Burn Patient

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.

 

Proliferation of Acetylcholine Receptors in the Burn Patient

Dr. Lee Woodson writes:

“Cardiac arrest in burned patients after succinylcholine administration was first reported in 1958.  Animal and human studies consistently demonstrate an association of increased numbers of skeletal muscle acetylcholine receptors with resistance to non-depolarizing muscle relaxants and increased sensitivity to succinylcholine. In addition, the distribution of the new receptors is altered. Nicotinic receptors are normally restricted to the neuromuscular synaptic cleft but in these disease states new receptors are distributed across the surface of the skeletal muscle membrane. The new receptors are also a distinctly different isoform (α7AChR) that has been referred to as an immature, extrajunctional, or fetal receptor. The immature receptors are more easily depolarized by succinylcholine and their ion channel stays open longer. The immature receptors are also strongly and persistently depolarized by the metabolite of acetylcholine and succinylcholine, choline. It has been suggested that the hyperkalemic response to succinylcholine after burn or denervation injury results when potassium is released from receptor-associated ion channels across the entire muscle cell membrane, rather than just the junctional receptors. Depolarization persists because the channels stay open longer and the breakdown product of succinylcholine, choline, is also a strong agonist for the immature receptors.
Proliferation of acetylcholine receptors across the muscle membrane has been used to explain both resistance to non-depolarizing muscle relaxants and the exaggerated hyperkalemic response to succinylcholine.”


Herndon, David N. "Anesthesia for Burned Patients." Total Burn Care. Fourth ed. Edinburgh: Saunders Elsevier, 2012. 184-85. Print.