Major surgery.

Major trauma.

Burns.

Pregnancy.

Post partum infection.

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! ! ! ! ! ! ! ! ! ! !

Oral contraceptives Severe trauma prolonged immobilization Long air travel Hip replacement surgery Polycythemia Smoking Obesity Diabetes mellitus Varicose veins Previous H/O DVT

deep veins of the calf. Only 55% are diagnosed before the death of the patient.

TROUSSEAU'S SYNDROME It is a condition which presents with spontaneous recurrent migratory venous thrombosis. Arterial embolization is caused by non bacterial thrombotic endocarditis or both.

It is seen in patients with known malignancy or occult malignancy.

The incidence of deep vein thrombosis is high following above diseases, during prolonged immobilization, in the ladies, after previous thrombosis and with varicose veins.

These patients have persistent low grade intravascular coagulation and anticoagulant therapy with heparin should be continued for ever otherwise new thrombus formation will occur.

The thrombus is usually formed in the deep veins of the calf and obstruction to venous flow occurs. The thrombus may be blocking many vessels leading to raised venous pressure and edema formation.

Two properties of the malignant lesions are required to develop Trousseau's syndrome ;

!

The malignant cells express surface membrane tissue factor.

Structural features of the tumor permit the malignant cells or vesicles it sheds to be exposed to circulating blood2.

If the venous pressure raises above local arterial pressure, venous gangrene occurs due to lack of blood flow.

!

Following thrombosis, most of the veins remain obstructed. Recanalization of veins also occurs but the venous valves are destroyed and become incompetent.

PARADOXICAL EMBOLISM It is the embolism which passes through an intracardiac defect such as patent foramen Ovale. It is associated with deep vein thrombosis and pulmonary embolization3.

Loose thrombi are taken away by the blood as emboli to the right heart and pulmonary artery, leading to pulmonary embolism.

Small emboli do not cause serious effects immediately but larger emboli are usually fatal.

80% of the pulmonary emboli arise from thrombi of SURGERY - PRINCIPLES IN GENERAL

DIAGNOSIS Diagnosis of deep vein thrombosis at the earlier stage is very important if this dreadful complication (pulmonary embolism) is to be prevented.

Proper history and clinical examination are most important in diagnosing this condition.

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The most prominent signs of deep vein thrombosis in pregnant women are swelling and tenderness of the affected leg, sometimes accompanied with fever and leucocytosis. The leg swelling may be absent in pelvic thrombosis5.

Swelling of calf, local tenderness and positive Homan's sign are common clinical features. Absence of these features does not exclude deep vein thrombosis. Edema of limb and even venous gangrene may be present if the venous pressure is raised.

DOPPLER FLOWMETER4 Ultrasound waves are used to measure the flow of venous blood in leg veins with the doppler probe.

It gives correct results in 80% cases but fails to detect venous obstruction if the obstruction is partial or larger collateral are present leading to reasonable venous flow.

Screening doppler sonography should be performed in all patients of hip fracture surgery to identify deep vein thrombosis (DVT) as patients are at higher risk of developing proximal DVT6.

RADIOACTIVE FIBRINOGEN UPTAKE TEST Radioactive fibrinogen (labeled I 125) is injected intravenously and radio-activity is checked up with receiving counter probe.

Thyroid uptake of iodine is blocked with potassium iodide before isotope is given.

This test can diagnose deep vein thrombosis with 7098% accuracy. False positive results are seen in the presence of haematoma, bruising, previous

SURGERY - PRINCIPLES IN GENERAL

operations, edema and inflammation.

PHLEBOGRAPHY It is the most accurate and specific method of diagnosing deep vein thrombosis. Negative shadow or lack of venous filling with the radio- opaque dye indicates venous thrombosis.

PLETHYSMOGRAPHY The change in the venous volume of the limb is measured with this method and deep venous thrombosis can be diagnosed. It is rarely used.

CONTRAST MEDIUM VENOGRAPHY Although it is confirmatory test for deep venous thrombosis, it is invasive and has its own hazards.

Allergic and anaphylactic reaction contract induced DVT, technical difficulties. Inadequate studies, intra observer variability and lack of availability. This investigation is non diagnostic or contraindicated in 20-25% of patients.

RADIOISOTOPE VENOGRAPHY It is associated with relatively less number of complications. It is rarely used these days.

DUPLEX SCANNING4 Real time B mode ultrasound with Doppler wave mapping is used for duplex scanning in deep vein thrombosis.

It is combination of real time ultrasonography with doppler flow studies.

Scan detects thrombus by failure to compress the vascular lumen.

Color doppler shows absence of color filling and flow in the deep veins.

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4

The sensitivity of duplex scan for proximal vein DVT is 97% but 73% for calf vein DVT. Its over all specificity is 95%.

investigations prior to major surgery are at a greater risk as they keep lying in the bed are likely to develop deep vein thrombosis.

It helps to differentiate DVT from haematoma, bakerâ&#x20AC;&#x2122;s cyst, abscess and other causes of leg pain and edema.

If possible, patients should be investigated as outpatients and they should be advised limb exercises if not contra indicated by their disease.

It is unable to differentiate between old and new thrombus. Color doppler is unable to diagnose perforating vessels.

Venous injury should be avoided by avoiding pressure on the calf veins and by avoiding infusing irritant substances through leg veins.

CT/M.R.I Perforation can be visualized by CT scan with 3D reconstruction.

Elevation of limbs by putting a pillow under the heals in operating theater is a very effective and simple method for avoiding the injury to deep calf veins. It has brought down the incidence of deep veins thrombosis post operatively.

It is expensive but an excellent method of investigations. It has no complications and is a non invasive investigation.

It is used more after now a days in suspected cases of DVT. Its accuracy is similar to contrast venography. It is most sensitive and useful in pregnant ladies during 2nd and 3rd trimester.

PREVENTION Factors predisposing to deep vein thrombosis should be avoided.

Weight should be reduced as the incidence of deep vein thrombosis is more in obese patients.

Oral contraceptives should be discontinued in patients who are at risk to develop deep vein thrombosis.

It is known that prolonged immobilization definitely increases the chances of deep vein thrombosis. The patients who are admitted to the hospital for SURGERY - PRINCIPLES IN GENERAL

The flow of blood in the limb vessels also improved due to effects of gravity in the elevated limbs.

Stasis of blood can be minimized by elevation of limbs, exercises, compression bandages and using pneumatic pumps during prolonged surgery and immobilization.

Hypercoagulability states can be prevented by using anticoagulants and antiplatelet stickiness drugs.

Heparin 5000 iu subcutaneously eight hourly for five days starting from the day of operation decreases the incidence of deep vein thrombosis.

Intravenous use of dextran during operation also decreases the deep vein thrombosis incidence.

Use of aspirin, persantin and antiprostaglandins also decreases the deep vein thrombus formation.

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Cessation of smoking is recommended in pregnant or post-partum women.

It also helps to lyse the pulmonary embolus.

Intr avenous infusion is as effective as intrapulmonary infusion1.

SURGICAL TREATMENT LIGATION OF VEINS Ligation of the veins proximal to the thrombus eliminates the risk of pulmonary embolism but has its own disadvantages which make this operation less popular.

Elastic stocking or compression bandages are used to improve venous return and decrease venous pressure. Later on leg exercises are encouraged to improve the venous return.

PLICATION OF VENA CAVA This is also an alternative to ligation of veins to avoid pulmonary embolism but has its own ill effects making it unsatisfactory as well.

Anticoagulants like heparin are given in continuous intravenous injections.

THROMBECTOMY AND LIGATION It is surgical removal of the thrombus. This method is used if the deep vein thrombus has already occurred. Re thrombus formation is very common after this method.

TREATMENT CONSERVATIVE Bed rest and elevation of the limb should be done when the thrombus has formed. This minimizes the separation of clot and the risk of pulmonary embolus formation.

Low molecular weight heparin have almost replaced standard heparin in the treatment of DVT in pregnant women. It has less number of side effects, easy subcutaneous application, no need for laboratory control, lower risk of bleeding and lower risk of osteoprosis and thrombocytopenia post treatment5.

Later on oral anticoagulants are started and compression bandages are given.

THROMBOLYTIC THERAPY Streptokinase and urokinase are used in established cases of deep vein thrombosis, dose is 600000 iu in first half hour and 1000000 iu every hour according to the prothrombin time.

Infusion of tissue-type plasminogen activator (PA) has very promising outcome in lysing the clot in peripheral deep veins. It minimizes the tendency toward post phlebitic syndrome

SURGERY - PRINCIPLES IN GENERAL

MOBIN UD DIN UMBRELLA OR GREENFIELD STEEL WIRE FILTER These prosthesis and cannulas are helpful in avoiding pulmonary embolism.

Once deep vein thrombus has occurred, the treatment is not satisfactory.

REFERENCES 1

Carter CJ. The natural history and epidemiology of venous sthrombosis. Prog cardiovasc dis 1994; 36: 423-38.

2. Callander N. Papaport SI. Trousseau's syndrome.

Western journal of medicine. [JC: xn5]. Apr 1993; 158(4): 364-74.

3. Narine K. Welleus F. Paradoxical embolism and acute

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arterial occlusion. Acta chirurgica. Belgica. [JC : oh8]. Sep-Oct 1990; 90 (5) : 244-7.

4. Anjum M N. Deep vein thrombosis changing imaging protocols. What is the lost for patient. JCPSP 2005; 15(5):251-252.

5. Vuci? N; Cala K; Ranci? I; Pticar R. Therapy and prevention of deep venous thrombosis and pulmonary embolism in gynecology and obstetrics.

Acta Med Croatica. 2003; 57(2):123-30.

SUMMARY Deep Vein Thrombosis Incidence Pathology & Pathogeniss Paradoxical embolism Investigations Prevention Treatment

6. Lieberman DV; Lieberman D. Proximal deep vein thrombosis after hip fracture surgery in elderly patients despite thromboprophylaxis. Am J Phys Med Rehabil. 2002; 81(10):745-50.

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Index

INDEX

1

C

A Acute wounds Abrasion Abdominal wound Angiogenesis Auto infection Active drain Acute abscess Appendicular abscess Aseptic surgery Antisepsis ASA classification Anaplasia Amelanotic melanoma Acral lentiginous melanoma Arterial system Ankle brachial index Angio-assisted in situ bypass Arterio venous fistula

03 04 07 16 29 60 65 69 83 83 93 202 224 224 249 260 263 297

B Bruise Burn wounds Burst strength Brain abscess Breast abscess Brodieâ&#x20AC;&#x2122;s abscess Bacteremia Blood transfusion Autologous Homologous Burns Degrees of Depth of Zones of Extent of Nature of Site of Benign tumors Basal cell carcinoma SURGERY - PRINCIPLES IN GENERAL

03 06 18 67 70 72 83 83 109 110 167, 169 169 170 170 171 172 175 187 215

Chest wound Chronic wounds Classes of wounds Clean wound Clean contaminated wound Contaminated wounds Cross infection Cryosurgery Cryogens Closed drains Critical care Control of haemorrhage Calcium balance Critical limb ischaemia

07 08 08 08 09 09 29 46 46 59 89 105 161 252

D Degloving wound Dressing (wound) Drains (surgical) Disinfections Dehydration Dermoid cyst Dysplasia Digital subtraction angiography Doppler ultrasound

06 37 59 84 146 193 202 259 259

E Empyema gall bladder Empyema thoracis Extracellular fluid Epidermal inclusion cyst Enlargement of lymph glands Endarterectomy

68 69 140 189 237 263

315

INDEX

2

F Facial wound Fibroplasia Factors affecting healing Fluid and electrolytes Fluid balance Fibroma Fusiform aneurysm

I 06 16 21 139 143 195 270

G Gunshot wound Granulation tissue Gangrene Dry Wet Gas Synergistic Fournierâ&#x20AC;&#x2122;s

H

J

99 99 99 99 99 99 99 100 100 100 101 149 152 155 157 241

197

L Lacerated wound Lasers in surgery Liver abscess Lung abscess Lock jaw Lipoma Lentigo maligna melanoma Lymphatics Leriche syndrome Leg ulcers

04 51 68 69 76 191 223 231 256 289

M Missile wound Magnesium balance Malignant tumors Mitosis Mohs micrographic surgery Malignant melanoma Magnetic resonance angiography Mycotic aneurysm

05 165 199, 201 201 211,217 219 260 271

N Neck wound

SURGERY - PRINCIPLES IN GENERAL

63 69 91 201 255

Junctional naevus

05 17 277 278 278 278 280 280

Haemorrhage Arterial Venous Capillary Primary Reactionary Secondary Revealed Concealed Acute Chronic Hyponatremia Hypernatremia Hypokalemia Hyperkalemia Hodgkinâ&#x20AC;&#x2122;s disease

Infections Interloop abscess Intra-operative care Invasiveness Intermittent claudication

07 316

INDEX

3

O Open drains

59

P Penetrating wounds Perineal wounds Peripheral wounds Primary healing Phases of healing Prevention of wound infection Passive drains Pyogenic abscess Pancreatic abscess Paracolic abscess Perianal abscess Pelvic abscess Periurethral abscess Pre-operative care Potassium balance Pleomorphism Photodynamic therapy Peripheral ischaemia Percutanous transluminal balloon angiography Peripheral arterial aneurysms Pyoderma gangrenosum

05 07 08 11 12 27 59 65 68 69 72 72 72 91 155 201 212 251 282 269 280

Secondary healing 11 Sutures 36 Staplers 36 Steristrips 37 Surgical practice 43 Subphrenic abscess 69 Satellite abscess 72 Sterilization 83 Septicaemia 83 SIRS 83 Sepsis 83,127 Shock 117 Irreversible 118,122 Progressive 118 Septic 119 Burn 119 Hypovolaemic 119 Cardiogenic 120 Psychogenic 120 Neurogenic 120 Vaso-vagal 120 Anaphylactic 120 Sepsis syndrome 127 Sodium balance 149 Split skin graft 185 Sebaceous cyst 189 Squamous cell carcinoma 209 Supraclavicular lymph gland enlargement 233 Saccular aneurysms 270

R Regeneration Repair Risus sardonicus

T 11 11 76

S Surgical wound Stab wound Septic wound Second degree healing SURGERY - PRINCIPLES IN GENERAL

04 05 09 11

Tensile strength Tourniquets Tetanus Trismus Tonicity

18 55 75 76 141

V Venous system Varicose veins

297 299 317

INDEX

4

W Wounds War wounds Wound healing Wound contraction Wound care Water balance Water intoxication Water depletion

SURGERY - PRINCIPLES IN GENERAL

01 05 11 18 35 145 146 146

318

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