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.

 

Self Immolation

“Self-immolation is an act of killing oneself as a sacrifice. While usage since the 1960s has typically referred only to setting oneself on fire, the term historically refers to a much wider range of suicidal choices.”
— Wikipedia

“Cases in which people use fire when attempting or committing suicide are not common but nevertheless constitute a cause of admission to burns units worldwide. Usually these people are suffering from stress and have been diagnosed as mentally ill. Schizophrenia, depression, and personality disorders are the most frequently diagnosed conditions.”

https://www.ncbi.nlm.nih.gov/pmc/journals/1231/

 

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Hemodynamic Consequences of Acute Burns

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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).”

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

What is the difference between Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)?

antibiotics

Stevens-Johnson syndrome and toxic epidermal necrolysis are severe cutaneous hypersensitivity reactions. Drugs, especially sulfa drugs, antiepileptic’s, and antibiotics, are the most common causes. Macules rapidly spread and coalesce, leading to epidermal blistering, necrosis, and sloughing. Diagnosis is usually obvious by appearance of initial lesions and clinical syndrome. Treatment is supportive care; cyclosporine, plasma exchange or IVIG, and early pulse corticosteroid therapy have been used. Mortality can be as high as 7.5% in children and 20 to 25% in adults but tends to be lower with early treatment.

    SJS and TEN are clinically similar except for their distribution. By one commonly accepted definition, changes affect < 10% of body surface area in SJS and > 30% of body surface area in TEN; involvement of 15 to 30% of body surface area is considered SJS/TEN overlap.

    The disorders affect between 1 and 5 people/million. Incidence, severity, or both of these disorders may be higher in bone marrow transplant recipients, in Pneumocystis jirovecii–infected HIV patients, in patients with SLE, and in patients with other chronic rheumatologic diseases.

Rehmus, Wingfield E., MD. MPH. "Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) - Dermatologic Disorders." Merck Manuals Professional Edition. N.p., n.d. Web. 09 Mar. 2017.