Lethal Injection of a Castor Bean Extract: Ricinine Quantification as a Marker for Ricin Exposure Using a Validated LC-MS/MS Method.

Ricin is a highly toxic agent derived from the castor bean plant (Ricinus communis). Poisoning occurs commonly by oral ingestion of the beans. Injection of ricin is believed to be more lethal. Ricin is a large glycosylated protein difficult to detect in clinical samples. Instead, ricinine, a small alkaloid found in the same beans, is used as surrogate marker for ricin exposure. We describe a simple LC-MS/MS method for the detection of ricinine in serum, blood and urine, validated according to EMA guidelines and successfully applied to patient samples of a suicidal death after injection of a castor bean extract. A 26-year-old man self-presented to the emergency department with severe abdominal cramps and nausea after injection of a castor bean extract. Due to rapid deterioration of his hemodynamic function despite early aggressive fluid resuscitation, he was transferred to ICU. Abdominal cramps worsened and a fulminant diarrhea developed, resulting in hypovolemic shock and cardiorespiratory collapse. Despite full supportive therapy, the patient died approximately 10 hours after injection due to multiple organ failure. Ricinine was quantified by LC-MS/MS after LLE with diethyl ether using ricinine-D3 as internal standard. Six hours after injection, ricinine concentrations in serum and blood were 16.5 and 12.9 ng/mL, respectively, which decreased to 12.4 and 10.6 ng/mL, 4 hours later. The urinary concentration was 81.1 ng/mL 7 hours after injection, which amply exceeded the levels previously reported in similar cases with lethal outcome. Concentrations of ricinine, compatible with a lethal exposure to castor beans, were detected in serum, blood and urine. Ricinine was also found in bile and liver tissue.

Is recent cannabis use associated with acute coronary syndromes? An illustrative case series.

Cannabis is a frequently used recreational drug that potentially imposes serious health problems. We report three cases where recent and/or chronic use of marijuana led to severe cardiac dysfunction. All three patients collapsed at home and required cardiopulmonary resuscitation (CPR) with initial restoration of spontaneous circulation (ROSC). The mechanism of the cardiovascular collapse was different in each case. The first case presented with asystole and was found to have diffuse coronary vasospasm on coronary angiography in the hours after acute cannabis abuse. In the second case, an acute anterior infarction with occlusion of both the right coronary artery (RCA) and the left anterior descendens (LAD) was observed in a young patient without known cardiovascular risks but with chronic cannabis abuse. The third case presented at home with ventricular fibrillation presumably caused by an acute coronary syndrome due to left anterior descending (LAD) artery occlusion. The hetero-anamnesis of the family reported that all three patients had recently used cannabis. Toxicological screening also showed no other substance abuse than cannabis. Using these three cases, we would like to illustrate that the widespread use of cannabis is not as innocent as is believed. Cannabis use can lead to severe cardiovascular problems and sudden death, not only in people at increased cardiovascular risk, but also in young people without any medical history or risk factors.