A 7-year-old boy with no significant past medical history was transported to an outside emergency department by emergency medical services after multiple episodes of emesis followed by a witnessed 10-minute episode of "shaking all over." In the emergency department, the patient was found to be profoundly acidotic with an arterial pH of 6.9, bradycardic (heart rate 50 beats/min), hypotensive (blood pressure 69/28 mm Hg), and hyperglycemic (serum glucose of 305 mg/dL). A preliminary diagnosis of diabetic ketoacidosis was established. Therapy was initiated with dextrose-containing intravenous fluids and a regular insulin drip. Following initial interventions targeted at stabilization of the patient's condition, he was transferred to our pediatric intensive care unit for further evaluation and management. On arrival, the patient's adoptive mother reported that he had been well-appearing up until shortly before the emesis began, when he became tired and sluggish. She denied any recent illnesses, fevers, sick contacts, or possible ingestions. The only medications reported to be in the home were aspirin, metformin, and prenatal vitamins.Physical exam revealed a well-developed boy who was drowsy and irritable. Vital signs included a temperature of 99°F, heart rate of 82 beats/min, blood pressure of 78/57 mm Hg, respiratory rate of 40 breaths/min, and oxygen saturation of 100% on room air. Pupils were equal and reactive and mucous membranes were dry. Cardiac exam was significant for bradycardia with strong pulses and normal capillary refill. Abdominal exam was benign. Neurologic exam was notable for a Glasgow Coma Score of 14 secondary to confusion; reflexes, motor, and sensory exams were unremarkable. Laboratory evaluation revealed negative serum and urine ketones, metabolic acidosis with arterial pH of 7.156, anion gap of 19, lactic acid of 10 mmol/L, serum glucose of 159 mg/dL, sodium 143 mmol/L, bicarbonate 14 mmol/L, potassium 4.1 mmol/L, magnesium 2.3 mg/dL, creatinine of 2.3 mg/dL, serum osmolarity of 301 mosm/kg, and negative urinary toxicology screen. Cerebrospinal fluid analysis was unremarkable. Electrocardiogram revealed junctional rhythm with a rate of 78 beats/min (Figure 1). Echocardiogram revealed normal anatomy and biventricular function. The patient was started on intravenous ceftriaxone and dopamine infusion at 5 µg/ kg/min to maintain systemic blood pressure.The patient's mental status deteriorated over the several hours following admission, requiring elective intubation and mechanical ventilation. Persistence of hypotension and onset of oliguria necessitated increasing doses of dopamine and the addition of intravenous norepinephrine at 0.01 µg/kg/min. After a period of 18 hours following admission, as infectious or cardiac causes of the patient's shock became increasingly unlikely, mass spectrometry of the urine was performed in the search for a toxic cause. Urine mass spectrometry revealed diltiazem, a calcium channel blocker (CCB).
Final DiagnosisDiltiazem ingestion resulting in bradycardia, hypoten...