Lily Toxicity
DEFINITION/OVERVIEW
■ Lily toxicity causes acute nephrotoxicity in cats. ETIOLOGY/PATHOPHYSIOLOGY
■ A variety of Lilium and Hemerocallis lily species (Figures 57.1 and 57.2 ) have been associated with nephrotoxicity, including Easter lily ( Lilium longifl orum ), tiger lily ( L. tigrinum ), asiatic hybrid lily ( Lilium sp .), day lily ( Hemorocallis dumortirei, H. fulva ), early day lily ( H. sieboldii ), orange day lily ( H. graminea ), red lily ( L.umbellatum ), rubrum lily ( L. speciosum ruburm ), stargazer lily ( L. orientalis ), western lily ( L. umbellatum ), and wood lily ( L. umbellatum ). Both the leaves and flowers are toxic, although the flowers seem more toxic. The toxic principle is water soluble.
Systems Affected
■ Renal/Urologic — The predominant component of lily toxicity is acute tubular nephrosis that causes acute renal failure. Azotemia is apparent within 24 hours of ingestion.
■ Gastrointestinal — Vomiting is a common occurrence within hours of ingestion. Pancreatitis and pancreatic lesions can occur within 8 hours of ingestion.
■ Nervous — Seizures may occur as early as 8 hours after ingestion.
■ Hepatobiliary — Liver enzyme elevations have been reported in later stages of disease.
■ Musculoskeletal — Increased creatine kinase was noted in experimental cases, but no histologic lesions were seen in muscle tissue. SIGNALMENT/HISTORY
■ Lily toxicity affects cats. Dogs that ingest lily plants have mild, short - term gastroenteritis without renal failure. Historical Findings
■ Vomiting, anorexia, and lethargy are usually the initial signs, and appear within 1 to 5 days after ingestion. The initial gastrointestinal signs may resolve, followed by signs of uremia. Polyuria may occur as early as 12 hours after ingestion. Neurologic signs of ataxia, depression, tremors, and seizures have been reported.
■ Owners may fi nd parts of the plant in vomitus, or evidence that the plant has been chewed (Figure 57.3 ).
CLINICAL FEATURES
■ Dehydration, renal pain, and renomegaly are common findings on initial examination. Mentation may vary from bright and alert to comatose. Urine output varies from anuric to polyuric; overhydration is common in anuric cats shortly after starting fluid therapy. Fever has been reported in some cases.
DIFFERENTIAL DIAGNOSIS
■ Initial gastrointestinal signs (vomiting, anorexia) ■ Nonspecific gastroenteritis ■ Dietary indiscretion ■ Pancreatitis
■ Acute uremia in cats
■ Nephrotoxins (e.g., ethylene glycol, NSAIDs, aminoglycosides) ■ Ureteral obstruction
■ Pyelonephritis ■ Lymphosarcoma
■ Recent ischemic events (i.e., anesthesia, hypovolemia, hypotension) DIAGNOSTICS
Complete Blood Count/Biochemistry
■ Azotemia: elevated BUN and creatinine with elevated phosphorus ■ Hyperkalemia (common) or hypokalemia ■ Metabolic acidosis, elevated anion gap
■ Variable increased creatine kinase: decreases within a few days
■ Alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase: increased in later stages
■ Occasionally hypocalcemia Urinalysis
Consistent with acute tubular nephrosis ■ Isothenuria ■ Glucosuria ■ Proteinuria ■ Granular casts Pathological Findings
■ The kidneys are usually swollen and may have perirenal edema. Histologically, acute tubular nephrosis that affects predominantly the proximal tubule is characteristic, frequently with evidence of epithelial regeneration. Small numbers of birefringent crystals are occasionally seen, but lily toxicity is not caused by oxalate nephrosis.
■ Pancreatic degeneration in early stages and fibrosing pancreatitis in late stages have been reported. Hepatic and lung congestion may occur. THERAPEUTICS Therapeutic objectives
■ Gastric decontamination to limit absorption of toxic components.
■ Early aggressive fluid treatment to counteract dehydration from polyuria and possibly to increase elimination of toxic component prior to onset of renal failure. ■ Standard therapy to manage acute renal failure.
■ Treatment with fluid therapy is important even if clinical signs are not present. Peace lily ( Sathiphyllum spp.) and lily - of - the - valley ( Convallaria majalis ) are not true lilies and do not cause nephrotoxicity. Drug(s) of Choice
■ Induce vomiting: apomorphine (administered via conjunctival sac or 0.03 – 0.04 mg/kg IV), 3% hydrogen peroxide (0.25 – 0.5 ml/kg PO), or xylazine (0.44 mg/kg IV, IM, or SQ)
■ Activated charcoal: 1 to 4 g/kg PO (protect airway with cuffed endotracheal tube if patient is unconscious)
■ Fluid therapy: balanced polyionic crystalloid (i.e., lactated Ringer ’ s solution or plasmalyte - 147) or saline IV at twice the maintenance rate for 48 hours prior to onset of renal failure Precautions/Interactions
■ If urine production is decreased, aggressive diuresis will result in volume overload.
Alternative Drugs
■ If medical management does not control uremia, hemodialysis or peritoneal dialysis has been used with favorable outcomes. Diet
■ Anorexia is common and may require placement of a feeding tube for management. A moderately protein restricted diet is appropriate. COMMENTS Client Education
■ If renal failure resolves completely (or does not develop), no special care is needed after discharge. If residual renal damage persists, standard care for chronic kidney disease will be required.
Patient Monitoring
■ Early treatment: Assessment of BUN, creatinine, electrolytes, and phosphorus at admission and after 48 hours of fluid therapy is recommended.
■ After onset of renal failure: Monitoring as for any cause of acute renal failure. Particular attention to volume status because many cats develop oliguria or anuria. Prevention/Avoidance
■ Lily plants should not be available in the cat ’ s environment. Lilies are common in floral arrangements, and day lilies are common in gardens. Expected Course and Prognosis
■ Early treatment (within 18 hours of ingestion): Prompt decontamination and fluid therapy may prevent renal failure and has a good prognosis
■ After development of renal failure: Overall mortality rates for cats with acute renal failure from nephrotoxic causes are about 50 to 60 percent. Cats that survive the acute phase may recover completely or have residual chronic kidney disease. Abbreviations
■ BUN : blood urea nitrogen ■ IM : intramuscularly ■ IV : intravenously
■ NSAIDs : nonsteroidal anti - inflammatory drugs ■ PO : by mouth
■ SQ : subcutaneously See Also
■ Acute Renal Failure