Authors: Adam Brzezinski, MD, (Pediatric Emergency Medicine Fellow, Atrium Health Levine Children’s Hospital/Carolinas Medical Center, Charlotte, NC) and Ann-Jeannette Geib, MD (Associate Professor of Emergency Medicine and Medical Toxicologist, Atrium Health Carolinas Medical Center, Charlotte, NC)// Brian Lewis, MD (Assistant Professor of Emergency Medicine, Michigan State University College of Human Medicine); Brit Long, MD; Alex Koyfman, MD

Case:

A 3-year-old previously healthy male is brought to the ED by his mother after he was found in the neighbor’s backyard garden chewing on what looked like berries or seeds from a tall red-stemmed plant.  The patient’s mother reports he was found eating this plant approximately 3 hours prior to arrival after he had three episodes of non-bloody, non-bilious vomiting and increased fussiness.  The patient’s mother brought in a photo of the plant, which appears to be a castor bean plant. 

On arrival to the ED the patient is overall well-appearing and is playing with a toy car.  He appears fussy when you approach him, but is easily consolable by his mother.  He is tachycardic. His blood pressure is normal for his age.  His abdomen is moderately tender throughout all quadrants. There is no distention or signs of peritonitis. He has a normal work of breathing, is normothermic, and has a capillary blood glucose of 80. 

Questions:

1. What potential clinical concerns are there regarding castor bean/ricin ingestion? 
2. What are the symptoms of ricin toxicity? 
3. What is the management of ricin toxicity? 

Background:

• Ricin is a glycoprotein toxin, or toxalbumin, that is extracted from the seeds of Ricinus communis, a common ornamental and agricultural plant.  It is one of the most potent biologic toxins with a well-documented history of use in assassination and terrorism, and was re-introduced into popular culture due to its frequent use by Walter White in the television series Breaking Bad.^1-2
• Structurally, ricin is a ribosome-inactivating protein composed of two disulfide-linked chains (an A-chain and a B-chain) that depurinates a single adenine from the 28s rRNA, halting protein synthesis and triggering apoptosis, and binds galactose-containing surface glycoproteins (to mediate cell endocytosis), respectively.³ These processes can inactivate up to 1500 ribosomes per minute, which explains the rapid and irreversible cell death.^3-4
• The estimated lethal oral dose in humans is 1-20 mg of ricin/kg (~8 beans), though symptomatic ingestion ranges have been reported anywhere between half a bean to 30 beans.  The human LD50 for injection/inhalation is approximately 5-10 μg/kg.^3-4 Interestingly, ingested bean count is poorly predictive of symptom severity and mortality because of the variable seed size, environment and cultivation season, and critically, degree of mastication.  Intact hard seed coats limit toxin release, so swallowed-whole seeds often pass right through harmlessly.³
• So why don’t we get ricin poisoning with consumption of castor oil? Ricin is a water-soluble protein, not a lipid; therefore, during processing, ricin does not partition into the oil and simply it stays behind in the solid bean pulp (the “castor cake”).  Any residual ricin is denatured by the heat used during processing, which is why commercial castor oil can be ingested without causing ricin poisoning.⁴

Clinical Presentation: 

• Symptom onset following ricin ingestion typically begins in the first 4-6 hours and rapidly-dividing tissues – particular gastrointestinal epithelium – are most susceptible to these mechanisms.^3-4 Therefore, ricin toxicity is initially accompanied by colicky abdominal pain and cramping, nausea, vomiting, and sometimes diarrhea, heartburn, and oropharyngeal pain.⁴
• More delayed symptom onset has also been seen in patient up to 10 hours post-ingestion.  Symptom progression can evolve into hematemesis and bloody stools, as well as profuse diarrhea, leading to electrolyte disturbance and dehydration with subsequent peripheral vascular collapse and multi-organ system failure.^1-2,4
• Inhalation exposure can lead to cough, dyspnea, pulmonary edema, hemoptysis, and in severe inhalations necrotizing pneumonitis.^3-4
• Fatality from ricin poisoning typically occurs between 10- and 72-hours following ingestion and is associated with profound cardiovascular collapse and consequently multi-organ system failure.¹

Diagnosis:

• Ricin exposure can mimic food-borne gastrointestinal illness, so diagnosis can typically be confirmed with a good clinical history.  History of castor seed ingestion is reported in nearly all documented ricin ingestions, and when history alone is not sufficient, retained plant material within emesis can be used by toxicologists and poison centers to help in identification.^1,5
• Leukocytosis, anemia, transaminitis, hyperbilirubinemia, elevated creatine kinase, and acute kidney injury have all been seen in varying degrees following ricin exposure.⁴ When toxic exposure is unknown, or if there is concern for castor bean/ricin ingestion, the following is a practical initial ED work-up:
  • • Complete blood count and coagulation studies
    • Complete metabolic panel with electrolytes
    • Creatine kinase level
    • Urinalysis to assess for myoglobinuria
    • Arterial/Venous blood gas with lactate

Management: 

• Treatment following ricin ingestion is largely base on supportive care measures.  There is no known antidote and there is no role for dialysis for ricin toxicity.
• Like most toxic ingestions, single-dose activated charcoal has been trialed in the non-vomiting patient with the goal of decontamination.  Though limited, data supporting charcoals efficiency in ricin ingestion have largely been unproven to provide clinically significant benefit.^1,4,6 Ipecac and routine gastric lavage are not recommended.
• Aerosolized ricin management is purely supportive and treatment centers on supplemental oxygen, bronchodilators, and endotracheal intubation.  For ED staff, because decontaminated patients pose negligible secondary-contamination risk from ricin’s low volatility, standard/universal precautions are adequate once patients have been decontaminated outside the ED (in a HAZMAT area), while personnel performing decontamination should wear the higher-level PPE used by first responders. ¹
• Aggressive intravenous crystalloid infusion to restore perfusion and fluid loss, as well as electrolyte replenishment remain the mainstay of supportive treatment, particularly in the setting of symptomatic hypotension, electrolyte derangement, and acute hepatic or renal injury.
• Inpatient or intensive care admission is required for all symptomatic ricin ingestions as the clinical course typically evolves over a 36-hour period.⁴

Case Follow-Up: 

With an unknown amount of ingested castor seeds and a history limited by patient’s age, although relatively asymptomatic, this patient must be treated as a high-risk ricin ingestion.  The patient was admitted to the pediatric inpatient team following antiemetic therapy and a 20 mL/kg bolus of normal saline.  Although he developed some non-bloody diarrhea, 24 hours after admission he was tolerating oral intake, voiding appropriately, and vomiting had resolved. A repeat electrolyte panel was within normal limits.  He was discharged home with close outpatient follow-up by his pediatrician and toxicology subspecialist team. 

Clinical Pearls: 

• Don’t anchor on gastroenteritis!  Take a good history and always consider (and ask about) potential toxic ingestions, travel history, and new or unique exposures.
• The mastication is the dose!  Intact, swallowed-whole beans traverse the GI tract unremarkably; chewed beans release the toxin.
• Ricin exposure = fluid losses!  Death typically occurs from profound fluid losses via diarrhea or vomiting, with subsequent cardiovascular collapse.  Aggressive fluid repletion and electrolytes replacements can save lives.
• Think about this patient (and the others!):  Ricin is a Category B bioterrorism agent; multiple similar ricin exposures, a non-typical pattern, or a history of ricin inhalation should raise concern and warrants immediate poison control and public health notification.^1-2

References: 

1. Abbes M, Montana M, Curti C, Vanelle P. Ricin poisoning: A review on contamination source, diagnosis, treatment, prevention and reporting of ricin poisoning. Toxicon. 2021 May;195:86-92. doi: 10.1016/j.toxicon.2021.03.004. Epub 2021 Mar 9. PMID: 33711365.
2. Chung S, Baum CR, Nyquist AC, The Disaster Preparedness Advisory Council, The Council on Environmental Health, The Committee on Infectious Disease. Krug SE, Fagbuyi DB, Fisher MC, Needle S, Schonfeld DJ, Lowry JA, Ahdoot S, Bernstein AS, Bole A, ByronLG , Landrigan PJ, Marcus SM, Pacheco SE, Spanier AJ, Woolf AD, Maldonado YA, Zaoutis TE, Banerjee R, Barnett ED, Campbell JD, Gerber JS, Kourtis AP, Lynfield R, Munoz FM, Nolt D, O’Leary ST, Sawyer MH, Steinbach WJ, Tan TQ. Chemical-Biological Terrorism and Its Impact on Children. Pediatrics. Feb 2020; 145(2): e20193750.10.1542/peds.2019-3750
3. Pohanka M. Ricin as a Biothreat Agent: From Molecular Mechanisms to Clinical Toxicology, Forensic Aspects, and Risk Mitigation. BioMed Research International, 2026, 5594252, 16 pages, 2026.
4. Audi J, Belson M, Patel M, Schier J, Osterloh J. Ricin Poisoning: A Comprehensive Review. JAMA. 2005;294(18):2342–2351. doi:10.1001/jama.294.18.2342
5. Wendt S, Lübbert C, Begemann K, Prasa D, Franke H. Poisoning by Plants. Dtsch Arztebl Int. 2022 May 6;119(Forthcoming):317–24. doi: 10.3238/arztebl.m2022.0124. Epub ahead of print. PMID: 35140011; PMCID: PMC9453220.
6. Shannon M. Ingestion of toxic substances by children. N Engl J Med. 2000 Jan 20;342(3):186-91. doi: 10.1056/NEJM200001203420307. PMID: 10639545.