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590 Lily Toxicosis

Lily Toxicosis Client Education
Sheet
VetBooks.ir Etiology and Pathophysiology Advanced or Confirmatory Testing

BASIC INFORMATION
Source: • There is no definitive confirmatory test for
Definition • Lilies have large, showy, funnel-shaped flowers. lily toxicosis.
Lilies are a family of flowering ornamental The plants grow from bulbs and have erect • Ultrasound can aid in measuring renal size
plants that can cause acute kidney injury stems 30-250 cm high. Lilies are frequently and cortical thickness and in ruling out other
(AKI) when ingested by cats. Lily poisoning is included in bouquets and floral arrangements. causes of AKI.
a well-recognized and potentially fatal toxicosis Daylilies are often grown in gardens. • Renal biopsy may help determine extent of
in cats. In dogs, only mild gastrointestinal upset • Peak incidence is during Christmas and renal damage and prognosis (rarely done
is expected with lily ingestion. Easter holidays because lilies are popular because history and exclusion of other causes
holiday ornamentals. are usually sufficient).
Synonyms Mechanism of toxicosis: • Histologically, the renal lesion includes acute
Lilies toxic to cats include daylilies (Hemerocallis • Intoxication occurs through ingestion. A necrosis of proximal convoluted tubules and
spp), Easter lilies (Lilium longiflorum), Rubrum single bite or even exposure only to pollen mineralization. Pancreatic acinar cells also
or Japanese showy lilies (Lilium speciosum, can cause the clinical syndrome. may show degeneration.
Lilium lancifolium), Stargazer lilies (Lilium • Mechanism of action is unknown. Toxin
auratum), and tiger lilies (Lilium tigrinum). is believed to be a water-soluble fraction. TREATMENT
Many new Lilium varieties are developed each All parts of the plant are considered toxic,
year. All Lilium or Hemerocallis species should including pollen. Flowers contain the highest Treatment Overview
be considered toxic. amount of toxin. In asymptomatic cats, the aim of treatment is
• Affected cats develop AKI due to degeneration early decontamination (induction of emesis if
Epidemiology and necrosis of the proximal renal tubules. within 2 hours and administration of activated
SPECIES, AGE, SEX Sloughing of necrotic tubular epithelial cells charcoal) and to prevent the development of
Lily toxicosis has been reported only in results in tubular blockage and anuria. AKI. Such treatment, including therapy aimed
cats and meerkats. at avoiding oliguria/anuria and uremic signs,
DIAGNOSIS is appropriate in all cases, including exposures
GENETICS, BREED PREDISPOSITION that are suspected but unconfirmed because
All cats are susceptible. Diagnostic Overview unchecked toxicosis may have devastating and
Diagnosis is based on history of vomiting irreversible results.
RISK FACTORS in a cat with known exposure to lilies or
Younger cats may be more likely to eat plant unexplained/unexpected elevations in serum Acute General Treatment
material. renal values, or both. In the absence of history • Decontamination of patient (no clinical
of exposure, other potential causes for AKI signs) (p. 1087):
GEOGRAPHY AND SEASONALITY must be ruled out, but empirical treatment ○ Emesis: for asymptomatic cats with recent
• Easter lilies are most commonly sold in should be initiated during diagnostic testing ingestion (within a few hours), induce
March and April. Other lilies are found because of the potentially severe consequences vomiting (p. 1087)
year-round. of unchecked toxicosis. There is no specific ○ Give activated charcoal 1-4 g/kg PO.
• Lilies grow naturally along the Pacific confirmatory test for in-clinic use. Protect airway with cuffed endotracheal
Coast of the United States. Lilies are tube if patient is unconscious.
frequently cultivated as garden plants or Differential Diagnosis • Prevent/slow development of kidney injury
houseplants. Toxicologic: (if cat is suspected or known to have ingested
• Daylilies (Hemerocallis spp) are common • Ethylene glycol lilies in the preceding 2 days). IMPORTANT:
landscape plants in the United States. • Nonsteroidal antiinflammatory drugs treatment is implemented regardless of
• Cholecalciferol or calcipotriene whether signs are present:
Clinical Presentation • Oxalic acid ○ Intravenous (IV) fluid diuresis for a
HISTORY, CHIEF COMPLAINT • Nephrotoxic antibiotics minimum of 48-72 hours at 2-3 times
• History of plant ingestion and/or presence Non-toxicologic, spontaneous (p. 23) maintenance rate plus volume deficit
of lilies in owner’s home • Acute-on-chronic kidney disease (e.g., (adjust based on hydration, fluid volume
• Cats typically present vomiting (± plant pyelonephritis, renal lymphoma, polycystic tolerance, and response to treatment). Cats
material in vomitus), anorexic, and lethargic. kidney disease) with normal serum renal values throughout
• Signs usually develop within 12 hours after • Acute glomerulonephritis (e.g., feline infec- diuresis may be weaned off fluids after 48
exposure (range, 2 hours to 5 days). tious peritonitis, autoimmune disease related) hours. In cats with azotemia, continue IV
• Polyuria, polydipsia, and AKI develop within • Renal thromboembolism fluids until azotemia resolves. In some cases,
36-72 hours after ingestion. this may mean days to weeks of treatment.
Initial Database ○ Monitor urine output in azotemic
PHYSICAL EXAM FINDINGS • Serum biochemistry panel: azotemia (blood patients. For oliguria (urine production
• Unremarkable if ingestion was recent. Initial urea nitrogen [BUN] > 34 mg/dL; creati- < 0.25 mL/kg/h), furosemide (begin with
signs of vomiting, anorexia, and lethargy may nine is often disproportionately elevated), 1 mg/kg; increase as needed up to 4 mg/kg
appear to resolve without treatment. hyperkalemia, and hyperphosphatemia are IV, IM, PO or SQ) may increase urine
• Signs progressing to oliguria and anuria, common. Occasionally, hypercalcemia, output (p. 1194).
dehydration, lethargy, and vomiting elevated pancreatic enzymes ○ Treat hyperkalemia (p. 495) if present.
• Some cats also show vocalization, adipsia, • Urinalysis: isosthenuria, epithelial granular • Supportive care
drooling, tremors, ataxia, weakness, and casts, and glucosuria in the absence of ○ Persistent nausea: consider maropitant
seizures. hyperglycemia are typical. 1 mg/kg SQ q 24h, dolasetron mesylate

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