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