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

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ThermoregulationThermoregulation (through sweating, vasoconstriction or vasodilatation) andcontrol of fluid loss are also essential functions performed by our skin. AlthoughSTSGs help restore a functional barrier, the blood vessels and sweat glandsnecessary for temperature regulation remain damaged.When an individual is exposed to heat stress, cutaneous vasodilation andsweating in well-healed grafted skin is severely impaired compared withadjacent non-damaged skin. Likewise, grafted skin does not vasodilate or sweatappropriately upon exogenous administration of local vasodilators and sudorificdrugs (i.e. sodium nitroprusside and acetylcholine), suggesting postsynapticimpairments, which are not resolved 4–8 years post-surgery (Lu & Fuchs 2014).These impairments in grafted skin become barriers to whole-body heatdissipation, especially when grafted skin represents a significant proportion ofTBSA.During physical activity, increases in metabolic heat production that are notproperly compensated for by adequate heat loss responses (e.g. skin vasodilationand sweating) can lead to dangerous increases in core body temperature.Therefore, the ability of individuals with STSGs to safely participate in physicalactivity may be limited by their capacity to dissipate heat, especially whenphysical activity is performed in warm/hot temperature environments (Ganio etal. 2013).Blood FlowThe control of skin blood flow occurs through two sympathetic neural pathways;one involves a sympathetic vasoconstrictor system and the other pathwaymodulates the skin blood flow through a non-adrenergic sympathetic activevasodilator system.Interestingly, grafted skin is shown to preserve its vasoconstrictor ability. Astudy conducted on split-thickness grafted skin 5–9 months post-surgery showedthat when exposed to cold stress (cold temperatures, high or cold wind,dampness and cold water) the grafted skin demonstrated indicators of reinnervationand restoration of autonomic control of the cutaneous

vasoconstrictor pathways. The same study showed that there were, however,impairments in cutaneous vasodilation and sweating during heat stress whencompared to that of healthy, uninjured skin (Crandall & Davis 2010).Increased skin blood flow and sweating are critical responses to correctlyregulate internal temperature during exercise and/or hyperthermic exposure. Thedata indicates that diminished sweating responses in grafted skin are due to anabsence of functional sweat glands. Weakened abilities to dissipate heat viacutaneous vasodilation and sweating from grafted skin do not recover for up to4–8 years after graft surgery, raising the possibility that individuals with asignificant amount of body surface area of grafted skin are at an increased risk ofa heat-related injury. On the other hand, preserved vasoconstrictor responses toboth indirect whole-body cooling and local cooling, regardless of graft maturity,suggest sustained capability to regulate internal temperature via cutaneousvasoconstriction during cold exposure (Crandall et al. 2009).Inflammation and EdemaThe inflammatory response in a critical burn injury is often unstable due to theglobal involvement of multiple tissue beds and their constituent immune andnon-immune cells, placing significant metabolic and energy requirements on therepair process; for example, the extent of inflammation and energy requirementsis directly proportional to the severity of injury sustained by the patient (Shankaret al. 2007).The spectrum of inflammation runs from a mild elevation in cytokinesassociated with inflammation that largely go unnoticed clinically to a systemwidesevere inflammatory response that eventually leads to microcirculatoryfailure of capillaries supplying individual vital organs, acute respiratorysyndrome, severe coagulopathy, and the development of multiple organ failuresometimes seen in the initial treatment of a burn injury.Exaggerated inflammation in burn injury wounds, which healed after 21 days,had a high rate of hypertrophic scarring formation (Tredget 2008). Edema, whichoccurs after a significant burn, is assumed to be a non-reversible process(Demling 2005).Lymphatic FlowAs noted in Chapter 3, lymph is composed of interstitial fluid, which is collected

Thermoregulation

Thermoregulation (through sweating, vasoconstriction or vasodilatation) and

control of fluid loss are also essential functions performed by our skin. Although

STSGs help restore a functional barrier, the blood vessels and sweat glands

necessary for temperature regulation remain damaged.

When an individual is exposed to heat stress, cutaneous vasodilation and

sweating in well-healed grafted skin is severely impaired compared with

adjacent non-damaged skin. Likewise, grafted skin does not vasodilate or sweat

appropriately upon exogenous administration of local vasodilators and sudorific

drugs (i.e. sodium nitroprusside and acetylcholine), suggesting postsynaptic

impairments, which are not resolved 4–8 years post-surgery (Lu & Fuchs 2014).

These impairments in grafted skin become barriers to whole-body heat

dissipation, especially when grafted skin represents a significant proportion of

TBSA.

During physical activity, increases in metabolic heat production that are not

properly compensated for by adequate heat loss responses (e.g. skin vasodilation

and sweating) can lead to dangerous increases in core body temperature.

Therefore, the ability of individuals with STSGs to safely participate in physical

activity may be limited by their capacity to dissipate heat, especially when

physical activity is performed in warm/hot temperature environments (Ganio et

al. 2013).

Blood Flow

The control of skin blood flow occurs through two sympathetic neural pathways;

one involves a sympathetic vasoconstrictor system and the other pathway

modulates the skin blood flow through a non-adrenergic sympathetic active

vasodilator system.

Interestingly, grafted skin is shown to preserve its vasoconstrictor ability. A

study conducted on split-thickness grafted skin 5–9 months post-surgery showed

that when exposed to cold stress (cold temperatures, high or cold wind,

dampness and cold water) the grafted skin demonstrated indicators of reinnervation

and restoration of autonomic control of the cutaneous

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