Severe caffeine poisoning treated with intermittent hemodialysis under circulatory support.

Caffeine poisoning can cause fatal ventricular arrhythmias. In this report, we describe a case of severe caffeine poisoning with extraordinarily high blood caffeine levels. Despite developing refractory ventricular fibrillation, the patient was successfully treated with intermittent hemodialysis (IHD) under circulatory support by venoarterial extracorporeal membrane oxygenation (VA-ECMO). A 22-year-old male was transported to our hospital approximately 2.5 h after ingesting 200 highly caffeinated tablets (200 mg/tablet) (40 g caffeine total) in a suicide attempt. On arrival, the patient vomited frequently with a Glasgow Coma Scale score E3V2M5, heart rate 185 beats/min, and a blood pressure of 97/62 mmHg. Shortly after arrival, the patient developed ventricular fibrillation which was refractory either to three electrical defibrillations or antiarrhythmic drugs, resulting in endotracheal intubation for mechanical ventilation and VA-ECMO. Starting from 2 h after arrival, intermittent hemodialysis (IHD) was performed for 11 h, which markedly improved clinical symptoms and circulatory parameters. Serum caffeine level was 454.9 mg/dL upon arrival at the hospital, but it decreased to 55.5 mg/dL by the end of IHD treatment. Renal replacement therapy (RRT) including intermittent hemodiafiltration, continuous hemodiafiltration, and IHD was continued because of rhabdomyolysis with myoglobinuria and secondary caused acute kidney injury. The patient was weaned off VA-ECMO on hospital day 7, extubated on hospital day 18, weaned from RRT on hospital day 46, and was transferred to another hospital for physical rehabilitation on hospital day 113. IHD under circulatory support by VA-ECMO should be considered in severe caffeine poisoning causing potentially fatal arrhythmias.

Severe caffeine poisoning successfully treated with high flow continuous hemodialysis.

In recent years, severe or lethal cases of caffeine poisoning after large or massive ingestion of caffeinated tablets have increased in Japan. Here we report the case of a 23-year-old male who ingested high-dose caffeine tablets (total: 32.4 g caffeine) in a suicide attempt. He was transferred to our hospital about 2 h after ingesting the tablets and presented with repeated vomiting and tremor in the trunk and extremities. His respiratory rate was 40 breaths/min, heart rate 240 beats/min, blood pressure 109/77 mmHg, and Glasgow Coma Scale E3V2M5. Blood tests revealed metabolic acidosis compensated with respiratory alkalosis, hyperlactatemia, hypokalemia, hyperglycemia, and leukocytosis. After tracheal intubation, gastric lavage was performed and activated charcoal was administered. The patient gradually became hypotensive (systolic blood pressure < 90 mmHg) with a heart rate > 250 beats/min, and non-sustained ventricular tachycardia frequently occurred. Given the lack of response to intravenous noradrenaline and landiolol, high flow continuous hemodialysis (CHD) was initiated 4 h after tablet ingestion with a blood flow rate of 150 mL/min and dialysate flow rate of 2000 mL/h. This dramatically improved his clinical signs and symptoms, especially during the first 3 h. His serum caffeine concentration was 240.9 µg/mL on admission and 344.0 µg/mL at the initiation of high flow CHD, but rapidly decreased to 153.8 µg/mL 3 h after initiating high flow CHD. Our findings suggest that high flow CHD may be effective in treating cases of severe caffeine poisoning with hemodynamics too unstable for intermittent hemodialysis.

Serum potassium level as a biomarker for acute caffeine poisoning.

AIM: Acute caffeine poisoning presents with hypokalemia, although a relationship between potassium levels and blood concentrations of caffeine has not been established. A correlation between serum potassium level and blood caffeine concentration could establish serum potassium as a simple marker to assess caffeine toxicity in patients with acute toxicity. We investigated whether serum potassium, a symptom of acute caffeine poisoning, could be a parameter correlated with blood caffeine levels. METHODS: We enrolled 85 patients treated for acute caffeine poisoning between January 2012 and March 2019 with blood caffeine levels measured after an overdose of a caffeine-containing over-the-counter drug and for whom serum potassium levels were available. We examined the correlation between serum potassium and blood caffeine concentration. A receiver operating characteristic curve was created with serum potassium values to stratify participants into two groups by blood caffeine concentrations: <20 or ≥20 mg/L (toxic dose) and <80 or ≥80 mg/L (lethal dose). The lethal cut-off value was calculated. RESULTS: The correlation coefficient between serum potassium level and blood caffeine concentration was -0.612 (R 2 = 0.374), indicating a negative correlation. The areas under the curve at blood caffeine concentrations of 20 mg/L (toxic dose) and 80 mg/L (lethal dose) and serum potassium levels were 0.716 and 0.888 (sensitivity, 0.829 and 0.919; specificity, 0.568 and 0.818; cut-off, 3.3 mEq/L and 2.9 mEq/L), respectively. CONCLUSION: Serum potassium levels are associated with blood caffeine concentrations; K+ of 3.3 mEq/L and 2.9 mEq/L indicate acute caffeine poisoning in the toxic and lethal dose, respectively.

Urinary glucose and ketone bodies as indicators of acute caffeine poisoning.

AIM: In various countries, many fatal health problems have been reported due to high intake of caffeine-rich energy drinks, tablets, and powders. In patients with acute caffeine poisoning, determination of blood caffeine concentration is an important yet difficult task. We aimed to assess whether the presence of glucose and ketone bodies in urine reflected the blood caffeine concentration in patients with acute caffeine poisoning. METHODS: From April 2010 to March 2018, 25 patients with an overdose of only caffeine-rich tablets were admitted to our hospital. Their clinical features were investigated. In addition, we investigated whether the glucose and ketone bodies in the urine reflected blood caffeine concentration in 23 patients who underwent the urine qualitative test at admission. RESULTS: The majority of the patients were young healthy women, whose average caffeine ingestion was 15.6 ± 8.1 g. Initial urine examinations showed glucose in 60% (14/23) of patients and ketone bodies in 57% (13/23) of patients. Ketone bodies or glucose were found in 78% (18/23) of the patients. The correlation between blood caffeine concentration and urinary glucose was R = 0.625, blood caffeine concentration and ketone bodies was R = 0.596, and blood caffeine and both was R = 0.76. CONCLUSION: Urine qualitative test is effective for differential diagnosis and severity assessment of acute caffeine poisoning in patients.

Bidirectional ventricular tachycardia induced by caffeine poisoning.

Bidirectional ventricular tachycardia (BVT) is a tachyarrhythmia characterized by 180-degree beat-to-beat alteration in the QRS axis. BVT is traditionally known as an electrocardiography (ECG) finding pathognomonic of digitalis poisoning and a hallmark of catecholamine-induced ventricular tachycardia. Apart from digitalis poisoning, aconitine poisoning is the only reported cause of poisoning-related BVT, and no report of caffeine-poisoning-related BVT is as yet available. A-27-year-old woman was transported to hospital with cardiac arrest from ventricular fibrillation after taking a massive dose of a caffeine-containing supplement (corresponding to 6 g of caffeine) 6 h before presentation. Return of spontaneous circulation (ROSC) was achieved by defibrillation. She developed BVT after ROSC. Hemodialysis was performed to remove the causative drug from the blood, with subsequent resolution of BVT and hemodynamic stabilization. At presentation, she had a blood caffeine concentration of 232 µg/mL. A suggested mechanism of development of BVT is that increased intracellular calcium concentration causes delayed afterdepolarization, which induces alternate occurrence of triggered activities within different His-Purkinje fibers, and thereby produces characteristic ECG findings. Caffeine acts on the ryanodine receptor to promote calcium release from the sarcoplasmic reticulum, and thus can induce BVT via the same mechanism. Caffeine poisoning can be treated by dialysis. In cases of BVT induced by caffeine poisoning, hemodynamic stabilization can be achieved by emergency dialysis.

Plasma lactate concentration as an indicator of plasma caffeine concentration in acute caffeine poisoning.

AIM: Severe caffeine poisoning is rare, but is associated with high mortality. Plasma caffeine concentration is one of the indications of treatment of caffeine poisoning; however, it is not easily measured at most emergency departments. If the plasma lactate concentration and the plasma caffeine concentration were correlated, the plasma lactate concentration may be an indication of caffeine poisoning. In this study, we investigated the correlation between the plasma lactate concentration and the plasma caffeine concentration. METHODS: From April 2010 to March 2012, 18 patients with severe caffeine poisoning by overdose were admitted at our Emergency Center. The plasma lactate concentration and plasma caffeine concentration of 10 patients were determined at the same time at 12-24 h after admission. These findings were plotted and we analyzed the correlation and trends in these concentrations. RESULTS: There were strong correlations between the plasma lactate concentration and the plasma caffeine concentration at admission (n = 18) and at 12-24 h after admission (n = 10) (correlation coefficients, 0.95 and 0.91, respectively). There was a strong positive correlation between the trend of the plasma lactate concentration and the plasma caffeine concentration (n = 10). The correlation coefficient was 0.91. CONCLUSION: These results are extremely beneficial for emergency department clinical physicians because such findings permit the determination of the severe caffeine poisoning patient. Additionally, the plasma lactate concentration might be one of the indicators of hospitalization and discharge.