A Near‐Fatal Overdose of Carisoprodol (SOMA): Case Report

Carisoprodol is a centrally acting skeletal muscle relaxant, structurally and pharmacologically related to meprobamate (1). It was first introduced in the 1950s for the relief of back pain and muscle spasms. Carisoprodol is metabolized to meprobamate, a potent and addictive sedative. Carisoprodol also has weak anticholinergic, antipyretic, and analgesic properties (2,3). Poisoning with carisoprodol is reported infrequently. Following ingestion of a large dose, death is attributed to CNS depression with respiratory failure. Ingestion of 3.5 g of carisoprodol has resulted in the death of a 4-year-old (4). Seizures and coma persisting for 33h (5) followed ingestion of up to 14.7 g of carisoprodol in an adult, whereas ingestion of 9.45 g has resulted in milder CNS effects (2). We report a 40-year-old white male who ingested 21 g (60 tablets) of carisoprodol along with an unknown quantity of chlordiazepoxide and temazepam. This case is worth reporting because it illustrates one of the highest-reported blood levels of carisoprodol. The patient was found unresponsive by the paramedics at a video store, where he underwent emergent endotracheal intubation and received artificial ventilation. On arrival to the Emergency Department, he was unresponsive to painful stimuli. He had a HR of 130 bpm, BP 220/118 mm HG, a temperature of 100.5 F, and was manually ventilated. The patient also demonstrated anticholinergic signs. Pupils were symmetric, dilated, and sluggishly reactive to light. Breath sounds were coarse with rales on the right side. Abdominal exam revealed absent bowel sounds as often seen in an anticholinergic toxidrome. He was deeply comatose, with absent tendon and plantar reflexes. His skin was warm and dry. The patient had a past medical history significant for psychiatric illness, substance abuse, chronic back pain, and hypertension. Initial blood gas analysis revealed a mild respiratory acidosis with a ph of 7.31 and a pCO2 of 50.1 mmHg (partially compensated with artificial ventilation). Other baseline labs were normal. The toxicology urine immunoassay was positive for cocaine metabolites and benzodiazepines. Chest radiographs showed a right upper lobe infiltrate. EKG revealed sinus tachycardia with a prolonged QT interval (exact measurements no longer available) mimicking a possible tricyclic overdose. In view of the possibility of multiple-drug ingestion and since he presented to the ER within an hour after his ingestion, the treatment in the emergency department consisted of gastric lavage and activated charcoal with sorbitol. Naloxone was used as part of the coma cocktail, and sodium bicarbonate was used to reverse cardiac toxicity from a tricyclic antidepressant. The use of flumazenil to reverse the possible benzodiazepine component of his presentation was considered ill-advised as the patient was on chronic benzodiazepine therapy, thus increasing the risk of withdrawal seizures. Intravenous clindamycin was initiated for aspiration pneumonia. After 36h in the intensive care unit the patient was extubated. He was hemodynamically stable and returned to his baseline mental status. Blood concentrations of carisoprodol measured by gas chromatography were 107 mg/L (therapeutic range: 10–40 mg/L and fell to 47.6 and 2.2 mg/L on the second and third days, respectively. The