Suspected albuterol toxicosis in a dog

CASE DESCRIPTION: A 6-year-old male castrated Shetland Sheepdog was evaluated because of severe hypokalemia and progressive paresis. CLINICAL FINDINGS: Physical examination revealed fever, tachypnea, mydriasis, hyperemic mucous membranes, severe forelimb paresis, and hind limb paraplegia. The dog had superficial and deep pain sensation in all 4 limbs. Forelimb spinal reflexes were considered normal, but hind limb reflexes were normal to slightly hyperreflexive. The panniculus reflex was considered to be normal, and cranial nerve reflexes were intact. A CBC revealed mild leukocytosis and erythrocytosis, and serum biochemical analysis revealed severe hypokalemia. Thoracic and abdominal imaging did not reveal relevant findings. Blood pressure and ECG findings were within reference limits. Questioning of the owner revealed possible exposure to albuterol via ingestion of medication intended for the owner's horse. Results of serum testing via immunoassay were suggestive of albuterol toxicosis. TREATMENT AND OUTCOME: Treatment included IV administration of an electrolyte solution and supplemental potassium chloride. The rate of potassium chloride supplementation was slowly decreased as serum potassium concentration increased. No other medical intervention was required, and the dog made a rapid and complete recovery. CLINICAL RELEVANCE: Ingestion of albuterol can lead to profound physical and serum biochemical abnormalities. Appropriate historical information should be obtained to identify possible sources and routes of exposure to intoxicants. Albuterol-induced hypokalemia can be successfully managed medically.     

Suspected tolazoline toxicosis in a llama

Clinical signs of tolazoline toxicosis developed in a 4-year-old llama that received 2 doses of tolazoline hydrochloride to reverse xylazine-induced sedation. The full first dose (4.3 mg/kg [2.0 mg/lb] of body weight) was erroneously injected i.v., and the second dose was administered half i.v., half i.m. 45 minutes later, because the llama became weak and recumbent. Signs of anxiety, hyperesthesia, profuse salivation, and tachypnea were the first detectable clinical signs of tolazoline toxicosis. Convulsions, hypotension, gastrointestinal tract hypermotility, and diarrhea also developed. The llama was treated successfully with i.v. administration of diazepam, phenylephrine, and lactated Ringer's solution supplemented with potassium chloride and oxygen administered via nasal insufflation. We suggest that the maximum dose of tolazoline administered at any one time to llamas not exceed 2 mg/kg (0.91 mg/lb). Furthermore, tolazoline should be administered slowly i.v. or i.m. to reduce the risk of adverse reactions.     

Suspected monensin toxicosis in feedlot cattle

Suspected monensin toxicosis was seen in feedlot cattle aged 6 to 9 months. Twenty cattle died following inclusion of monensin in the feed at 400g/tonne, which was 13 times the recommended level. The deaths occurred over 2 weeks. Clinical signs were inappetance, respiratory distress and sudden death. Post-mortem features were those of right-sided heart failure and included dependent subcutaneous oedema, ascites, hydrothorax, and periancinar hepatocyte congestion and necrosis. However, in contrast to previous reports no myocardial necrosis was found, but focal skeletal muscle necrosis was observed. Additional findings were marked pulmonary oedema accompanied by fibrin and erythrocyte exudation into alveoli and interlobular lymphatics. From these findings it appears that monensin, as well as affecting both cardiac and skeletal muscle, has a primary effect on lung vasculature.     

Fluoride toxicosis in wild ungulates

To compare the occurrence of chronic fluoride toxicosis in wild and domestic animals in selected areas of Utah, Idaho, Montana, and Wyoming, deer, elk, and bison bones and teeth were collected for evaluation. Vegetation and drinking water samples also were collected, so that potential sources of fluoride could be evaluated. Deer, elk, and bison were found to be susceptible to the adverse effects of ingestion of excessive amounts of fluoride. Teeth and bones were primarily affected with characteristic lesions. Pathognomonic soft tissue changes were not observed. The animals had been exposed to a variety of sources of excessive fluoride, including water high in fluoride, forages contaminated by industrial effluents that were high in fluoride, vegetation contaminated with high fluoride-content soil by rain splash or wind, or a combination of these sources. Waters high in fluoride, especially from geothermal springs and wells, often contained appreciable amounts of various soluble salts. Evidence accumulated from specimens collected throughout the aforementioned states indicated that there are areas where chronic fluoride toxicosis is a problem for wildlife. These areas were where natural sources of fluorine (especially geothermal waters) provided amounts for ingestion that exceed species tolerance limits or were near certain industrial operations.     

Suspected lead toxicosis in a captive goshawk.

Lead toxicosis was diagnosed in a 3-week-old male goshawk after evaluation of the history, clinical signs, radiographic lesions, and laboratory values. Treatment with Ca-EDTA and supportive measures was successful. The presumed source of lead was from birds that had been shot with a pellet gun and used for food.     

Suspected citrus pulp toxicosis in dairy cattle.

Thirteen lactating dairy cows from a herd of 650 died over a 6-week period. Most animals were down in milk production at 1 milking and were found dead at the next milking. Two cows had elevated heart rate and enlarged mandibular lymph nodes. Two others had azotemia, elevated heart rate, hyperglycemia, and weight loss. Necropsy of 10 cows revealed hemorrhages on the intestinal serosa and epicardium, lymphadenopathy, interstitial nephritis, small intestinal hemorrhage, and interstitial pneumonia. Histopathology showed lymphocytic to lymphogranulomatous inflammation in the heart, spleen, kidney, lymph nodes, liver, lung, pancreas, and adrenal gland. Phlebitis was present in 2 livers. The lesions resembled those of hairy vetch toxicosis, but no vetch was being fed. Similar lesions have been reported with the feeding of citrus pulp. Citrus pulp was being fed to the lactating cows and had been added to the diet 6 weeks before the first death. The syndrome resolved with elimination of citrus pulp from the diet.     

Suspected lily-of-the-valley (Convallaria majalis) toxicosis in a dog

Objective: To describe successful treatment of third-degree atrioventricular (AV) block using temporary noninvasive transthoracic pacing and placement of a permanent transvenous pacemaker in a case of suspected lily-of-the-valley ( Convallaria majalis ) intoxication in a dog.
Case summary: A 2-year-old neutered male Beagle weighing 17.8 kg was presented to the emergency service for treatment of bradycardia, vomiting, and lethargy. An electrocardiogram revealed third-degree AV block that was nonresponsive to atropine. Ten hours after admission, the dog became obtunded. Treatment initially consisted of temporary noninvasive transthoracic pacing and eventually placement of a permanent transvenous pacemaker. The initial history did not suggest that the dog had access to any known cardiotoxins. However, C. majalis , which contains cardiac glycosides, was identified within the dog's environment and the dog's serum did contain digoxin or an immunologically cross-reactive compound.
New or unique information provided: This is the first reported successful management of C. majalis toxicosis in a dog. Temporary noninvasive transthoracic pacing was used in the management of this case as a safe and effective bridge to permanent pacemaker implantation.     

Suspected ivermectin toxicosis in a miniature mule foal causing blindness

A 9-week-old miniature mule foal presented to the Veterinary Medical Teaching Hospital for acute blindness, ataxia, and depression following an overdose of an over-the-counter ivermectin-based de-worming medication. Ophthalmic examination and electrodiagnostic evaluation eliminated outer retinal abnormalities as the primary cause of the bilateral blindness, implicating instead a central neurologic effect of the drug. With symptomatic and supportive care, the foal recovered fully and regained its vision.     

Suspected toxicosis after topical administration of minoxidil in 2 cats

Objective: To discuss the clinical presentation and necropsy findings of 2 cats after topical administration of a minoxidil solution. Additionally, a potential management plan is offered for future cases. Case summary: Two cats with dermal exposure to topical minoxidil solution were identified from the ASPCA Animal Poison Control Center (APCC) files. Both cats were presented with lethargy and dyspnea within 36 hours of exposure. The cats were hypothermic, and had pulmonary edema and pleural effusion present on thoracic radiography. Both cats died despite supportive care. Necropsy of both cats confirmed pleural effusion and pulmonary edema and indicated cardiac compromise. New or unique information provided: Topical administration of minoxidil solution may cause life‐threatening pulmonary edema, pleural effusion, and cardiac dysfunction in the cat.     

Dinoseb toxicosis in two dogs

Two male English Setters were noticed to be breathing rapidly, hyperexcitable, and atactic after roaming a rural area for 2 hours. Both dogs' cost were stained with yellow liquid. One dog died while en route to the veterinarian. Treatment was begun for the surviving dog for what was initially diagnosed to be organophosphorus or carbamate insecticide toxicosis. Before the diagnosis could be confirmed, the second dog died. The yellow liquid on the dogs' skin was identified as dinoseb in high concentrations. Dinoseb is an acutely toxic, substituted dinitrophenolic herbicide believed to act as an uncoupler of electron transport from oxidative phosphorylation.     

Lead-induced toxicosis in two domestic rabbits

Lead toxicosis developed in 2 pet rabbits. Both rabbits had decreased appetite or anorexia; also, one had mild anemia and one had pleural effusion. Treatment with the calcium chelate of ethylenediaminetetraacetic acid was effective in both rabbits. The rabbit's propensity for gnawing may result in lead toxicosis, and may be seen more frequently as rabbits become more popular as pets.     

Brodifacoum toxicosis in two neonatal puppies

Eight out of a litter of 13 puppies were either born dead or died within 48 hours of birth. Three puppies that died shortly after birth were necropsied. Two puppies had hemorrhage in the thoracic and peritoneal cavities, intestinal serosa, and meninges. The third puppy was smaller than the other two puppies but did not have detectable hemorrhage. Brodifacoum, a second-generation coumarin anticoagulant, was detected in livers from the two puppies with hemorrhage. The dam did not have clinical signs of coagulopathy before or subsequent to whelping. The owners were confident that the dog had not been exposed to rodenticide for at least 4 weeks before whelping. A presumptive diagnosis of in utero brodifacoum toxicity was made. To the authors' knowledge this is the first time a second-generation coumarin anticoagulant has been detected in the liver of a newborn animal. This case is also unique because the dam was unaffected, suggesting that fetuses are more susceptible to brodifacoum toxicity than adult animals.     

Amanita muscaria toxicosis in two dogs

Objective: To report the manifestations, history, and pathophysiologic basis of disease in 2 dogs with Amanita muscaria toxicosis. Case summaries: Two dogs were evaluated for an acute onset of gastroenteritis and seizures. A. muscaria toxicosis was suspected in each dog after confirmation of environmental exposure and visualization of ingested mushrooms in vomitus. The diagnosis was confirmed following identification of toxic Amanita metabolites in the urine and serum of each dog. Administration of supportive and symptomatic therapies resulted in the complete recovery of each animal. Unique information provided: Ingestion of the mushroom, A. muscaria, by dogs can result in acute gastrointestinal distress that precedes a potentially life‐threatening central neurologic syndrome characterized by seizures, tremors, and somnolence. Central nervous system dysfunction results primarily from the actions of ibotenic acid and its decarboxylation product, muscimol, which are analogues of the neurotransmitters glutamate and γ‐aminobutyric acid (GABA), respectively. Identification of these toxins in the urine and serum of affected dogs using high‐performance liquid chromatography (HPLC) provides a definitive diagnosis.     

Suspected ergotism in two heifers

A syndrome similar to gangrenous ergotism was seen in 2 Friesian heifers grazing meadow hay containing perennial rye grass seed heads parasited by an ergot presumed to be Claviceps purpurea. Clinical signs were bilateral hind limb lameness and gangrene. There was angiographic evidence of vasoconstriction in the lower hind limbs with necrosis of all tissues in the distal region of both hind limbs.     

Suspected chlorpyrifos toxicosis in a llama, and plasma pseudocholinesterase activity in llamas given chlorpyrifos

Five days after treatment with chlorpyrifos, a 1.5-year-old male llama was unable to stand, had saliva flowing from its mouth, and had constricted pupils, hyperglycemia, a metabolic acidosis, and a plasma pseudocholinesterase activity of 111 IU/L. Mean (+/- 1 SD) plasma pseudocholinesterase activity of 29 healthy llamas was 233.76 +/- 51.55 IU/L. Five to 8 days after topical application of chlorpyrifos (25 mg/kg of body weight) to 3 healthy llamas, the pseudocholinesterase activity decreased to 38% to 62% of pretreatment (base-line) activity and returned to within 90% of base-line activity by the 36th to 48th day after treatment.     

Retinopathy associated with ivermectin toxicosis in two dogs

CASE DESCRIPTION: 2 dogs (dogs 1 and 2) were examined for sudden onset of blindness. Both dogs had mild obtundation and mydriasis in both eyes. It was thought that dog 1 may have ingested ivermectin; dog 2 had been treated with ivermectin for demodectic mange. CLINICAL FINDINGS: On initial examination, both dogs had mydriasis and decreased pupillary light reflexes in both eyes. Dog 1 had an absent menace response bilaterally. Fundic examination of both eyes in both dogs revealed regions of multifocal retinal edema and folds with low-lying retinal separation. The electroretinogram was extinguished in dog 1 and attenuated in dog 2. Ivermectin was detected in serum samples from both dogs. TREATMENT AND OUTCOME: Both dogs made a complete clinical recovery following cessation of exposure to ivermectin; electroretinographic findings improved, and retinal edema resolved with some residual chorioretinal scarring. CLINICAL RELEVANCE: To our knowledge, this is the first report of resolution of retinal edema and electroretinographic changes associated with ivermectin toxicosis in dogs. In dogs that develop blindness suddenly, fundic examination, electroretinography, and assessment of serum ivermectin concentration are diagnostically useful, even if exposure to ivermectin is unknown.     

Suspected Clostridium difficile-associated diarrhea in two cats

Two adult cats from the same household developed acute diarrhea. Clostridium difficile toxins were detected in the feces of both cats, whereas other recognized causes of diarrhea were not identified. Supportive medical treatment and metronidazole were administered and both cats responded well. A fecal sample obtained from 1 of the affected cats after treatment and a fecal sample obtained from a clinically normal cat in the household did not contain C difficile toxins. The role of C difficile in enteric disease in cats has not been extensively studied and is unclear; however, our findings suggest that toxigenic strains of C difficile may cause diarrhea in cats.     

Suspected renal tubular acidosis in two dogs

Clinical signs of hyperventilation, muscle weakness and lethargy were recognised in a one-year-old female Bichon Frise and a three-year-old male Poodle. One dog was also hyperexcitable and pyrexic. The diagnosis of renal tubular acidosis was confirmed by demonstrating the tendency to an elevated urine pH, a low blood pH and low blood bicarbonate level, and by eliminating other causes of metabolic acidosis. Both dogs were treated with oral sodium bicarbonate resulting in improvement in their clinical condition and a return to near normal blood pH and bicarbonate levels.