The physiologic response to burn injury

Sirs with infection is a major factor determining morbidity and mortality in thermally injured patients. Pathologic alterations of the metabolic, cardiovasculer, gastrointestinal, and coagulation systems occur, with resulting hypermetabolisme, increased cellular, endothelial and epithelial permeability, classic hemodynamic alterations, and often extensive microthrombosis.
A. Burn shock
It is not easily or fully repaired by fluid resuscitation. Tissue trauma and hypovolemic shock result in the formation and release of local and sistemic mediators, which produce an increase in vascular permeability and microvascular hydrostatic pressure.
-histamine, it predominantly disrupt venular endothelial tight junctions, permitting egress of fluid and proteins. Its involved only in the very early increase in microvascular permeability.
-seretonin, released immediately postburn via platelet aggregation, and acts directly to increase pulmonary vascular resistance, and indirectly to amplify the vasoconstrictive effects of norepinephrine, histamine, angiotensine II and select eicosanoids at the microvascular level
-eicosonoids, these subtances do not directly alter vascular permeability but increased levels of the vasodilator prostaglandins, such as PGE2, and prostacyclin /PGI2 result in arterial dilatation in burn tissue that increases blood flow and hydrostatic pressure in the injured microcirculation and accentuates edema formation.
-kinins, specifically the bradikinins, increase vascular permeability, primarily in the venule.
-as hematologically measured, it resembles disseminated intravascular coagulation and may correlate with organ failure and outcome.
B. Metabolic response to burn injury
*hypermetabolism
Resting energy expenditure/REE after burn injury can be as much as 100% above predictions based on standard calculations for size, age, sex, and weight. On average, the RRE is approximately 1,3 times the predicted BMR obtained using the harris-benedict equation.
Glucose is elevated in almost all critically-ill patient, including those with burn injuries.
Plasma insulin levels typically are elevated in burn patients. Which can be defined as hepatic insulin resistance
Lipolysis occured. The majority of released fatty acids are not oxidized, but rather re-esterified into triglycerides, resulting in fat accumulation in the liver.
Proteolisis is increased. Protein intake greater 1g/kg per day or 2g/kg per day with normal renal function.
*Neuroendocrine response
-catecholamine are massively elevated following burn injury, and appear to be the major endocrine mediators of the hypermetabolic response in thermally injured patient.
-growth hormone levels are attenuated following thermal injury.
-thyroid hormone serum concentrations are altered in patient with large burns. Total T3 and T4 are reduced and reverse T3 concentration are elevated.
C. Immunologic response to burn injury
The immune status of the burn patient has a profound impact on outcome in terms of survival and major morbidity.