PubMed HealthSearch

PubMed · 707024

Malignant hyperthermia.

Abstract

Malignant hyperthermia is now recognized as a distinct entity in anesthetic practice and can be considered as a pharmacogenetic disease of obscure etiology occuring in man and pigs with a dominant inheritance. A close association with myopathy has been noted. Commonly used muscle relaxants or anesthetic drugs can act as triggering agents in genetically susceptible patients, who develop a real hypermetabolic state, characterized by a rapid rise in body temperature, muscular rigidity, tachycardia and tachypnoea, cyanosis and severe respiratory and metabolic acidosis, the lethality being about 60%. Other clinical, biochemical and histopathological features of this condition are described. The prevention and early diagnosis of this syndrome is very important. Therefore, it is necessary in the preanesthetic evaluation, to obtain information from the patient, with regard to previous anesthetic experiences, and to have a more exact anamnesis in patients with muscular diseases or with other members of the family under suspicion. Some screening methods are described. The prognosis of malignant hyperthermia depends on an early diagnosis. Although the incidence is, fortunately, small, this condition is sufficiently significant and acute in nature to require that anesthesiologist be aware of its clinical pathophysiology and prepared to recognize and treat it promptly. Therefore body temperature should be controlled continuously in all anesthetized patients, particularly in the younger age group and especially in those in which symptoms of muscle rigor have been observed particularly after application of succinylcholine and halothane. A regime of treatment is suggested, based on current concepts of the pathogenesis. It consists in establishing effective and rapid cooling, reversal of tissue hypoxia and correction of respiratory and metabolic acidosis and hyperkalemia. Specific therapy with dantrolene sodium may prove to be an answer to this serious problem.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R Demeyere. 1978. Malignant hyperthermia.. https://pubmed.ncbi.nlm.nih.gov/707024/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

General anaesthetics inhibit the responses induced by glutamate receptor agonists in the mouse cortex.

The effects of several general anaesthetics on the responses evoked by the excitatory amino acid agonists N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) were investigated in mouse cortical wedges placed in a two compartment bath and superfused with a nominally Mg(2+)-free Krebs solution. Chloroform (3-6 mM) and halothane (1-3 mM) preferentially antagonized AMPA responses; thiopental (0.1-0.4 mM), diethyl ether (10-30 mM) and isoflurane (1-3 mM) antagonized both AMPA or NMDA responses while ketamine antagonized NMDA responses in a highly selective way. The antagonism of the excitatory amino acid responses exerted by the anaesthetics was non competitive in nature. The inhibition of excitatory amino acid receptor function may be one of the mechanisms whereby general anaesthesia is produced.

Anesthetics

Nature of alcohol and anesthetic action on cooperative membrane equilibria.

A generalized, colligative thermodynamic framework is used to treat the action of solutes on cooperative membrane equilibria. Configurational entropy, the randomness imparted by solutes through the partitioning or mixing process, is implicated as the energetic driving force for the action of anesthetics on cooperative membrane equilibria. The equilibria predicted to be most sensitive to solute action--in which the dilute solute causes a perturbation equivalent to a large change in temperature--are (1) low-enthalpy processes that coincide with (2) large partitioning differences between states. The model stresses that solutes do not act at a single site, but on both states in an equilibrium, and that the perturbation is determined by the difference in entropy. Evidence for the thermodynamic framework is obtained from the partitioning behavior of the general anesthetic 1-hexanol into a model lecithin (DMPC; 1,2-dimyristoyl-sn-glycero-3-phosphocholine) membrane as a function of temperature and alcohol concentration. The low-enthalpy equilibrium between the gel (L beta') and ripple states (P beta') (pretransition) is more sensitive to 1-hexanol than the high-enthalpy equilibrium between the ripple (P beta') and fluid bilayer states (L alpha) (main transition). The perturbations of both equilibria are accurately described by the colligative thermodynamic framework. The results suggest that alcohols and anesthetics act through entropy to upset the natural thermal balance that maintains native membrane architecture.

Anesthetics