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147.e2 Castor Bean Toxicosis

Castor Bean Toxicosis Client Education
Sheet
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toxin (toxalbumin) that inhibits protein
BASIC INFORMATION
synthesis, causing cell death. This results in • Activated charcoal 1-2 g/kg PO; may be
effective even several hours after exposure
Definition vomiting, diarrhea, abdominal pain, and if seeds have been ingested. Protect airway
Acute toxicosis is manifested by vomiting and gastrointestinal (GI) hemorrhages and liver with cuffed endotracheal tube if patient is
diarrhea initially, frequently progressing to coma or kidney injury. unconscious.
and death. Toxicosis occurs in dogs or cats Protect GI mucosa:
after eating castor beans or other parts of the DIAGNOSIS • Administer GI protectants: sucralfate
plant. 0.5-1 g/DOG or 125-250 mg/CAT PO q
Diagnostic Overview 8-12h and H2-blockers (e.g., famotidine
Synonyms A working diagnosis is made based on history/ 0.5 mg/kg PO, SQ, IM, or IV q 12-24h)
African coffee tree, Mexico weed, mole bean, evidence of exposure (evidence of chewed-up • Control severe vomiting with metoclo-
Palma Christi, wonder tree, Ricinus communis leaves/seeds in vomitus) and onset of vomiting, pramide 0.1-0.4 mg/kg PO, SQ, or IM q
diarrhea, anorexia, or lethargy several hours 6h or maropitant 1 mg/kg, SQ, q 24h for
Epidemiology after ingestion. up to 5 doses.
SPECIES, AGE, SEX Supportive care:
All breeds, ages, and both sexes susceptible; Differential Diagnosis • IV fluids for 2-3 days or longer at 1.5 to 2
dogs > cats • Dietary intolerance/garbage toxicosis times maintenance rates
• Sago palm toxicosis • Diazepam for seizures 0.5-2 mg/kg IV prn
RISK FACTORS • Pancreatitis • Lactulose 15-30 mL PO q 6-8h in dogs,
Presence of castor beans in pet’s environment • Viral/bacterial gastroenteritis 0.25-1 mL PO q 8-12h in cats, avoid if
• GI tract obstruction diarrhea; may reduce the risk of hepatic
GEOGRAPHY AND SEASONALITY encephalopathy if acute hepatic injury
• Year round; more cases in October and Initial Database (pp. 440 and 442)
November, when castor beans mature and • CBC: leukocytosis • S-adenosylmethionine (SAMe) 18 mg/kg PO
are released from their spiny pods • Serum biochemistry profile in dogs and cats q 24-72h for 1-3 months
• Castor beans used for jewelry/ornamental ○ Elevated alanine aminotransferase, for hepatic injury
purposes are available throughout the year. aspartate aminotransferase, and lactate • Dietary management: soft, bland diet in small
dehydrogenase, indicative of liver damage amounts for 1-5 days
Clinical Presentation ○ Increased blood urea nitrogen and serum
HISTORY, CHIEF COMPLAINT creatinine: may be renal or prerenal Chronic Treatment
• History of exposure to castor bean plant or ○ Increased serum albumin and globulin pos- Management of chronic hepatopathy (p. 174)
ornamentals (e.g., jewelry) sible, suggesting dehydration, followed by
• Lag period: 6-12 hours (up to 48 hours) hypoalbuminemia and hypoglobulinemia Possible Complications
before signs appear due to GI losses Ongoing liver or renal compromise
• Vomiting and diarrhea (with or without • Changes occur 12-24 hours after ingestion.
blood), anorexia, lethargy Recommended Monitoring
Advanced or Confirmatory Testing • CBC
PHYSICAL EXAM FINDINGS Necropsy findings may include necrosis and • Serum biochemical profile (i.e., liver enzymes,
• No remarkable physical exam findings hemorrhages in the heart, GI tract, lungs, liver, renal parameters, electrolytes) q 24h until
initially (<6 hours) kidney, and pancreas. resolution of clinical signs
• Within 6-48 hours of exposure, anorexia, • Blood pressure and heart rate
depression, lethargy, mild to severe vomiting, TREATMENT
diarrhea, and abdominal tenderness PROGNOSIS & OUTCOME
• In severe cases, dehydration, weakness, Treatment Overview
tremors, or seizures can ensue. Treatment is implemented based on reasonable • Prognosis depends on the amount ingested
• Tachycardia, hypotension, and hypovolemic clinical suspicion (history of possible or proven and whether the beans were chewed or
shock may be present (potentially fatal). exposure). In asymptomatic patients, treatment broken (prognosis worse) and if spontaneous
• Presence of castor beans or leaves in the consists of decontamination of the patient and vomiting occurred after the ingestion (prog-
vomitus monitoring. With overt clinical signs, intensive nosis better due to self-decontamination).
supportive care is indicated. Therapeutic goals • Most dogs respond well to supportive
Etiology and Pathophysiology are decontamination of patient, protecting GI treatment.
• Castor bean is a large, decorative, ornamental, mucosa, and supportive care. • Poor prognosis if multiple organ damage,
Caribbean plant that now grows throughout shock, or seizures occur.
the warmer parts of the United States. The Acute General Treatment • Mortality rate for dogs is ≈9%.
beans are commercially grown for castor oil Decontamination of patient (p. 1087):
or may be used for ornamental purposes (e.g., • Emesis: in asymptomatic patients (p. PEARLS & CONSIDERATIONS
jewelry). The plant produces spiny pods that 1188). May be effective within several
burst open after drying, releasing seeds. The hours after exposure, especially if seeds have Comments
seeds have color markings resembling ticks been ingested, because seeds are hard to • Severity of signs increases if the seed is
or beetles. digest chewed open. Ricin is released from the
• All parts of the plant contain ricin and are • Gastric lavage (p. 1117): only if a potentially seed when the seed coat is broken.
toxic if ingested; the highest concentra- lethal amount has been ingested (see Pearls • All known or potential ingestions should
tion of ricin is in the seed/bean. Ricin, a & Considerations below) and emesis cannot be considered serious and treated to avoid
heterodimeric glycoprotein, is a cellular be induced (comatose animal) serious consequences.
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