Metabolic Changes Associated with Burn Injury

Lee C. Woodson, Edward R. Sherwood, Asle Aarsland,
Mark Talon, Michael P. Kinsky, and Elise M. Morvant state:

“Increased metabolic rate is the hallmark metabolic alteration that takes place after thermal injury.  The size of the burn wound, medical management and the core body temperature of the patient influence the magnitude of hypermetabolism.  Within the range of 30–70% TBSA burn injury, hypermetabolism tends to be proportionate to the size of the burn wound.  With burns beyond this range, the hypermetabolism appears to plateau and only increases in smaller increments as burn size increases.   As mentioned earlier, burn patients increase their metabolic rate in an effort to generate heat according to an increased core temperature threshold set point, which is influenced by the size of the burn.

The recognition of this fact has led to an increased awareness of the importance of the ambient temperature in modulating the hypermetabolism of the burn patient.  Resting energy expenditure typically increases as core body temperature decreases below the new set point.  Therefore, it is critical to prevent significant decreases in core body temperature in the operating room.  As a result of the hypermetabolic response, the burned patient has an increased O2 consumption along with an increased CO2 production that collectively causes increased minute ventilation and demands a higher respiratory effort.  The anesthetic care of the acute burned patient must accommodate these changes, and frequently this has to be done in patients with compromised pulmonary function due to burn and inhalation injuries.”

Herndon, David N. "Anesthesia for burned patients" Total Burn Care. Fourth ed. Edinburgh: Saunders Elsevier, 2012. 183. Print.

Hemodynamic Consequences of Acute Burns

George C. Kramer writes:

“Hemodynamic consequences of acute burns

The cause of reduced cardiac output during the resuscitative phase of burn injury has been the subject of considerable debate. There is an immediate depression of cardiac output before any detectable reduction in plasma volume. The rapidity of the response may result from impaired electrical activity of cardiac nerves and muscle and increased afterload due to vasoconstriction. Soon after injury developing hypovolemia and reduced venous return undeniably contribute to the reduced cardiac output.  The subsequent persistence of reduced CO after apparently adequate fluid therapy, as evidenced by restoration of arterial blood pressure and urinary output, has been attributed to circulating myocardial depressant factor(s), which possibly originates from the burn wound.  It was concluded that the depression of CO resulted not only from decreased blood volume and venous return, but also from and increased SVR and from the presence of a circulating myocardial depressant substance. After the resuscitation phase of burn shock, patients can have supranormal CO.  This is associated with a hypermetabolic state and systemic inflammatory response syndrome (SIRS).”

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Herndon, David N. "Pathophysiology of burn shock and burn edema" Total Burn Care. Fourth ed. Edinburgh: Saunders Elsevier, 2012. 110. Print.