Caffeine fatalities—four case reports
Introduction
Caffeine has been used as a pharmaceutical in the treatment of apnoea of premature infants, is a component in some analgesics and above all is used as a stimulant in a number of beverages. It is also an ingredient in “look-alike drugs” or healthfood products sold as appetite supressants [1].
Caffeine has long been recognized as an addictive substance. Numerous toxic effects have been described. Death due to caffeine overdose is considered rare and case reports of death from caffeine toxicity are not very frequent. However, over the years there have been a number of reports concerning deaths mainly due to intake of “look-alike drugs” containing caffeine [2], [3], [4], [5], [6], [7].
Caffeine is a natural alkaloid methylxanthine. The pharmacodynamic profile of caffeine is similar to that of theophylline, another methylxanthine. Both block the adenosine receptor, which is considered to be the mechanism of action in concentrations normally reached [8] and act as a phosphodiesterase inhibitor. Caffeine increases the intracellular calcium concentration, causes noradrenaline release and sensitises dopamine receptors [1]. The resulting pharmacological effects of caffeine include central nervous system and cardiac stimulation.
The toxic effects of caffeine include vomiting, abdominal pain and CNS symptoms, including agitation, altered conscious state, rigidity and seizures. The cardiovascular effects include supraventricular and ventricular tachyarrhythmias.
The direct cause of death is often described to be ventricular fibrillation. It has been shown in anesthetized rats that ventricular fibrillation accounts for the lethal outcome of caffeine poisoning [9].
In humans a blood concentration greater than 100 μg/ml is considered lethal [10], [11].
In this paper we report four fatal intoxications with caffeine which we have seen during the last year. In Sweden 95% of all autopsies in forensic medicine are routinely screened for alcohol and about 150 different substances, mainly pharmaceuticals.
Section snippets
Materials and methods
At the autopsy blood from the femoral vein was collected and potassium fluoride was added as a preservative to a concentration of 1–2%. The samples were stored at +4 °C until analysed. Ethanol was analysed in duplicate by head-space gas-chromatography and the mean value was reported. The limit of quantification was 0.10 mg/ml. Drugs including caffeine were analysed by capillary gas-chromatography with a nitrogen specific detector as described in detail previously [12]. Ephedrine was analysed by a
Case 1
A 54-year-old male was found dead at a nursing home where he was living. He was known as an ethanol and drug abuser and suffered from schizophrenia and hepatitis C. In the morning the same day as he was found dead he had bought 250 caffeine tablets (100 mg) at the pharmacy and 150 tablets were remaining. At the autopsy chronic hepatitis, chronic pulmonary emphysema and coronary artery sclerosis were found.
Case 2
A 21-year-old male was found dead in his home. He was recently discharged from a
Results and discussion
The results from the toxicological analysis are summarized in Table 1 as well as the cause and manner of death according to the decision of the responsible forensic pathologist. Ethanol was not detected in any of the cases and caffeine was the only drug in case 3. In the other cases, high concentrations of orphenadrine (2.2 μg/g) in femoral blood and therapeutic concentrations of thioridazine (1.1 μg/g) were found in case 1, and in case 4 a high concentration of ephedrine (4.8 μg/g) was detected
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