Serum caffeine levels were reported on day 3 following the initial presentation, as shown in Table 3 and Fig 1. Metabolic acidosis had been corrected by dialysis. The patient subsequently maintained urine output of 100 to 200 mL/h and received appropriate calcium and magnesium replacement. Because both cardiovascular (normal sinus rhythm and blood pressure) and neurologic symptoms improved, we discontinued further HD. After the second HD session, serum potassium levels normalized without needing further potassium supplementation. This suggested continued activity of the drug (caffeine) or one of its metabolites.Ĭaffeine levels were redrawn 6 hours after the first HD session, and a second HD session was performed with similar parameters. We followed up serum potassium levels ( Table 1) as a marker of adrenergic activity (in consideration of concurrent losses from high urinary flows and against a high dialysate potassium concentration) the patient needed large doses of IV potassium replacement (200 mmol of IV potassium chloride in the first 24 hours). Our patient tolerated the first HD session without interruption. It was measured using a high-performance liquid chromatography method. We aimed to maintain urine output at >100 mL/h by an infusion of Ringer’s lactate at 125 to 150 mL/h.Ībbreviation: K Uf, ultrafiltration coefficient.īlood was drawn for serum caffeine levels and sent to an external laboratory to measure levels at presentation, immediately before dialysis, and after finishing the first dialysis session however, results would not be available for up to 48 hours. Details of the dialysis session and dialysate composition are illustrated in Table 2. Dialysis was initiated 5 hours after presentation (7 hours after presumed ingestion time). The goal was to help with drug elimination given the patient’s clinical deterioration. The decision to initiate hemodialysis (HD) was based on the reported high dose of caffeine ingestion. Another peripheral IV line was established, and a temporary dialysis catheter was inserted. Fifty grams of activated charcoal was given through a nasogastric tube to facilitate gastrointestinal elimination. This required large doses of propofol, midazolam, and fentanyl. Despite initial hemodynamic stability, rapid response intubation was performed due to deterioration in the level of consciousness, recurrent episodes of supraventricular tachycardia, and the risk for aspiration. The patient received lorazepam, ondansetron, and intravenous (IV) potassium chloride in the emergency department and then transferred to the intensive care unit. Screening for other toxic ingestion was done and was reported as all negative.Ĭritical care, nephrology, and poison control teams were involved immediately. ![]() Initial laboratory results are shown in Table 1. The electrocardiogram showed sinus tachycardia, with subsequent development of supraventricular tachycardia. This individual was of average size, and although the initial Glasgow Coma Scale score was 15, incoherence and confusion soon developed. Vital signs were blood pressure, 155/88 mm Hg heart rate, 132 beats/min (later accelerated to >200 beats/min) respiratory rate, 32 breaths/min temperature, 35.8 ☌ and oxygen saturation, 97% while breathing room air. There was no history of alcohol or other recreational drug ingestion. On arrival to the emergency department 2 hours after ingestion, this individual was extremely agitated, irritable, diaphoretic, and hyperventilating and had episodes of repeated vomiting. This individual was not receiving any regular medications and had normal baseline kidney function. An individual ingested 60,000 mg of caffeine in tablet form.
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