April 2000

Often we forget that common household plants and flower arrangements can be deadly to our feline friends. This month we present an article we published in Feline Practice which is a prominent veterinary journal. The case describes acute renal failure that was secondary to ingestion of tiger lilies from a flower arrangement the owner had received for Easter. Easter Lilies cause the same toxicity. The moral of this story is that you should not allow cats to have access to plants and flowers unless you know for sure they are safe to ingest. For additional information on toxic plants and other poisons visit our poisonous plant page.

Acute Renal Failure in a Cat Secondary to Tiger Lily (Lilium tigrinum) Toxicity

Lynn Gulledge, DVM, Diplomate ABVP Feline Practice, Deborah Boos, DVM, and Rand Wachsstock, DVM

Feline Practice . Volume 25, Nos. 5-6 . 1997

Easter Lily (Lilium longiflorum) toxicity as a cause of acute renal failure in cats has been recently reported.^1,2,3 The National Animal Poison Control Center (NAPCC) at the University of Illinois has also had reports of similar toxicities involving Tiger Lilies (L. tigrinum) which is in the same genus.^2,4

The exact toxin is unknown. Ingestion of Easter Lily leaves and/or flowers results in acute onset of gastrointestinal upset, depression, and anorexia with renal failure developing between 48 and 96 hours post ingestion.¹ The toxin causes an acute regional destruction of the renal tubular epithelial cells. The basement membrane usually remains intact allowing the possibility of regeneration.⁴ The syndrome of Easter Lily toxicity has been reproduced in an experimental cat.¹ Urine collected from this cat 12 hours post exposure had numerous tubular epithelial casts, protein, and glucosuria. NAPCC case follow-ups found that four cats decontaminated (via emesis, activated charcoal, saline cathartic, and fluid diuresis) prior to six hours post exposure had no indication of renal failure; four cases treated after 18 hours post exposure developed renal failure and died.¹

Acute renal failure (ARF) results from an abrupt decline in renal function (usually caused by an ischemic or toxic insult to the kidneys) with the inability of the kidneys to regulate water and solute balance.^5,6 There are numerous references as to causes of renal ischemia and potential nephrotoxins in the veterinary literature.^3,6 The kidneys receive approximately 20% of cardiac output which increases the risk of exposure of the renal tubular epithelial cells to toxins in circulation ^5,6. ARF is potentially reversible; therefore immediate recognition and initiation of therapy is crucial.⁶ A diagnosis is made when a sudden increase in serum creatinine level persists despite correction of all prerenal factors.³ The primary goal of treatment of ARF is to allow the patient to survive long enough for restoration of sufficient renal function.⁷ This maintenance phase of ARF may continue for weeks before evidence of improvement is apparent.^3,8 Volume depletion, overhydration, hyperkalemia, and severe metabolic acidosis must be addressed during treatment. Discussion of the induction, maintenance, and recovery phases as well as treatment options can be found in veterinary references.^3-8 In the absence of dialysis, euthanasia should be considered if clinical improvement and increased patient comfort is not seen in 3 to 5 days.³ This is especially true if the patient remains oliguric, develops progressive oliguria, develops overhydration (despite conservative fluid therapy), or has intractable hyperkalemia or metabolic acidosis.³ The following describes a case of acute renal failure associated with ingestion of an unknown quantity of Tiger Lilies. This is a relatively unreported toxicity in the cat.

A 3 year old female spayed Domestic Longhair cat was presented for evaluation of 3 to 4 episodes of vomiting the previous evening followed by anorexia and depression. The vomitus was bright yellow with plant fiber present. The owner reported receiving a flower arrangement several days earlier that contained bright yellow Tiger Lilies. Several of the flowers had been chewed and spread about the house. The cat had not been allowed outside, and there were no other known sources of toxicity.

On presentation, the cat appeared bright and alert. She weighed 5.1 kg, had a temperature of 38.6 C, and appeared to be of normal hydration. Pain was elicited with kidney palpation. There had been no vomiting since the previous evening. Urinalysis revealed a urine specific gravity of 1.020, large amount blood, and >2000mg/dl glucose. Sediment examination showed many epithelial and red blood cells and numerous (greater than 10/lpf) granular epithelial casts. Blood was drawn and the NAPCC was contacted to confirm the possibility of toxicity. Initial blood values are listed in Table 1. Other blood values were within normal limits. These tests were performed at the referral laboratory. Subsequent blood tests were performed with cooperation of the local emergency clinic to allow more frequent monitoring.

Treatment for acute renal failure was started with 200 ml 0.9%NaCl given IV over the first 4 hours to correct any prerenal factors and continued at twice maintenance levels (25ml/hour).³ The cat was monitored through the night at the local emergency clinic.

Fluid therapy was continued. The urine was not collected, but was judged to be an adequate volume. Weight was 5.3 kg. See Table 1 for laboratory values.

The cat remained alert and responsive but had become oliguric. Fine crackles could be auscultated in all lung fields. Her weight was 5.8 kg. See Table 1 for laboratory values. The 0.9% NaCl drip was replaced with 5% dextrose in water with added B vitamins to increase endogenous insulin release and to drive potassium intracellular.⁹ 12.5 mg of furosemide was administered intravenously to increase renal output and cimetidine was started at 30 mg intravenously every 8 hours to protect against uremic gastritis. One hour after furosemide administration, no urine was palpable in the bladder. An additional 24 mg was given intravenously. An hour later, the cat started producing large volumes of urine and the breathing improved. Within two hours, the serum potassium had decreased to 5.5 MEQ/L. Furosemide was continued at 6 mg subcutaneously every 6 hours . Referral for peritoneal dialysis was discussed and declined.

The cat appeared comfortable and continued to urinate but remained anorectic. Renal values remained essentially unchanged (See Table 1). Fine crackles in all lung fields were auscultated. A dopamine drip (which acts to increase renal blood flow, glomerular filtration rate, and sodium excretion)¹⁰, was started at a rate of 2.5µg/kg/min (13ml/hr of a solution containing 60µg/ml) for 24 hours. A second IV line and infusion pump was used for the administration of the dopamine drip. Heart rate and rhythm were frequently monitored. Furosemide and cimetidine were continued at previous dosages. The cat's attitude and comfort continued to improve throughout the day although anorexia continued.

The cat continued to be alert and responsive and produced large volumes of urine. Morning and evening blood values are listed in Table 1. The 5% dextrose in water drip was replaced with 0.9% NaCl at a rate of 25ml/hr. By late afternoon, a pronounced cardiac gallop was noted. Respiratory rate remained normal.

Large hematomas were noted on the medial left thigh and over the left jugular vein presumably from previous venipunctures. DIC had become a concern at this point. Cardiac gallop rhythm continued and dyspnea had returned. The cat had also started retching. Renal parameters failed to show improvement (See Table 1). The owners elected euthanasia.

Acute renal failure can be a frustrating medical condition to manage. The recognition of the problem and exposure to a known toxin must be ascertained immediately. If a known toxin had not been identified, other causes of ARF would have had to be ruled out. Vomiting by cats of plant material is a common clinical entity. There is a paucity of information in the veterinary literature regarding Easter Lily (and other members of the lily family) toxicity. In this particular case, treatment was initiated after the six hour window of opportunity (vomiting had occurred the previous evening and renal parameters were abnormal at presentation). In theory, if the renal tubular basement membrane is left intact and the patient can remain stable, regeneration is possible. After consultation with the NAPCC and the owner, treatment for acute renal failure was started despite the guarded prognosis. Ideally, urine production should have been quantitated but, due to the temperament of the cat, this was not a practical option.

In future cases of lily poisoning, peritoneal dialysis (and hemodialysis when available) should be stressed immediately before the patient becomes debilitated and a poor surgical candidate. Based on this case report and the reported cases, treatment should be discouraged if exposure has occurred more than 6 hours previously and the owners are not willing to pursue dialysis.

A 3 year old female spayed Domestic Longhair cat was diagnosed with acute renal failure associated with ingestion of Tiger Lilies. Renal failure was documented less than 24 hours after plant material was found in vomitus. Treatment for ARF was instituted with aggressive fluid therapy, diuretics, and a vasoactive drug. The cat was euthanized on the sixth day of hospitalization due to unresolved renal failure. This case draws attention to the need to educate veterinarians and cat owners regarding the dangers of plant toxins and the need to contact a poison control center about potential toxicities that have not been widely reported in the veterinary literature.

	Day 1	Day 2	Day 3	Day 4	Day 5 AM	Day 5 PM	Day 6
PCV	45	41	41		35
TP	7	5.6	5.4		5.6
SUN (8-35mg/dl)	118		175	175	270	220	275
Creatinine (0.5-1.8mg/ml)	14.4		15	15		14	15
Phosphorous (2.0-6.5mg/dl)	10.3		6	6.3	11.5	14	21
Potassium (3.2-5.5MEQ/L)	5.8		7.6	5	4.4
Carbon Dioxide (18-25MEQ/L)	12
Total Bilirubin (0.1-0.6mg/dl)	1.0
ALT (5-75U/L)	187
Weight	5.1kg	5.3kg	5.8kg

1. Hall J. Nephrotoxicity of Easter Lily (Lilium Longiflorum) when ingested by the cat. Proceedings 10th ACVIM Forum, San Diego, California, May 1992;804.

2. Stanek D, Thompson L. Potential holiday poisoning problems. Veterinary Update, Cornell Veterinary Extension. November 1992.

3. Chew D. Acute Intrinsic Renal Failure. Proceedings of the 13th Kal Kan Symposium. Columbus, Ohio, October 1990;69-92.

5. Grauer G. Management of acute renal failure. AAHA 1991 Scientific Proceedings. Toronto, Canada, 1991;380-382.

6. Frenier S, Dhein C. Diagnosis and management of acute renal failure, in August J (ed): Consultations in Feline Internal Medicine.Philadelphia, WB Saunders Co, 1991;281-288.

7. Polzin D. Management of patients with acute uremia. AAHA 1993 Scientific Proceedings. Seattle, Washington, 1993;457-460.

8. Chew D. Renal disease. Proceedings from D.C. Academy of Medicine, May 6, 1993. Washington, D.C.

9. DiBartola S. Electrolyte abnormalities. Proceedings of the 14th Kal Kan Symposium. Columbus, Ohio, October 1990;49-60.

10. Lane IF, Grauer GF, Fettman MJ. Acute renal failure. Part I. risk factors, prevention, and strategies for protection. Compendium on Continuing Education 1994;16:15-30.

Case of the Month

Feline Practice . Volume 25, Nos. 5-6 . 1997