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Palm (Cycad/Sago) Toxicosis 737

• Heart failure (pp. 263 and 408) • Cardiogenic shock requires supplemental PEARLS & CONSIDERATIONS
• Aortic thromboembolism (p. 74) oxygen (p. 1146) and attempts to improve Comments
VetBooks.ir TREATMENT cardiac tamponade) and medications (e.g., Most causes of pallor are serious, requiring Diseases and Disorders
perfusion, such as with pericardiocentesis (if
positive inotropes, antidysrhythmics) (pp.
timely evaluation and therapy.
Treatment Overview
263, 408, and 1033).
Stabilization of the animal (e.g., blood • Regional perfusion impairment is addressed Technician Tips
transfusion for severely anemic patients, according to cause (p. 74). Be cognizant of membrane color because pallor
intravenous fluids for noncardiogenic shock) is often a sign of serious disease.
followed by treatment of specific cause. Recommended Monitoring
Frequent initial assessment of vital parameters SUGGESTED READING
Acute and Chronic General and PCV in patients with anemia, BP in shock Ohad DG: Pallor. In Ettinger SJ, et al, editors:
Treatment Textbook of veterinary internal medicine, ed 8,
• Patients with severe anemia or acute blood PROGNOSIS & OUTCOME St. Louis, 2017, Elsevier, pp 206-207.
loss may require transfusion of packed RBCs AUTHOR: Jeff D. Bay, DVM, DACVIM
or whole blood if packed RBCs are not Determined by the underlying cause; ranges EDITOR: Leah A. Cohn, DVM, PhD, DACVIM
available (pp. 57 and 1169). from excellent (e.g., hemotropic mycoplasma,
• Hypovolemic, traumatic, and septic shock hookworm infestation) to grave (e.g., cardio-
cases are usually treated with intravenous genic shock with dilated cardiomyopathy)
crystalloids ± colloids (pp. 907 and 911).

Palm (Cycad/Sago) Toxicosis Client Education
Sheet

BASIC INFORMATION PHYSICAL EXAM FINDINGS offer further support. There is no definitive
• As above (see History, Chief Complaint) diagnostic test.
Definition • Abdominal pain, dehydration
Acute, potentially fatal toxicosis occurring • Hypovolemic shock (depressed mentation, Differential Diagnosis
from ingesting cycad palm leaves, seeds, bark, weakness/collapse, poor perfusion, weak • Toxic: mushroom (Amanita) poisoning,
or roots and characterized by vomiting and pulse) acetaminophen, blue-green algae toxicosis
diarrhea, anorexia, lethargy, acute liver failure • Petechiae, ecchymoses (microcystin), iron, xylitol (dogs)
(2-3 days later), coagulopathies, and neurologic • Central nervous system (CNS) signs: ataxia, • Nontoxic: chronic hepatitis, viral hepatitis,
signs. seizures leptospirosis, other causes of acute hepatic
injury
Synonyms Etiology and Pathophysiology
Cycad palm/plant, sago palm (includes Zamia • Sago palms (cycad plants) are palmlike Initial Database
and Cycas spp) plants in the family Cycadaceae. They are • CBC: leukocytosis, thrombocytopenia (mild,
woody, coarse plants with leaves originating due to blood loss)
Epidemiology from a thickened stem and are found in • Serum biochemistry panel: increased alanine
SPECIES, AGE, SEX dry, sandy soils of tropical and subtropical aminotransferase (ALT) and alkaline phos-
All animals are susceptible; most poisoning regions throughout the world. phatase (ALP) levels, hyperbilirubinemia,
cases are reported in dogs. • Cycas revoluta is the species most commonly hypoalbuminemia/hypoproteinemia,
involved in poisoning cases. azotemia (prerenal and/or renal)
RISK FACTORS • Toxins: cycasin and methylazoxymethanol, a • Coagulation profile: increased prothrombin
Presence of palm in the pet’s environment neurotoxic amino acid, and an unidentified time (PT), activated partial thromboplastin time
high-molecular-weight compound (aPTT) (liver damage–related coagulopathy)
GEOGRAPHY AND SEASONALITY • The glucose molecule on cycasin is • Urinalysis: glucosuria, bilirubinuria, hema-
• Indoor ornamental plants; landscaping in the hydrolyzed by the gut bacterial enzyme turia possible
southern part of the United States and Hawaii alpha-glycosidase, yielding sugars and meth-
• Intoxication occurs mostly in summer ylazoxymethanol, which then alkylates DNA Advanced or Confirmatory Testing
months; availability of indoor potted sago and RNA. This process causes hepatotoxic, Histopathologic lesions of liver include marked
palms makes intoxication possible through- teratogenic, carcinogenic, and gastrointestinal focal centrolobular and midzonal coagulation
out the year. (GI) effects. necrosis.
• Azotemia secondary to decreased renal perfu-
Clinical Presentation sion resulting from systemic hypotension/
HISTORY, CHIEF COMPLAINT hypoperfusion is possible. TREATMENT
• Exposure to sago palm (any part of the plant) Treatment Overview
• Within 24 hours, onset of vomiting, diarrhea, DIAGNOSIS Asymptomatic animals thought to have ingested
lethargy, and anorexia; chewed leaves, seeds, sago palm should undergo prompt decontami-
plant material may be in vomitus. Diagnostic Overview nation (emesis, activated charcoal). In patients
• Ataxia, weakness, or seizures Diagnosis is based on history/evidence of showing clinical signs (GI, CNS), treatment is
• Occurrence/recurrence of lethargy, anorexia, exposure to plant and presence of vomiting, aimed at stabilization. Signs of hepatic dysfunc-
vomiting 2-3 days after ingestion, due to anorexia, lethargy, and diarrhea within 24 hours. tion should prompt treatment/prophylaxis for
acute hepatic injury/failure (p. 442) High liver enzymes 1-3 days after exposure hepatic encephalopathy and coagulopathy.
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