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BURN SHOCK The burn wound is a 3-dimensional mass of damaged tissue. At its margin is the zone of hyperemia and at its center is the zone of coagulation. Surrounding the coagulation region is the zone of stasis, so named because it starts with a circulation, which becomes static. Due to direct thermal effects, the microvasculatures in this region dilate and its endothelial lining 'leaks' plasma and intravascular proteins. Within minutes to hours, the circulation in this region ceases as the capillaries become packed with red blood cells and microthrombi, aggravating the inflammatory response. Although the cellular damage in this region is potentially reversible, injury to the microcirculation is progressive over 48 hours. Extent of the zone of stasis is minimized by adequate resuscitation. The inflammatory response in the zone of stasis is responsible for burn edema and shock. Regional edema occurs in the burned tissue due to increased microvascular permeability, vasodilation, increased extravascular osmotic activity in damaged tissue, and infiltration of tissues by leukocytes with release of vasoactive substances. Endogenous inflammatory mediators implicated in the pathogenesis of burn shock include interleukins, histamine, serotonin, kinins, oxygen free radicals, lipid peroxides and products of the eicosanoid acid cascade. This last group includes products of cyclooxygenase, such as thromboxane, prostacyclin, and prostaglandins E and F2; and products of lipoxygenase, the leukotrines B4, C4, D4 and E4. Thromboxane, through its effects on vasoconstriction and platelet aggregation, may markedly increase dermal ischemia, augmenting tissue destruction of the thermal injury. In burns greater than 30% BSA, a more generalized capillary permeability occurs due to systemic hypoproteinemia and inflammatory mediators, resulting in edema formation in non-burned tissues as well. Excessive leakage of plasma, especially in the first eight hours post-burn, causes hypovolemia, hypoproteinemia, hemoconcentration, electrolyte imbalances and acid base disturbances. Plasma volume is reduced by as much as 23-27%, with a reduction in cardiac output and an increase in peripheral vascular resistance. In the absence of prompt fluid replacement, burn shock is imminent. Fluid Resuscitation Fluid Resuscitation
In each case, half of this volume is administered in the first eight hours post-burn. The rate is adjusted hourly to assure a urinary output of 30 ml/hr in adults and 1 ml/kg/hr in children. Serum albumin is replaced to keep levels >2.5 gm/dl. We calculated appropriate replacement boluses at 6.25 gm for patients < 20 kg, 12.5 gm for patients between 20 and 40 kg, and 25 gm for patients over 40 kg. Resuscitation of burned children differs in 2 aspects. First, the standard Parkland formula commonly underestimates fluid requirements in a burned child and may not provide even usual daily maintenance requirements. There is great variability between body surface area and weight in a growing child. More accurate estimation of resuscitation requirements in burned children can be based on body surface area, determined from nomograms of height and weight. For children, we recommend initial resuscitation with 5000 ml/m² BSA burned/day plus 2000 ml/m² BSA total/day lactated ringer's, one half over the first 8 hours. Second, infants require glucose due to small glycogen stores and are prone to hypoglycemia in the initial resuscitation period. Serum and urine glucose levels are monitored and replaced as indicated. Over-aggressive dextrose infusion can produce an osmotic diuresis, paradoxically increasing burn shock. In the subsequent 24 hours, transcutaneous evaporative losses from burn wounds are replaced at 1 ml/kg/% burn daily. In burned children, fluid requirements are 3750 ml/m²BSA burned/day plus 1500 ml/m²BSA total/day. The sodium content of the replacement solution is altered as needed to maintain a normal range serum sodium level, e.g. D51/3 NS solution + 10-20 mEq/l of potassium phosphate. Hypophosphatemia is common following burn injury. Generally, enteral feedings are begun within 6 hours, often immediately following burn injury and gradually increased. Intravenous fluids are diminished as enteral intake increases. By 48 hours, most of the fluid replacement can be provided enterally. Care should be taken to avoid rapid shifts in serum sodium concentration which may cause cerebral edema and neuroconvulsive activity. All resuscitation formulas are meant to serve as guides only. The response to fluid administration and physiologic tolerance of the patient is most important. Additional fluids are commonly needed in inhalation injuries, electrical burns, associated trauma and delayed-resuscitation patients. The appropriate resuscitation regimen administers the minimal amount of fluid necessary for maintenance of vital organ perfusion measured as adequate urine output. Inadequate resuscitation can cause further insult to pulmonary, renal and mesenteric vascular beds. Fluid overload can produce pulmonary or cerebral edema. Over-resuscitation will also increase wound edema and thereby, dermal ischemia, producing increased depth and extent of cutaneous damage. The appropriate use of colloid solutions for acute burn resuscitation remains debated. Development of hypoproteinemia in the early resuscitation period increases edema in non-burned tissues. Interestingly, in the absence of inhalation injury, lung water content does not increase. Early infusion of colloid solutions may decrease overall fluid requirements in the initial resuscitation period and reduce non-burn edema. However, injudicious use of colloid infusion may cause iatrogenic pulmonary edema, increasing pulmonary complications and mortality. We recommend an albumin beginning 8 hours after the burn injury if it is to be used. Monitoring The single best monitor of fluid replacement is urine output. Acceptable hydration is indicated by a urine output of more than 30 ml/hr is an adult (0.5 ml/kg/hr) and at least 1 ml/kg/hr in a child. Diuretics are generally not indicated during the acute resuscitation period. Patients with high voltage electrical burns and crush injuries have an increased risk of renal tubule obstruction from myoglobinuria and hemoglobinuria. Urine output should be maintained at 1-2 ml/kg/hr, if pigment can be seen in the urine and the urine alkalinized with IV sodium bicarbonate or acetazolamide with IV mannitol to aid in diuresis and to act as a free radical scavenger. Pulse rate and pulse pressure are more sensitive indicators of hemodynamic status than blood pressure. Hypotension is a late finding in burn shock. Normal sensorium and adequate peripheral capillary refill are additional clinical indicators of adequate organ perfusion. Invasive hemodynamic monitoring with central venous catheters, arterial lines, and Swan Ganz catheters is usually not needed in the absence of a severe inhalation injury, and discretion is advised. Pulmonary artery lines especially carry an inordinate risk of sepsis, thrombophlebitis and endocarditis in thermal injury patients.
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