Rocuronium and atracurium triggered malignant hyperthermia in a 30-year-old male with severe hypertriglyceridemia-induced pancreatitis, which resolved after dantrolene administration.
Case Report (n=1)
Non-depolarizing paralytics such as rocuronium and atracurium can trigger malignant hyperthermia, particularly in the setting of severe metabolic stress.
Abstract Introduction Malignant hyperthermia (MH) is a rare pharmacogenetic disorder of skeletal muscle that manifests as a hypermetabolic crisis in susceptible individuals exposed to certain anesthetics or paralytics. The incidence is reported between 1 in 10,000 to 250,000 anesthetic exposures, with mortality near 10% despite timely dantrolene therapy. Here we present a case of MH following rocuronium and atracurium administration in the context of hypertriglyceridemia-induced pancreatitis. Case Presentation A 30-year-old male presented with three days of worsening epigastric abdominal pain radiating to the back, associated with persistent vomiting and anorexia. He denied alcohol use and prior pancreatitis. Physical examination revealed abdominal tenderness without rebound or guarding. Initial laboratory evaluation showed triglycerides 4,500 mg/dL, lipase 1,000 U/L, and glucose 370 mg/dL. Computed tomography (CT) of the abdomen demonstrated findings consistent with acute interstitial edematous pancreatitis (Figure 1). He was admitted to the ICU for insulin infusion for hypertriglyceridemia and aggressive fluid resuscitation. He rapidly deteriorated into multisystem organ failure requiring endotracheal intubation which included a one-time dose of rocuronium (1mg/kg). Due to vent desynchrony, he was deeply sedated and paralyzed with a continuous atracurium infusion. He developed marked hyperthermia (108 °F), sinus tachycardia, and required vasopressor support with norepinephrine, vasopressin, and epinephrine infusions. Physical exam was significant for muscular stiffness and rigidity. Atracurium was discontinued and multiple doses of dantrolene (2.5 mg/kg) were administered. External cooling and intravenous hydration were initiated, and his hyperthermia resolved soon thereafter. His hospital course was further complicated by rhabdomyolysis (creatine kinase CK peaked at 32,000 U/L), which necessitated continuous renal replacement therapy. He continued to improve and ultimately was discharged from the hospital. Discussion This case illustrates a unique presentation of MH, triggered by administration of the non-depolarizing paralytics rocuronium and atracurium. The rapid clinical evolution, which included severe hyperthermia, hypercapnia, and acidosis, alongside stabilization after dantrolene and offending drug withdrawal, supports a diagnosis of likely MH induced by non-depolarizing paralytics. Although most are associated with inhaled volatile anesthetics and succinylcholine, case reports describing MH related to rocuronium and cisatracurium exist. The pathophysiology involves uncontrolled calcium release through the ryanodine receptor (RYR1) on skeletal muscle, leading to sustained contraction, ATP depletion, and excessive heat generation. In this patient, metabolic stress from his severe pancreatitis and acidosis alongside tissue hypoxia likely exacerbated abnormal intracellular calcium cycling, culminating in MH. This case underscores the necessity of maintaining MH on the differential diagnosis for unexplained hyperthermia in patients receiving neuromuscular blockade. This abstract is funded by: None
Johnkutty et al. (Fri,) conducted a case report in Malignant hyperthermia and hypertriglyceridemia-induced pancreatitis (n=1). Rocuronium and atracurium was evaluated. Rocuronium and atracurium triggered malignant hyperthermia in a 30-year-old male with severe hypertriglyceridemia-induced pancreatitis, which resolved after dantrolene administration.