Case Files from the University of California San Diego Health System Fellowship Coma and Severe Acidosis: Remember to Consider Acetaminophen

Abstract

A 28-year-old man was brought to the Emergency Department (ED) for evaluation of a depressed level of consciousness that developed while in jail. Sixteen hours previously, he had been arrested on charges of murder. The patient's mental status was reported as normal at the time of arrest, and it had remained so during several hours of interrogation and during the booking process at jail. Following interrogation, the patient was placed into a cell with no other inmates. During the jail intake process, the patient had not reported any history of medical problems nor was he prescribed with any medications. Paramedics arrived to find him unresponsive, but maintaining airway reflexes and hemodynamically stable. They measured a blood glucose of 300 mg/dL and noted one episode of blood-tinged emesis during transport to the ED. No seizure activity was witnessed.On arrival to the ED, vital signs were: heart rate 132/min, blood pressure 129/74 mmHg, temperature 35.3°C (95.5°F), respiratory rate 24/min, and 100 % oxygen saturation on 15 l/ min of oxygen delivered by non-rebreather face mask.Physical examination was notable for a depressed level of consciousness. His eyes remained closed to pain, he withdrew all extremities equally to pain, and he was non-verbal. He had no signs of trauma, and his pupils were normal in size and reactive. Rapid sequence tracheal intubation was performed for airway protection. An electrocardiogram was normal except for sinus tachycardia at a rate of 111/min. An initial peripherally drawn arterial blood gas obtained immediately after intubation revealed: pH 6.97, pCO 2 40 mmHg, pO 2 215 mmHg. A computed tomography scan of the brain was normal. Initial blood chemistry panel was significant for a serum bicarbonate of 7 mEq/L, glucose of 362 mg/dL, and a normal potassium, blood urea nitrogen (BUN), creatinine, and calcium. The initial serum anion gap was 34 mEq/L. Measured serum osmolality was 320 mOsm/kg, yielding an osmol gap of 9 mOsm/kg (using formula of [2(Na)+BUN/2.8+glu-cose/18] for calculated serum osmolarity). Initial lactate was 156.5 mg/dL (normal reference range 4.5-19.8 mg/dL) and beta-hydroxybutyrate (βHB) 2.9 mg/dL (normal reference range 0.0-2.8 mg/dL). Initial liver panel included an aspartate aminotransferase (AST) of 64 U/L, alanine aminotransferase (ALT) of 27 U/L, and bilirubin of 0.4 mg/dL. Prothrombin time was 13.1 s (reference range 9.7-12.5), and lipase was normal at 25 U/L. Initial creatinine phosphokinase (CK) was slightly elevated at 373 U/L (0-175). Urinalysis was positive for small ketones and crystals were not present. Measurements of acetone and acetoacetate were not performed. Serum ethanol and salicylate levels were undetectable, and a urine drug of abuse panel by immunoassay was negative for amphetamines as a class, barbiturates as a class, benzodiazepines as a class, benzoylecgonine (cocaine metabolite), methadone, opiates as class, oxycodone, phencyclidine, and tetrahydrocannabinoids. Iron concentration was normal at 87 mcg/dL.Over the first hour of management,...

Fomepizole should be used more liberally in paracetamol overdose

“…10 Severe paracetamol poisoning not only includes oxidation of paracetamol to N-acetyl-p-benzoquinone imine (NAPQI) but also produces mitochondrial toxicity resulting in metabolic acidosis, 11 hyperlactaemia 12 and depressed level of consciousness. 13 These metabolic effects, which precede hepatotoxicity, are partly mediated by direct inhibition of mitochondrial respiration. 14,15 Cytosolic and microsomal CYP 2E1 (EC 1.14.14.1) produce NAPQI, which mediates hepatotoxicity.…”