به نام هستي بخش

به نام هستي بخش

BURN PATHOPHYSIOLOGY

ITEMS • * Burn ulcer • * Burn edema • * Reduction in RBC mass • * Burn immunology • * Hormonal changes • * Inhalation injury

First Degree • * Epiderm is injured • * Derm and its appendages are intact

SECOND DEGREE • * Some thickness of derm is injured • * There is injury to the dermal appendages • * But some thickness of derm and many of dermal appendages are spared

THIRD DEGREE • * Full thickness of derm is injured • * Heeling is only by contraction

FORTH DEGREE • * Soft tissue and bone is injurred

EDEMA IN BURN PATIENT

PROBLEMES WITH EDEMA • * Reduction in tissue oxygenation • * Reduction in tissue perfusion • * Increase the risk of infection • * Increase the work of breathing leading to pulmonary failure

TWO KIND OF EDEMA • * FIRST Edema in burn area that is non preventable • * SECOND Edema in non burn area that is preventable

CAUSES OF EDEMA • * In burn area first vasoconstriction and then vasodilatation due to ischemia • * Increase in gaps between cells in microvasculature for some days to some weeks • * Vasoactive substances like LTs PGs oxygen radicals and histamin • * Increase in intrestitial osmolarity in burned area • * Probability of a systemic mediator • * Hypoproteinemia

REDUCTION IN RBCMASS

40%DAMAGE OF RBC MASS • * 8% - 15% From direct injury • * 25% Due to reduced RBC • survival

IMMUNOLOGY • * Burn by itself • * Systemic drugs • * Topical drugs • * General anesthesia

BURN BY ITSELF • * Increase phagocytosis • * reduced intracellular killing • * reduced opsonins • * reduced serum Ig level 2 days after Bu mostly IgM • * Reduced serum compleman • * Reduced cellmediated immunity • * Increased skin allograft survival

DRUGS • * Tetracyclin • * Chloramphenicol • * Streptomycin • * Gentamicin • * Kanamycin • All reduce cell mediated immunity

TOPICAL DRUGS • * Acetate mafenide and silver sulfadiazin both inhibit PMN chemotaxis

General anesthesia • * Halotan Ether and N2 Reduce mitogenic activity of lymphocyts Band T • * Phenobarbital reduce Ab production by spleen

HORMONAL CHANGES • * Increase in Catecholamines • * “ “ GH • * “ “ Cortizole • * Decrease in T3 and T4 • * “ “ serum Insuline • * Serum TSH is normal

METABULISM • * Hypermetabolism 2-4 times normal • * Most of extra blood flow is for B. ulcer • * Up reset of body thermostat is due to B receptor stimulation • * Brain deed patient have not hypermet. • * > 10% W.loss cause abnormal W.H • * > 30% W.loss is lethal • * Increase int. cellular Na due to Na and K pomp derangement

INHALATION INJURY • * 20-80% mortality is due to I.Inj • * 30- 40% increase in mortality if I.Inj is present

PATHOGENESIS OF I.INJ. • * CO intoxication • * Direct thermal effect • * Products of combustion inhalation

CO INTOXICATION • * Competition with O2 for Hb • * 210 times affinity for Hb • * Cytocorom system derangement in cytoplasm • * CNS derangement • * A.B.G : Lactic acidosis with low PO2 PaO2 is normal Oxy Hb saturation is low

DIRECT THERMAL INJ. • * Lower air ways are spared except for steam • * Upper air ways are more affected • * Most of edema is in first 18-24h • that increase breathing work or makes obstruction

PRODUCTS OF COMBUSTION • * The most common and most important part of inhalation inj. • * Aldeids Ketons and Organic materials • * Symptoms are like gastric acid aspiration Bronchoconstriction Silia paralysis Increase vessel permeability and ARDS Decrease in surfactant Prone to infection due to mucosa dam.

RESOSCITATION RESOSCITATION • COLLOID Evans N/S 1ML/KG/% CO 1 ml/kg/% D/W 2000cc Brook R/L 1.5 ml/kg/% CO 0.5ml/kg/% D/W2000cc Slater R/L 2L/24h FFP 75ml/kg/24 • CRYSTALLOID Parkland R/L 4ml/kg/% Modified brook 2ml/kg/% • HYPERTONIC SALIN Modif Monafo 180meq Na/L (R/L+ 50ml NaHCo3) /8h U 30-50ml/h then R/l after 8h ---until 24h • DEXTRAN FORMULA DEX 40 insalin 2ml/kg/h for 8h + R/L for U 30ml/h then after 8h FFP 0.5ml/kg/h for 18h

به نام هستي بخش