Daffodil toxicosis in an adult cat

Abstract

A domestic longhair cat with a 3-day history of lethargy and vomiting after ingesting dried daffodil stems (Narcissus spp.) was severely hypothermic (33.0°C), with bradycardia (78 beats/min) and hypotension. Treatment with atropine, dexamethasone, fluid therapy, and supportive care resulted in a complete recovery by 6 days after exposure.

A 2-year old, neutered, male domestic longhair was presented with a history of lethargy and vomiting of 3 d duration. Four days earlier (day 1), the cat had expelled a hairball, but this was not considered unusual. Subsequently, on day 2, the cat had vomited food and yellow fluid several times and had displayed a marked decrease in appetite, with polydipsia and polyuria. No vomiting occurred on day 3, but the cat was lethargic and anorexic. The owners attributed these changes to hairballs and treated the cat with a teaspoon of a hairball remedy on the morning of day 4. On further questioning, the owner reported seeing the cat chewing on dried daffodil stalks, which had been removed from the flower garden for disposal on the morning of day 2, and recalled seeing plant material in the vomitus that day.

When examined, the cat was sternally recumbent, quiet, in thin body condition, and conscious, but only weakly responsive. The extremities were cool to the touch and the rectal temperature averaged 33.5°C for 3 readings. Pale oral mucous membranes were noted, and auscultation of the heart revealed bradycardia (84 beats/min (bpm); reference range, 120 to 140 bpm). Respiratory rate was normal (22 breaths/min). Dehydration was estimated at 10%, and peripheral pulses were weak. The severity of the cat’s condition was discussed with the owner, who agreed to emergency therapy for possible daffodil toxicosis.

The cat was wrapped in warm towels and catheterization of the left cephalic vein was attempted but was not possible, probably because of hypotension. Accordingly, 180 mL of lactated Ringer’s solution (Baxter; Toronto, Ontario) was administered SC. During this procedure, the rectal temperature of the cat dropped to 33.0°C. Accordingly, the cat was immersed in a water bath at 40°C for approximately 15 min, removed, and immediately dried with warm towels and a hair dryer. Subsequently, the cat was rewrapped in dry towels with warm oat bags and placed under a heat lamp. After 15 min, the body temperature had risen to 36.0°C, and it was possible to catheterize the right cephalic vein. A 2-mL blood sample was drawn for a complete blood cell (CBC) count (QBC VetAutoread Hematology Anayzer; Idexx Laboratories, Toronto, Ontario) and serum biochemical profile (VetTest Chemistry Analyzer; Idexx Laboratories). Warmed lactated Ringer’s solution was administered, IV, at shock rate (45 mL/kg bodyweight (BW)/h). The heart rate had dropped to 78 bpm, and atropine, 0.02 mg/kg BW, IM, and dexamethasone (Vétoquinol, Lavaltrie, Quebec), 2 mg/kg BW, IV, were also administered. Detoxification procedures, such as induction of emesis, administration of activated charcoal, or gastric lavage, were not elected because more than 48 h had elapsed since the time of exposure to the daffodil stalks. The cat was monitored continuously and the rectal temperature was taken 4 times/h. Thirty minutes after warming and atropine administration, the heart rate had increased to 120 bpm and the rectal temperature had increased to 37.5°C; however, 30 min later, rectal temperature had dropped to 35.1°C. The described warming protocol was repeated with similar results. Oral mucous membranes remained a normal pink color.

The CBC counts were within normal range; however, the biochemical profile results revealed elevated urea (42.62 mmol/L; reference range, 5.71 to 12.85 mmol/L), hyperglycemia (glucose 25.14 mmol/L; reference range, 4.22 to 8.06 mmol/L), hyponatremia (sodium 137.2 mmol/L; reference, range, 150.0 to 165.0 mmol/L), hypokalemia (potassium 2.35 mmol/L; reference range, 3.5 to 5.8 mmol/L), and hypochloremia (chloride 75.5 mmol/L; reference range, 112.0 to 129.0 mmol/L). The urinary bladder was not palpable, so it was not possible to collect urine either by cystocentesis or digital compression. Because of the difficulty in maintaining normothermia for more than 30 min and to ensure metabolic stability overnight, the cat was transferred to an emergency clinic for continuous observation and warming.

The cat was returned from the emergency clinic to the admitting clinic on the morning of day 5. With the use of warm towels, oat bags, and warm IV fluids, average rectal temperature had reached 38.0°C. The average heart rate (measured hourly) was 120 bpm and oral mucous membranes remained pink. A serum biochemical profile revealed a return to normal ranges for urea (11.45 mmol/L), sodium (153 mmol/L), and potassium (3.8 mmol/L). Chloride remained slightly low (110 mmol/L); glucose had decreased (10.08 mmol/L) but remained above the reference range. A free-flow clear yellow urine sample (specific gravity 1.015; pH 8.5) contained trace blood and protein.

On day 6, the cat began sitting up and walking periodically. Crackles were noted in the ventral lung fields bilaterally. The IV fluid rate was decreased to maintenance rate and furosemide (Apo-Furosemide; Apotex, Toronto), 2 mg/kg BW, IM, was administered. The cat remained quiet, alert, and responsive, urine output increased during the 3 h following diuretic administration, and lung sounds returned to normal 4 h after diuretic administration. During the next 8 h, in the absence of exogenous heat sources, rectal temperature, taken hourly, averaged 38.4°C, and the cat consumed 30 mL of Prescription Diet Canine/Feline a/d (Hill’s Pet Nutrition Canada, Mississauga, Ontario).

On day 7, with a body temperature of 38.9°C, normal hydration, and a normal CBC count and serum biochemical profile, the cat remained quiet. Fluid therapy was discontinued and the cat remained stable. On day 8, the cat was bright and energetic, with a normal appetite. A complete physical examination was unremarkable and the cat was discharged.

The common spring-flowering perennial, daffodil (Narcissus spp.), is grown from a bulb and is easily recognized by its yellow, trumpet-shaped flowers. The emetic, diarrheic, sedative, and irritant properties of daffodil extracts have been known for many years and, historically, were used in human medicine to induce vomiting and therapeutically for whooping cough (1). A review of the literature reveals few documented cases of companion-animal daffodil intoxication, but human cases have occurred when the bulbs were mistaken for onions, leeks, or Chinese lilies (1). The Veterinary Poisons Information Service (VPIS), located in London, England, and the National Animal Poison Control Center (NAPCC), located in Illinois, USA, have received a few enquiries regarding daffodil ingestion, most of which involved dogs (2,3). Four cases of severe poisoning have been reported to the VPIS: 1 of these animals died and 1 was euthanized (2). In most reported cases, bulbs were ingested, but poisoning has also occurred after ingestion of the flowers or leaves. Prominent clinical effects, with onset between 15 min and 24 h of ingestion, included vomiting, anorexia, diarrhea, lethargy, collapse, hypothermia, hypotension, bradycardia, abdominal pain, hyperglycemia, and dehydration. In contrast to these animal cases, human cases showed only nausea, vomiting, diarrhea, and lightheadedness. In all human cases, the symptoms resolved, often spontaneously, within 48 h (1). Therefore, it appears that the clinical syndrome in companion animals is more severe and of longer duration than in humans. Perhaps this is because the eating behavior of companion animals results in the ingestion of larger doses, or it may reflect a species-specific response.

Daffodil contact dermatitis, commonly referred to as “daffodil pickers’ rash,” has also been documented in florists and growers. Recent research implicates calcium oxalate crystals in the stem sap, in conjunction with alkaloid compounds, as a cause of the characteristic skin lesions (4).

The most abundant bioactive alkaloids characterized in daffodil extracts are galanthamine, lycorine, and narciclasine (1). These compounds are thought to induce vomiting by irritating the gastric mucosa and stimulating the chemoreceptor trigger zone in the medulla oblongata (2). Although the cat in this case vomited several times following ingestion of the daffodil leaves, thereby reducing absorption of the full dose of the toxicant, some absorption likely occurred before emesis began, and some of the ingested material may have remained in the stomach and duodenum following vomition. This might account for the protracted course of clinical signs.

In this cat, the more profound clinical findings were hypothermia, bradycardia, hypotension, and dehydration. These significant cardiovascular effects of daffodil extracts have also been investigated by phytotherapy researchers. Nonpurified extracts of Narcissus tazetta produce dose-related hypotensive responses in rats (5). The mechanism of this effect was characterized through the administration of daffodil extract in the presence of alpha and beta adrenergic, cholinergic, histaminic, and angiotensin converting enzyme receptor blockers. Significant decreases in the hypotensive effect of Narcissus extract were noted only in the presence of atropine and phentolamine, suggesting cholinergic and alpha adrenergic mechanisms, respectively (5). While atropine sulphate was administered to the cat in this case to resolve bradycardia, perhaps clinical improvement in peripheral vasodilation, and therefore hypothermia, might also have been achieved with the use of phentolamine, additional atropine, or both.

The serum biochemical and electrolyte abnormalities seen in this cat may be largely attributed to fluid losses and anorexia, as fluid therapy corrected the electrolyte imbalances and returned blood urea values to normal. Permanent kidney damage was ruled out when renal parameters returned to normal and urine output was not compromised.

In this case, the owners did not attribute the cat’s vomiting and lethargy to the ingestion of the dried daffodils, although they saw the cat eat them, because they were not aware that this plant was poisonous. Daffodils are common in Canadian spring gardens, and should be included in toxic plant client education programs. Significant risk likely exists not only during bulb planting, but also during storage and disposal of dead plants, as occurred in this case. Supportive care, including the administration of anticholinergics, may result in a full recovery, but prognosis most likely depends upon the dose ingested and timely diagnosis.