From the Guidelines
Malignant hyperthermia is a rare but potentially fatal genetic disorder characterized by a hypermetabolic response to certain anesthetic agents, and the correct answer is (e) it is more common in children than adults. Malignant hyperthermia occurs more frequently in pediatric patients than in adults, with a higher incidence observed in children and young adults, as reported by 1. This condition is triggered primarily by volatile anesthetic gases (such as sevoflurane, desflurane, and isoflurane) and the depolarizing muscle relaxant succinylcholine, as stated in 1 and 1. It is not induced by local anesthetics, nondepolarizing muscle relaxants, or nitrous oxide, making options (a), (b), and (c) incorrect. While malignant hyperthermia does involve electrolyte disturbances during an acute crisis, including hyperkalemia (elevated potassium levels), it is fundamentally a disorder of calcium regulation in skeletal muscle, not primarily a disorder of potassium metabolism, making option (d) incorrect, as explained in 1. The underlying pathophysiology involves a genetic mutation affecting the ryanodine receptor in skeletal muscle, leading to uncontrolled calcium release from the sarcoplasmic reticulum when exposed to triggering agents, resulting in sustained muscle contraction, rigidity, hyperthermia, and a hypermetabolic state. Some key points to consider in the management of malignant hyperthermia include:
- The importance of early recognition and treatment, as delayed diagnosis can lead to increased mortality, as noted in 1
- The use of dantrolene as a treatment for malignant hyperthermia, as recommended in 1 and 1
- The need for careful monitoring and management of patients suspected of having malignant hyperthermia, including the use of activated charcoal filters and careful preparation of anesthesia workstations, as discussed in 1 and 1.
From the FDA Drug Label
In the anesthetic-induced malignant hyperthermia syndrome, evidence points to an intrinsic abnormality of skeletal muscle tissue. In affected humans, it has been postulated that "triggering agents" (e.g., general anesthetics and depolarizing neuromuscular blocking agents) produce a change within the cell which results in an elevated myoplasmic calcium. Malignant Hyperthermia Succinylcholine administration has been associated with acute onset of malignant hyperthermia, a potentially fatal hypermetabolic state of skeletal muscle. The risk of developing malignant hyperthermia following succinylcholine administration increases with the concomitant administration of volatile anesthetics
The correct answers are:
- (b) can be induced by nondepolarizing muscle relaxants: No, the text actually says depolarizing neuromuscular blocking agents.
- (b) is actually incorrect, but (a) can be induced by local anesthetics: No, the text does not mention local anesthetics as triggering agents.
- (c) can be induced by nitrous oxide: No, the text mentions volatile anesthetics, but does not specifically mention nitrous oxide.
- The correct answer is:
- Malignant hyperthermia can be induced by depolarizing muscle relaxants, such as succinylcholine 2
- Malignant hyperthermia can be induced by general anesthetics 3
- There is no information about local anesthetics or nitrous oxide
- There is no information about disordered K+ metabolism in relation to malignant hyperthermia
- There is no information about the prevalence of malignant hyperthermia in children versus adults
From the Research
Malignant Hyperthermia Inducing Agents
- Malignant hyperthermia can be induced by volatile anesthetic gases and the depolarizing muscle relaxant succinylcholine 4, 5, 6, 7, 8
- Nondepolarizing muscle relaxants do not trigger malignant hyperthermia 4
- Nitrous oxide, intravenous induction agents, benzodiazepines, and opioids do not trigger malignant hyperthermia 4
- Local anesthetics are not mentioned as triggering agents in the provided studies
Malignant Hyperthermia Characteristics
- Malignant hyperthermia is related to disordered calcium metabolism, not potassium metabolism 5, 6, 7, 8
- The syndrome is characterized by hypermetabolism, hypercarbia, hypoxia, hyperthermia, and hyperkalemia 4, 5, 6, 7, 8