Malignant hyperthermia

Malignant Hyperthermia in Bariatric Surgery: A Case Study With Clinical, Pathophysiological, Biochemical and Biophysical Correlations

“…Hyperkalemia was noted in our patient on the afternoon of postoperative day 1. Although the literature describes case reports with contradictory serum potassium concentration, reviews of MH specify that hyperkalemia is indicative of MH crisis triggering [1,3,7,8,12,17]. According to Mahmood (2018) [40], hyperkalemia can induce fatal cardiac dysrhythmias.…”

“…Malignant hyperthermia (MH) is an acute pharmacogenetic disorder, which while uncommon is potentially fatal [1,2]. In humans, susceptibility to MH is an inherited disorder and it has an autosomal dominant pattern [3][4][5][6][7]. To date, genes located at six chromosomal loci associated with MH have been described: 1) Ryanodine receptor type 1 (RyR1) gene, ryanodine receptor found in skeletal muscle (chromosomal locus 19q13.1.…”

“…To date, genes located at six chromosomal loci associated with MH have been described: 1) Ryanodine receptor type 1 (RyR1) gene, ryanodine receptor found in skeletal muscle (chromosomal locus 19q13.1. ); 2) CACNA1S gene, which encodes for the alpha-1S subunit of dihydropyridine (chromosomal locus 1q32); 3) A variant of the STAC3 gene, which encodes an important protein for excitationcontraction coupling via trafficking the voltage sensor into the correct T-tubular location (chromosomal locus 7q21-q22); 4) SCN4A gene (possible), related to voltage-dependent sodium channel of skeletal muscle (chromosomal locus 17q11.2-q24); and, not yet identified genes for 5) chromosomal loci 3q13.1 and 6) 5p [2,5,[7][8][9][10]. However, these genes associated with MH show incomplete penetrance and variable expression [4,5,7].…”

“…Muscle relaxation occurs when stimulation of the motor nerve stops and the intracellular adenosine triphosphate (ATP)-dependent Ca 2+ pump transports intracytoplasmic Ca 2+ into the sarcoplasmic reticulum lumen [5,7,13,14]. MH is a calcium channelopathy of skeletal muscle [15] in which a constant increase of intracytoplasmic Ca 2+ concentration occurs causing a change in cellular metabolism [5,[7][8][9]13]. A hypermetabolic state develops when susceptible patients are exposed to halogenated volatile inhalational anesthetic agents (halothane, isoflurane, enflurane, sevoflurane, desflurane and methoxyflurane), depolarizing muscle relaxants (e.g., succinylcholine), and/or extreme physical activity in hot environments [3,7,8,[16][17][18].…”

“…Nevertheless, the prevalence of genetic variants or mutations of an individual susceptible to MH is estimated to be 1 in 2,000 -3,000 [5,6,10]. MH affects all ethnic groups and both sexes, although there is a greater predisposition for men and children, and it is atypical in the elderly [3,[5][6][7]. The MH episode can occur both in the first exposure to the substances that triggers the crisis and in subsequent contacts [8,19,20].…”