Safe Duration of Postoperative Monitoring for Malignant Hyperthermia Patients Administered Non-Triggering Anaesthesia: An Update

Barnes, C; Stowell, Kathryn M.; Bulger, Terasa; Langton, E E; Pollock, Neil

doi:10.1177/0310057x1504300115

Cited by 17 publications

(5 citation statements)

References 67 publications

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“…While traditionally, MH susceptible patients who have undergone non-triggering anesthesia were monitored routinely for four hours in the post-anesthesia care unit, this practice is no longer thought to be necessary [ 171 ]. Pretreatment with dantrolene is also not necessary.…”

Section: Reviewmentioning

confidence: 99%

Malignant hyperthermia: a review

Rosenberg

Pollock

Schiemann

et al. 2015

Orphanet J Rare Dis

429

529

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Malignant hyperthermia (MH) is a pharmacogenetic disorder of skeletal muscle that presents as a hypermetabolic response to potent volatile anesthetic gases such as halothane, sevoflurane, desflurane, isoflurane and the depolarizing muscle relaxant succinylcholine, and rarely, in humans, to stressors such as vigorous exercise and heat. The incidence of MH reactions ranges from 1:10,000 to 1: 250,000 anesthetics. However, the prevalence of the genetic abnormalities may be as great as one in 400 individuals. MH affects humans, certain pig breeds, dogs and horses. The classic signs of MH include hyperthermia, tachycardia, tachypnea, increased carbon dioxide production, increased oxygen consumption, acidosis, hyperkalaemia, muscle rigidity, and rhabdomyolysis, all related to a hypermetabolic response. The syndrome is likely to be fatal if untreated. An increase in end-tidal carbon dioxide despite increased minute ventilation provides an early diagnostic clue. In humans the syndrome is inherited in an autosomal dominant pattern, while in pigs it is autosomal recessive. Uncontrolled rise of myoplasmic calcium, which activates biochemical processes related to muscle activation leads to the pathophysiologic changes. In most cases, the syndrome is caused by a defect in the ryanodine receptor. Over 400 variants have been identified in the RYR1 gene located on chromosome 19q13.1, and at least 34 are causal for MH. Less than 1 % of variants have been found in CACNA1S but not all of these are causal. Diagnostic testing involves the in vitro contracture response of biopsied muscle to halothane, caffeine, and in some centres ryanodine and 4-chloro-m-cresol. Elucidation of the genetic changes has led to the introduction of DNA testing for susceptibility to MH. Dantrolene sodium is a specific antagonist and should be available wherever general anesthesia is administered. Increased understanding of the clinical manifestation and pathophysiology of the syndrome, has lead to the mortality decreasing from 80 % thirty years ago to <5 % in 2006.

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Section: Reviewmentioning

confidence: 99%

Malignant hyperthermia: a review

Rosenberg

Pollock

Schiemann

et al. 2015

Orphanet J Rare Dis

429

529

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“…3) Postoperative period: There is no need for extended stay of MH-susceptible patients in the recovery room or in hospital as there is no risk of MH reaction if these patients are given trigger-free anesthetics 32. Clinical case scenario A 14-yr-old girl (weight: 50 kg) is booked for a laparoscopic appendectomy.…”

mentioning

confidence: 99%

Updated guide for the management of malignant hyperthermia

Riazi

Kraeva

Hopkins

2018

Can J Anesth/J Can Anesth

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“…Studies suggest that ambulatory anesthesia is safe for MH-susceptible patients; the recommended time required for monitoring serious adverse events has declined over the years, from four to up to 1 h, depending on the procedure and monitoring site. 9 , 21 , 22 , 23 …”

Section: Discussionmentioning

confidence: 99%