Key Notes on Plastic Surgery PDF

KEY NOTES ON Plastic Surgery ADRIAN M. RICHARDS MSc FRCS (Plast.) Consultant Plastic Surgeon Stoke Mandeville NHS Trust Aylesbury Buckinghamshire United Kingdom FOREWORD BY PROFESSOR IAN T. JACKSON Director of Craniofacial and Reconstructive Surgery Providence Hospital Michigan USA Blackwell Science KEY NOTES ON Plastic Surgery ADRIAN M. RICHARDS MSc FRCS (Plast.) Consultant Plastic Surgeon Stoke Mandeville NHS Trust Aylesbury Buckinghamshire United Kingdom FOREWORD BY PROFESSOR IAN T. JACKSON Director of Craniofacial and Reconstructive Surgery Providence Hospital Michigan USA Blackwell Science © 2002 by Blackwell Science Ltd a Blackwell Publishing Company Editorial Ofﬁces: Osney Mead, Oxford OX2 0EL, UK Tel: +44 (0)1865 206206 Blackwell Science, Inc., 350 Main Street, Malden, MA 02148-5018, USA Tel: +1 781 388 8250 Blackwell Science Asia Pty, 54 University Street, Carlton, Victoria 3053, Australia Tel: +61 (0)3 9347 0300 Blackwell Wissenschafts Verlag, Kurfürstendamm 57, 10707 Berlin, Germany Tel: +49 (0)30 32 79 060 The right of the Author to be identiﬁed as the Author of this Work has been asserted in accordance with the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher. First published 2002 Library of Congress Cataloging-in-Publication Data Richards, Adrian M. Key notes on plastic surgery/Adrian M. Richards; foreword by Ian Jackson. p. cm. Includes index. ISBN 0-632-05668-1 (pbk.) 1. Surgery, Plastic—Handbooks, manuals etc. I. Title. [DNLM: 1. Surgery, Plastic WO 600 R514k 2001] 617.9′5—dc21 ISBN 0-632-05668-1 A catalogue record for this title is available from the British Library Set in 9.5 on 12pt Galliard by Graphicraft Limited, Hong Kong Printed and bound in Great Britain by MPG Books, Bodmin, Cornwall For further information on Blackwell Science, visit our website: www.blackwell-science.com Contents Foreword, v Preface, vi Acknowledgements, vi Abbreviations, vii 1 General principles, 1 2 Skin and soft-tissue lesions, 56 3 The head and neck, 79 4 The breast and chest wall, 168 5 The upper limb, 193 6 The lower limb, 243 7 The urogenital system, 262 8 Burns, 273 9 Microsurgery, 284 10 Aesthetic surgery, 292 Index, 307 iii Foreword I am particularly critical of the large numbers of plastic surgery textbooks being produced by well-known and little-known companies, and authored by well- known and little-known authors. The latter range from dermatologists through oral surgeons to ear, nose and throat surgeons and plastic surgeons. One wonders why these books are ever written, why they are ever published, and especially why anyone would ever want to buy them. When Key Notes on Plastic Surgery was sent to me, my feeling was, ‘Oh, no, not another useless, general plastic surgery textbook’. How wrong I was. This is a plastic surgery textbook with a difference. The difference is that it is not a large book, it is not ﬁlled with unnecessary padding and photographs, be they good or awful. This contains only the meat without all the unnecessary trimmings. It is not ﬁlled with references which are designed to make the reader think that the author has researched all of them (most of these references are never used except in the production of yet another chapter or yet another book). This book has a deﬁnite purpose and, as such, it truly ﬁlls a void in plastic surgery. It is a distillation of plastic surgery and contains only the signiﬁcant facts laid out in a clear fashion with economy of wordsaa rare feature of the modern textbook! This being so, it will be used clinically by a multitude of trainees and also by fully ﬂedged plastic surgeons. I can also see it being consulted prior to surgery and certainly prior to examinations. It might, on occasion, even ﬁnd its way into the operating room! I especially appreciate the economy of words, it makes for easier registration of facts. Adrian Richards is to be congratulated on seeing the need for such a book and to have set it out in such a clear and informative fashion. I heartily recommend it to those in training, and to those who are somewhat older and want to quickly review techniques and brush up on those which have stood the test of time. I have a feeling that this will be the ﬁrst of many editions, and it will become a signiﬁcant textbook in the training of plastic surgeons in the UK and Europe, and, hopefully, given the proper exposure, in the United States. I consider it an honour, and certainly it has been a pleasure, to be invited to write this foreword. Ian T. Jackson, MD v Preface When preparing for the plastic surgical exam at the end of my training, I bought almost every plastic surgical text on the market in the hope that this would guarantee success. I found it difﬁcult and time consuming to extract information from the larger texts and rued the lack of a short and succinct book to help me with my studies. This book aims to provide the reader with a sturdy scaffold of plastic surgical knowledge, which can then be supplemented from other sources. I hope that it will be useful to plastic surgeons of all levels the world over; if it makes exam preparation any less frustrating it will have served its purpose. Adrian M. Richards Dedication To the memory of my mother, Jill Lovesey To my father, David To my wife, Helena, and my children, Josie, Ciara and Alﬁe Acknowledgements I would like to thank my many trainers and mentors for their teaching, advice and inspiration, particularly Michael Klaassen, Professor Gus McGrouther, Robert McDowall, John Hobby, Richard Cole, Michael Cadier, Tim Goodacre, David Coleman, Steven Wall, Henk Giele, Graham Southwick, Simon Donahoe, Morris Ritz, Damien Ireland, Anthony Berger and Steven Tham. I have appreciated the advice and support of my fellow trainees Michael Tyler, David Johnson and Andrew Pay, who have given me valuable advice while prepar- ing the book. Paul Cohen, David Lam, Emma Hormbrey and Tom MacLeod spent many hours proofreading the text for which I am grateful. I would also like to thank Mr Parkhouse for reviewing the manuscript in its early stages. I am indebted to Stuart Taylor, Rosie Hayden, Debbie Maizels, Rupal Malde, and all those at Blackwell Science for their help in getting the book to print. Finally I would like to thank my wife, Helena, for her patience and support. vi Abbreviations ABPI ankle brachial pressure indices ADM abductor digiti minimi AER apical ectodermal ridge AFX atypical ﬁbroxanthoma AK actinic keratosis ALM acral lentiginous melanoma AP anteroposterior APB abductor pollicis brevis APL abductor pollicis longus ARDS adult respiratory distress syndrome ASA American Society of Anesthesiologists AVA arteriovenous anastomosis AVM arteriovenous malformation AVN avascular necrosis BAPS British Association of Plastic Surgeons BCC basal cell carcinoma BEAM bulbar elongation and anastomotic meatoplasty BMP bone morphogenic protein BOA British Orthopaedic Association BP blood pressure BSA body surface area BXO balinitis xerotica obliterans CL cleft lip CMCJ carpometacarpal joint CMF cisplatin, melphalan, 5-ﬂuouracil CO carbon monoxide CP cleft palate CT computed tomography DBD dermolytic bullous dermatitis DCIA deep circumﬂex iliac artery DCIS ductal carcinoma in situ DEC diethylcarbamazepine DFSP dermatoﬁbrosarcoma protuberans DIC disseminated intravascular coagulation DIEA deep inferior epigastric artery DIEP deep inferior epigastric perforator (ﬂap) DIPJ distal interphalangeal joint DISI dorsal intercalated segment instability DOPA dihydroxyphenylalanine vii viii A B B R E V I AT I O N S DOT double-opposing tab ECRB extensor carpi radialis brevis ECRL extensor carpi radialis longus ECU extensor carpi ulnaris EDC extensor digitorum communis EDM extensor digiti minimi EHL extensor hallucis longus EIP extensor indicis proprius ELND elective lymph node dissection EMG electromyograph EPB extensor pollicis brevis EPL extensor pollicis longus ESR erythrocyte sedimentation rate FBC full blood count FCR ﬂexor carpi radialis FCU ﬂexor carpi ulnaris FDA Food and Drug Administration FDM ﬂexor digiti minimi FDP ﬂexor digitorum profundus FDS ﬂexor digitorum superﬁcialis FGF ﬁbroblast growth factor FNA ﬁne needle aspiration FPB ﬂexor pollicis brevis FPL ﬂexor pollicis longus GAG glycosaminoglycan GHN giant hairy naevus GI gastro-intestinal Hb haemoglobin HIV human immunodeﬁciency virus HLA human leucocyte antigen HPV human papilloma virus ICD intercanthal distance ICP intercranial pressure IDDM insulin dependent diabetes mellitus IF interferon IL interleukin IOP interorbital distance IPJ interphalangeal joint IPPV intermittent positive pressure ventilation IVP intravenous pyelogram KA keratoacanthoma LA local anaesthesia LASER light ampliﬁcation by stimulated emission of radiation LCIS lobular carcinoma in situ LM lentigo maligna A B B R E V I AT I O N S ix LME line of maximum extensibility LMM lentigo maligna melanoma MAGPI meatal advancement and glanuloplasty incorporated MCPJ metacarpophalangeal joint MFH malignant ﬁbrous histiocytoma MHC major histocompatibility complex MM malignant melanoma MRC Medical Research Council MRI magnetic resonance imaging mRNA messenger ribonucleic acid MRSA methicillin resistant Staphylococcus aureus MSG Melanoma Study Group MSH melanocyte-stimulating hormone MUM monosodium urate monohydrate NAC nipple areolar complex NK natural killer (cell) NSAID non-steroidal anti-inﬂammatory drug OA osteoarthritis OM occipital mental OPG orthopantomogram OR&IF open reduction and internal ﬁxation PA posteroanterior PB peroneus brevis PCR polymerase chain reaction PDGF platelet-derived growth factor PDS polydioxanone suture PE pulmonary embolus PIPJ proximal interphalangeal joint PL peroneus longus PL palmaris longus PT peroneus tertius PT pronator teres PTFE polytetraﬂuoroethylene RA retinoic acid RA rheumatoid arthritis RCL radial collateral ligament RFF radial-forearm ﬂap ROOF retro-orbicularis oculi fat (pad) RSD reﬂex sympathetic dystrophy RSTL relaxed skin tension line RT-PCR reverse transcriptase-polymerase chain reaction S-GAP superior gluteal artery perforator (ﬂap) SCC squamous cell carcinoma SCIA superﬁcial circumﬂex iliac artery SLE systemic lupus erythematosus x A B B R E V I AT I O N S SLL scapholunate ligament SLAC scapholunate advanced collapse SMAS superﬁcial musculoaponeurotic system SMR submucous resection SNAC scaphoid nonunion advanced collapse SOOF suborbicularis oculi fat (pad) SSG split-skin graft SSM superﬁcial spreading melanoma TBSA total body surface area TCA trichloroacetic acid TFCC triangular ﬁbrocartilagenous complex TFL tensor fascia lata TGF transforming growth factor TLND therapeutic lymph node dissection TMJ temporomandibular joint TMN tumour, metastases, nodes TNF tumour necrosis factor t-PA tissue plasminogen activator TPN total parental nutrition TRAM transverse rectus abdominis muscle UAL ultrasonic assisted liposuction UCL ulnar collateral ligament UV ultraviolet VAC vacuum-assisted closure VCF velocardiofacial (syndrome) VISI volar intercalated segment instability VPI velopharyngeal incompetence VRAM vertical rectus abdominis myocutaneous (ﬂap) WLE wide local excision XP xeroderma pigmentosa ZF zygomaticofrontal 1 1 General principles Structure and function of the skin, 1 Blood supply to the skin, 4 Classiﬁcation of ﬂaps, 8 Geometry of local ﬂaps, 12 Wound healing and skin grafts, 21 Bone healing and bone grafts, 28 Nerve healing and nerve grafts, 31 Tendon healing, 35 Transplantation, 39 Alloplastic implantation, 41 Wound dressings, 46 Sutures and suturing, 47 Tissue expansion, 51 Further reading, 54 Structure and function of the skin The functions of the skin include: 1 Physical protection 2 Protection against UV light 3 Protection against microbiological invasion 4 Prevention of ﬂuid loss 5 Regulation of body temperature 6 Sensation 7 Immunological surveillance. The epidermis The epidermis is composed of stratiﬁed squamous epithelium. It is derived from ectoderm. Epidermal cells undergo keratinization in which their cytoplasm is replaced with keratin as the cell dies and becomes more superﬁcial. The epidermis is composed of the following ﬁve layers, from deep to superﬁcial. 1 Stratum germinativum This is also known as the basal layer. The cells within this layer have cytoplasmic projections, which ﬁrmly link them to the underlying basal lamina. 1 1 2 GENERAL PRINCIPLES This is the only actively proliferating layer of skin. The stratum germinativum contains melanocytes. 2 Stratum spinosum The stratum spinosum is also known as the prickle cell layer. This layer contains large keratinocytes which produce keratin. The cells within this layer are joined to each other by tonoﬁbrils (prickles). 3 Stratum granulosum The stratum granulosum contains mature keratinocytes, which possess cyto- plasmic granules of keratohyalin. This layer is called the stratum granulosum because of these granules. The stratum granulosum is the predominant site of protein synthesis. 4 Stratum lucidum This is a clear layer. The stratum lucidum is only present in the thick skin of the palms and feet. 5 Stratum corneum The stratum corneum contains non-viable keratinized cells. The thick cells of this layer protect against trauma. The stratum corneum: Insulates against ﬂuid loss Protects against bacterial invasion. Sebum produced by the sebaceous glands of the stratum corneum is bactericidal to both streptococci and staphylococci. Cellular composition of the epidermis Keratinocytes are the predominant cell type in the epidermis. Langerhans cells form part of the immune system and function as antigen- presenting cells. Merkel cells are mechanoreceptors of neural crest origin. Melanocytes: Are neural crest derivatives Are usually located in the stratum germinativum Produce melanin, which protects the surrounding skin by absorbing UV light. The dermis The dermis accounts for 95% of the thickness of the skin. The papillary dermis is superﬁcial and contains more cells and ﬁner collagen ﬁbres. The reticular dermis is deeper and contains fewer cells and coarser collagen ﬁbres. The dermis is composed of the following. STRUCTURE AND FUNCTION OF THE SKIN 3 1 Collagen ﬁbres These ﬁbres are produced by ﬁbroblasts. They are responsible for much of the strength of the skin. The normal ratio of type 1 to type 3 collagen is 5 : 1. Elastin ﬁbres These are secreted by ﬁbroblasts. They are responsible for the elastic recoil of the skin. Ground substance This consists of the glycosaminoglycans (GAGs), hyaluronic acid, dermatan sulfate and chondroitin sulfate. GAGs are secreted by ﬁbroblasts and become ground substance when hydrated. Vascular plexus This separates the denser reticular dermis from the overlying papillary dermis. Skin appendages The skin contains the following appendages. Hair follicles Each hair is composed of a medulla, cortex and outer cuticle. The hair follicle consists of an inner root sheath, derived from the epidermis, and an outer root sheath, derived from the dermis. Several sebaceous glands drain into each follicle. Discharge from these glands is aided by the contraction of erector pili muscles. Velus hairs are ﬁne and downy. Terminal hairs are coarse. Hairs are in either the telogen or the anogen phase. 75% of hairs are in the anogen (growth) phase at any one time. The remaining 25% of hairs are in the telogen (resting) phase. Eccrine glands These sweat glands secrete an odourless hypotonic ﬂuid. They are present in all sites of the body. Eccrine glands occur more frequently in the eyelids, palms, feet and axilla. Apocrine glands These are located in the axilla and groin. They emit a thicker secretion than eccrine glands. They are responsible for body odour. Hidradenitis suppurativa is an infection of the apocrine glands. Sebaceous glands These are holocrine glands that usually drain into the pilosebaceous unit. 1 4 GENERAL PRINCIPLES They drain directly onto the skin in the labia, penis and tarsus (meibomian glands). They occur more frequently on the forehead, nose and cheek. Sebaceous glands are not the sole cause of so-called sebaceous cysts. These cysts are in fact of epidermal origin and contain all of the substances secreted by the skin (predominantly keratin). Some authorities maintain that they should therefore be called epidermoid cysts. Types of secretion from glands Eccrine or merocrine glands secrete opened vesicles via exocytosis. Apocrine glands secrete unbroken vesicles which later discharge. Holocrine glands secrete whole cells which then disintegrate. Histological terms Acanthosisahyperplasia of the epithelium. Papillomatosisaan increase in the depth of the corrugations at the junction between epidermis and dermis. Hyperkeratosisaan increase in the thickness of the keratin layer. Parakeratosisathe presence of nucleated cells at the skin surface. Blood supply to the skin Anatomy of the circulation The blood reaching the skin originates from deep vessels. These then feed interconnecting vessels which supply the vascular plexuses of fascia, subcutaneous tissue and skin. Deep vessels The deep vessels arise from the aorta and divide to form the main arterial supply to the head, neck, trunk and limbs. Interconnecting vessels The interconnecting system is composed of: Fasciocutaneous (or septocutaneous) perforating vessels These vessels reach the skin by traversing fascial septae. They provide the main arterial supply to the skin in the limbs. Musculocutaneous vessels These vessels reach the skin via direct muscular branches from the deep system. These branches enter muscle bellies and divide into multiple perforating branches, which travel up to the skin. The musculocutaneous system provides the main arterial supply to the skin of the torso. BLOOD SUPPLY TO THE SKIN 5 1 Vascular plexuses of fascia, subcutaneous tissue and skin Vascular plexuses of the fascia, subcutaneous tissue and skin are divided into six layers. 1 Subfascial plexus A small plexus lying on the undersurface of the fascia. 2 Prefascial plexus A larger plexus particularly prominent on the limbs. Predominantly supplied by fasciocutaneous vessels. 3 Subcutaneous plexus Lies at the level of the superﬁcial fascia. Mainly supplied by musculocutaneous vessels. Predominant on the torso. 4 Subdermal plexus Receives blood from the underlying plexuses. The main plexus supplying blood to the skin. Represented by dermal bleeding observed in incised skin. 5 Dermal plexus Mainly composed of arterioles. Plays an important role in thermoregulation. 6 Subepidermal plexus Contains small vessels without muscle in their walls. Has a predominantly nutritive and thermoregulatory function. Angiosomes An angiosome is a composite block of tissue supplied by a named artery. The area of skin supplied by an artery was ﬁrst studied by Manchot in 1889. His work was expanded by Salmon in the early 1930s, and more recently by Taylor and Palmer. The anatomical territory of an artery is the area in which the vessel branches ramify before anastomosing with adjacent vessels. The dynamic territory of an artery is the area into which staining extends after intravascular infusion of ﬂuorescein. The potential territory of an artery is the area that can be included in a ﬂap if it is delayed. The vessels that pass between anatomical territories are called choke vessels. The transverse rectus abdominis muscle (TRAM) ﬂap illustrates the angiosome concept well. Zone 1 This receives musculocutaneous perforators from the deep inferior epigastric artery (DIEA) and is therefore in its anatomical territory. Zones 2 and 3 There is some controversy as to which of the following zones is 2 and which is 3; the numbers of these zones are interchanged in various texts. The portion of skin lateral to zone 1 is in the anatomical territory of the superﬁcial circumﬂex iliac artery (SCIA). Blood has to travel through a set of choke vessels to reach it from the ipsilateral DIEA. 1 6 GENERAL PRINCIPLES The portion of skin on the other side of the linea alba is in the anatomical area of the contralateral DIEA. This area is reliably perfused in a TRAM ﬂap based on the contralateral DIEA and is therefore within its dynamic territory. Zone 4 This lies furthest from the pedicle and is in the anatomical territory of the con- tralateral SCIA. Blood passing from the ﬂap pedicle to zone 4 has to cross two sets of choke vessels. This portion of the TRAM ﬂap has the worst blood supply and for this reason it is often discarded. Arterial characteristics From his detailed anatomical dissections Taylor made the following observations: 1 Vessels usually travel with nerves. 2 Vessels obey the law of equilibriumaif one is small, its neighbour will tend to be large. 3 Vessels travel from ﬁxed to mobile tissue. 4 Vessels have a ﬁxed destination but a varied origin. 5 Vessel size and orientation is a product of growth. The microcirculation Terminal arterioles are present in the reticular dermis and terminate as they enter the capillary network. The precapillary sphincter is the last part of the arterial tree containing muscle within its wall. It is under neural control and regulates the blood ﬂow into the capillary network. Arteriovenous anastomoses (AVAs) connect the arterioles to the efferent veins. Blood ﬂowing through AVAs bypasses the capillary bed and has a thermoregula- tory rather than nutritive function. AVAs are of two types: 1 Indirect AVAs are convoluted structures known as glomera and are densely innervated by autonomic nerves. 2 Direct AVAs are much less convoluted and have a sparser autonomic supply. The blood supply to the skin far exceeds its nutritive requirementsamuch of it bypasses the capillary beds via the AVAs and has a primarily thermoregulatory function. Control of blood ﬂow The muscular tone of vessels is controlled by the following factors. Pressure of the blood within vessels (myogenic theory) The myogenic theory was originally described by Bayliss and states that: Increased intraluminal pressure results in constriction of vessels. Decreased intraluminal pressure results in their dilatation. This mechanism helps to keep blood ﬂow constant and is the cause of the imme- diate hyperaemia observed on release of a tourniquet. BLOOD SUPPLY TO THE SKIN 7 1 Neural innervation Arterioles, AVAs and precapillary sphincters are densely innervated by symp- athetic ﬁbres. Neural control regulates skin blood ﬂow in the following ways. Increased arteriolar tone results in a decrease of cutaneous blood ﬂow. Increased precapillary sphincter tone reduces the blood ﬂow into the capillary networks. Decreased AVA tone results in an increase in the non-nutritive blood ﬂow bypassing the capillary bed. Humoral factors Epinephrine (adrenaline) and norepinephrine (noradrenaline) cause vasocon- striction of the vessels. Histamine and bradykinin cause vasodilatation. Low oxygen saturation, high carbon dioxide saturation and acidosis also result in vasodilatation. Temperature Increased heat produces cutaneous vasodilatation and increased ﬂow which pre- dominantly bypasses the capillary beds via the AVAs. The delay phenomenon Delay is any preoperative manoeuvre that results in increased ﬂap survival. Historical examples include Tagliacozzi’s technique for nasal reconstruction described in the 16th century. This involves elevation of a bipedicled ﬂap with a length : breadth ratio of 2 : 1 (the ﬂap can be considered as two ﬂaps of the ratio 1 : 1). Cotton lint is then placed under the ﬂap, preventing its reattachment. Two weeks later one end of the ﬂap is detached from the arm and attached to the nose. A ﬂap of these dimensions transferred immediately, without a prior delay pro- cedure, would have an increased chance of distal necrosis. A form of delay used in clinical practice today is the division of the DIEA supplying the rectus muscle, 2 weeks prior to pedicled TRAM-ﬂap breast reconstruction. Despite many advances in our understanding, the mechanism of delay remains incompletely understood. The following theories have been proposed to explain the delay phenomenon. Increased axiality of blood ﬂow Removal of the blood ﬂow from the periphery of a random ﬂap will promote the development of an axial blood supply from its base along its axis. Axial ﬂaps are known to have improved survival when compared with random ﬂaps. 1 8 GENERAL PRINCIPLES Tolerance to ischaemia Cells become accustomed to hypoxia after the initial delay procedure. Less tissue necrosis therefore occurs after the second operation. Sympathectomy vasodilatation theory Sympathectomy resulting from dividing the sympathetic ﬁbres at the borders of the ﬂap results in vasodilatation and an improved blood supply. But why, if sympathectomy is immediate, does the delay phenomenon only begin to appear at 48 h, and why does it take 2 weeks to reach its maximum effect? Interﬂap shunting hypothesis This theory postulates that sympathectomy dilates the AVAs more than the pre- capillary sphincters, resulting in an increase in non-nutritive blood ﬂow bypassing the capillary bed. A greater length of ﬂap will survive at the second stage as there are fewer symp- athetic ﬁbres to cut and therefore there will be less of a reduction in non-nutritive ﬂow. Hyperadrenergic state Surgery results in increased tissue concentrations of vasoconstrictor substances, such as epinephrine and norepinephrine. After the initial delay procedure, the resultant reduction in blood supply is not sufﬁcient to produce tissue necrosis. The level of vasoconstrictor substances returns to normal before the second procedure. The second procedure produces another rise in the concentration of vasocon- strictor substances. This rise is smaller than it would be if the ﬂap were elevated without a prior delay. The ﬂap is therefore less likely to undergo distal necrosis if a prior delay is performed. Unifying theory This theory was described by Pearl in 1981. It incorporates elements of all of the above theories. Classiﬁcation of ﬂaps Flaps can be classiﬁed by the ﬁve ‘C’s: Circulation Composition Contiguity Contour Conditioning. C L A S S I F I C AT I O N O F F L A P S 9 1 Circulation The circulation to ﬂaps can be further subcategorized into: Random Axial (direct; fasciocutaneous; musculocutaneous; or venous). Random ﬂaps Random ﬂaps have no directional blood supply and are not based on any known vessel. These include most local ﬂaps on the face. They should have a maximum length : breadth ratio of 1 : 1 in the lower extremity, as it has a poor blood supply. They can have a length : breadth ratio of up to 1 : 6 in the face, as it has a good blood supply. Axial ﬂaps Direct Direct ﬂaps contain a named artery running along the axis of the ﬂap in the sub- cutaneous tissue. Examples include: The groin ﬂap based on the superﬁcial external iliac vessels. The deltopectoral ﬂap based on perforating vessels of the internal mammary artery. Both ﬂaps can include a random segment in their distal portions after the artery peters out. Fasciocutaneous Fasciocutaneous ﬂaps are based on vessels running either within or near the fascia. Blood reaches these ﬂaps from fasciocutaneous vessels (also called septocutaneous vessels) running from the deep arteries of the body to the fascia. The fasciocutaneous system predominates on the limbs and this is the location of most of these ﬂaps. Fasciocutaneous ﬂaps have been classiﬁed by Cormack and Lamberty into the following types: Type A These ﬂaps are dependent on multiple non-named fasciocutaneous vessels that enter the base of the ﬂap. The lower-leg ‘super ﬂaps’ described by Pontén are examples of type A ﬂaps. Their dimensions vastly exceed the 1 : 1 ratios recommended for random ﬂaps in the lower leg. Type B These are based on a single fasciocutaneous vessel which runs along the axis of the ﬂap. Examples include the scapular and parascapular ﬂaps, and the fasciocutaneous ﬂaps based on perforators in the lower leg. 1 10 GENERAL PRINCIPLES Type C These ﬂaps are supplied by multiple small, perforating vessels which reach the ﬂap from a deep artery running along a fascial septum between muscles. Examples include the radial forearm ﬂap (RFF) and the lateral arm ﬂap. Type D These are fasciocutaneous ﬂaps that contain bone. As these ﬂaps are usually type C, they have recently been reclassiﬁed as ‘type C ﬂaps with bone’. Examples include: The RFF raised with a segment of the radius. The lateral arm ﬂap raised with a segment of the lateral supracondylar ridge of the humerus. Musculocutaneous Musculocutaneous ﬂaps are based on perforators that reach the skin through the muscle. The musculocutaneous system predominates on the torso and this is the location of most of these ﬂaps. Musculocutaneous ﬂaps were classiﬁed by Mathes and Nahai in 1981. Type 1 These ﬂaps are supplied by a single vascular pedicle. Examples include the gastrocnemius, the tensor fascia lata (TFL) and the abductor digiti minimi (ADM). These are generally good ﬂaps for transfer, as the whole muscle is nourished by a single pedicle. Type 2 These ﬂaps are supplied by a single dominant pedicle which enters the muscle near its origin or insertion point. Additional smaller vascular pedicles enter the muscle belly. Examples include the trapezius, temporalis and gracilis ﬂaps. These are generally good ﬂaps for transfer, as they can be based on the single dominant pedicle. Type 3 These ﬂaps are supplied by two vascular pedicles, each arising from a separate regional artery. Examples include the rectus abdominis and the gluteus maximus ﬂaps. These are useful muscles for transfer, as they can be based on either pedicle. Type 4 These ﬂaps are supplied by multiple segmental pedicles. Examples include the sartorius, the tibialis anterior and the long ﬂexors and extensors of the toes. In practice they are seldom used for transfer, as each pedicle only supplies a small portion of muscle. Type 5 These ﬂaps have one dominant vascular pedicle and secondary smaller segmen- tal pedicles. C L A S S I F I C AT I O N O F F L A P S 11 1 Examples include the latissimus dorsi and the pectoralis major. These are useful ﬂaps, as they can be based on either the dominant vascular pedicle or the secondary smaller segmental pedicles. Venous These ﬂaps are based on venous rather than arterial pedicles. In fact, many of the venous pedicles have very small arteries running alongside them. One example is the saphenous ﬂap, which is based on the short saphenous vein and often used to reconstruct defects around the knee. Venous ﬂaps have been classiﬁed by Thatte and Thatte as follows: Type 1 These ﬂaps are supplied by a single venous pedicle. Type 2 These are venous ﬂow-through ﬂaps and are supplied by a vein which enters one side of the ﬂap and exits from the other. Type 3 These are arterialized venous ﬂaps. Venous ﬂaps tend to become very congested post-operatively and have not been universally accepted. Composition Flaps can be classiﬁed by their composition, as: Cutaneous Fasciocutaneous Fascial Musculocutaneous Muscle only Osseocutaneous Osseous. Contiguity Flaps can be classiﬁed by their source, as: Local ﬂaps These are composed of tissue adjacent to the defect. Regional ﬂaps These are composed of tissue from the same region of the body as the defect, e.g. head and neck, upper limb. Distant ﬂaps Pedicled distant ﬂaps are from a distant part of the body to which they remain attached. Free ﬂaps are completely detached from the body and anastomosed to recipi- ent vessels close to the defect. Contour Flaps can be classiﬁed by the method in which they are transferred into the defect. Methods of transferring ﬂaps include the following. 1 12 GENERAL PRINCIPLES Advancement The following methods can be used to facilitate advancement of a ﬂap into a defect. Stretching of the ﬂap Excision of Burow’s triangles at its base V-Y advancement Z-plasty at its base A combination of the above. Transposition The ﬂap is moved into a defect from an adjacent position, leaving a defect which must be closed by another method. Rotation The ﬂap is rotated into the defect. Classically, rotation ﬂaps are of sufﬁcient dimensions to permit closure of the donor defect. In reality, many ﬂaps have elements of transposition and rotation and may be best described as pivot ﬂaps. Interpolation These ﬂaps are moved into a defect either under or above an intervening bridge of tissue. Crane principle This technique aims to transform an ungraftable bed into one that will accept a skin graft. At the ﬁrst stage a ﬂap is placed into the defect. After a sufﬁcient time period to allow vascular ingrowth into the ﬂap from the recipient site, the superﬁcial portion of ﬂap is replaced in its original position. This leaves a segment of subcutaneous tissue in the defect, which can now accept a skin graft. Conditioning ‘Delay’ is any preoperative manoeuvre which will result in increased ﬂap survival. Traditionally delay has been used to increase the survival of ﬂaps prior to surgery. The mechanism of delay is discussed in more detail in ‘The blood supply to the skin’ (p. 7). Geometry of local ﬂaps Orientation of elective incisions In the 19th century, Langer showed that circular awl wounds produced ellipt- ical defects in cadaver skin. He believed that this occurred because the skin tension along the longitudinal axis of the ellipse exceeded that along the transverse axis. GEOMETRY OF LOCAL FLAPS 13 1 Borges has provided over 36 descriptive terms for skin lines. These include: Relaxed skin tension lines (RSTLs)athese are parallel to the natural skin wrinkles (rhytids) and tend to be perpendicular to the ﬁbres of the underlying muscle. Lines of maximum extensibility (LMEs)athese lie perpendicular to the RSTLs and parallel to the ﬁbres of the underlying muscle. The best orientation of an incision can be judged by a number of methods, including: Knowledge of the direction of pull of the underlying muscle. Ascertaining whether the incision is parallel to any rhytids or RSTLs. Ascertaining whether the incision is perpendicular to the LMEs. Ascertaining whether the incision is parallel to the direction of hair growth. ‘The pinch test’aif the skin is pinched transversely it will form a transverse fold without distortion if it is orientated correctly; if a sigmoid-shaped fold forms it is orientated incorrectly. Plasty techniques Z-plasty This technique involves the transposition of two triangular-shaped ﬂaps. A Z-plasty can be used to: Increase the length of an area of tissue or a scar Break up a straight-line scar Realign a scar. The degree of elongation of the longitudinal axis of the Z-plasty is directly related to the angles of its constituent ﬂaps. 30° → 25% elongation 45° → 50% elongation 60° → 75% elongation 75° → 100% elongation 90° → 125% elongation. The amount of elongation obtained for each ﬂap angle can be worked out by starting at 30° and 25% and adding 15° and 25% to each of the ﬁgures. Gains in tissue length are only estimates and depend on local tissue elasticity and tension. Flaps of 60° angulation are most commonly used clinically as they provide sufﬁcient lengthening without undue tension. The angles of the two ﬂaps do not need to be equal and can be designed to suit local tissue requirements. All three limbs should be of the same length. The following steps should be taken when designing a Z-plasty to realign a scar. 1 Mark the desired direction of the scar. 2 Draw the central limb of the Z-plasty along the original scar. 3 Draw the lateral limbs of the Z-plasty from the ends of the central limb to a line along the desired direction of the scar. 4 Two patterns will be available, one with a wide angle at the apex of the ﬂaps, the other with a narrow angle. 1 14 GENERAL PRINCIPLES 5 Select the pattern with the narrower angle as these ﬂaps transpose better than those with a wider angle. The four-ﬂap plasty This technique is used to elongate an area of tissue. It is, in effect, two interdependent Z-plasties. It can be designed with different angles. The two outer ﬂaps become the inner ﬂaps after transposition. The two inner ﬂaps become the outer ﬂaps after transposition. The ﬂaps, which are originally in an ‘ABCD’ conﬁguration, end as ‘CADB’ (CADBury). C C A A B A B A or C D C D D D B B GEOMETRY OF LOCAL FLAPS 15 1 The ﬁve-ﬂap plasty Because of its appearance this technique is also called a jumping-man ﬂap. It is used to elongate tissue and is often utilized clinically to release ﬁrst web space contractures and epicanthal folds. It is, in effect, two opposing Z-plasties with a V-Y advancement in the centre. The ﬂaps, which are originally in an ‘ABCDE’ conﬁguration, end as ‘BACED’. A E B C D B D A E C The W-plasty This technique is used to break up the line of a scar and improve its aesthetics. Unlike the Z-plasty and the four- and ﬁve-ﬂap plasties, it does not lengthen tissue. If possible, one of the limbs of the W-plasty should lie parallel to the RSTLs so that half of the resultant scar will lie parallel to them. This technique involves discarding normal tissue, which may be a disadvantage in certain areas. RSTL Local ﬂaps Local ﬂaps may be: Advancement ﬂaps (simple; modiﬁed; V-Y; or bipedicled). Pivot ﬂaps (transposition; interpolation; rotation ; or bilobed). Advancement ﬂaps Simple Simple advancement ﬂaps rely on skin elasticity. 1 16 GENERAL PRINCIPLES Modiﬁed Modiﬁed advancement ﬂaps incorporate one of the following techniques at the base of the ﬂap to increase tissue advancement. A counter incision A Burow’s triangle A Z-plasty. Counter incision Burow's triangle Z-plasty at base at base at base GEOMETRY OF LOCAL FLAPS 17 1 V-Y These ﬂaps are incised along each of their cutaneous borders. The blood supply to these ﬂaps arises from the deep tissue and passes to the ﬂap through a subcutaneous pedicle. Horn ﬂaps and oblique V-Y ﬂaps are modiﬁcations of the original V-Y ﬂap. Traditional V–Y flap Horn flap Bipedicled These ﬂaps receive a blood supply from both ends. They are less prone to necrosis than ﬂaps of similar dimensions, which are only attached at one end. A commonly used bipedicled ﬂap is the von Langenbeck mucoperiosteal ﬂap, used to repair cleft palates. Bipedicled ﬂaps should be designed with their limbs curved parallel to the circumference of the defect. This design permits ﬂap transposition with less tension. 1 18 GENERAL PRINCIPLES Original defect 2x x y 2y 2x Secondary defect Pivot ﬂaps Transposition ﬂaps These ﬂaps are transposed into the defect, leaving a donor site which is closed by some other means (often a skin graft). Line of greatest tension Area of excess skin or Pivot dog ear Secondary point defect Transposition ﬂaps with direct closure of donor site These include the rhomboid ﬂap (Limberg ﬂap) and the Dufourmontel ﬂap. These ﬂaps are similar in concept but vary in geometry. Both ﬂaps should be designed so as to leave the donor site scar lying parallel to the RSTLs. GEOMETRY OF LOCAL FLAPS 19 1 The rhomboid ﬂap The rhomboid flap Excised area x x 120° 60° x x Lo o ski se n RS x TL 60° LM x E The Dufourmontel ﬂap The Dufourmontel flap b 150° a 30° c b a c Interpolation ﬂaps These ﬂaps are raised from local, but not adjacent, skin. The pedicle must therefore be passed either over or under an intervening skin bridge. Skin paddle Defect De-epithelialized Intact skin bridge skin pedicle Pivot point 1 20 GENERAL PRINCIPLES Rotation ﬂaps These large ﬂaps rotate tissue into the defect. Tissue redistribution usually permits direct closure of the donor site. The ﬂap circumference should be 5–8 times the width of the defect. Clinically, these ﬂaps are often used on the scalp. The back cut at the base of the ﬂap can be directed either towards or away from the defect. Back cut Burow's triangle x x 2x Pivot point The bilobed ﬂap Many varied designs of this ﬂap have been described. It consists of two transposition ﬂaps. The ﬁrst ﬂap is transposed into the original defect. The second ﬂap is transposed into the secondary defect at the original site of the ﬁrst ﬂap. The tertiary defect at the original site of the second ﬂap should be small enough to close directly. The ﬂap should ideally be designed so that this suture line lies parallel to the RSTLs. (a) Defect r r Pivot point (b) (c) RSTL WOUND HEALING AND SKIN GRAFTS 21 1 Wound healing and skin grafts Wound healing can occur by the following methods. Healing by primary intention The skin edges are directly opposed. Healing is normally good with minimal scar formation. Healing by secondary intention The wound is left open to heal by a combination of contraction and epithelialization. Increased inﬂammation and proliferation occur in these wounds when com- pared with those that heal by primary intention. Healing by tertiary intention This occurs in wounds that are initially left open, then closed as a secondary procedure. Phases of wound healing Wound healing consists of four phases: (i) haemostasis; (ii) inﬂammation; (iii) pro- liferation; and (iv) remodelling. Haemostasis The vessels vasoconstrict immediately after division. A platelet plug is then formed. The platelets degranulate; platelet-derived growth factor (PDGF) and throm- boxanes stimulate the conversion of ﬁbrinogen to ﬁbrin. This stimulates prop- agation of the thrombus. The thrombus is initially pale when it contains platelets alone (white thrombus). As red blood cells are trapped within it the thrombus becomes darker (red thrombus). Inﬂammation This phase occurs in the ﬁrst 2–3 days after injury. Its stimulus may be: Physical injury Antigen–antibody reaction Infection. The thrombus releases growth factors such as PDGF. Endothelial cells swell, allowing the egress of polymorphonuclear lymphocytes (polymorphs or PMNs) and mononuclear cells (monocytes and macrophages) into the surrounding tissue. Proliferation This phase begins on the 2nd or 3rd day following injury and lasts for 2–4 weeks. Macrophages within the tissue release growth factors which are chemoattractant to ﬁbroblasts. Fibroblasts which are usually located in perivascular tissue migrate along networks of ﬁbrin ﬁbres into the wound. 1 22 GENERAL PRINCIPLES The ﬁbroblasts secrete GAGs and produce collagen and elastin. GAGs consist of a protein core surrounded by disaccharide units. When hydrated, GAGs become ground substance. Remodelling This phase begins 2–4 weeks after injury, as the proliferative phase subsides. During the remodelling phase there is no net increase in collagen (state of collagen homeostasis). The extensive capillary network produced in the proliferative phase begins to involute. The collagen ﬁbres, which are initially laid down in a haphazard manner, become arranged in a more organized manner. Function of the macrophage in wound healing Macrophages are derived from mononuclear leucocytes. They debride tissue and remove micro-organisms. They co-ordinate the activity of ﬁbroblasts by releasing growth factors. These include interleukin 1 (IL-1), tumour necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta). Macrophages are essential for normal wound healing. Wounds depleted of macrophages heal slowly. Epithelial repair This process, whereby epithelial continuity is re-established across a wound, con- sists of the following four phases. Mobilization 1 Epithelial cells at the wound edges enlarge and ﬂatten. 2 They detach from the neighbouring cells and the basement membrane. 3 They then move away from adjoining cells. Migration 1 Decreased contact inhibition promotes cell migration. 2 The cells migrate across the wound until they meet those from the opposite wound edge. 3 At this point, contact inhibition is reinstituted and migration ceases. Mitosis Epithelial cells begin to proliferate once they have covered the surface of the wound. Cellular differentiation 1 The normal structure of stratiﬁed squamous epithelium is re-established. 2 The cells differentiate and the layered structure of stratiﬁed squamous epithe- lium is reconstituted. WOUND HEALING AND SKIN GRAFTS 23 1 Collagen Collagen constitutes approximately 30% of the total body protein. Collagen is formed by the hydroxylation of the aminoacids lysine and proline. Procollagen is initially formed within the cell. Procollagen is transformed into tropocollagen after it is excreted from the cell. Fully formed collagen has a complex structure. It consists of three polypeptide chains wound in a left-handed helix. These three chains are further wound in a right-handed coil to form the basic tropocollagen unit. Collagen formation is inhibited by colchicine, penicillamide, steroids, vitamin C and iron deﬁciency. There are at least ﬁve types of collagen. Each type of collagen shares the same basic structure but differs in the relative composition of hydroxylysine and hydro- xyproline and in the degree of cross-linking between chains. Type 1: predominant in mature skin, bone and tendon. Type 2: present in hyaline cartilage and the cornea. Type 3: present in healing tissue, particularly in fetal wounds. Type 4: predominant constituent of basement membranes. Type 5: similar to type 4 and also found in the basement membrane. The ratio of type 1 collagen : type 3 collagen in normal skin is 5 : 1. Hypertrophic and immature scars contain a ratio of 2 : 1 or less. 90% of the total body collagen is type 1. The myoﬁbroblast This cell was ﬁrst identiﬁed by Gabbiani in 1971. It resembles a ﬁbroblast but differs in that it contains cytoplasmic ﬁlaments of α- smooth muscle actin. α-smooth muscle actin is also found in smooth muscle. The muscle ﬁbres within the ﬁbroblast are thought to be responsible for wound contraction. The number of myoﬁbroblasts within a wound is proportional to its contraction. Increased numbers of myoﬁbroblasts have been found in the fascia in patients with Dupuytren’s disease. They are thought to be responsible for the abnormal contraction of this tissue. TGF-β This growth factor is secreted by macrophages. It is believed to play a central role in wound healing and has a number of effects including: Chemoattraction of ﬁbroblasts and macrophages Induction of angiogenesis Stimulation of extracellular matrix deposition. Three isoforms of TGF-β have been identiﬁed. Types 1 and 2 promote wound healing and scarring. Type 3 decreases wound healing and scarring and in the future may have a role as an antiscarring agent. 1 24 GENERAL PRINCIPLES TGF-β is not present in fetal wounds and this may be one of the factors re- sponsible for the decreased inﬂammation and improved scarring observed in this tissue. Factors affecting healing Factors affecting wound healing may be: (i) systemic (congenital or acquired); or (ii) local. Systemic factors: congenital Pseudoxanthoma elasticum This is an autosomal recessive condition. It is characterized by increased collagen degradation. The skin is pebbled and extremely lax. Ehlers–Danlos syndrome This is a heterogeneous collection of connective tissue disorders. It results from defects in the synthesis, structure or cross-linking of collagen. Clinical features include: Hypermobile ﬁngers Hyperextensible skin Fragile connective tissues. Surgery should be avoided if possible in these patients as wound healing is poor. Cutis laxa This condition presents in the neonatal period. The skin is abnormally lax. Typically the patient has coarsely textured, drooping skin. Progeria This condition is characterized by premature ageing. Clinical features of the condition include: Growth retardation Baldness Atherosclerosis. Werner syndrome This is an autosomal recessive condition. Skin changes are similar to scleroderma. Elective surgery should be avoided whenever possible as healing is poor. Epidermolysis bullosa This is a heterogeneous collection of separate conditions. The skin is very susceptible to mechanical stress. Blistering may occur after minor trauma (Nikolsky sign). WOUND HEALING AND SKIN GRAFTS 25 1 The most severe subtype, dermolytic bullous dermatitis (DBD), results in hand ﬁbrosis and syndactyly. Systemic factors: acquired Nutrition Vitamin A deﬁciency delays wound healing. Vitamin C is required for collagen synthesis. Vitamin E acts as a membrane stabilizer; deﬁciency may inhibit healing. Zinc is a constituent of many enzymes; administration accelerates healing in deﬁcient states. Albumin is an indicator of malnutrition; low levels are associated with poor healing. Pharmacological Steroids decrease inﬂammation and subsequent wound healing. Non-steroidal anti-inﬂammatory drugs (NSAIDs) decrease collagen synthesis. Endocrine abnormalities Diabetics often have delayed wound healing. Recent evidence suggests neuropathy rather than small vessel occlusive disease may be responsible for the delayed healing (see ‘Leg ulcers’, p. 244). Age The rate of cell multiplication decreases with age. All stages of wound healing are more protracted in the elderly. Healed wounds have decreased tensile strength in the elderly. Smoking Nicotine is a sympathetic stimulant which causes vasoconstriction and con- sequently decreases tissue perfusion. Carbon dioxide, contained in cigarette smoke, shifts the oxygen dissociation curve and reduces tissue oxygenation. Local factors Infection Subclinical wound infection can impair wound healing. 5 Wounds with over 10 organisms per gram of tissue are considered infected and are unlikely to heal without further treatment. Radiation Radiation causes endothelial cell, capillary and arteriole damage. Irradiated ﬁbroblasts secrete less collagen and extracellular matrix. Lymphatics are also damaged, resulting in oedema and an increased risk of infection. 1 26 GENERAL PRINCIPLES Blood supply Decreased tissue perfusion results in decreased wound oxygenation. Fibroblasts are oxygen-sensitive and their function is reduced in hypoxic tissue. Reduced oxygen delivery to the tissues can result from decreases in: Inspired oxygen concentration Oxygen transfer to haemoglobin Haemoglobin concentration Tissue perfusion. Decreased oxygen delivery to the tissue reduces: Collagen formation Extracellular matrix deposition Angiogenesis Epithelialization. Hyperbaric oxygen treatment increases the inspired oxygen concentration but its effectiveness relies on good tissue perfusion. Trauma The delicate neoepidermis of healing wounds is disrupted by trauma. Neural supply There is some evidence that wounds in denervated tissue heal slowly. This may contribute to the delayed wound healing observed in some pressure sores, and in patients with diabetes and leprosy. Fetal wound healing Tissue healing during the ﬁrst 3 months of fetal life occurs by regeneration rather than by scarring. Regenerative healing is characterized by the absence of scarring. Regenerative wound healing differs from normal adult healing in the following ways. Inﬂammation is reduced. Epithelialization is more rapid. Angiogenesis is reduced. Collagen deposition is rapid, not excessive and organized. More type 3 rather than type 1 collagen is laid down. The wound contains a greater proportion of water and hyaluronic acid. The lack of TGF-β in fetal wounds may be responsible for some of these differences. Skin grafts Skin grafts are either full or split thickness. Split-skin grafts contain a variable amount of dermis and are usually harvested from the thigh or buttock. Full-thickness skin grafts contain the entire dermis and are usually harvested from areas with sufﬁcient tissue laxity to permit direct closure of the donor defect. WOUND HEALING AND SKIN GRAFTS 27 1 Primary contraction is the immediate recoil observed in freshly harvested skin. Secondary contraction occurs after the graft is applied to its bed. The thinner the graft, the greater the degree of secondary contraction. Mechanisms Skin grafts heal in four phases. Adherence Fibrin bonds form immediately on applying a skin graft to a suitable recipient bed. Serum imbibition Skin grafts swell in the ﬁrst 2–4 days after application. This increase in volume results from absorption of ﬂuid (serum imbibition). The nutritive value of serum imbibition in maintaining graft viability is debated. Revascularization Vessel ingrowth into skin grafts begins on about the 4th day. The mechanism of revascularization is uncertain and may be via: Inosculationadirect anastomosis between the vessels within the graft and those in the recipient tissue. Revascularizationanew vessel ingrowth from the recipient tissue along the vascular channels of the graft. Neovascularizationanew vessel ingrowth from the recipient tissue along new channels in the graft. Remodelling This is the process whereby the histological architecture of the graft returns to that of normal skin. Reasons for graft failure Skin grafts fail for the following reasons. Haematoma This is the most common cause of graft failure. The risk of haematoma formation is minimized by: Meticulous haemostasis The use of a meshed skin graft which allows blood to escape The application of a pressure dressing. Infection Generally, skin grafts will not take if the bacterial count of the donor site exceeds 105 organisms per gram. Some organisms such as the beta haemolytic streptococcus can destroy grafts when present in much fewer numbers. 1 28 GENERAL PRINCIPLES Seroma Any collection of ﬂuid under the graft reduces the likelihood of its taking successfully. Shear This is a lateral force placed on a graft. It results in the disruption of the delicate connections between the graft and its bed and consequently reduces the likelihood of successful graft take. Inappropriate bed Skin grafts will not survive on cartilage, tendon and endochondral bone denuded of periosteum. Membranous bone, found in some areas of the skull, will accept a skin graft. Grafts on previously irradiated tissue are prone to failure. Technical error An assortment of technical errors can result in graft failure. Examples include placing the graft upside down or allowing it to dry out before application. Bone healing and bone grafts All bones are derived from mesenchyme. All are composed of an organic matrix (osteoid) which is mineralized by the calcium salt hydroxyapatite. Bones are formed by one of two different mechanisms: (i) intramembranous ossiﬁcation; or (ii) endochondral ossiﬁcation. Intramembranous ossiﬁcation Bones formed by intramembranous ossiﬁcation include the ﬂat bones of the face, calvarium and ribs. Intramembranous ossiﬁcation occurs by direct deposition of bone within a vascularized membranous template. Endochondral ossiﬁcation Endochondral bones develop from a cartilage precursor. Bones formed by endochondral ossiﬁcation include all the long bones and the iliac crest. Bone structure All bones have an outer cortical layer and an inner cancellous layer. The cancellous portion of membranous bone is found within the diploic space. Cancellous bone consists of loosely woven trabeculae made up of organic and inorganic bone. BONE HEALING AND BONE GRAFTS 29 1 Cortical bone consists of: Multiple bone units (osteons), which are composed of a central longitudinal canal (haversian canal) that contains a central blood vessel. The osteons are interconnected by transverse nutrient canals (Volkmann canals). Bone is laid down in concentric layers around each haversian canal. Osteocytes are scattered throughout the osteons. Blood supply to bone Blood reaches bone by one of the following routes: 1 Periosteal vessels at the sites of muscle attachments 2 Apophyseal vessels at the sites of tendon and ligament attachment 3 Nutrient arteries supplying the medullary cavity 4 Epiphyseal vessels supplying the growth plates. Bone healing The phases of bone healing are similar to those of wound healing. 1 Haematoma formation 2 Inﬂammation 3 Cellular proliferation Periosteal proliferation occurs on the outer aspect of the cortex. Endosteal proliferation occurs on the inner aspect of the cortex. 4 Callus formation Callus consists of immature woven bone composed of osteoid laid down by osteoblasts. This osteoid is mineralized with hydroxyapatite. 5 Remodelling The cortical structure and medullary cavity are restored. Primary healing This occurs if bone is rigidly ﬁxed with direct apposition of the bone ends. Primary bone healing is characterized by restoration of the normal bone structure. The inﬂammatory and proliferative phases of bone healing do not occur. Callus is not formed. Secondary healing This occurs if the fragments are not rigidly ﬁxed, or if a gap exists between the bone ends. Complications of fractures These include: Delayed union Non-union Mal-union Infection 1 30 GENERAL PRINCIPLES Avascular necrosis (AVN) Shortening Damage to adjacent structures. Bone graft healing Bone grafts heal by the following mechanisms. Incorporation This is adherence of the graft to the host tissue. Incorporation is maximized in immobilized, well-vascularized tissue. Osseoconduction The bone graft acts as a scaffold along which vessels and osteoprogenitor cells travel. Old bone is absorbed as new is deposited. This process is also known as creeping substitution. Osseoinduction This is the differentiation of mesenchymal cells within the local tissue into osteocytes. Osteoclasts, osteoblasts and osteocytes within the bone graft are not capable of mitosis. The increased numbers of these cells within the bone graft are derived from the mesenchymal tissue of the recipient site. Osseoinduction is controlled by bone morphogenic proteins (BMPs). Osteogenesis This is the formation of new bone by surviving cells within the bone graft. It is the predominant mechanism by which new bone is formed in vascularized bone grafts. Osteogenesis does not occur to a signiﬁcant degree in non-vascularized bone grafts. Survival of bone grafts Factors inﬂuencing the survival of bone grafts can be divided into three groups: (i) systemic factors; (ii) intrinsic graft factors; and (iii) factors relating to the place- ment of the graft. Systemic factors These are similar to those affecting wound healing and include: Age Nutrition Immunosuppression Drugs Diabetes Obesity. NERVE HEALING AND NERVE GRAFTS 31 1 Intrinsic graft factors Bone grafts with intact periosteum undergo less absorption than those stripped of this covering. Membranous bone undergoes less absorption than endochondral bone when used as an onlay graft in the facial skeleton. Graft placement factors Orthotopic or heterotopic placement Orthotopicagraft is placed into a position normally occupied by bone. Heterotopicagraft is placed into a position not normally occupied by bone. Grafts placed into an orthotopic position are less prone to absorption. Quality of the recipient bed Radiotherapy, scarring and infection adversely affect graft survival. Graft ﬁxation Rigidly ﬁxed grafts survive better than those that are mobile. Site of graft placement Grafts survive better in areas in which bone is normally laid down (depository sites). These sites include areas such as the zygoma and mandible in the child. Nerve healing and nerve grafts Nerve anatomy and function Nerve cells (neurons) consist of a cell body from which nerve ﬁbres project. Efferent nerve ﬁbres are called axons. Afferent nerve ﬁbres are called dendrites. The endoneurium surrounds individual nerve ﬁbres or axons. The perineurium surrounds groups of nerve ﬁbres (fascicles). The epineurium surrounds a group of fascicles to form a peripheral somatic nerve. Schwann cells produce a multilaminated myelin sheath in myelinated nerves. Unmyelinated nerves are surrounded by a double layer of basement membrane. In myelinated nerves, adjacent Schwann cells abut at the nodes of Ranvier. Nerve conduction involves the passage of an action potential along a nerve. In myelinated nerves, this is via saltatory conduction between adjacent nodes of Ranvier. Nerve ﬁbres are subdivided into the following groups. Group A Group A-alpha ﬁbres conduct motor and proprioceptive impulses. Group A-beta ﬁbres transmit pressure and proprioceptive impulses. Group A-gamma ﬁbres conduct motor impulses to the muscle spindles. Group A-delta ﬁbres transmit touch, pain and temperature impulses. 1 32 GENERAL PRINCIPLES Group B These ﬁbres are found in myelinated, preganglionic autonomic nerves. Group C These ﬁbres are found in myelinated, postganglionic autonomic nerves. Medical Research Council grading of nerve function The MRC have recommended the following grading of nerve function. Motor function Sensory function M0 No contraction S0 No sensation M1 Flicker S1 Pain sensation M2 Movement with gravity eliminated S2 Pain and some touch sensation, possible hypersensitivity M3 Movement against gravity S3 Pain and touch with over-reaction M4 Movement against gravity and resistance S3+ Some 2-point discrimination M5 Normal S4 Normal Injury After transection of a nerve, traumatic degeneration occurs proximally as far as the last node of Ranvier. Distally, nerves undergo wallerian degeneration. This process was described by Waller in 1850 and consists of: Degeneration of axons and myelin which are then phagocytosed by macro- phages and Schwann cells. Collapsed columns of nerve cells develop a bandlike appearance on electron microscopy; these are known as the bands of Buengner. Neurotropism is selective, directional growth of nerve ﬁbres towards their appropriate receptors. It is mediated by nerve growth factors and consists of the following stages. 1 The proximal nerve stump sprouts many new ﬁbres. 2 Fibres growing in an inappropriate direction atrophy. 3 Those growing in the correct direction survive and grow. Neurotropism is non-selective, non-directional growth of nerve ﬁbres. Factors which mediate neurotropism include growth factors, extracellular matrix components and hormones. Classiﬁcation of nerve injury The degree of nerve injury has been classiﬁed by both Seddon and Sunderland. Seddon classiﬁed nerve damage into three groups: 1 Neurapraxia 2 Axonotmesis 3 Neurotmesis. Sunderland expanded this classiﬁcation to ﬁve groups. NERVE HEALING AND NERVE GRAFTS 33 1 First-degree injury The axon remains in continuity although conduction is impaired. Recovery should be complete. Second-degree injury Axonal injury occurs and the segment of nerve distal to the site of damage undergoes wallerian degeneration. All connective tissue layers remain intact and recovery should be good. Third-degree injury The axon and endoneurium are divided. The perineurium and epineurium remain intact. Recovery should be reasonable. Fourth-degree injury Complete division of all intraneural structures occurs. The epineurium remains intact. Recovery of some function is expected. This injury may result in neuroma-in-continuity. Fifth-degree injury The nerve trunk is completely divided. A sixth-degree injury is added by some to the classiﬁcation, although it was not described by Sunderland. This stage consists of a mixed pattern of nerve injury with segmental damage. Seddon’s classiﬁcation of neurapraxia equates to a Sunderland ﬁrst-degree injury. Axonotmesis equates to a second-, third- or fourth-degree injury. Neurotmesis equates to a ﬁfth-degree injury. Nerve repair Nerve repair should be performed by direct approximation of the divided stumps whenever possible. The ends of the nerve should be trimmed and an epineural repair performed with ﬁne sutures, under magniﬁcation. Attempts should be made to correctly align the fascicles of the nerve trunks. The repair should not be under undue tension. Some authorities maintain that primary repair should only be performed in cases in which a single 8/0 suture is strong enough to oppose the divided nerve ends. Fascicular identiﬁcation The following methods can be used to aid fascicular matching during nerve repair. Matching of anatomical structures during repair Anatomical guides to the correct orientation of the nerve stumps include: The size and orientation of the fascicles The distribution of the vessels on the surface of the nerve. 1 34 GENERAL PRINCIPLES Electrical stimulation Motor nerves respond to electrical stimulation for approximately 72 h following division. Electrical stimulation of the distal nerve stump during this period can be used to differentiate motor from sensory ﬁbres. Awake stimulation of the nerves can be used to differentiate motor from sensory ﬁbres in the proximal nerve stump. Electrical stimulation of sensory ﬁbres produces sharp pain. Similar stimulation of motor ﬁbres is felt as a dull ache. Knowledge of internal nerve topography The fascicular layout of many nerves is known and can be used to aid accurate repair. Ulnar-nerve motor fascicles lie centrally between the volar sensory branches coming from the palm and the dorsal sensory branches coming from the dorsum of the hand. Nerve grafts Nerve grafts are required if primary nerve repair is not possible without undue tension. If the divided nerve is large, multiple cables of a smaller donor nerve may be required to bridge the defect. It may be possible to reduce the tension across the repair by mobilizing the nerve stumps proximally or distally. Methods by which extra nerve length can be obtained by proximal dissection include: Transposition of the ulnar nerve at the elbow. Intratemporal dissection of the facial nerve. Materials used to bridge nerve gaps are either autologous or synthetic. Of these, autologous nerve is the best material for bridging nerve gaps at present. Composition Autologous tissues that can be used as nerve grafts include: Fresh nerve Freeze–thawed muscle Segments of vein. Synthetic nerve grafts composed of ﬁbronectin mats impregnated with growth factors may be available in the future. Autologous grafts The following nerves can be used as autologous grafts. Sural nerve This nerve passes behind the lateral malleolus. Proximally it divides into the medial sural nerve and the peroneal communicat- ing branch. TENDON HEALING 35 1 Graft lengths of up to 30–40 cm are available in the adult. Endoscopic harvesting has been reported; this produces less scarring. Lateral antebrachial cutaneous nerve This nerve lies adjacent to the cephalic vein alongside the ulnar border of the brachioradialis. Graft lengths of up to 8 cm in length are available. Removal of this nerve results in only a limited loss of sensation due to cutaneous sensory overlap. Medial antebrachial cutaneous nerve This is located in the groove between triceps and biceps, alongside the basilic vein. Distally, it divides into anterior and posterior branches. Graft lengths of up to 20 cm are available. The terminal branch of the posterior interosseous nerve This nerve is useful for bridging small defects in small diameter nerves. It is located in the radial side of the base of the fourth extensor compartment at the wrist. Only a relatively short length of nerve graft is available. Principles The following principles are universal to all nerve grafts. Both nerve ends should be trimmed back to healthy tissue. The graft should be placed in a healthy vascular bed. Tension on the graft should be avoided. The level of repair should be staggered between the separate cables. Wherever possible, the cables should be separated from one another as they bridge the defect. Tendon healing Anatomy Tendons are composed of dense, metabolically-active connective tissue. Within their substance, collagen bundles are arranged in a regular spiraling fashion. The collagen is predominantly type 3 with a small amount of type 1. Tendons contain few cells; those that are present include: Tenocytes Synovial cells Fibroblasts. Endotendon surrounds tendons whilst they lie within synovial sheaths. Paratendon is a loose adventitial layer that surrounds tendons outside synovial sheaths. 1 36 GENERAL PRINCIPLES Verdan described ﬁve zones of ﬂexor tendon injury. Zone 1: distal to the insertion of ﬂexor digitorum superﬁcialis (FDS). Zone 2: between the proximal end of the ﬂexor sheath and the insertion of FDS. Zone 3: between the distal edge of the ﬂexor retinaculum and the proximal end of the ﬂexor sheath. Zone 4: under the ﬂexor retinaculum. Zone 5: proximal to the ﬂexor retinaculum. Zone 2 was described as ‘no man’s land’ by Bunnell because of the poor results of ﬂexor tendon repair at this site. Tendon repair in this area is complicated by the fact that the superﬁcial and deep ﬂexors are in close approximation within a tight sheath. Extensor tendons are subdivided into eight zones. Zone 1: over the distal interphalangeal joint (DIPJ). Zone 2: between the proximal interphalangeal joint (PIPJ) and the DIPJ. Zone 3: over the PIPJ. Zone 4: between the metacarpophalangeal joint (MCPJ) and the PIPJ. Zone 5: over the MCPJ. Zone 6: between the MCPJ and the extensor retinaculum. Zone 7: under the extensor retinaculum. Zone 8: between the extensor retinaculum and the musculotendinous junction. The odd-numbered zones are located over the joints. The ﬁrst ﬁve zones are in the ﬁnger. Mechanisms of tendon healing Extrinsic healing Extrinsinc healing is dependent on ﬁbrous attachments forming between the tendon sheath and the underlying tendon. Historically this was believed to be the sole mechanism by which tendons healed. This led to the development of post-operative protocols which immobilized the tendons in the mistaken belief that this maximized tendon repair. Intrinsic healing Intrinsic tendon healing is dependent on: Bloodﬂow though the long and short vinculae. Diffusion from the synovial ﬂuid. Lunborg showed that tendons heal when wrapped in a semipermeable mem- brane and placed in the knee joint of a rabbit. Enclosing the tendons in semipermeable membrane stimulates intrinsic healing as it permits the passage of nutrients but not cells. Awareness of the ability of tendons to heal by intrinsic mechanisms has led to the development of post-operative protocols which include early mobilization. Phases of tendon healing These are similar to those of wound healing. TENDON HEALING 37 1 Inﬂammation This occurs in the ﬁrst 2–3 days following tendon injury. Inﬂammatory cells inﬁltrate the wound. These cells secrete growth factors which attract ﬁbroblasts. Proliferation This starts 2–3 days after tendon injury and lasts approximately 3 weeks. Fibroblasts are responsible for tissue proliferation. They manufacture and secrete collagen and GAGs. Collagen is initially arranged randomly, consequently the tendon lacks tensile strength. Remodelling This begins approximately 3 weeks following tendon injury. It is characterized by collagen homeostasis (the net amount of collagen in the wound remains stable). The structure of the tendon differentiates into an organized structure. Early motion of the tendon limits the formation of ﬁbrous attachments between itself and the tendon sheath. Early motion promotes intrinsic healing at the expense of extrinsic healing. Mobilized tendons are stronger than immobilized tendons. Techniques of repair Many methods of tendon repair have been described. The following principles apply to most techniques. The number and size of the incisions in the ﬂexor sheath should be minimized. The A2 and A4 pulleys should be preserved wherever possible. Any incision in the sheath should be made between the annular pulleys. The tendon ends should be touched as little as possible to protect their delicate covering and reduce the risk of adhesion formation. The epitendinous suture in the posterior wall is usually performed ﬁrst to correctly align the tendon. This suture should be inverting and is generally continuous. Many designs of core suture have been described, amongst the more commonly used are the: Bunnell stitch Kessler stitch Modiﬁed Kessler stitch. These suture patterns are usually self locking. Two or four strands of core suture are usually used to bridge the gap between the tendons. The tendon sheath should be reconstructed when possible but may be left unre- paired in part, if it involves compromising tendon glide. In tendon grafts and transfers, the extra length of available tendon allows the ends to be woven into each other, rather than be repaired end-to-end. 1 38 GENERAL PRINCIPLES Tendon weaves are more secure than end-to-end repairs. The technique most commonly used was described by Pulvertaft and is known as the Pulvertaft weave. In this technique the tendons are woven together by passing their ends through three or four longitudinal slits in the body of the other tendon. Rehabilitation following repair of ﬂexor tendons Until relatively recently, tendons were immobilized post-operatively. There is now a trend towards earlier mobilization. The post-operative rehabilitation regimens may consist of the following. Immobilization Immobilization is used mainly in children and adults considered unsuitable for early mobilization. Early passive mobilization This involves regular passive motion of the joints. No active movement is permitted. Early active extension with passive ﬂexion This regimen was advocated by Kleinert et al. A dorsal splint protects against hyperextension. Finger ﬂexion is maintained by rubber-band traction. The rubber bands are attached to the ﬁngernail and the volar aspect of the splint. Active extension can occur against the elastic recoil of the bands. Passive ﬂexion occurs by the elastic recoil of the bands. Early active mobilization The ‘Belfast’ regimen is widely used. This involves the ﬁtting of a dorsal splint which leaves the ﬁngers free to ﬂex. The splint should hold the wrist between neutral and 30° of ﬂexion. It should limit MCP extension to 70° of ﬂexion. It should limit hyperextension of the interphalangeal joints (IPJs) beyond the neutral position. The ﬁngers are left free on their volar surfaces. Active mobilization is started in the early post-operative period. This consists of the following three elements. Passive ﬂexion This mobilizes the joints and prevents their contraction. Passive ﬂexion and hold This produces an isometric force on the proximal muscle bellies. This helps to maintain their function. T R A N S P L A N TAT I O N 39 1 Active ﬂexion This results in tendon glide within the ﬂexor sheath. It limits the formation of ﬁbrous attachments and increases the rate of intrinsic healing. The strength of the tendon repair is increased by early active ﬂexion. Transplantation Transplantation is the movement of tissue from one body location to another. Orthotopic transfers are transplants into an anatomically similar site. Heterotopic transfers are transplants into an anatomically different site. The following types of transplantation are available. Autografts This is transplantation of tissue from one location to another within the same individual. It includes all ﬂaps and grafts. Flaps carry with them some intrinsic blood supply; grafts do not. Isografts This is transplantation of tissue between genetically identical individuals. Allografts These are also called homografts. This is transplantation between different individuals of the same species. Xenografts These were previously called heterografts. This is transplantation between individuals of differing species. Transplant immunology History Gibson and Medawar did much of the pioneering work on transplant immuno- logy in the 1940s and 1950s. They described the second set phenomenon, which they deﬁned as ‘the acceler- ated rejection of allogenic tissue due to the presence of humoral antibodies from prior exposure to the same allogenic source’. The ﬁrst set reaction occurs when a skin allograft is applied to an individual for the ﬁrst time. The ﬁrst set reaction is characterized by the following stages. 1 During the ﬁrst 1–3 days, allografts behave in a similar fashion to autografts in that they develop dilated capillaries with no blood ﬂow. 2 Between 4 and 7 days, the grafts are inﬁltrated by leucocytes and thrombi, and punctate haemorrhages appear within their vessels. 1 40 GENERAL PRINCIPLES 3 Between 7 and 8 days, blood ﬂow ceases and the skin graft undergoes necrosis. The second set reaction occurs in patients who have been previously grafted with the same allograft material. The second set reaction is characterized by the following stages. 1 Immediate hyperacute rejection. 2 The graft never undergoes any revascularization and has been termed a ‘white graft’. Immunology Rejection occurs when the host immune system recognizes foreign antigens. Foreign antigens are from the major histocompatibility complex (MHC). In humans these are known as human leucocyte antigens (HLAs). HLAs are six closely linked genes on the short arm of chromosome 6 and are divided into two classes. Class 1: includes HLAs A, B and C which are found on all nucleated cells and platelets. Class 2: includes HLAs DR, DQ and DP which are found on monocytes, macrophages and both B and T lymphocytes. HLAs, A, B and DR are the most important mediators of tissue rejection. Antigen-presenting cells (APCs), such as macrophages, pick up HLAs from allograft tissue and present them to the host immune system. APCs can be of: Donor origin (known as direct presentation) Host origin (known as indirect presentation). The host immune system reacts by: Increasing production of IL-1 and IL-2. This causes a rapid clonal expansion in the numbers of T and B lymphocytes within lymphoid tissue. Graft destruction is produced in the following ways: 1 Direct destruction This is mediated by the cellular system. CD4 and CD8 cytotoxic T cells cause damage to the graft. 2 Indirect destruction This is mediated by the humoral system. Stimulated B lymphocytes produce an antibody that binds with the antigen and stimulates tissue destruction via the complement system. Xenografts In transplants between species, natural antibodies often exist without prior sensitization. If natural antibodies are present, hyperacute rejection results, occurs secondary to complement activation. Concordant transplantation occurs when natural antibodies between species are not present, e.g. primate to human. A L L O P L A S T I C I M P L A N TAT I O N 41 1 Discordant transplantation occurs when natural antibodies are present, e.g. pig to human. Immunosuppression Immunosuppressive techniques can be subdivided into non-speciﬁc and speciﬁc modalities. Non-speciﬁc techniques of immunosuppression include the following. Radiation Whole-body radiation removes mature lymphocytes. This technique is not used in humans. Localized lymphoid-tissue irradiation is more speciﬁcally targeted. Graft irradiation aims to try and reduce its antigenicity. Drugs Steroids have an anti-inﬂammatory and immunosuppressive action. Azathioprine downgrades the lymphocyte-activation cascade. Cyclosporin is a fungus derivative, isolated in 1976. Cyclosporin inhibits the production of IL-2. Biological agents Anti-lymphocyte serum is made by injecting another species with lymphoid tissue from the recipient. The anti-lymphocyte antigens produced are powerful suppressers of T-cell activity. One speciﬁc technique of immunosupression is the administration of monoclonal anti-T-lymphocyte antibodies. In the future, monoclonal antibodies may be avail- able to down-regulate speciﬁc parts of the immune response. Alloplastic implantation The ideal implant should be: 1 Non-allergenic, causing a minimal soft tissue reaction. 2 Strong and fatigue resistant. 3 Resistant to reabsorption, corrosion or deformation. 4 Non-supportive of growth of micro-organisms. 5 Radiolucent. 6 Cheap. 7 Readily available. Classiﬁcation Implants may be classiﬁed into: Liquids (silicone, collagen preparations, hyaluronic acid preparations) Solids (metals, polymers, ceramics). 1 42 GENERAL PRINCIPLES Liquids Silicone Silicon is an element. Silica is silicone oxide and is the main constituent of sand. Silicone consists of interlinked silicon and oxygen molecules with methyl, vinyl or phenol side groups. Short polymer chains produce a viscous liquid. Long polymer chains produce a ﬁrmer, cohesive gel. Cross-linking of the chains produces solid silicone. Silicon is biologically inert but elicits a mild foreign-body reaction with sub- sequent capsule formation. Synovitis can occur when silicone prostheses are used in joint arthroplasty. Bioplastique consists of textured silicone-rubber microparticles mixed with water in a hydrogel carrier. There has been much debate as to whether silicone implantation is associated with an increased risk of developing connective tissue diseases. Extensive reviews of the safety of silicone have been performed: In the USA by the Institute of Medicine (IOM) of the National Academy of Science In the United Kingdom by the Independent Review Group. Both of these reviews concluded that there was no evidence that silicone implants were responsible for any major diseases. The ﬁndings of these groups are discussed in more detail in ‘Plastic surgery of the breast and chest wall. Breast augmentation’, see pp. 177–8. Collagen preparations Zyderm 1 This is made from sterilized, ﬁbrillar bovine collagen. It is composed of 95% type 1 collagen and 5% type 3 collagen. The collagen concentration is 35 mg/mL. It is administered via injection and is used for treating ﬁne, superﬁcial wrinkles. Zyderm 2 This has a similar collagen composition to Zyderm 1. The collagen concentration is higher, at 65 mg/mL. It is used to treat coarser wrinkles. Absorption of the water carrier from both Zyderm 1 and Zyderm 2 reduces their injected volume by approximately 30%. Soft-tissue defects should therefore be overcorrected initially. Zyplast This is formed by cross-linking the collagen with glutaraldehyde. It is ﬁrmer than either Zyderm 1 or Zyderm 2. A L L O P L A S T I C I M P L A N TAT I O N 43 1 It is used to treat deep dermal defects and coarse rhytids. Little reabsorption occurs 50 overcorrection is not recommended. Hyaluronic acid preparations A number of preparations, such as Restylane and Perlane, composed of syntheti- cally manufactured hyaluronic acid are now available. Average absorption rates are 20%–50% of the original volume by 6 months. These preparations are typically injected superﬁcially, to treat wrinkles or increase lip deﬁnition. Solids Metals Stainless steel Stainless steel is an alloy of iron, chromium and nickel. It has a relatively high incidence of corrosion and implant failure. Galvanic currents set up between screws and the plates can result in corrosion. Vittalium Vittalium is an alloy of chromium, cobalt and molybdenum. It has a higher tensile strength than either stainless steel or titanium. Titanium Titanium is a pure material and not an alloy. It is more malleable and less prone to corrosion than either stainless steel or vittalium. In addition, it is less likely to produce an artefact on MRI or CT scanning. Gold Gold is resistant to corrosion but has a low tensile strength. It is used primarily as an upper-eyelid weight to facilitate eye closing in facial palsy. Polymers Polyurethane This polymer induces an intense foreign-body reaction followed by tissue adhesion. Breast implants covered with polyurethane foam have a low rate of capsular con- tracture. Breakdown products of polyurethane include toluene-diamine dimers. Concern over the risk of carcinogenesis from the build-up of these dimers has resulted in withdrawal of these breast implants. 1 44 GENERAL PRINCIPLES Fluorocarbons Bonding between ﬂuorine and carbon results in an extremely stable biomaterial. No human enzyme can break the bond between the two substances. Proplast 1 This is a black composite of Teﬂon and carbon. It is used for facial bony augmentation. Proplast 2 This is a white composite of Teﬂon and aluminium oxide. It is used for more superﬁcial augmentation. A high rate of complications (infection, extrusion, etc.) with proplast temporo- mandibular joint (TMJ) implants resulted in its withdrawal from the market in the USA. Goretex This is a sheet of expanded polytetraﬂuoroethylene (PTFE). It is soft and very strong. PTFE has been used as a vascular prosthesis since 1975. Goretex has been approved for facial implantation in the USA since 1994. Polyethylene This material has a simple carbon chain structure and, unlike the ﬂuorocarbons, does not contain ﬂuorine. It is available in three grades: 1 Low density 2 High density 3 Ultra-high molecular weight. Medpor is high-density, porous polyethylene. It is commonly used for augmenting the facial skeleton. It elicits very little foreign-body reaction. Some soft tissue ingrowth does occurathis acts to stabilize the implant. Medpor implants are available in a variety of preformed shapes. Ultra-high molecular weight polyethylene is used in the fabrication of load- bearing orthopaedic implants. Polypropylene Polypropylenes have a similar structure to polyethylenes. They differ by containing a methyl group instead of a hydrogen atom in each unit of the polymer chain. Marlex polypropylene mesh has high tensile strength and allows early tissue ingrowth. A L L O P L A S T I C I M P L A N TAT I O N 45 1 Methylmethacrylate This is a self-curing acrylic resin. It is used for: Securing artiﬁcial joint components Craniofacial bone augmentation Fabrication of gentamicin-impregnated b

Key Notes on Plastic Surgery PDF

Document Details

Tags

Related

Summary

Full Transcript

Upgrade to continue