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Correspondence

Hyperthermia

N Engl J Med 1994; 330:218-219January 20, 1994

Article

To the Editor:

Dr. Simon's review of hyperthermia (Aug. 12 issue)1 states that “the majority of anesthetic agents can trigger malignant hyperthermia. . . . ” The syndrome is triggered only by halogenated volatile anesthetics and succinylcholine. It is not triggered by other anesthetics, including etomidate, ketamine, propofol, nitrous oxide, benzodiazepines, and opioids; nondepolarizing muscle relaxants and barbiturates delay the triggering of malignant hyperthermia. Furthermore, not a single local anesthetic triggers the syndrome. Consequently, susceptible persons can be safely anesthetized, even for elective surgery.

Malignant hyperthermia has a “high mortality rate” only if untreated. Even when fulminant, the syndrome has a mortality rate approaching zero if diagnosed early and treated appropriately. Treatment most definitely does not include “mandatory” antipyretic therapy. Antipyretic agents reduce fever by decreasing the central thermoregulatory set-point. Central thermoregulation is believed to be normal during malignant hyperthermic crises; hyperthermia (as opposed to fever) results from the combination of skeletal-muscle hypermetabolism and abnormally increased circulating catecholamine concentrations, which limit heat dissipation by constricting skin vasculature.

When a crisis is identified, triggering anesthetics obviously should be discontinued. Hyperventilation and active cooling are useful therapeutic adjuncts, but dantrolene is the specific treatment for acute malignant hyperthermia. Consequently, administration of dantrolene must be the first priority.

Daniel I. Sessler, M.D.
University of California, San Francisco, CA 94143-0648

1 References
  1. 1

    Simon HB. Hyperthermia. N Engl J Med 1993;329:483-487
    Full Text | Web of Science | Medline

To the Editor:

Among North Americans, malignant hyperthermia has been documented as clearly autosomal dominant in approximately 40 percent of cases1. In other, more homogeneous populations, autosomal dominance is the rule2. Pedigrees demonstrating familial susceptibility to malignant hyperthermia are difficult to construct, since the phenotype is expressed only under general anesthesia. Tight linkage between malignant hyperthermia and an arginine-to-cysteine mutation at position 615 of the primary calcium-release channel of skeletal-muscle sarcoplasmic reticulum has been documented in pigs with autosomal recessive hyperthermia,3 but it has been found in few human families4. In humans, DNA linkage studies and the association of malignant hyperthermia with many neuromuscular disorders suggest that mutations in the ryanodine receptor may not be primarily responsible for susceptibility to malignant hyperthermia, which is likely to be genetically heterogeneous4. Taking a family history and carrying out the caffeine-halothane contracture test remain the best ways to screen for susceptibility. Reliable contracture testing can be performed only at a few centers in North America; information can be obtained from the Malignant Hyperthermia Association of the United States (Box 191, Westport, CT 06881-0191).

Readers should also be aware that the Malignant Hyperthermia Association maintains a 24-hour hot line (through the MedicAlert System, 209-634-4917; ask for index 0) to assist physicians with the diagnosis and treatment of suspected malignant hyperthermia.

Jerome Parness, M.D., Ph.D.
University of Medicine and Dentistry, New Brunswick, NJ 08903-0019

4 References
  1. 1

    Rosenberg H, Seitman D. Pharmacogenetics. In: Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia. Philadelphia: J.B. Lippincott, 1989:459-83.

  2. 2

    McCarthy TV, Healy JM, Heffron JJ, et al. Localization of the malignant hyperthermia susceptibility locus to human chromosome 19q12-13.2. Nature 1990;343:562-564
    CrossRef | Web of Science | Medline

  3. 3

    Fujii J, Otsu K, Zorzato F, et al. Identification of a mutation in porcine ryanodine receptor associated with malignant hyperthermia. Science 1991;253:448-451
    CrossRef | Web of Science | Medline

  4. 4

    Levitt RC. Prospects for the diagnosis of malignant hyperthermia susceptibility using molecular genetic approaches. Anesthesiology 1992;76:1039-1048
    CrossRef | Web of Science | Medline

To the Editor:

Dr. Simon's otherwise excellent review of hyperthermia states, “Immersion in ice water is the most effective means of physical cooling.” I disagree.

Heat loss may occur by any of four mechanisms -- conduction, radiation, convection, or evaporation. Evaporative heat loss is the most efficient,1-4 with cooling rates that are two to three times as rapid as those produced by immersion in ice water (which relies on conduction)2. The evaporation of 1 g of water dissipates approximately seven times more heat than melting the same quantity of ice3,4.

When patients are kept wet and air is blown over them, efficient evaporative cooling occurs, with numerous theoretical and practical advantages. Immersion in ice water may result in shivering and cause peripheral vasoconstriction1,3,4. Not only is immersion in ice water physically painful, but it also creates a number of practical problems. These include the need for a large tank, the difficulty in safely lifting a patient into and out of the cooling tub, the inability to perform continuous cardiac or temperature monitoring, the difficulty in providing immediate airway support if the patient vomits or has a respiratory arrest, and the inability to perform defibrillation immediately. There are data that suggest that the use of evaporative cooling results in better survival rates among victims of heatstroke than immersion in ice water5.

Excellent results from evaporative cooling have been obtained by many different complicated or simple methods, such as a specialized body-cooling unit for heat-stricken pilgrims in Mecca, a helicopter's rotors for shipboard sailors kept wet with a garden hose, or tap water and portable house fans for runners with heatstroke2-4.

Corey M. Slovis, M.D.
Vanderbilt University Medical Center, Nashville, TN 37232

5 References
  1. 1

    Wyndham CH, Strydom NB, Cooke HM, et al. Methods of cooling subjects with hyperpyrexia. J Appl Physiol 1959;14:771-776
    Web of Science | Medline

  2. 2

    Weiner JS, Khogali M. A physiological body-cooling unit for treatment of heat stroke. Lancet 1980;1:507-509
    CrossRef | Web of Science | Medline

  3. 3

    Callaham M. Heat illness. In: Rosen P, Baker F, Barkin R, et al., eds. Emergency medicine: concepts and clinical practice. St. Louis: C.V. Mosby, 1987:693-717.

  4. 4

    Tek D, Olshaker JS. Heat illness. Emerg Med Clin North Am 1992;10:299-310
    Medline

  5. 5

    Graham BS, Lichtenstein MJ, Hinson JM, Theil GB. Nonexertional heatstroke: physiologic management and cooling in 14 patients. Arch Intern Med 1986;146:87-90
    CrossRef | Web of Science | Medline

To the Editor:

I am quite concerned about Simon's recommendation that alcohol sponge baths be used to treat hyperthermia. Acute alcohol intoxication with near-fatal coma due to alcohol sponge baths given to reduce fever was reported as early as 1952 in children1 and in an 1969 in an adult2. As a result of many such reports, this practice has been abandoned in favor of the other, more efficacious and safer methods described in Simon's article. Major textbooks of medicine, emergency medicine, and pediatrics no longer mention the use of alcohol sponge baths except for Nelson's Textbook of Pediatrics, which states that they should not be given3.

In a preface to a case report of acute alcohol intoxication due to an alcohol sponge bath, the editor of the American Journal of Diseases in Children lamented, “In some of us who reviewed it, the following brief report stirred memories of cold, unresponsive children who were being bathed in isopropyl alcohol in a closed room in busy emergency departments. We thought the practice had ended, but apparently not!”4 Seven years later, it is unfortunate to see alcohol sponge baths still being advocated as a way to reduce fever. They should never be used for either children or adults.

Marc R. Salzberg, M.D.
Baystate Medical Center, Springfield, MA 01106

4 References
  1. 1

    Senz EH, Goldfarb DL. Coma in a child following use of isopropyl alcohol in sponging. J Pediatr 1958;53:322-323
    CrossRef | Web of Science | Medline

  2. 2

    Wise JR Jr. Alcohol sponge baths. N Engl J Med 1969;280:840-840
    Web of Science | Medline

  3. 3

    Infectious diseases. In: Behrman RE, Kliegman RM, Nelson WE, Vaughan VC III, eds. Nelson textbook of pediatrics. 14th ed. Philadelphia: W.B. Saunders, 1992:648.

  4. 4

    Arditi M, Killner MS. Coma following use of rubbing alcohol for fever control. Am J Dis Child 1987;141:237-238
    Web of Science | Medline

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