Surgical incisions and principles of wound healing
restore the original architecture. Secondary healing relies on ingrowth of granulation tissue from the wound margins and deep tissue, followed by accumulation of extra-cellular matrix (ECM) and laying down of collagen.
Delayed primary This is undertaken in the management of wounds that are too heavily contaminated for primary closure but appear clean and well-vascularized after 4e5 days’ observation. Local phagocyte recruitment into the wound by day 2e3 reduces the bacterial concentration within the wound to allow safe closure.
Abstract A wound is any break in the skin or an organ or part as the result of trauma or surgical incision. The process of wound healing can be defined as the physiological responses by which the body replaces and restores function to damaged tissues. In normal skin, the epidermis and dermis exists in a steady-state equilibrium, forming a protective barrier against the external environment. Once the protective barrier is broken, the normal physiological process of wound healing is immediately set in motion. This is a complex and dynamic process dependent on local and systemic factors affecting the patient’s health status. An understanding of normal wound healing physiology will provide the surgeon with a framework for performing any surgical procedure and achieving satisfactory wound healing. Understanding of the mechanism of wound healing has increased dramatically during last decade. Today wound-healing abnormalities are among the greatest causes of disability and deformity. This chapter reviews the principles and factors that effect wound healing and the common surgical incisions.
Partial thickness wounds These occur in superficial burns or abrasions where the wound has not penetrated the entire dermis and healing occurs mainly by epithelialization from remaining dermal elements leading to reduced contractility and scarring compared with secondary healing.
Healing of acute wound There are four main non-discrete phases involved in acute wound healing (Figure 1): haemostasis inflammation regeneration and proliferation remodelling, maturation and contracture. Haemostasis Haemostasis begins immediately following the tissue injury occurs. Damaged endothelium within the wound releases vonWillebrand factor (vWF) and tissue thromboplastin. vWF facilitates platelet adhesion to sub-endothelial collagen and discharges adenosine diphosphate (ADP) and thromboxane A2 leading to platelet aggregation. Alpha granules within the platelets release
Keywords Haemostasis; hypertrophic; inflammation; keloid; primary healing; secondary healing; wound healing; wound regeneration; wound remodelling
Types of wound closure Primary apposition/intention This occurs with approximation of wound margins using simple methods such as sutures, tapes, glue or mechanical methods within 12e24 hours of the incision being made. It occurs in clean, fresh wounds in well-vascularized areas. The wound may be treated with irrigation and debridement and the tissue margins are approximated precisely. These wounds are often the most cosmetically pleasing.
Summary of the phases of wound healing Wound healing
Haemostasis (4 to 6 hours) vWF, PDGF, TGF-β: platelet aggregation and fibrin production
Secondary healing/intention Commonly used in the management of infected or difficult to approximate wounds, this method of healing allows closure of an open wound via re-epithelialization and wound contraction by myofibroblasts. Regeneration of epithelial cells alone cannot
Early inflammatory phase (day 1–2) PMN migration, complement activation
Late inflammatory phase (day 2–3) Monocytes → macrophages: phagocytosis & growth factor production
Regeneration and proliferation (day 3–14) Matrix deposition, granulation tissue, angiogenesis, epithelialization
Zuhair Nawaz MBBS MRCS is a Registrar at the Royal National Orthopaedic Hospital, Stanmore, Middlesex, UK. Conflicts of interest: none declared.
Remodelling and scar maturation (day 7+) Metalloproteinases; wound strength 70–80% PDGF, platelet-derived growth factor; PMN, polymorphonuclear leukocyte; TGF, transforming growth factor; vWF, von-Willebrand factor.
George Bentley DSc ChM FRCS is Professor of Orthopaedic Surgery at the Royal National Orthopaedic Hospital, Stanmore, Middlesex, UK. Conflicts of interest: none declared.
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platelet-derived growth factor (PDGF), and transforming growth factor-beta (TGF-b). PDGF is chemotactic for fibroblasts, neutrophils and monocytes and, along with TGF-b, lead to prolific collagen construction. Tissue thromboplastin activates the coagulation pathways producing fibrin. Fibrin provides the structural support for the inflammation phase.
stimulates monocytes to release vascular endothelial growth factor which is mitogenic for endothelial cells leading to further angiogenesis. Re-epithelialization: the formation of granulation tissue in an open wound allows the re-epithelialization phase to take place, as epithelial cells migrate across the new tissue to form a barrier between the wound and the environment. Basal keratinocytes from the wound edges and dermal appendages such as hair follicles, sweat glands and sebaceous glands are the main cells responsible for the epithelialization phase of wound healing. Increase in mitotic activity of the basal epithelial cells modulated by several growth factors encourages migration over the matrix leading to re-establishment of stratified epithelium.
Inflammation Early phase (days 1e2): activation of the complement cascade e polymorphonuclear leukocytes (PMNs) infiltration which adhere to endothelial cells in adjacent blood vessels (margination) and begin to move through vessel walls (diapedesis). They are attracted to the site by fibronectin, growth factors, and kinins. Neutrophils phagocytize debris and bacteria and also kill bacteria by releasing free radicals. They cleanse the wound by secreting proteases that break down damaged tissue. The cut edges of dermis begin to exhibit increased mitotic activity and epithelial cells from the edges begin to migrate and proliferate, depositing a basement membrane.
Remodelling, maturation and contracture (>1 week) Constant synthesis and remodelling of ECM with concurrent granulation tissue formation can occur for years after initial injury. The maturation phase begins when equilibrium between collagen deposition and degradation occurs, usually around 3 weeks. Type III collagen, which is prevalent during proliferation, is gradually degraded and the stronger type I collagen is laid down in its place. Metalloproteinases, whose activity is reliant on zinc ions, has the potential to impair or improve wound healing in this stage. Contraction is a key phase of wound healing. If contraction continues for too long, it can lead to disfigurement and loss of function. Contraction commences approximately a week after wounding, when fibroblasts have differentiated into myofibroblasts. Contraction can last for several weeks and continues even after the wound is completely re-epithelialized. The scar usually achieves its maximum tensile strength by 12 weeks, with approximately 70e80% of its original strength.
Late phase (days 2e3): monocytes replace PMNs as the predominant cells in the wound by 2 days after injury. Monocytes are attracted to the wound by the release of complement, clotting components, immunoglobulin G and cytokines. The monocytes then undergo phenotypic change to macrophages, which are the key regulator cells in this phase. Macrophages have two key roles in the late phase: 1. Phagocytosis and proteolytic enzyme release which aid in the debridement of the wound. 2. Primary producers of growth factors (platelet-derived growth factor, TGF-b) stimulated by the low oxygen content of their surroundings. These factors are responsible for inducing and accelerating angiogenesis and stimulating cells to re-epithelialize and deposit of new ECM. Regeneration and proliferation (day 3eweek 2) This phase starts at day 3 and can continue for further 2e4 weeks. During this phase there is deposition of ECM, fibroblast migration and formation of granulation tissue.
Excessive wound healing Keloid and hypertrophic scarring Hypertrophic and keloid scarring are forms of excessive healing unique to humans. Keloid is defined as an abnormal scar that grows beyond the boundaries of the original site of skin injury, compared to hypertrophic scarring which is limited to the wound margins, with a potential to regress spontaneously. Both types can cause significant amorphous growth which can lead to symptoms such as pain and pruritus as well as the significant cosmetic implications. Both are difficult to manage and treat, with several methods available. Keloid and hypertrophic scarring are very different entities. Pathophysiological differences between the two are still to be clearly defined. The major differences are described in Table 1.
Formation of granulation tissue/fibroplasia/matrix deposition: this occurs simultaneously with angiogenesis. Fibroblasts begin accumulating in the wound site and release PDGF and TGFb which are mitogenic for epithelium and fibroblasts. Proliferation of epithelial cells and fibroblasts lead to ECM production. ECM is composed of collagen, adhesive glycoproteins and proteoglycans. Examples of glycoproteins are fibronectin and laminin which help link the components of the matrix. Proteoglycans help regulate the structure and permeability of the matrix. Hypoxia also contributes to fibroblast proliferation and excretion of growth factors, though too little oxygen will inhibit their growth and deposition of ECM components, and can lead to excessive, fibrotic scarring.
Treatments Most of the literature on keloids suggests that a high recurrence rate (50%) is expected, regardless of treatment. Treatment for keloid scarring can be non-operative measures, surgical intervention or a combination of both. First-line treatment of keloid scarring is injection of highly active steroid, usually triamcinolone. This can be dramatically
Angiogenesis: it occurs at 3e5 days concurrently with fibroblast proliferation. Angiogenesis is imperative because the activity of fibroblasts and epithelial cells is oxygen- and nutrient-dependent. Stem cells of endothelial cells, originating from parts of uninjured blood vessels, develop pseudopodia and push through the ECM into the wound site to establish new blood vessels. Hypoxia
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Differences between keloid and hypertrophic scarring Keloid
Appearance Typical sites
Raised extending beyond wound margins Sternum, back, ear lobes, shoulder
Puberty to 30 years Uncommon in children Black; Hispanic; Polynesian; Chinese; Indian Excessive collagen synthesis rate and glycosaminoglycan deposition Large, thick collagen fibres composed of numerous fibrils closely packed together Increased immunoglobulin G and C3 levels F>M (? Due to ear piercings in women) Possible No Yes; high likelihood
Raised confined to wound margin More common over flexor surfaces, skin creases and after burns Any age More common in children Can occur in any race Normal collagen synthesis with randomly organized collagen fibres Both have increased collagenase activity
Racial groups affected Pathology
Immunology M:F Genetic predisposition Wound contracture Recurrence Treatment
Debulking or excisional surgery; intralesional steroids; cryotherapy; pressure; silicone sheeting; laser therapy, radiotherapy
No associations M¼F None Yes No; usually growth subsides with time May even regress As with keloids
successful with flattening and softening of the scar. The mechanism of action is not fully understood and therefore should only be used by those experienced in the technique. Other treatments available include laser therapy (pulse dye, neodymiumeyttrium aluminium garnet (NdeYAG), and argon), cryotherapy and direct pressure to the area. Postoperatively the application of skin creams, silicone sheets and massage are all thought to improve wound healing and maturation of scars. Scar revision usually involves debulking rather than excision, this implies cutting within the keloid/hypertrophic scar rather than around it. Excision can have a recurrence rate ranging from 50e80%. Scar revision with other methods has been used, most commonly intralesional steroid injections or the use of radiotherapy in extensive keloids. Surgical excision followed by postoperative intralesional steroid injection is reported to have recurrence rates between 50% and 70%. A combination of surgical excision and external beam radiotherapy is implemented in certain centres, usually for the very resistant keloids. Radiation therapy adversely affects fibroblast growth and collagen production.
providing the appropriate environment for good wound healing and preventing complications in the future. It is also important to avoid excessively tight bandages. Systemic factors are harder to address. Usually these need to be corrected preoperatively. Physiological factors are difficult to correct and have to be considered prior to surgery. Obesity does contribute to poor wound healing primarily as a consequence of poor suture holding in the subcutaneous fat layers. Endogenous factors such as hypoproteinaemia or malnourished states delay wound healing due to lack of protein synthesis. Uraemia can interfere with wound healing by slowing granulation tissue formation and inducing the synthesis of poor-quality collagen.
Local and systemic factors that impede wound healing Local factor Systemic factors C Inadequate blood supply C Advancing physiological age C Increased skin tension C Obesity C Poor surgical apposition/ C Smoking C Diabetes mellitus technique C Wound dehiscence C Malnutrition C Poor venous drainage C Vitamin/trace elements deficiency C Presence of foreign body C Systemic malignancy and foreign body reactions C Shock C Haematoma C Chemotherapy and radiotherapy C Infection C Immunosuppressants, C Excess local mobility, corticosteroids, anticoagulants C Chronic renal/hepatic failure such as over a joint C Topical medicine
Factors affecting wound healing (Table 2) Factors that interfere with wound healing may be divided by source into local and systemic categories. These categories can be further subdivided into exogenous and endogenous factors. Local factors typically affect the environment around the wound at the time of closure and healing. Inadequate blood supply will impair wound healing. Surgical technique is one area we can focus on to minimize the chances of impaired wound healing. Reducing the soft tissue trauma at time of closure, minimizing wound tension, use of the correct suture type, everting skin edges and good haemostasis prior to closure will all aid in
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Commonly used incisions for access to the abdomen and thorax
A surgeon is responsible for choosing the best incision for a planned procedure. The success of any open surgical procedure requires a well-chosen incision based upon sound anatomic principles and closure with a technique that will result in a secure, well-healed wound. A well-planned incision has four essential elements: access ability to extend the wound preservation of function secure closure. Langer’s lines (sometimes called cleavage lines) were first described in 1861 by Austrian anatomist Karl Langer (1819e1887), and are topological lines of the human body. They correspond to the natural orientation of collagen fibres in the dermis and epidermis. Incisions made in the direction of Langer’s lines are less likely to gape and aid in wound healing. Numerous body incisions have been used for centuries, many associated with eponymous names, and have become well established in current practice. Figure 2 shows some of the most important and commonly used surgical incisions when specifically approaching the abdomen or thorax. A
10 2 5
Linea alba 4
6 7 8
1: Sternotomy 2: Thoracotomy 3: Midline laparotomy 4: Paramedian (L/R) 5: Kocher’s/subcostal 6: Gridiron 7: Pfannenstiel 8: Open inguinal hernia 9: Nephrectomy 10: Roof top/Mercedes (when combined with sternotomy)
FURTHER READING Giele H, Cassell O. Plastic & reconstructive surgery (oxford specialist handbook). Oxford University Press, 2008. Goldberg A, Stansby G. Surgical talk: revision in surgery. 2nd edn. Imperial College Press, 1999. Grey JE, Harding KG. ABC of wound healing. Blackwell Publishing Ltd, 2006. Tortora GJ, Grabowski SR. Principles of anatomy and physiology. 8th edn. New York: Wiley, 1996.
Exogenous factors include any external chemicals. Corticosteroids markedly inhibit capillary budding, fibroblast proliferation, and the rate of epithelialization. Cytotoxic drugs such as alkylating agents (e.g. cyclophosphamide, melphalan) slow wound healing by blocking DNA synthesis.
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