Essential Revision Notes for Intercollegiate MRCS Book 1

Contents
Acknowledgements Preface Contributors Introduction CHAPTER 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. Basic surgical knowledge and skills Claire Ritchie Chalmers Infection and inflammation Catherine Sargent and Claire Ritchie Chalmers Neoplasia Amer Aldouri and Claire Ritchie Chalmers Haematology Sheila Fraser and Claire Ritchie Chalmers Trauma Claire Ritchie Chalmers Peri-operative care Sally Nicholson and Catherine Parchment Smith Critical care Sam Andrews and Claire Ritchie Chalmers Surgical outcomes, research, ethics and the law Shireen MacKenzie and Nerys Forester Vascular surgery Sam Andrews and Nerys Forester Paediatric surgery Susan Picton and David Crabbe Urology and transplantation Sunjay Jain and Kilian Mellon 1 89 193 265 329 437 577 753 801 897 973 1113 1119 1121 1124 vi vii viii x

Abbreviations Picture permissions Bibliography Index

Physiology of wound healing

Chapter 1 Basic Surgical Knowledge and Skills

Claire Ritchie Chalmers

1 1.1 1.2 1.3 1.4 1.5 2 2.1 2.2 2.3 2.4 2.5 2.6

Physiology of wound healing Skin anatomy and physiology Pathophysiology of wound healing Healing in specialised tissues Delayed wound healing Wound dehiscence and incisional hernias Creation and care of the surgical wound Classification of wounds Incisions and closures Needles and sutures Surgical drains Dressings Scars and contractures

3 3.1 3.2 3.3 3.4 3.5 4 4.1 4.2 4.3 4.4 4.5 4.6 4.7

Basic surgical techniques Anastomosis Biopsy Basic plastic surgery Abscess drainage Minimal access surgery Tumours and lesions of the skin and subcutaneous tissues Benign skin lesions Excision of benign skin lesions Curettage and cryosurgery Pre-malignant skin lesions Basal cell carcinoma Squamous cell carcinoma Malignant melanoma

Basic Surgical Knowledge and Skills

Physiology of wound healing

Section 1 Physiology of wound healing

1.1 SKIN ANATOMY AND PHYSIOLOGY
In a nutshell

A core knowledge of skin anatomy and physiology is essential to understand fully the processes involved in wound healing. The skin is an enormously complex organ acting both as a highly efficient mechanical barrier and also as a complex immunological membrane. It is constantly regenerating with a generous nervous, vascular and lymphatic supply, and has specialist structural and functional properties in different parts of the body.

All skin has the same basic structure, although it varies in thickness, colour and the presence of hairs and glands in different regions of the body. The external surface of the skin consists of a keratinised squamous epithelium called the epidermis. The epidermis is supported and nourished by a thick underlying layer of dense, fibroelastic connective tissue called the dermis which is highly vascular and contains many sensory receptors. The dermis is attached to underlying tissues by a layer of loose connective tissue called the hypodermis or subcutaneous layer which contains adipose tissue. Hair follicles, sweat glands, sebaceous glands and nails are epithelial structures called epidermal appendages that extend down into the dermis and hypodermis. The four main functions of the skin: Protection: against UV light, and mechanical, chemical and thermal insults; it also prevents excessive dehydration and acts as a physical barrier to micro-organisms Sensation: various receptors for touch, pressure, pain and temperature Thermoregulation: insulation, sweating and varying blood flow in dermis Metabolism: subcutaneous fat is a major store of energy, mainly triglycerides; vitamin D synthesis occurs in the epidermis

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Epidermis

Dermal papillae

Dermis

Sebaceous gland

Arrector pili

Merocrine sweat gland Hair follicle Hair bulb Hypodermis

Figure 1.1a

Skin anatomy

Skin has natural tension lines, and incisions placed along these lines tend to heal with a narrower and stronger scar, leading to a more favourable cosmetic result (see Fig. 1.1b). These natural tension lines lie at right angles to the direction of contraction of underlying muscle fibres, and parallel to the dermal collagen bundles. On the head and neck they are readily identifiable as the wrinkle lines, and can easily be exaggerated by smiling, frowning and the display of other emotions. On the limbs and trunk they tend to run circumferentially, and can easily be found by manipulating the skin to find the natural skin creases. Near flexures these lines are parallel to the skin crease.

Physiology of wound healing

Figure 1.1b Langers lines. The lines correspond to relaxed skin and indicate optimal orientation of skin incisions to avoid tension across the healing wound

1.2 PATHOPHYSIOLOGY OF WOUND HEALING

In a nutshell

Wound healing consists of three phases: Acute inflammatory phase (see Chapter 2 Infection and Inflammation) Proliferative phase (cell proliferation and deposition of extracellular matrix, ECM) Maturation phase (remodelling of the ECM) Different tissues may undergo specialised methods of repair (eg organ parenchyma, bone and nervous tissue).

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Tissue injury

Clot formation

Platelet activation

Complement activation

ACUTE INFLAMMATORY PHASE

Vasodilatation

Increased vascular permeability

Influx of inflammatory cells of fibroblasts

Release of cytokines and growth factors

PROLIFERATION PHASE

Extracellular matrix production

Fibroblasts

Endothelial cells

Keratinocytes

Collagen synthesis

Angiogenesis

Epithelialisation

Healed wound

MATURATION PHASE

Matrix remodelling

Figure 1.2a

Wound healing

Physiology of wound healing

All surgeons deal with wounds and it is essential to understand fully the exact pathophysiological mechanisms involved in wound healing, how this may be optimised, and how it may be compromised, leading to wound dehiscence, delayed healing and incisional hernia formation. The aims of wound healing are a rapid restoration of tissue continuity and a rapid return to normal function.

The inflammatory phase

Tissue damage starts a typical acute inflammatory reaction by damage to cells and blood vessels. The inflammatory phase of wound healing involves: Vasodilation and increased vascular permeability Influx of inflammatory cells (neutrophils) and fibroblasts Platelet activation and initiation of the coagulation and complement cascades, leading to clot formation and haemostasis

The acute inflammatory response is generic to all forms of injury and noxious insult. It is discussed in detail in Chapter 2 Infection and Inflammation.

The proliferative phase

The proliferative phase is characterised by migration and proliferation of a number of cell types: Epithelial cells: within hours of injury epithelial cells at the margins of the wound begin to proliferate and migrate across the defect; epithelial closure is usually complete by 48 hours Fibroblasts: fibroblasts migrate into the wound, proliferate and synthesise extracellular matrix (ECM) components including collagen and ground substance (45 days) Endothelial cells: the development of new blood vessels (angiogenesis) occurs simultaneously with activation of fibroblasts proliferation and migration of endothelial cells depend on the proteolytic activity of matrix metalloproteinases (for which zinc is an essential cofactor)

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Cell types involved in wound healing and time of appearance in wound Platelets Neutrophils Macrophages Fibroblasts Myofibroblasts Endothelial cells Immediate 01 day 12 days 24 days 24 days 35 days

Granulation tissue is a temporary structure which forms at this stage. It consists of a rich network of capillary vessels and a heterogeneous population of cells (fibroblasts, macrophages and endothelial cells) within the stroma of the ECM. It has a characteristic pinkish, granular appearance. Additionally the wound contracts due to the action of myofibroblasts.

PROLIFERATIVE PHASE

Epithelial cell migration

Fibroblast migration

Macrophage migration

Endothelial cell migration

Covers epithelial defect

Synthesis of components of the extracellular matrix (ECM) eg collagen

Angiogenesis and new vessel development

GRANULATION TISSUE

Figure 1.2b

The proliferative phase

The maturation phase Matrix remodelling

This stage lasts for many months after the wound is clinically healed The scar becomes less vascular hence the change in colour The scar tensile strength increases due to modifications made to collagen. The collagen molecule is a triple -helix. Multiple molecules orientate to form a fibril. The cross-linkage of collagen fibrils by formation of covalent bonds (aided by the action of vitamin C) increase the tensile strength of the scar 8

Physiology of wound healing

Regaining strength in the wound

During matrix remodelling the scar regains its strength. The tissue types and thickness involved in the scar will determine the length of time to regain strength. Bowel and muscle regains virtually full strength within 1 month and skin takes up to 6 months. Strength tends to increase very quickly over the first 710 days although full maturation of a scar can take up to 1218 months. Choice of wound closure materials should reflect this. Abdominal incisions through muscle layers will take many weeks to regain their strength, achieving sufficient strength at 34 months to no longer require suture support and about 80% of their former strength after many months. Closure is therefore performed either with loop nylon that will persist in the wound, or a strong, slowly absorbing suture material such as PDS that will support the wound. Superficial skin wounds require minimal support and so can be closed with a quickly absorbable suture material or by interrupted sutures or staples that can be removed within days.

1.3 HEALING IN SPECIALISED TISSUES Classification of wound healing

In a nutshell

Wound healing can be classified into: First (primary) intention Second (secondary) intention Third (tertiary) intention In addition different tissues have different healing properties. You should be aware of the healing properties of: Skin Bone Nerve Bowel Solid organs (liver, kidney, spleen, heart) Non-regenerative organs (eg eye)

First (primary) intention

This typically occurs in uncontaminated wounds with minimal tissue loss and when the wound edges can easily be approximated with sutures, staples or adhesive strips, without

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excessive tension. The wound usually heals by rapid epithelialisation and formation of minimal granulation tissue and subsequent scar tissue.

Second (secondary) intention

Usually secondary intention occurs in wounds with substantial tissue loss, when the edges cannot be apposed without excessive tension. The wound is left open and allowed to heal from the deep aspects of the wound by a combination of granulation, epithelialisation and contraction. This inevitably takes longer, and is accompanied by a much more intense inflammatory response. Scar quality and cosmetic result are poor. Wounds which may be left to heal by secondary intention: Extensive loss of epithelium Extensive contamination Extensive tissue damage Extensive oedema leading to inability to close Wound reopened (eg infection, failure of knot)

Third (tertiary) intention

The wound is closed several days after its formation. This may well follow a period of healing by secondary intention, for example when infection is under control or tissue oedema is reduced.

Healing in different tissues

Different tissues heal in a remarkably similar way, albeit at different rates the scalp and face heal very quickly, at least in part because of increased vascularity. Healing rates are quickest early in life, and decline with advancing years. Surgery performed on the fetus in utero leaves no scarring at all as it occurs by regeneration. Some tissues possess the ability to regenerate their specialised cells following injury, with the result that significant tissue loss can be replaced by regenerated specialised cells, with no or minimal loss of function (eg bone, intestine). Conversely, some tissues have little regenerative ability (eg cardiac tissue) and wounds heal by simple scar formation significant tissue loss will result in significant loss of function. Nervous tissue possesses very limited regenerative capacity and partial function may be regained through slow neuronal growth in peripheral nerve injuries.

Skin
Skin consists of two layers the keratinised stratified epidermis and the connective tissue of the dermis. Following injury to the skin, healing essentially follows the pattern outlined above. Blood lost into the wound clots into a fibrin meshwork (the scab). Inflammatory cells, fibroblasts and capillaries invade the clot to form a contractile granulation tissue that draws the wound margins together. Neutrophils release cytokines and growth factors that activate fibroblasts and keratinocytes, which alter their anchorage to the surrounding cells, ECM and 10

Physiology of wound healing

basal lamina. Protease secretion by the keratinocytes allows them to migrate through the fibrin mesh of the clot and the cut epidermal edges to move forward to cover the denuded wound surface. A new stratified epidermis with underlying basal lamina is then re-established. Epidermal appendages (eg sweat glands and hair follicles) do not regenerate.

Bone and callus

Bone is unique in its ability to repair itself as it re-activates processes that normally occur during embryogenesis.

Primary bone healing

This occurs when the fracture gap is small (12 mm) and when there is absolute stability between the fracture fragments. Bone remodelling units cross the small gap and Haversian remodelling occurs (without callus formation); this type of bone healing is seen when there has been an anatomical reduction and stable internal fixation of the fracture (an intact blood supply is required).

Secondary bone healing

Haematoma formation Formed by rupture of blood vessels within medullary cavity Haematoma fills the fracture gap and spills out into the surrounding tissue Haematoma provides a fibrin mesh that seals off the fracture site and provides a framework for the influx of inflammatory cells, fibroblasts, and capillary vessels Inflammatory phase Necrotic material at the fracture site releases inflammatory mediators, promoting chemotaxis of neutrophils Inflammatory cells release cytokines (eg TGF- and fibroblast growth factor which activate osteoprogenitor cells) Repair phase By the end of the 1st week the organised haematoma is being replaced by soft callus (it provides some anchorage but no structural rigidity) Soft callus gradually changes from fibrinous matrix, through a cartilaginous phase, to bony callus (resembles embryonic endochondral ossification and is similar to process occurring at the physis) Around the periphery, under the periosteum, osteoblasts deposit a layer of woven bone the hard callus (process resembles embryonic intra-membranous ossification) So the fracture ends are bridged by a bony callus that gains strength as it mineralises (giving the fracture increasing stability, and allowing early weight-bearing)

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Basic Surgical Knowledge and Skills

Remodelling phase Remodelling occurs over the months and years following a fracture Callus and new bone (formed initially) is bulky and relatively disordered; it is replaced with lamellar bone through Haversian remodelling Internal architecture of any bone alters in response to loads placed on it (the same holds true at the fracture site); this phenomenon is known as Wolffs law

Times for healing of nerves, tendons and bone (general guide)

Tendon repair 35 weeks to protected mobilisation 612 weeks to full mobilisation > 12 weeks to full strength Nerve repair 46 weeks of cast immobilisation of neighbouring joints > 6 weeks to free mobilisation Fracture of upper limb 34 weeks in a cast (mobilise rest of limb) Fracture of lower limb 68 weeks in a cast Protected weight-bearing from 34 weeks if the cast is a stable fracture May take 1216 weeks for full unprotected weight-bearing

Factors that impede fracture healing

Infection Diabetes mellitus Vascular insufficiency Calcium, phosphate, or vitamin D deficiency Displaced and comminuted fractures: Large areas of periosteal stripping result in large volume of devitalised bone Devitalised bone is gradually revascularised or resorbed Increased volume of callus is produced and increases the process of remodelling Inadequate immobilisation Normal constituents of callus dont form if there is constant significant movement of the fracture site Callus mainly consists of fibrous tissue and cartilage, perpetuating instability, resulting in delayed union and non-union Drugs: steroids and possibly NSAIDs delay fracture healing

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Physiology of wound healing

Nerve injury and repair

In a nutshell

In order of increasing degree of injury: Neuropraxia (I): no axonal disruption Axonotmesis (II): axonal disruption/supportive tissue framework preserved Neurotmesis (IIIV): supportive tissue framework disrupted Principles of surgical repair of nerves: Accurate apposition of nerve ends Healthy surrounding tissue No tension Minimal dissection

There are many variations of nerve injury. A common classification was described by Seddon, dividing injuries into three groups: neuropraxia, axonotmesis, and neurotmesis. Sunderlands classification expands the category of neurotmesis and refers to categories of increasing severity.

Neuropraxia (I)
This is the mildest form of nerve injury, referring to a crush, contusion or stretching injury of the nerve without disruption of its axonal continuity. There is a reduction or block in conduction of the impulse down a segment of the nerve fibre. This may be caused by local biochemical abnormalities. There is a temporary loss of function which is reversible within hours to months of the injury (average 68 weeks). Motor function often suffers greater impairment than sensory function, and autonomic function is often retained.

Axonotmesis (II)
This is the loss of the relative continuity of the axon and its covering of myelin with preservation of the connective tissue framework of the nerve (epineurium and perineurium). It is a more serious injury than neuropraxia. Wallerian degeneration occurs and there is a degree of retrograde proximal degeneration of the remaining axon. Recovery occurs through regeneration of the axons (which grow along the existing preserved framework of the nerve). Regeneration requires time and may take weeks or months, depending on the size of the lesion. The proximal end of the lesion grows distally (23 mm per day) and the distal end of the lesion grows proximally (1 mm per day).

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Neurotmesis (III, IV and V)

This is the loss of continuity of both axons and nerve structural connective tissue. It ranges in severity, with the most extreme degree of neurotmesis being transection. Most neurotmetic injuries do not produce gross loss of continuity of the nerve but rather internal disruption of the architecture of the nerve sufficient to involve perineurium and endoneurium as well as the axons and their myelin sheath. There is a complete loss of motor, sensory and autonomic function. If the nerve has been completely divided, axonal regeneration causes a neuroma to form in the proximal stump. In grade III injuries, axonal continuity is disrupted by loss of endoneurial tubes (the neurolemmal sheaths) but the perineurium is preserved. This causes intra-neural scarring and regenerating axons may re-enter the sheaths incorrectly. In grade IV injuries, nerve fasciculi (axon, endoneurium, perineurium) are damaged, but nerve sheath continuity is preserved. In grade V injuries, the endoneurium, perineurium, and epineurium, which make up the entire nerve trunk, are completely transected. This may be associated with perineural haematoma or displacement of the nerve ends.

Bowel
The layers of the bowel involved in the anastomosis heal at different rates. Optimal healing requires good surgical technique and apposition of the layers. The intestinal mucosa is a sheet of epithelial cells that undergoes rapid turnover and proliferation. It may sustain injury as a result of trauma (from luminal contents or surgery), chemicals (eg bile), ischaemia or infection. Injury to the mucosa resulting in breaches of the epithelial layer is though to render patients susceptible to bacterial translocation and systemic sepsis syndromes. Minor disruption to the mucosa is thought to be repaired by a process separate to proliferation called restitution, instigated by cytokines and growth factors and regulated by the interaction of cellular integrins with the ECM. After uncomplicated surgery to the GI tract, mucosal integrity is thought to have occurred by 24 hours. The other muscular layers of the bowel undergo the general phases of inflammation, proliferation and maturation as outlined above. Anastomotic healing results in the formation of collagenous scar tissue. Scarring may eventually contract resulting in stenosis.

Solid organs
Solid organs either heal by regeneration (through a process of cell proliferation) or by hypertrophy of existing cells. Some organs heal by a combination of the two processes. In organs in which the cells are terminally differentiated, healing occurs by scarring or fibrosis.

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Physiology of wound healing

Liver
The liver has remarkable regenerative capacity. The stimulation for regeneration is reduction in the liver mass to body mass ratio (eg surgical resection) or the loss of liver functional capacity (eg hepatocyte necrosis by toxins or viruses). Regeneration is achieved by proliferation of all the components of the mature organ hepatocytes, biliary epithelial cells, fenestrated epithelial cells and Kupffer cells. Hepatocytes, which are normally quiescent and rarely divide, start to proliferate to restore hepatic mass and function. This occurs initially in the areas surrounding the portal triads and then extends to the pericentral areas after 48 hours. After 70% hepatectomy in animal models, the remaining hepatocytes divide once or twice and then return to quiescence. About 24 hours after the hepatocytes start to proliferate, so do all the other cell types and ECM is produced, including the structural protein, laminin. Eventually the cell types re-structure into functional lobules over 710 days. The stimulus for hepatocyte proliferation is thought to be TNF and the IL-6 family of cytokines. Subsequently HGF and TGF- are responsible for continued cell growth. Regeneration is terminated after about 72 hours by the action of cytokines such as TGF-1.

Kidney
The cells of the kidney are highly specialised, reflecting their terminal state of differentiation. Healing in the kidney predominantly occurs by scarring and fibrosis.

Spleen
Splenic regeneration is controversial. Increases in size and weight of the residual splenic tissue have been recognised after partial splenectomy (eg for trauma) and, hypertrophy of missed splenunculi after splenectomy for haematological and glycogen storage diseases (eg Gauchers) may also occur. However, there is little evidence that this increase in size of the residual splenic tissue results in functional regeneration and the increase in size may be due to infiltration of the tissue with cells characteristic of the underlying haematological or other disorder.

Heart and lung

Cardiac tissue is commonly damaged by ischaemia and occasionally by trauma. The inflammatory response is particularly important in the healing of cardiac tissue and is instigated by release of cytokines such as tumour necrosis factor-alpha (TNF- or interleukin-6 (IL-6) from the damaged myocardium. These cytokines have been implicated in the regulation of myocyte survival or apoptosis, myocyte hypertrophy, defects in myocyte contractility, proliferation of myofibroblasts and angiogenesis/vasculogenesis and, to a limited extent, progenitor cell proliferation. The cytokine response lasts about a week and the infarcted myocardium is gradually replaced by scar tissue. Within this scar tissue there is a degree of regeneration of myocytes and blood vessels and current research is focused on facilitating this process for an improvement in myocardial function post infarct.

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Non-regenerative tissues
Non-regenerative tissues, such as the cornea of the eye, heal by collagen deposition and scarring. This is obviously accompanied by complete loss of function.

1.4 DELAYED WOUND HEALING

In a nutshell

Wound healing is affected by: Local factors (factors specific to the wound) Wound classification Surgical skill General factors (factors specific to the patient) Concomitant disease Nutrition

Factors affecting wound healing Local risk factors

Wound infection Haematoma Excessive mobility Foreign body Dead tissue Dirty wound Surgical technique Ischaemia Acute; damage to blood supply; sutures too tight Chronic; previous irradiation Diabetes Atherosclerosis Venous disease

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Physiology of wound healing

General risk factors

Elderly Cardiac disease Respiratory disease Anaemia Obesity Renal (uraemia) or hepatic failure (jaundice) Diabetes mellitus Malnutrition (vitamins and minerals) Malignancy Irradiation Steroid or cytotoxic drugs Other immunosuppressive disease or drugs

Nutritional factors
Proteins are essential for ECM formation and effective immune response Vitamin A is required for epithelial cell proliferation and differentiation Vitamin B6 is required for collagen cross-linking Vitamin C is necessary for hydroxylation of proline and lysine residues. Without hydroxyproline, newly synthesised collagen is not transported out of fibroblasts; in the absence of hydroxylysine, collagen fibrils are not cross-linked Zinc is an essential trace element required for RNA and DNA synthesis and for the function of some 200 metalloenzymes Copper plays a role in the cross-linking of collagen and elastin

Optimising wound healing

Wound failure may be minimised by attention to the risk factors listed above. Ensure good delivery of blood and oxygen to the wound (and be aware of the importance of good hydration and respiratory function). Debride devitalised tissues and handle other tissues with care to prevent tissue necrosis. Sutures that are tied very tightly will cause tissue hypoxia. Avoid tension on the wound. Careful aseptic technique should be used. Heavily contaminated wounds or the abdominal cavity should be washed with copious amounts of warmed saline until clean. Patient nutrition is also very important and critically ill patients may require support either via NG feeding or parenteral nutrition. On occasions the patient may be in such a poor condition (eg be elderly, have septic shock, be on steroids) and the circumstances of the operation so hostile (emergency, faecal contamination, disseminated malignancy) that the chance of good wound healing is very low. Under these circumstances, there are various surgical options: Bring out a stoma rather than perform a primary bowel anastomosis Leave the skin and subcutaneous fat open in a heavily contaminated abdomen for delayed primary closure this wound can then be packed as required (be aware that changing dressings on large wounds may require return visits to theatre) 17

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Close the wound with additional deep tension sutures The abdominal wall itself may be left open (a laparostomy) or partially closed with an artificial mesh to reduce intra-abdominal pressure after surgery for intra-abdominal catastrophe and prevent abdominal compartment syndrome

1.5 WOUND DEHISCENCE AND INCISIONAL HERNIAS

In a nutshell

The same risk factors predispose to: Failure of wound healing Wound dehiscence Incisional herniation

Wound dehiscence is the partial or total disruption of any or all layers of the operative wound. Risk factors for wound dehiscence are the same as those for factors affecting wound healing Evisceration (burst abdomen) is rupture of all layers of the abdominal wall and extrusion of the abdominal viscera (usually preceded by the appearance of blood-stained fluid the pink-fluid sign) Wound dehiscence without evisceration should be repaired by immediate elective re-closure. Dehiscence of a laparotomy wound with evisceration is a surgical emergency with a mortality rate of > 25%. Management involves resuscitation, reassurance, analgesia, protection of the organs with moist sterile towels, and immediate reoperation and closure (usually with deep tension sutures) Incisional hernias are still common despite modern suture materials. They occur at sites of partial wound failure or dehiscence. Risk factors for incisional hernia are therefore the same as those for dehiscence. Symptoms include visible protrusion of the hernia during episodes of raised intra-abdominal pressure and discomfort. Incisional hernias usually correspond to a wide defect in the abdominal wall and so do not often incarcerate. Treatment depends on symptoms and size of defect (eg. conservative measures including a truss/corset and surgical repair). Further details on incisional hernias and methods of repair are covered in the Abdomen chapter of Book 2.

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Creation and care of the surgical wound

Section 2 Creation and care of the surgical wound

2.1 CLASSIFICATION OF WOUNDS
In a nutshell

Wounds can be classified in terms of: Depth: superficial vs deep Mechanism: incised, lacerated, abrasion, degloved, burn Contamination or cleanliness: clean, clean contaminated, contaminated, dirty

Depth of wound
Superficial wounds
Superficial wounds involve only the epidermis and dermis and heal without formation of granulation tissue and true scar formation. Epithelial cells (including those from any residual skin appendages such as sweat or sebaceous glands and hair follicles) proliferate and migrate across the remaining dermal collagen. Examples: Superficial burn Graze Split skin graft donor site

Deep wounds
Deep wounds involve layers deep to the dermis and heal with the migration of fibroblasts from perivascular tissue and formation of granulation tissue and subsequent true scar formation. If a deep wound is not closed with good tissue approximation, it heals by a combination of contraction and epithelialisation, which may lead to problematic contractures, especially if over a joint. 19