Sago Palm Toxicity
Sago palms are popular outdoor plants in the southern United States—and are also becoming popular indoor house plants throughout other areas of the country. While sago palms (Cycas revoluta) are the more commonly recognized plant, coontie palms (Zamia integrifolia) and cardboard palms (Zamia furfurecea) cause similar problems. Collectively these plants are referred to as cycads.
Toxicity Dangers
Cycads contain three different types of toxins: Cycasin, beta-methylamino-L-alanine (BMAA) and a third unidentified compound. Cycasin is the toxin responsible for hepatoxicity and gastrointestinal signs that are most commonly reported in dogs.
All parts of cycads contain cycasin, with seeds containing the highest concentration. In dogs, any potential exposure to the plant should be considered serious—with exposure to the seed being the most serious.
Clinical Signs
Onset of signs can tend to be rapid (under an hour), but a delay of several days is also possible.
Common clinical signs reported with cycad intoxication include vomiting, diarrhea, abdominal pain, anorexia, icterus, hypersalivation and depression. Laboratory changes may include elevated liver values, hypoalbuminemia, coagulopathies, hypoglycemia or hyperglycemia.
Treatment Options
Since all parts of cycads are toxic, any exposure is likely to warrant veterinary care. Stabilization of the patient’s clinical status and evaluation of history is important since there’s potential for delayed onset of signs or significant gastrointestinal signs.
If exposure is recent and the patient is not already exhibiting gastrointestinal signs or is otherwise compromised, emesis should be induced. Potentially repeated doses of activated charcoal have shown to be beneficial with exposures to cycads.
Caution may be needed when administering activated charcoal particularly if patient is showing neurological signs or gastrointestinal signs.
Protecting the liver with liver protectants and aggressive control of gastrointestinal signs including potential gastro protectants may be needed. Laboratory monitoring should include biochemistries with particular focus on liver function, electrolytes, and coagulation profiles every 24-48 hours, particularly in initial phases of toxicity.
Vitamin K and fresh frozen plasma may be warranted if a coagulopathy develops secondary to significant liver injury.