Ricin intoxication by lethal dose of castor seeds ingestion: a case report.

INTRODUCTION: Ricin intoxication is a serious condition with symptoms ranging from mild gastroenteritis to fatal outcomes due to shock and multi-organ failure. Intoxication from the ingestion of castor seeds is uncommon. However, its diagnosis is crucial, particularly with a clear history of exposure to castor seeds, regardless of the route of exposure (enteral or parenteral). Prompt diagnosis is essential to monitor and manage the patient effectively and to prevent potentially fatal outcomes. We report a case where ingestion of castor seeds resulted in gastroenteritis severe enough to necessitate emergency medical care. CASE REPORT: We present the case of a 47-year-old Belgian woman of Moroccan descent, previously healthy who was admitted to the emergency department with symptoms of colicky abdominal pain, diarrhea, and vomiting following the ingestion of six castor beans. The patient was diagnosed with ricin intoxication, admitted for observation, and received symptomatic treatment. She was discharged home after a complete recovery three days later. CONCLUSION: Our report underscores the clinical manifestations, hemodynamic changes, laboratory findings, and treatment of intoxication due to castor seed ingestion. It contributes to the limited literature on castor seed poisoning in humans, with a specific focus on cases in Belgium. This report aims to raise awareness among clinicians about this condition and emphasizes the importance of a comprehensive history-taking to prevent misdiagnosis and malpractice.

Near-fatal poisoning after ricin injection.

OBJECTIVE: To report a near-fatal poisoning after intentional injection of ricin from a castor bean (Ricinus communis) extract. CASE REPORT: A 21 year-old man self-injected ∼3 mL of a castor bean extract intramuscularly and subcutaneously in the left antecubital fossa. Upon admission to our ED (1 h post-exposure; day 1, D1) he was awake and alert, but complained of mild local pain and showed slight local edema and erythema. He evolved to refractory shock (∼24 h post-exposure) that required the administration of a large volume of fluids and high doses of norepinephrine and vasopressin, mainly from D2 to D4. During this period, he developed clinical and laboratory features compatible with systemic inflammatory response syndrome, multiple organ dysfunction, capillary leak syndrome, rhabdomyolysis, necrotizing fasciitis and possible compartment syndrome. The patient underwent forearm fasciotomy on D4 and there was progressive improvement of the hemodynamic status from D7 onwards. Wound management involved several debridements, broad-spectrum antibiotics and two skin grafts. Major laboratory findings within 12 days post-exposure revealed hypoalbuminemia, proteinuria, thrombocytopenia, leukocytosis and increases in cytokines (IL-6, IL-10 and TNF-α), troponin and creatine kinase. Ricin A-chain (ELISA) was detected in serum up to D3 (peak at 24 h post-exposure), with ∼79% being excreted in the urine within 64 h post-exposure. Ricinine was detected in serum and urine by LC-MS up to D5. A ricin A-chain concentration of 246 µg/mL was found in the seed extract, corresponding to the injection of ∼738 µg of ricin A-chain (∼10.5 µg/kg). The patient was discharged on D71, with limited range of motion and function of the left forearm and hand. CONCLUSION: Ricin injection resulted in a near-fatal poisoning that evolved with septic shock-like syndrome, multiple organ dysfunction and necrotizing fasciitis, all of which were successfully treated with supportive care.

Ricin Poisoning after Oral Ingestion of Castor Beans: A Case Report and Review of the Literature and Laboratory Testing.

BACKGROUND: Ricin is a protein toxin derived from the castor bean plant Ricinus communis. Several cases secondary to its consumption have been published and, more recently, its use as a potential bioterrorism agent has also been reported. Oral absorption of ricin is highly erratic, leading to a wide spectrum of symptoms. In addition, conventional urine drug screening tests will not be able to detect this compound, posing a diagnostic challenge. CASE REPORT: A male teenager intended to die by ingesting 200 castor beans after mixing and blending them with juice. Eight hours later, he presented with weakness, light-headedness, nausea, and vomiting and sought medical treatment. The patient was admitted and treated conservatively. An immune-based standard urine toxicology drug screen panel was reported as negative. A comprehensive untargeted urine drug screen test showed the presence of ricinine, a surrogate marker of ricin intoxication. He was transferred to the psychiatric service 3 days after admission. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: This case highlights the importance of knowing the peculiar pharmacokinetic properties of ricin after oral ingestion of castor beans and toxin release through mastication. Emergency physicians should be aware that oral absorption of ricin is dependent on several factors, such type and size of seeds and the geographic harvesting region, making it extremely difficult to estimate its lethality based solely on the number of ingested beans. Finally, comprehensive untargeted urine drug screening testing is highly valuable as a diagnostic tool in this context.

Plasma exchange parameter selection and safety observation of children with severe ricinism.

The aim of this study was to investigate the selection of plasma exchange (PE) parameters and the safety of children with severe ricinism. The PE parameters and heparin dosage in 7 children with severe ricinism were recorded, and changes in the patients' vital signs and coagulation function were monitored before and after PE. All patients successfully completed PE. The speed of blood flow was 50-80 mL/min, speed of exchange flow was 600-800 mL/h, and isolating rate of blood plasma was 12.5-19.05%. Transmembrane pressure was stable at approximately 100 mmHg, and venous pressure was stable at approximately 95 mmHg. The first dose of heparin was 0.39 ± 0.04 mg/kg, and the maintaining heparin dose was 0.40 ± 0.05 to 0.22 ± 0.03 mg·kg(-1)·h(-1). During the PE process, mean arterial pressure, heart rate, respiratory rate, and pulse oxygen saturation were steady. After PE, the activated partial thromboplastin time and thrombin time prolonged to 2-3 times greater than that before PE. However, no bleeding tendency was seen. For children with severe ricinism, the choice of PE to eliminate the toxin from blood, tissues, and organs was safe and effective.

Early plasma exchange for treating ricin toxicity in children after castor bean ingestion.

Plasma exchange (PE) for the treatment of ricin toxicity has not been previously reported. Here we describe the use of PE to treat children who experienced ricin toxicity after ingesting castor beans. Seven children (median age: 8.1 years) who consumed castor beans (median: 5 beans) were treated with PE. All had bradycardia and sinus arrhythmia, and most had experienced episodes of vomiting and/or diarrhea. PE settings were blood flow, 50-80 mL/min; PE rate, 600-800 mL/h; volume of exchange, 1440-1950 mL. Median time from ingestion to PE was 73 h. All clinical symptoms disappeared and vital signs rapidly returned to normal after PE; no severe organ dysfunction occurred. All children were discharged and recovered uneventfully. Concentrations of all serum biochemical parameters significantly decreased immediately after PE. Some, but not all, of these parameters were also significantly decreased at 48 and 72 h after PE compared with before PE. Our findings suggest that PE can be an effective early intervention in the treatment of ricin toxicity due to castor bean ingestion.

Spontaneous poisoning by Ricinus communis (Euphorbiaceae) in cattle / Intoxicação espontânea por Ricinus communis (Euphorbiaceae) em bovinos

The aim of this study is to report cases of spontaneous poisoning of cattle by Ricinus communis (castor beans) in Paraíba, a semiarid region of northeastern Brazil. The cases were observed in 2 herds on neighboring properties in 2013. Clinical signs developed within 6-24 h and consisted of weakness, tachycardia, dyspnea, profuse watery diarrhea, dehydration, depression, instability, cramps, permanent lateral recumbency and death within 48-72 h. Of the 60 cattle at risk, 19 were affected and 14 died. Five fully recovered after the course of 12 days. Three animals were necropsied. The main gross lesions were hemopericardium, hemothorax, pulmonary edema, petechial hemorrhages in the epicardium and endocardium, ecchymoses at the papillary muscles and suffusions on the intercostal muscles. Hemorrhages were also observed in the abdominal cavity, spleen and mucosa of the abomasum and small intestine. The rumen content was liquid with a large amount of castor bean seeds. There were circular, whitish and focally diffuse areas in the liver parenchyma. The main microscopic lesions consisted of multifocal coagulative myocardial necrosis with the presence of mononuclear cell infiltration and varying degrees of bleeding between cardiac muscle fibers. The abomasum and small intestine mucosae and submucosa had mild edema and mononuclear and polymorphonuclear inflammatory cell infiltration. The diagnosis of R. communis was based on the history of plant consumption, clinical signs, pathology of the disease and the presence of large amounts of castor bean seeds in the forestomachs...

O objetivo deste trabalho é relatar casos de intoxicação espontânea em bovinos por Ricinus communis (mamona) na Paraíba, região semi-árida do nordeste do Brasil. Os casos foram observados em dois rebanhos de propriedades vizinhas no ano de 2013. Os primeiros sinais clínicos se desenvolveram dentro de 6-24 h e consistiam em fraqueza, taquicardia, dispnéia, diarréia aquosa profusa, desidratação, depressão, instabilidade, cólicas, decúbito lateral permanente e morte em 48-72h. Dos 60 bovinos sob risco, 19 foram afetados e 14 morreram. Cinco bovinos se recuperaram totalmente após um período de 12 dias. Três bovinos foram necropsiados. As principais lesões macroscópicas foram hemopericárdio, hemotórax, edema pulmonar, petéquias no epicárdio e endocárdio, equimoses nos músculos papilares e sufusões nos os músculos intercostais. Hemorragias também foram observadas na cavidade abdominal, baço e na mucosa do abomaso e intestino delgado. O conteúdo ruminal estava líquido, e continha grande quantidade de sementes de R. communis. No parênquima hepático havia áreas circulares, esbranquiçadas e distribuídas focalmente. As principais lesões microscópicas consistiam em necrose miocárdica coagulativa multifocal com a presença de infiltrado de células mononucleares e graus variados de hemorragias entre as fibras musculares cardíacas. O abomaso e a mucosa e submucosa do intestino delgado apresentavam edema discreto e infiltrado de células inflamatórias mononucleares e polimorfonucleares. O diagnóstico da intoxciação por R. communis foi baseado na história de consumo de planta, sinais clínicos, patologia da doença e pela presença de grandes quantidades de sementes de R. communis no sistema digestório dos bovinos...

Suicidal death after injection of a castor bean extract (Ricinus communis L.).

The castor bean plant (Ricinus communis L.) or wonder tree is cultivated in many countries as an ornamental annual plant in gardens. The highest concentration of the lectin ricin is present in the seeds and pods. Ricin is considered as one of the most toxic natural poisons. Ricinine is a piperidine alkaloidal toxin present in castor bean and is described as a biomarker for the exposure to ricin. A case report is presented of a 49-year-old man who committed suicide by intravenous and subcutaneous injection of a castor bean extract. He was brought to the emergency department 24 h after injecting himself. On admission, the patient was conscious and he presented with a history of nausea, vomiting, diarrhoea, dyspnoea, vertigo and muscular pain. Despite symptomatic and supportive intensive care, the man died 9 h after admission due to multiorgan failure. A body external examination was performed. Blood, urine, vitreous humour and the castor bean extract were submitted to the laboratory for toxicological analysis. The identification of ricinine in the extract was performed by solid phase extraction in combination with full-scan gas chromatography/mass spectrometry, high-performance liquid chromatography with photodiode array detection and liquid chromatography/mass spectrometry operated in the full-scan mode, respectively. An extraction procedure with Oasis HLB solid phase extraction cartridges was applied. Chromatography was achieved using a Symmetry C18 column using a gradient mode with 0.15% formic acid and 0.15% formic acid in acetonitrile as mobile phase. Exposure to the castor bean extract was confirmed by identification of the biomarker ricinine in blood, urine and vitreous humour using solid phase extraction and liquid chromatography tandem mass spectrometry with electro spray source in positive ionization mode. Multiple reaction monitoring was used for specific detection. To the authors' knowledge, it is the first time that ricinine has been identified in vitreous humour in a case of castor bean poisoning. Based on the clinical symptoms and the results of the toxicological analysis, we concluded that death was caused by intoxication with plant toxins originated from R. communis L.

A case of ricin poisoning following ingestion of Korean castor bean.

Ricin is a member of a group of protein toxins whose cytosolic target is the 28S rRNA of the 60S ribosomal subunit. It was recently introduced as a weapon of terrorism in some countries. There is little evidence about the mechanism, diagnosis and treatment of ricin poisoning. The case history is reported of a patient with ricin poisoning who presented with nausea and vomiting following ingestion of Korean castor bean.

Castor bean (Ricinus communis) toxicosis in a sheep flock.

This paper describes clinical, laboratory and pathological findings of sheep, which is intoxicated with castor bean. The source of intoxication was a miscellaneous garden waste. Forty-five animals showed clinical toxicosis and 17 died. The clinical signs included weakness, salivation, profuse watery diarrhoea, dehydration, mydriasis, teeth grinding, hypothermia and recumbency. The most significant haematological and biochemical findings were a high haematocrit, high concentration of serum BUN, creatinine and phosphorus and high activity of serum CK and AST. Pathology revealed severe gastroenteritis, cardiac haemorrhage and necrosis, hepatic necrosis and acute tubular necrosis in kidneys. Treatment included symptomatic and supportive care with fluid therapy and cathartic administration.

Ricinus communis cake poisoning in a dog.

A fatal case of canine poisoning by castor bean (Ricinus communis L) cake used as fertilizer is described, heat treatment The process of R communis cake production should include heat treatment to reduce the risk if the product is accidentally ingested by pets or humans.

Evaluation of castor bean toxicosis in dogs: 98 cases.

Castor beans (Ricinus communis) contain ricin. Ricin is a glycoprotein reported to cause hypotension, gastroenteritis, depression, and death. However, few deaths are reported following castor bean ingestion in animals. From January 1987 to December 1998, the American Society for the Prevention of Cruelty to Animals-National Animal Poison Control Center received 98 incidents of castor bean ingestion in dogs. The most commonly reported clinical signs were vomiting, depression, and diarrhea. Death or euthanasia occurred in 9% of the cases. The severity of clinical signs following castor bean ingestion may depend on whether the beans were chewed or swallowed whole.

Hepatotoxicity from castor bean ingestion in a child.

BACKGROUND: Castor beans contain ricin, one of the most toxic substances known. A biphasic toxicity is described consisting of acute and potentially fatal gastroenteritis followed by damage to the viscera several days later. However, the most current review of the literature states that the above delayed toxicity has not been reported. CASE REPORT: We report a 20-month-old girl with no gastrointestinal symptoms who developed reversible hepatotoxicity beginning 48-72 hours after the ingestion of castor beans. CONCLUSION: It seems prudent to follow for several days any patients who actually chewed castor beans before ingestion.

Ingestion of castor oil plant seeds.

Ingestion of seeds of the castor oil plant is rare, and may cause toxicity but rarely death. The presumed toxic component is ricin, a highly potent cellular poison. We report the case of a young adult who ingested a large number of the seeds, causing initial toxicity, but with subsequent full recovery. The management of such ingestions and the apparent discrepancy between the extreme toxicity of ricin and the generally milder toxicity of ingested seeds are discussed.