[libribook.com] Traumatic Scar Tissue Management 1st Edition

16.06.2020 Views

Nerve density in pathophysiological scarsDuring wound healing, scar tissue becomes both vascularized and innervated(Bove & Chapelle 2012). Under, over or aberrant innervation can potentially beproblematic.Example 1: as sensory nerves play a role in modulating immune response,denervated skin exhibits reduced leukocyte infiltration leading to impairedfirst line of defence, constituting a kind of no one minding the storepredicament (Galkowska et al. 2006, Sibbald & Woo 2008).Example 2: it is suggested that increased density of substance P and CGRPresponsive fibers is associated with chronic pain and pruritus (Henderson et al.2006, Scott et al. 2007, Almarestani et al. 2008, Cheng et al. 2011, Hamed etal. 2011, Widgerow 2013).In healing wounds, it appears that regeneration of nerve fibers correlates withepithelialization during healing. Immediately following injury, the wound bed isdevoid of nerves. Gradually, nerve fibers localize to the edges and later to thecenter of the wound beds. By 14 days post-injury, burn wounds displayexcessive numbers of nerve fibers (hyperinnervation) below the advancingepithelium. In normal wound healing, these numbers normalize with time andafter 4 weeks, the distribution of nerve fibers in re-epithelialized areas is similarto that of normal skin (Dunnick et al 1996, Scott et al. 2007).Innervation density is not the exclusive consideration in terms of restoration ofnormal neural responsiveness. It has been suggested that loss of sensory functionin pathophysiological scars is not so much due to diminished re-innervation butmore to do with aberrancies in nerve function within the scar or from changes inthe perception of stimuli (e.g. sensitization and plasticity changes). It has alsobeen suggested that a change in tissue structure (e.g. decrease in pliability in thetissues around, near or associated with the nerve) results in sensory deficits(Anderson et al. 2010).

Clinical ConsiderationSome pathological scars differ neurologically from normal tissue.Neurologically active scars can subtly alter or inhibit spinal motion andabnormal joint motion can contribute to pain. Pain of this nature can berelieved by treating neurologically active scars in the abdominal and pubicregion (Kobesová et al. 2007).Hypertrophic scarsHypertrophy of a scar is accompanied by hypertrophy of noci-responsive nerveswithin the scar. Hypertrophic scars exhibiting a greater number of nociresponsivefibers, presented with more serious pathologies (Derderian et al.2005).Aberrations in the re-innervation of scars may either cause aberrant woundhealing or neural hypertrophy may be a result of disturbed interplay in woundhealing mechanisms such as excessive concentrations of NGF and unduemechanical tension, as noted previously (Zhang & Laato 2001, Xiao et al. 2013).Pruritus associated with hypertrophic scars involves a complex interactionbetween the CNS, PNS and skin. Pruritus not only accompanies hypertrophicscars but is also thought to contribute to the development of hypertrophic scars.In addition to itch being caused by histamine, neurokinin, tachykinins,bradykinin and neuropeptides, peripheral nerve damage may be central to theburn injury itch syndrome and may be a central component contributing tohypertrophic scar development. Various neuropeptides are released in responseto injury activate mast cells, which release kinins, histamine and other agents,which in turn excite nociresponsive-fibers leading to exaggerated neurogenicinflammation. Fourteen days post-injury, a rebound increase in substance Presponsive nerve fibers is observed in pathophysiological scars. It is suggestedthat this exaggerated re-innervation is associated with pruritus and thedevelopment of hypertrophic scars. Therefore, attenuating pruritus not only

Clinical Consideration

Some pathological scars differ neurologically from normal tissue.

Neurologically active scars can subtly alter or inhibit spinal motion and

abnormal joint motion can contribute to pain. Pain of this nature can be

relieved by treating neurologically active scars in the abdominal and pubic

region (Kobesová et al. 2007).

Hypertrophic scars

Hypertrophy of a scar is accompanied by hypertrophy of noci-responsive nerves

within the scar. Hypertrophic scars exhibiting a greater number of nociresponsive

fibers, presented with more serious pathologies (Derderian et al.

2005).

Aberrations in the re-innervation of scars may either cause aberrant wound

healing or neural hypertrophy may be a result of disturbed interplay in wound

healing mechanisms such as excessive concentrations of NGF and undue

mechanical tension, as noted previously (Zhang & Laato 2001, Xiao et al. 2013).

Pruritus associated with hypertrophic scars involves a complex interaction

between the CNS, PNS and skin. Pruritus not only accompanies hypertrophic

scars but is also thought to contribute to the development of hypertrophic scars.

In addition to itch being caused by histamine, neurokinin, tachykinins,

bradykinin and neuropeptides, peripheral nerve damage may be central to the

burn injury itch syndrome and may be a central component contributing to

hypertrophic scar development. Various neuropeptides are released in response

to injury activate mast cells, which release kinins, histamine and other agents,

which in turn excite nociresponsive-fibers leading to exaggerated neurogenic

inflammation. Fourteen days post-injury, a rebound increase in substance P

responsive nerve fibers is observed in pathophysiological scars. It is suggested

that this exaggerated re-innervation is associated with pruritus and the

development of hypertrophic scars. Therefore, attenuating pruritus not only

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