Lilies (Lilium, Hemerocallis)

Easter lilies (Lilium longiflorum), tiger lilies (Lilium tigrinum), rubrum or Japanese showy lilies (Lilium speciosum and Lilium lancifolium), and various day lilies (Hemerocallis species) have been incriminated in causing acute renal failure and death in cats. The toxic principle is unknown. Even minor exposures (a few bites on a leaf, ingestion of pollen, etc.) may result in toxicosis, so all feline exposures to lilies should be considered potentially life-threatening and should merit aggressive clinical intervention. It should be noted that not all plants with "lily" in the name are members of Liliaceae, e.g. calla lily (Zantedeschia spp. see oxalate-containing plants) or lily of the valley (Convallaria spp., see cardiac glycosides-containing plants).

Affected cats often vomit within a few hours of exposure to lilies, but the vomiting usually subsides after a few hours, during which time the cats may appear normal or may be mildly depressed and anorexic. Within 24 to 72 hours of ingestion, oliguric to anuric renal failure develops, accompanied by vomiting, depression, anorexia, dehydration, and hypothermia; additionally, disorientation, ataxia, facial and paw edema, dyspnea, and seizures have been less commonly reported.

When initiated within 18 hours of ingestion, decontamination (emesis, oral activated charcoal, and cathartic) and fluid diuresis using lactated Ringer's solution at twice maintenance infusion rate for 48 hours have been effective in preventing lily-induced acute renal failure. Conversely, delaying treatment beyond 18 hours frequently results in death or euthanasia due to severe renal failure. Baseline renal values should be obtained upon presentation and then repeated at 12, 24, 36 and 48 hours.

Because the tubular injury from lily ingestion spares the renal tubular basement membrane, regeneration of damaged tubules may be possible. In severe cases, peritoneal dialysis may aid in managing renal failure until tubular regeneration occurs (10-14 days or longer).

Castor beans (Ricinus communis)

The castor bean plant is used as a decorative plant and oil extracted from the seeds is used in industry and medicine. Other names for castor bean plants are Mole Bean Tree, Wonder Tree, African Coffee Tree, Mexican Weed and Palma Christi; the seeds are sometimes called dog tick seeds. The toxic principle is ricin, a glycoprotein that is one of the most potent plant toxins known.

All parts of the castor bean plant are toxic, but the seeds contain the highest concentration of ricin and are most commonly associated with toxicosis. In humans, ingestion of one to eight seeds is estimated to be potentially lethal. Damage to the seed coat is required in order to allow the ricin to be available for absorption; for this reason, beans that are swallowed whole without being chewed may pass harmlessly through the digestive tract. Because of this, and because ricin has poor oral absorption, deaths from castor bean ingestion are not as common as one would imagine. In a study of the ASPCA National Animal Poison Control Center database between 1987 and 1998, the overall death/euthanasia rate in 98 dogs that ingested castor beans was 9%. The most common clinical signs reported were vomiting (+/- blood; 90%), diarrhea (+/- blood; 51%), depression (45%), anorexia (16%), and abdominal pain (14%). Weakness, hyperthermia, ataxia/tremors/seizures, recumbency/coma, tachycardia, icterus, vocalization and hypersalivation were also noted. Clinical signs generally develop within 6 hours of ingestion, although delays of up to 42 hours post ingestion have been reported. Elevations in hematocrit, WBC, ALT, and/or AST were the most commonly reported clinical laboratory abnormalities; alterations in laboratory values are frequently not seen until at least 12 to 24 hours post ingestion.

Because of the potential for serious toxicosis, any oral exposure to castor beans should be considered an emergency and should treated aggressively. Treatment should include early decontamination (emesis and activated charcoal with cathartic) if possible. Gastrointestinal protectants (sucralfate or kaolin-pectin) should be used as needed. Exposed animals should be closely monitored for at least 24 hours, and fluid therapy using balanced electrolyte solutions should be instituted immediately upon the development of clinical signs. Hypovolemia secondary to massive gastrointestinal fluid and blood losses is possible, so fluid rates should be adjusted as needed based on the severity of clinical signs. Seizures, if present, generally respond to diazepam. Following resolution of gastrointestinal signs, a diet consisting of bland food offered in small, frequent meals should be followed for up to 4 days after vomiting has resolved.

Baseline CBC and serum chemistries should be obtained, and values should be reassessed at 24, 48, and 72 hours in symptomatic animals. Evidence of hepatic damage, based on biochemical values, would indicate that symptomatic therapy for general liver failure (oral antibiotics, lactulose, dietary management, etc) should be instituted. Similarly, significant alterations in renal values should be treated with fluid therapy and supportive care. Repeated monitoring of serum chemistries should be done until values return to normal.