Burns - Pathophysiology

so let's learn a bit more about the pathophysiology and the mechanism of disease when a burn occurs on the skin it causes changes within the skin and that could be divided into sort of three regions or three zones these zones of a burn were described by Jackson in 1947 and so it is also called the Jackson model the first zone is the zone of coagulation then it's the zone of stasis on the outside and then the furthest part is a zone of hyperemia so the zone of coagulation is essentially the point of maximum damage in this zone there is irreversible tissue loss due to coagulation of proteins thus you get coagulative necrosis surrounding the coagulation zone of necrosis is a zone of stasis now in this zone it's essentially characterized by decreased perfusion this ischemic zone may progress to full necrosis unless the ischemia is reversed at the very outside is the zone of hyperemia in this outermost zone tissue perfusion is increased the tissue here is invariably recovered unless there is severe sepsis or prolonged hypo perfusion again the stasis zone is characterized by ischemia and may progress to full necrosis unless the ischemia is reversed therefore the main aim of burns resuscitation is to increase tissue perfusion here and prevent any further damage any damage becoming irreversible so that is a general pathophysiology or mechanism of disease concept of burns when you accessable it is important to know the cause of the burn as we have learned such as if it's a thermal or radiation burn the other important aspect of a burn assessment is to know the depth of the burn to make it super easy just think of burns as initially being superficial burns or deep burns so let's zoom into the skin here to look at what hap in a superficial burn and what happens in a deeper let's take a look at at a superficial burn first if it's a superficial burn it will cause damage to the epidermis and the upper dermis only so like the papillary layer of the dermis again you have blood vessels here capillaries superficial burns will damage the keratinocytes which are your cells in the epidermis and will also activate an immune response so activate immune cells around the area such as mast cells and macrophages the damaged keratinocytes the mast cells and the macrophages will secrete pro-inflammatory cytokines triggering an immune response the cytokines will stimulate nerve endings around the dermis the sensory nerve endings here can be the ones that detect pain for example and pain is an important feature of superficial burns some cytokines will cause increase in vascular permeability the increase in vascular permeability will cause fluid to leak out and may lead to interstitial edema as the fluid leaks out it can result in hypotension remember that the increase in vascular permeability causes fluid to leak out the flute can actually accumulate in one area causing a blister on the skin surface the sensitive blister can rupture and release fluid onto the damaged skin surface thus superficial burns have a moist appearance the cytokine secreted by the cells above will also cause concurrent vasodilation causing further hypotension in severe cases the vasodilation contributes to the warmth in the area as well as causing blanching of the skin and erythema blanching means that when you press on the burnt skin surface blood will quickly fill it up because of the increase in blood flow to the area the blanching skin is a feature of superficial burns in deep burns you have more than just damage to the epidermis and the upper part of the dermis you have damage all the way down extends all the way to the hypodermis so it's a pretty deep burn deep burns can thus damage blood vessels in the skin because you have damaged blood vessels everything will leak out you have no blood supply to the area so you eventually get this dry non blanching surface it is dry and inelastic the non blanching dryness is an important feature of deep burns further deep burns extending to the reticular layer of the dermis can destroyed nociceptors and other sensory nerve fibers initially pain can be detected but as a sensory nerve fibers are damaged you get hyper Thessia so you get reduction in sensation loss of sensation is an important feature of deep burns obviously not all your blood supply is damaged or your blood vessels are damaged the functional blood vessels react to the cytokines produced around the area the vessels will increase vascular permeability which will cause fluid to shift out causing interstitial edema so fluid shifts out from the intravascular space so the blood vessel and this will into the interstitial and this huge amount of fluid coming out of the vessels will result in hypotension so circulatory shock even hypotension as a result of this shift of fluid occurs more in deep burns rather than superficial burns