IS CRITICAL CARE MYOPATHY A CONTRAINDICATION FOR SUCCINYLCHOLINE?

Abstract

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Succinylcholine, a depolarizing muscular blocker, has widespread use for rapid sequence intubation (RSI) in the intensive care unit (ICU), emergency department, and operating room. The advantageous pharmacologic profile includes rapid onset of action (40-60 secs), short duration (6-10 mins), and better intubation conditions such as ease of laryngoscopy and diaphragm inactivation. There are recognized adverse effects including benign manifestations (muscle fasciculations) to life-threatening conditions (acute hyperkalemia and malignant hyperthermia). Scenarios with increased risk include muscular dystrophies, rhabdomyolysis, crush/burn injuries, malignant hyperthermia, and abdominal infections. We present a case of life-threatening hyperkalemia after administration in the setting of critical care myopathy. CASE PRESENTATION: A 63-year-old woman was admitted for acute respiratory distress syndrome from COVID-19 pneumonia. Treatment included steroids, neuromuscular blockade, and prone positioning. Due to frequent ventilator associated pneumonias and difficulty with airway hygiene, endotracheal (ET) tube exchange was planned on hospital day 34. Succinylcholine was utilized given suitable creatinine clearance, normal serum potassium, and sinus rhythm. The removed ET tube had dark, thick, adherent secretions. Less than one minute from administration, telemetry changed to a wide QRS complex and degenerated into pulseless ventricular fibrillation. There was no preceding hypoxemia. The patient received ACLS with defibrillation for recurrent ventricular fibrillation with ROSC. DISCUSSION: Succinylcholine binds to the post-synaptic nicotinic acetylcholine receptor on the motor endplate causing depolarization. Receptor activation triggers efflux of intracellular potassium into the plasma. Receptor upregulation occurs in pathologic conditions including lower motor neuron disorders, immobilization, burns, and muscular dystrophies. Myopathies have inherent membrane fragility and increased permeability producing release of potassium. The development of critical illness myopathy, polyneuropathy, and polyneuromyopathy in the ICU has an incidence of 25-83%. Proposed mechanisms include myosin loss, necrosis of the muscle, muscle membrane dysfunction, denervation of the muscle, nerve ischemia, and axonal injury. Activation of the acetylcholine receptors and sustained muscle contraction in this state can result in devastating hyperkalemia. CONCLUSIONS: Succinylcholine as a paralytic medication for RSI in patients with critical care myopathy should give providers clinical equipoise. There is a risk for acute hyperkalemia due to the damaged muscle membrane and upregulated acetylcholine receptors. REFERENCE #1: Tran, D. T. T., et al. "Rocuronium vs. succinylcholine for rapid sequence intubation: a Cochrane systematic review." Anaesthesia 72.6 (2017): 765-777. REFERENCE #2: Martyn, J. A. Jeevendra, and Martina Richtsfeld. "Succinylcholine-induced hyperkalemia in acquired pathologic statesetiologic factors and molecular mechanisms." Anesthesiology: The Journal of the American Society of Anesthesiologists 104.1 (2006): 158-169. REFERENCE #3: Shepherd, Starane, Ayush Batra, and David P. Lerner. "Review of critical illness myopathy and neuropathy." The Neurohospitalist 7.1 (2017): 41-48. DISCLOSURES: No relevant relationships by Bhupinder Natt, source=Web Response No relevant relationships by Alan Nyquist, source=Web Response