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42 Wound Healing

The normal adult 4:1 ratio of type I to type III collagen is restored Hypertrophic Scars and Keloids
during remodelling. Equilibrium is established as new collagen is Keloids and hypertrophic scars are challenging complications of
formed and collagen is degraded. The matrix metalloproteinases wound healing frequently encountered by paediatric surgeons in Africa.
(MMPs)—collagenases, gelatinases, and stromelysins—degrade the Lesions are more common in individuals with darker complexions,
ECM components and are in part responsible for establishing a balance with a family history, at a younger age, and in areas exposed to stretch
between collagen deposition and degradation. or tension. The overall incidence of keloid formation in wound heal-
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Wound tensile strength increases for up to 1 year after injury. The ing is estimated at 4.5–16%. The incidence of keloids was 6.2% of
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tensile strength of wounded skin at best reaches 80% of unwounded 4,877 people in a western Nigerian community, and as high as 16%
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skin. The ultimate outcome of adult wound healing is formation of a in Zaire. Although the incidence of hypertrophic scars is unknown,
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scar. A scar can be defined morphologically as a lack of organisation it is thought to be higher than keloids. Keloids and hypertrophic scars
compared to the surrounding tissue; it is characterised by disorganised present functional as well as cosmetic problems. Management remains
collagen deposition. Collagen of a scar is in densely packed fibers and controversial; however, some recent guidelines have been established. 5
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not the reticular pattern seen in unwounded skin. The final scar is brittle, Normal wounds have stop signals to halt the repair process when the
less elastic, and lacks such appendages as hair follicles or sweat glands. defect is closed and re-epithelialisation is complete. When these signals
Foetal Wound Healing: Scarless Repair are absent or altered, the healing process continues and may result in
Foetal wound healing differs from that of adults in a number of aspects. excessive scarring. Prominent scars may be cosmetically and physically
There is minimal inflammation during foetal healing. The minimal challenging for the patient.
cellular infiltration seen is predominantly mononuclear cells with Hypertrophic scars are defined as scars confined to the boundaries
few neutrophils. Collagen is deposited in a more organised and rapid of the original wound. They are an example of excessive healing,
fashion and has an increased type III to type I ratio. Further, collagen and histologically contain an overabundance of dermal collagen.
is deposited in a reticular pattern, indistinguishable from surrounding Hypertrophic scars are usually self-limited and can regress. The scar
tissue, and has greater tensile strength than that for adult wounds. 3 will tend to fade and flatten. Improvement in scar appearance has been
8
Research has demonstrated lower amounts of transforming growth obtained with pressure garments, topical silicone gel, or re-excision.
factor-b (TGF-b) types 1 and 2 and decreased ratio of total TGF-b1 Keloids are uncommon forms of excessive scarring and
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and TGF-b2 released from foetal platelets. These factors are thought predominantly occur in dark-skinned individuals with a genetic
to be in part responsible for the absence of inflammatory infiltrate and predisposition to them. The incidence is as high as 16% in African
5,8,22
fibrosis in foetal wound repair. In the midgestational foetal rabbit, populations. In contrast to hypertrophic scars, keloids overgrow
incisional wounds heal without fibrosis or scar formation, and there the original wound boundaries and rarely regress. Keloids may behave
is no evidence of wound contracture. The ECM consists mostly of as benign tumours and extend into or invade surrounding tissue.
hyaluronan without evidence of collagen deposition, and fibroblasts are Histologically, keloids are rich in collagen, as collagenases cannot keep
present only at the wound margin. 13,14 up with collagen deposition.
The foetal environment may also contribute to the quality of wound The exact cause of hypertrophic scar and keloid formation is
healing. However, adult skin transplanted into foetuses in utero does unknown, and treatment is difficult. Recent recommendations from
5
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not heal differently than as seen in normal adults. Also, a marsupial an international advisory panel provide several treatment guidelines.
foetus heals without scar formation even in the absence of amniotic They suggest that first line therapy for immature hypertrophic scars and
fluid. 16,17 A sterile environment is important in foetal healing. If a keloids should be silicone gel sheeting. If scars are resistant, intralesional
stimulus is provided, such as bacteria-soaked sponges, an inflammatory injection of corticosteroids is indicated. For first-line treatment failures
cascade can be initiated, resulting in extensive inflammation, fibrosis, of hypertrophic scars, surgical excision with postoperative silicone gel
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and scar formation. sheeting should be considered. Larger hypertrophic scars may benefit
The genes and complex cell signalling pathways that regulate the from Z-plasty, excision, and grafting or flap coverage. Large keloids are
mechanisms resulting in the regenerative type of wound healing seen more challenging because of their postsurgical recurrence. Some newer
in the foetus, however, remain unknown. A better understanding of the treatments, such as local radiation therapy, bleomycin, or 5-flourouracil
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biology of scarless foetal wound repair may help in the development treatment, may have roles in keloid management.
of therapeutic strategies that can be used to minimise scar formation. Chronic and Complex Wounds
Clinical Wound-Healing Problems Chronic wounds can be defined as those failing to proceed through an
Many pathological processes are characterised by either abnormal col- orderly and timely process to produce anatomic and functional integ-
rity, or proceeding through the repair process without establishing a
lagen deposition or degradation. Insufficient collagen deposition could sustained result. Practically, a chronic wound is one that has failed to
1
manifest as abdominal wound dehiscence or leaking intestinal anasto- heal within 3 months. The cellular, biochemical, and molecular events
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mosis, two common examples of deficient healing that cause severe that characterise chronic wounds have been well defined, including pro-
morbidity and frequent mortality. Chronic wounds, such as venous longed inflammatory phase, cellular senescence, deficiency of growth
stasis ulcers, diabetic ulcers, and pressure sores, similarly result from factor receptor sites, deficient fibrin production and growth factor
inadequate collagen synthesis, although excessive collagen degrada- release, and high levels of proteases. Chronic wounds are frequently
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tion may be the more important factor. In contrast, accumulation caused by vascular insufficiency, chronic inflammation, repetitive tis-
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of collagen due to excessive deposition or impaired degradation can sue insults, or underlying pathology.
distort normal tissue architecture, compromise function, and produce a “Complex wound” is a term used to group acute or chronic wounds
fibrotic state characteristic of such conditions as keloids, hypertrophic that are nonhealing or difficult to treat. They show extensive loss of
burn scars, pulmonary fibrosis, oesophageal strictures, and hepatic integument, are frequently complicated by infection, demonstrate
cirrhosis. Acute wounds are discussed in the chapters on trauma and circulatory impairment, and are often associated with systemic
burns. The following discussion concentrates on conditions of exces- pathology. Recognising chronic or complex wounds, identifying
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sive scarring (keloid and hypertrophic scars) and those of deficient the underlying causes for poor healing, and early intervention are
healing (chronic wounds).
crucial to decreasing morbidity and mortality. The majority of chronic