The authors declare no conflict of interest.
Mountain laurel toxicosis in a dog
Article first published online: 14 JAN 2013
© Veterinary Emergency and Critical Care Society 2013
Journal of Veterinary Emergency and Critical Care
Volume 23, Issue 1, pages 77–81, January/February 2013
How to Cite
Manhart, I. O., DeClementi, C. and Guenther, C. L. (2013), Mountain laurel toxicosis in a dog. Journal of Veterinary Emergency and Critical Care, 23: 77–81. doi: 10.1111/vec.12009
- Issue published online: 28 JAN 2013
- Article first published online: 14 JAN 2013
- Manuscript Accepted: 23 NOV 2012
- Manuscript Received: 7 NOV 2011
- poisonous plant;
- gastrointestinal injury;
To describe a case of mountain laurel (Kalmia latifolia) toxicosis in a dog, including case management and successful outcome.
A dog presented for vomiting, hematochezia, bradycardia, weakness, and ataxia, which did not improve with supportive treatment. Mountain laurel ingestion was identified as cause of clinical signs after gastrotomy was performed to remove stomach contents. Supportive treatment was continued and the dog made a full recovery.
New or Unique Information Provided
This report details a case of mountain laurel toxicosis in a dog, including management strategies and outcome, which has not been previously published in the veterinary literature.
Mountain laurel (Kalmia latifolia) is a member of the heath family of plants, which also includes azaleas and rhododendrons. These plants grow in acidic, moist soil and are found in higher elevations and near coastlines. They are typically grown for ornamental use. All parts of the plant are toxic. Ingestion of any part of the plant can cause bradycardia, gastrointestinal upset, depression, ataxia, and convulsions. Most animals avoid eating mountain laurel unless other forage is scarce. Mountain laurel toxicosis has been reported in goats, sheep, and people. To the authors’ knowledge mountain laurel toxicosis in dogs has not been reported in veterinary literature.
A 4-year-old neutered male Bernese Mountain dog weighing 44 kg was evaluated by the emergency service for vomiting, hematochezia, and weakness. The dog had a history of foreign body ingestion and exploratory laparotomies performed in December 2005 and December 2007. The dog had an episode of vomiting and hemorrhagic stool 1 wk prior to presentation. The dog was seen by the primary care veterinarian and improved with outpatient treatment, which consisted of oral maropitant1 and metronidazole.2 The night before presentation to the emergency service the dog vomited and had soft stool that contained mucus but no blood. The dog became acutely ataxic on the morning of presentation and was described by the owner as acting “drunk.” The dog was presented to the emergency service shortly after his owners noticed ataxia, which was approximately 11 h after first exhibiting any clinical sign.
On physical examination, the dog was quiet but alert, had injected mucous membranes, and was profusely hypersalivating. Capillary refill time was 1 s. The dog's heart rate was 108/min with no murmurs ausculted, respiratory rate was 28/min and rectal temperature was 37.6°C (99.8°F). The dog was painful on abdominal palpation but no palpable masses or fluid was noted. The dog was ataxic in the hindlimbs and exhibited generalized weakness. Hematochezia was noted during hospitalization. The owners were questioned about the possibility of the dog having been exposed to a toxin, prescription medication, or recreational drugs. They reported no known exposure.
Biochemical testing was performed. Abnormalities included an increased amylase of 1645 U/L (reference interval 200–1200 U/L) and an increased glucose concentration of 7.9 mmol/L [143 mg/dL] (reference interval 3.33–6.1 mmol/L [60–110 mg/dL]). Results of CBC were within the reference interval. PCV was 44% and total plasma protein was 68 g/L [6.8 g/dL] (reference interval 50–82 g/L [5.0–8.2 mg/dL]).
Abdominal radiographs revealed the stomach was filled with ingesta but not distended. The small bowel was normal in diameter and the colon contained scant fecal material. One lateral radiograph of the thorax revealed no abnormality.
Initial treatments included a 1 L bolus of an isotonic crystalloid solution,3 dolasetron,4 1 mg/kg IV, famotidine5 0.5 mg/kg IV, and metronidazole6, 10 mg/kg IV. An isotonic crystalloid solution3 with 20 mEq KCl/L was continued at 200 mL/h (4.5 mL/kg/h). The dog was subsequently noted to be ataxic. Systolic blood pressure measured via Doppler7 at that time was 80 mm Hg and the heart rate was 84/min. An ECG was performed because of the bradycardia in the face of hypotension and noted abdominal pain. The ECG showed intermittent 2° AV block. Due to hypotension, the dog was bolused an additional liter of an isotonic crystalloid solution and then continued on this fluid at 200 mL/h. The dog was progressively more weak and ataxic. Due to concern for potential toxic material in the stomach contributing to the dog's worsening clinical signs, the dog underwent abdominal exploratory surgery.
The dog was premedicated with an opiate agonist8 0.05 mg/kg IV and anesthesia was induced with propofol 3.4 mg/kg IV. The dog was intubated with an 11-mm cuffed endotracheal tube and anesthesia was maintained with inhalant isoflurane9 in oxygen. Cefazolin10 1 g (23 mg/kg) IV was administered preoperatively. Shortly after the start of surgery, the patient's systolic blood pressure via Doppler decreased to 75 mm Hg. A 220 mL (5 mL/lg) bolus of a colloid,11 was administered and subsequent to this the blood pressure increased to 115 mm Hg. After 1 h in surgery, the systolic blood pressure decreased to 75 mm Hg and the patient was administered a second bolus of a colloid (280 mL, [6.4 mL/kg]). Isotonic crystalloid solution was continued during surgery at 20 mL/kg/h.
A ventral midline celiotomy was performed and the abdomen was explored. The stomach was full of ingesta. A gastrotomy was performed at the fundus and several handfuls of plant material (approx. 1 kg) were removed (Figure 1). Manual inspection of the small intestine showed no obvious ingesta, but small pieces of plant material remaining in the small intestine could not be ruled out. The rest of the abdomen was grossly normal. The stomach was lavaged with sterile warmed saline and closed in 2 layers. The abdomen was lavaged with sterile warmed saline and an incisional gastropexy was performed on the right abdominal wall. The linea was closed in a continuous pattern. The SC tissue was closed with suture and the skin was closed with staples.
Post operatively the patient's rectal temperature was 35.5°C, heart rate 112/min, and systolic blood pressure via Doppler 75 mm Hg. Heat support was supplied by an external heating device.12 Isotonic crystalloid solution was administered at 200 mL/h and systolic blood pressure and temperature normalized to 92 mm Hg and 37.8°C, respectively. Post operative bloodwork revealed a decreased HCT of 0.3 L/L (30%) (reference interval 0.35–0.5 L/L [35–50%]), manual PCV of 35% and total plasma protein of 48 g/L (4.8 mg/dL) (reference interval 50–82 g/L [5.0–8.2 mg/dL]). The dog was placed on continuous ECG monitoring post operatively and had a normal sinus rhythm.
Based on visual inspection of the gastric contents, the leaves were identified as mountain laurel. The owner was contacted about the possibility of mountain laurel plants in the dog's environment. The owner indicated that mountain laurel was present in the yard. Upon inspection of the yard, the owners found a mountain laurel bush that had been half eaten and on comparison to the stomach contents, mountain laurel ingestion was confirmed. The bush was found in an area of the yard frequented by the dog. The ASPCA Poison Control Center (APCC) was contacted and they advised vigilant monitoring of blood pressure, heart rate and rhythm, serum potassium concentration, and symptomatic treatment of vomiting and general supportive care.
When fully recovered from surgery, the patient was administered 240 mL of activated charcoal solution once to prevent absorption of any toxins from small pieces of plant material that may have remained in the gastrointestinal tract. Sucralfate13 1 g was administered PO as slurry q 8 h. It was not clear from the record whether the activated charcoal included a cathartic. Hydromorphoneh (4 mg [0.1 mg/kg]) was administered IV q 6 h and cefazolin 1 g (22.7 mg/kg) was administered IV q 8 h. Overnight the patient's blood pressure and heart rate were normal. No vomiting or diarrhea was noted and the patient began eating. Signs of ataxia and weakness were completely resolved. Electrolytes were checked q 12 h and remained within reference interval, except for a mild increase in potassium (4.7 mmol/L, reference interval 3.5–4.5 mmol/L) 24 h after surgery. Medications administered during hospitalization included famotidine 0.5 mg/kg IV q 24 h, metronidazole 11.4 mg/kg IV q 12 h, and tramadol14 2.3 mg/kg PO q 8 h. The dog was discharged from the hospital 20 h after surgery. The dog was discharged home with metronidazole,b 11.4 mg/kg PO q 12 h, tramadol 2.3 mg/kg PO q 8 h, and sucralfate 1 g PO q 8 h.
The dog was seen for a recheck appointment 7 days after discharge and was deemed clinically normal. The owners reported that the dog was acting normally at home, was eating well and had no episodes of ataxia or weakness. The dog was seen 6 months later for an orthopedic evaluation and was clinically normal at that time.
Mountain laurel (Kalmia latifolia) is a member of the Ericaceae family, closely related to the rhododendron. Despite the similar name, Texas mountain laurel or blue laurel is actually a member of the Sophora spp. Members of the Sophora family are distinct from Kalmia plants in that they possess smaller leaves. They also contain quinolizidine alkaloids and their ingestion causes predominantly neurological signs.
Mountain laurel is a flowering evergreen shrub that is found in the eastern US (Figure 2). It contains grayanotoxins that bind to sodium channels in excitable cell membranes of nerve, heart, and skeletal muscle. This increases the membrane permeability of sodium ions in the excitable membranes, thus maintaining the cells in a state of depolarization.  Accumulation of intracellular sodium results in an exchange with extracellular calcium and plays a large role in the control of neurotransmitter release. These channels also become more permeable to potassium. In extensive studies of squid axons, it was noted that grayanotoxin is able to increase sodium permeability by almost 100-fold. The result is persistent depolarization due to the opening of sodium channels at more negative potentials, as well as the slower closure of these channels. Other mechanisms may be involved, as depolarization occurs even after sodium channel inactivation, but these mechanisms have not been studied. The activity of grayanotoxins is antagonized by tetrodotoxin, a sodium channel blocker. The cholinergic responses to the toxin, including salivation and decreased heart rate, are responsive to atropine. Cardiac effects include decreased sinoatrial node activity due to negative chronotropic actions. This leads to sinus arrest due to persistently open sodium channels. Bradycardia and a variety of cardiac arrhythmias are results of mediation of the vagus nerve. All parts of the plant, including the nectar, contain grayanotoxins. The term grayanotoxin is both a general and specific descriptor; the term ericaceous diterpenoid is preferred when referring to the toxin in general. A number of grayanotoxins have been identified in members of the Ericaceae family, the most common of which is Grayanotoxin I. Concentrations of grayanotoxins in ericaceous plants commonly found in the United States have not been determined. The risk of toxicity from ingestion of these plants may vary considerably among plant species.
Honey bees that ingest Kalmia produce “toxic honey,” which, when ingested by humans, causes severe digestive distress, dizziness, cardiac arrhythmias, decreased blood pressure, weakness, visual derangements, and rarely seizures. Viscera of chicken fed mountain laurel are toxic to cats. Most animal species are susceptible to the effects of mountain laurel toxicosis, including goats, horses, sheep, cattle, rats, llamas, and kangaroos. A high incidence of death is reported for rabbits, possibly due to the lagomorph's inability to vomit the toxic material. The majority of intoxications involve sheep and goats, especially in winter months when the animals are experiencing cold stress. Most animals avoid K. latifolia unless other forage is not available. Deer are considered to be resistant to the effects of mountain laurel; they can become intoxicated but often are reluctant to eat sufficient foliage to cause problems.
The toxic dose of K. latifolia for sheep is 0.3–0.4% body weight and the toxic dose of grayanotoxin-containing plants for cattle is 0.2–0.6% body weight. The lethal dose is 0.6–1.6% body weight for these animals. The minimum grayanotoxin dose causing clinical signs in dogs is 7 mg/kg body weight (noted from rhododendron ingestion). Several cases of azalea or rhododendron ingestion reported to the APCC involved dogs that had ingested as many as 30 nearly intact leaves and were treated with emergency gastrotomy. The dog in this case report ingested approximately 1 kg of Kalmia plant material. The patient weighed 44 kg, therefore the dose ingested was 2.15% of the dog's body weight. When compared to the toxic dosage for sheep, this was a significant exposure.
Clinical signs of grayanotoxin ingestion develop within 2–6 h of ingestion. The cholinergic effects of grayanotoxin may include salivation, anorexia, repeated swallowing, retching, vomiting, bloat, abdominal pain, respiratory depression, and hypotension. Partial blindness and seizures have been reported in fatal intoxications. The animals become weak, unable to stand, and seem paralyzed. The acute effects usually last for a few hours up to 24 h, but neurological effects and weakness may persist for up to 3 days. Less commonly seen pathologic changes include pulmonary edema, renal tubular, and hepatocellular necrosis. Treatment involves supportive care and is directed to relieve symptoms as there is no specific antidote. In animals suspected to be exposed to Kalmia, vomiting should be induced to decontaminate. Because clinical signs of toxicosis develop within 2–6 h of ingestion, oral activated charcoal may be of some benefit in limiting absorption of the toxins. Increased salivation and bradycardia are responsive to atropine. Though there is no experimental confirmation, sodium and calcium channel blockers may be of some benefit.
In the present case, the contents of the stomach were not revealed until gastrotomy was performed. If this had been known, efforts to induce emesis would have been pursued. However, if the stomach was not emptied after vomiting, the remainder of the contents would have required surgical removal. Due to the history of foreign body ingestion and because the patient was vomiting on presentation, it was determined that induction of emesis was contraindicated. In retrospect, atropine may have alleviated the dog's bradycardia and 2°AV block, but by the time mountain laurel toxicosis was confirmed the bradycardia and heart block had resolved.
Activated charcoal was administered to this dog post operatively because of concern that there were pieces of plant that may have remained in his small intestine. Grayanotoxins are rapidly absorbed through the gastrointestinal tract, but the specific area where absorption occurs has not been reported. If the toxin is absorbed through the stomach, activated charcoal would not have been indicated, as the stomach was emptied during surgery. If the toxin is absorbed by both the stomach and intestine, the activated charcoal may have been beneficial in this case. Activated charcoal may also be of benefit once the stomach is empty if the toxin undergoes enterohepatic recirculation. Specific absorption kinetic information has not been reported in the literature. Because grayanotoxins are absorbed rapidly, activated charcoal may not be of benefit a few hours after ingestion, especially if the patient is showing clinical signs. Finally, due to the fact that this dog had gastrotomy, the benefits of giving activated charcoal may not have outweighed the risks. If the gastrotomy site had leaked, there would have been an increased risk of peritonitis.
Grayanotoxin concentrations can be detected using several procedures. The first involves use of a saturated solution of antimony trichloride in chloroform for detection of grayanotoxin in urine, ingesta, serum, or honey on thin-layer chromatography with observation under UV light. More recently another method has been developed, which involves extraction of the toxins from ingesta with 2–3 volumes of methanol and chloroform, then detected using a mixture of ethanolic vanillin and perchloric acid. Detection limit with these methods is 2 μg. If gastric contents are not available, grayanotoxin concentrations can be determined in serum and urine via a liquid chromatography/mass spectrometry method. This method can detect 1 ng of grayanotoxin per gram of serum or urine. Grayanotoxins can be detected in urine up to 5 days after exposure. Presence of grayanotoxins in any of the submitted samples is consistent with exposure to grayanotoxin-containing plants in the environment. If clinical signs for grayanotoxin poisoning are also present, a diagnosis of this toxicosis can be made. The most common test used currently by most diagnostic labs is the rapid liquid chromatography/tandem mass spectrometry method, which detects 0.2 μg/g of feces or rumen contents and 0.05 μg/mL in urine and other fluids.
Mountain laurel toxicosis in dogs has not been reported in the literature. Forty-two cases of ingestion of mountain laurel in dogs have been reported to APCC between 2000 and October 2011.15 Of these patients, vomiting was the most commonly reported sign. Lethargy, anorexia, ataxia, diarrhea, and salivation were also common. Weakness, seizures, and hyperglycemia were reported rarely.o Because mountain laurel is eaten by goats and sheep most commonly when other vegetation is not available, it likely has a bitter and unappealing taste. Due to the paucity of published material about intoxication in dogs, it can only be speculated that dogs avoid mountain laurel because of its taste.
Mountain laurel is native to the eastern US and is used in ornamental landscaping.  Although mountain laurel intoxication is rarely reported in dogs, it should be considered in dogs presenting with clinical signs of toxicosis, especially in areas where mountain laurel is grown. As Kalmia species become more popular as an ornamental plant, exposure of domestic animals to this plant will likely increase and therefore clinicians should be aware of this toxicity.
Cerenia, Pfizer Animal health, New York, NY.
Metronidazole, Teva Pharmaceuticals, Sellersville, PA.
Normosol R, Abbott Laboratories, North Chicago, IL.
Anzemet, Sanofi-Aventis US, Bridgewater, NJ.
Famotidine, Merck & Co Inc, Whitehouse Station, NJ.
Metronidazole, Hospira Inc, Lake Forest, IL.
Ultrasonic Doppler flow detector, Parks Medical Electronics Inc, Aloha, OR.
Hydromorphone, Abbott Laboratories.
Isoflurane, MWI, Meridian, ID.
Cefazolin, Steri-Pharma LLC, Syracuse, NY.
Hetastarch, Hospira Inc.
Bair Hugger, Arizant Healthcare, Eden Prairie, MN.
Sucralfate, Nostrum Laboratories, Kansas City, MO.
Tramadol, Amneal Pharmaceuticals, Hauppauge, NY.
ASPCA APCC AnTox Database [unpublished data].
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