Suspected caffeine and ephedrine toxicosis resulting from ingestion of an herbal supplement containing guarana and ma huang in dogs: 47 cases (1997-1999)

OBJECTIVE: To describe the clinical signs following ingestion of an herbal supplement containing guarana and ma huang in dogs, estimate minimum dose at which clinical signs of toxicosis and death were reported, and evaluate treatment options. DESIGN: Retrospective study. ANIMALS: 47 dogs with evidence of ingestion of an herbal supplement containing primarily guarana and ma huang. PROCEDURE: Records of dogs that had ingested an herbal supplement containing ma huang and guarana between July 1997 and October 1999 were retrieved from the National Animal Poison Control Center database. Data were retrieved and reviewed regarding signalment, dose ingested, clinical signs, laboratory test results, treatment, and final outcome. Cases were assessed by staff veterinarians as toxicosis or suspected toxicosis on the basis of strength of evidence supporting a diagnosis. RESULTS: Most dogs (80%) developed clinical signs of toxicosis within 8 hours of ingestion, and clinical signs persisted for up to 48 hours. Hyperactivity, tremors, seizures, and behavior changes were reported in 83% of dogs; other signs included vomiting (47%), tachycardia (30%), and hyperthermia (28%). Seventeen percent of the dogs died or were euthanatized. Estimated doses of guarana and ma huang ranged from 4.4 to 296.2 mg/kg (1.98 to 133.2 mg/lb) and 1.3 to 88.9 mg/kg (0.58 to 40.0 mg/lb) of body weight, respectively; minimum dose at which death was reported was 19.1 mg of guarana/kg (8.7 mg/lb) and 5.8 mg of ma huang/kg (2.6 mg/lb). CONCLUSIONS AND CLINICAL RELEVANCE: Accidental ingestion of herbal supplements containing primarily guarana and ma huang in dogs can lead to a potentially lethal condition that may require prompt detoxification and supportive treatment for several days. Most dogs recovered with supportive treatment.     

5-Hydroxytryptophan toxicosis in dogs: 21 cases (1989-1999)

OBJECTIVE: To determine epidemiologic characteristics, clinical findings, and treatment outcome of 5-hydroxytryptophan (5-HTP) toxicosis in dogs. DESIGN: Retrospective study. ANIMALS: 21 dogs with evidence of accidental 5-HTP ingestion. PROCEDURE: Information was retrieved from the National Animal Poison Control Center database. Records of dogs ingesting 5-HTP between January 1989 and February 1999 were reviewed for information on signalment, dose ingested, clinical signs (onset, severity, duration), treatments administered, and outcome. RESULTS: Clinical signs of toxicosis developed in 19 of 21 (90%) dogs. Neurologic signs included seizures (9 dogs), depression (6), tremors (5), hyperesthesia (5), and ataxia (4). Gastrointestinal tract signs included vomiting or diarrhea (12 dogs), signs of abdominal pain (3), and hypersalivation (2). Other clinical signs were hyperthermia (7 dogs) and transient blindness (3). Three dogs died. No important clinical laboratory or necropsy findings were reported. The doses of 5-HTP ingested ranged from 2.5 to 573 mg/kg (1.1 to 260 mg/lb) of body weight; the minimum toxic dose reported in our study was 23.6 mg/kg (10.7 mg/lb), and the minimum lethal dose was 128 mg/kg (58.1 mg/lb). Onset of signs ranged from 10 minutes to 4 hours after ingestion, and signs lasted up to 36 hours. Of 17 dogs with clinical signs of toxicosis that received treatment, 16 recovered; treatment consisted of decontamination, seizure control, thermoregulation, fluid therapy, and supportive care. CONCLUSIONS AND CLINICAL RELEVANCE: Ingestion of 5-HTP in dogs can result in a potentially life-threatening syndrome resembling serotonin syndrome in humans, which requires prompt and aggressive care.     

Clinical syndrome associated with zolpidem ingestion in dogs: 33 cases (January 1998-July 2000)

Zolpidem is a nonbenzodiazepine hypnotic of the imidazopyridine class that is used to treat insomnia in humans. Zolpidem binds selectively to the benzodiazepine omega-1 receptor and increases the frequency of chloride channel opening, which results in inhibition of neuronal excitation. A retrospective study was conducted of zolpidem ingestion in dogs that were reported to the ASPCA Animal Poison Control Center (APCC) between January 1998 and July 2000. Data analysis included amount ingested, clinical effects, and time of onset of signs. Thirty-three reports of zolpidem ingestion in dogs (ranging in age from 5 months to 16 years) were evaluated. Approximate ingested dosages ranged from 0.24 to 21 mg/kg. Clinical signs reported included ataxia (18 dogs; 54.5%), hyperactivity (10 dogs; 30.3%), vomiting (7 dogs; 21.2%), and lethargy (5 dogs; 15.2%), as well as panting, disorientation, nonspecific behavior disorder, and hypersalivation (4 dogs each sign; 12.1%). Other signs reported include tachycardia, tremors, apprehension, vocalization, hypersalivation, weakness, and hyperesthesia. In 85% percent of reports, clinical signs developed within 1 hour and usually resolved within 12 hours. Although central nervous system (CNS) depression is reported as a primary effect of zolpidem in humans and would also be expected in dogs, information obtained from this study indicates that some dogs may exhibit a paradoxical excitation reaction. This effect appears to vary among individual dogs.     

Severe gastrointestinal bleeding secondary to lornoxicam in the dog

Six dogs with lornoxicam induced severe gastrointestinal bleeding are described. The ingested dose ranged between 0.5 - 5.1?mg/kg BW (median 0.63?mg/kg BW). The severity of the bloodloss anemia was moderate to severe with PCV values ranging between 12 - 27 % (median 16 %) and serum albumin concentrations between 12 - 22 g/l (median 16 g/l). One dog had evidence of chronic thrombocytopathia over 13 days and clinicopathologic findings of gastrointestinal bleeding over 55 days. None of the dogs developed kidney injuries. The clinical condition required transfusion of blood products in 5 of 6 cases. One dog with a perforated duodenal ulcer and septic peritonitis survived until discharge but had to be euthanized later on due to recrudescent clinical signs (hematemesis, melena). The median length of hospitalisation was 12 days (5 - 14). No correlation was seen between the ingested dose and severity of clinical signs. Lornoxicam ingestion leads to severe and longlasting gastrointestinal bleeding in the dog and requires immediate intensive therapy.     

Bread dough toxicosis in dogs

Objective: To provide information on the ingestion, and subsequent toxicity, of raw bread dough in dogs. Case summary: A report from the ASPCA animal poison control center (APCC) files of 3 cases of ingestion of raw bread dough by dogs. Clinical signs included vomiting, ataxia, blindness, hypothermia, and recumbency. All dogs were successfully treated for ethanol toxicosis. New information: Ingestion of bread dough can cause gastric obstruction, bloat, or ethanol toxicosis. The treatment of ethanol toxicosis, including decontamination, IV fluids, management of metabolic acidosis, and hypoglycemia is discussed. Yohimbine can be used in cases where the dog is comatose or has developed severe respiratory depression.     

Successful treatment of severe salt intoxication in a dog

Objective: To report successful treatment of severe salt intoxication and hypernatremia in a dog. Case summary: A 5‐year‐old intact female Doberman Pinscher was admitted to the intensive care unit with a history of seizures and coma. The owner had administered approximately 100 g of cooking salt to induce vomiting following ingestion of a nontoxic dose (10 g) of chocolate. Upon admission, the dog was comatose with intermittent seizures and vomiting. Diagnostic tests confirmed salt intoxication (Na: 200 mEq/L, Cl: 180 mEq/L) and metabolic acidosis (pH: 7.18; pCO₂: 39 mmHg; HCO₃: 14.3 mmol/L). Immediate treatment included intravenous fluid therapy, an anticonvulsant, antiemetic, diuretic, low molecular weight heparin, and supplemental oxygen. A fluid therapy protocol was initiated to decrease serum sodium concentration by approximately 2 mEq/L/hr. After 24 hours of intensive care, the patient regained consciousness and volume and acid‐base abnormalities improved. The patient developed a variety of abnormal clinical signs as a result of the severe hypernatremia. After 5 days of treatment, the serum sodium concentration returned to the established reference range. The patient recovered completely in 10 days. New information provided: Severe hypernatremia due to salt ingestion is a rare condition in dogs. All dogs in previous case reports of salt intoxication have died. This case report is the first to report survival of a dog with severe salt intoxication.     

Treatment of ibuprofen intoxication with charcoal haemoperfusion in two dogs

ABSTRACT

Case history: Two dogs presented separately to the Small Animal Hospital, University of Florida (Gainsville, FL, USA) for ingestion of ibuprofen. The first dog ingested 561.8?mg/kg ibuprofen in addition to paracetamol and caffeine and vomited prior to admission. This patient also received fluid therapy for 8 hours prior to charcoal haemoperfusion. The second dog ingested 500?mg/kg of ibuprofen and the owners induced vomiting with hydrogen peroxide prior to presentation. Due to the severity of clinical signs, both patients were treated with charcoal haemoperfusion.

Clinical findings: The concentrations of ibuprofen in the blood of the dogs prior to treatment were 478 and 301?mg/L. During the treatment ibuprofen concentrations were reduced by 95.8% and 45.5%, respectively, with no treatment side effects and minimal clinical signs after treatment.

Diagnosis: Toxicity due to ingestion of ibuprofen toxicity that was successfully treated with charcoal haemoperfusion.

Clinical relevance: In the cases described here minimal benefit was seen after 3 hours of treatment using one haemoperfusion cartridge. This is in contrast to a previously published report in which dogs were treated for 6 hours with two charcoal haemoperfusion cartridges. This suggests that one cartridge may be sufficient. The amount of ibuprofen ingested was not a reliable predictor of the concentration in blood at the initiation of treatment. Charcoal haemoperfusion is an effective means of reducing plasma concentrations of ibuprofen, however, its use may be limited by its cost and availability.     

Clinical, neurological and clinicopathological signs, treatment and outcome of metaldehyde intoxication in 18 dogs

OBJECTIVES: To describe the clinical signs, clinicopathological abnormalities and outcome of metaldehyde intoxication in dogs. METHODS: Medical records of dogs presenting between 1989 and 2005 with a diagnosis of metaldehyde toxicity were reviewed retrospectively. Data obtained from the medical record included signalment, history, clinical signs, laboratory tests results, hospitalisation period length, treatments and outcome. RESULTS: Eighteen dogs fulfilled the inclusion criteria. The most prevalent clinical signs were seizures, hyperthermia, tachycardia and muscle tremors. Serum biochemistry abnormalities included increased serum muscle enzymes activities, acidaemia (six dogs) and decreased blood bicarbonate (eight dogs). Treatment was symptomatic and supportive. Hyperbilirubinaemia was observed in two dogs. Diazepam was the most commonly used anticonvulsant followed by phenobarbitone and pentobarbital. General inhalant anaesthesia was required in nine of 18 dogs with seizures unresponsive to anticonvulsants. The survival was 83 per cent (15 of 18 dogs). CLINICAL SIGNIFICANCE: This clinical study recorded, for the first time in the veterinary literature, several clinicopathological abnormalities from severely intoxicated dogs. Metabolic acidosis was common, while acute or delayed hepatotoxicity was an uncommon complication.     

Brunfelsia spp (yesterday, today, tomorrow) toxicity in four dogs

Four dogs were treated for acute toxicity following ingestion of the popular garden shrub 'Yesterday, today, tomorrow' (Brunfelsia spp). Clinical signs included vomiting, diarrhoea, muscle tremors, anxiousness, opisthotonus and seizures. All dogs recovered following treatment with any or all of general anaesthetic, gastric lavage, enema, diazepam, phenobarbitone or propofol sedation. Brunfelsia spp toxicity should be considered in young, previously healthy dogs presenting with gastrointestinal signs that rapidly progress to muscle tremors and seizures. Examination of faeces was required for diagnosis in all cases. Owners should also be questioned thoroughly about their dogs' access to such plants.     

Bromide toxicosis (bromism) in a dog treated with potassium bromide for refractory seizures.

A 4-year-old German Shepherd Dog was evaluated because of chronic hind limb lameness and recurrent seizures. Diagnostic evaluation of the dog confirmed rheumatoid arthritis and idiopathic epilepsy. The rheumatoid arthritis was treated with prednisone and piroxicam. The seizures were treated with phenobarbital plus clonazepam. The seizures were refractory and potassium bromide was substituted for clonazepam. The dog was reevaluated 4 months after initiation of potassium bromide treatment because of recurrence of arthritis signs. During hospitalization, the dog had neurologic signs, which progressed from depression to recumbency and stupor. Anisocoria, muscle pain, and hyporeflexia were noticed. Bromide toxicosis was diagnosed on the basis of toxic serum bromide concentration (2.7 mg/ml; therapeutic range, 1.0 to 2.0 mg/ml). Following cessation of potassium bromide treatment, the neurologic signs resolved. The seizures recurred 6 weeks after potassium bromide was discontinued. Bromide treatment was reinitiated at half the initial dosage. After 6 weeks, the serum bromide concentration was 1.9 mg/ml, and no seizures had been reported by the dog's owners. Therapeutic serum bromide concentrations in dogs has been reported to be 0.5 to 2.3 mg/ml. The serum bromide concentration at which toxic signs are expected is variable in human beings because individuals differ in their tolerance of the drug. Clinical trials are necessary to determine the toxic serum bromide concentrations in dogs. This case of bromism in a dog suggests that the dosage of potassium bromide should be based on serial measurement of serum bromide concentrations.     

Coma and respiratory failure due to moxidectin intoxication in a dog

Objective: To describe the clinical consequences following ingestion by a dog of a moxidectin‐containing equine deworming product. Few reports exist concerning the treatment and outcome of severe moxidectin toxicity. Treatment, known factors influencing intoxication, and prognosis are reviewed. Case summary: A 10‐month‐old female Border Collie ingested an unknown quantity of a moxidectin‐containing equine deworming product several hours before presentation. Severe neurological signs subsequently developed and included: ataxia, seizures, coma, and respiratory failure. The dog was treated with supportive care including intravenous fluids, activated charcoal, and positive pressure ventilation. Normal spontaneous respiration returned in 34 hours and the patient was discharged 58 hours after ingestion. Full recovery occurred within 1 week of intoxication. New information provided: This report describes moxidectin intoxication and associated respiratory failure in a dog that required mechanical ventilation. The dog's recovery was rapid. Despite severity of signs, the prognosis for patients with moxidectin intoxication is good with appropriate supportive care.     

Tremorgenic mycotoxicosis in four dogs from a single household

Mycotoxins are fungal metabolites that induce undesirable effects. The effects of these mycotoxins vary depending on the chemical structure of the toxin and degree of toxicity. Mycotoxins that induce muscle tremors, ataxia, and convulsions are termed tremorgenic mycotoxins. Our report documents the clinical course of 4 dogs from a single household that were simultaneously affected by tremorgenic mycotoxins. Diagnosis of tremorgenic mycotoxicosis was confirmed by stomach content analysis from 1 of the dogs. The mycotoxins identified were penitrem A and roquefortine, which are both produced by Penicillium spp. Treatment goals following tremorgenic mycotoxin ingestion include minimizing absorption, controlling tremors and seizures with methocarbamol and pentobarbital sodium administration, and providing supportive care. Two of the affected dogs required ventilatory support. With early aggressive treatment, prognosis is good and recovery is complete without sequelae. It is helpful for the clinician to be familiar with the typical clinical signs at the time of admission, treatment, and clinical course of dogs with tremorgenic mycotoxicosis.     

Tremorgenic mycotoxin intoxication with penitrem A and roquefortine in two dogs

In this report, we describe the natural intoxication of 2 dogs that consumed moldy dairy products found in the household garbage and the procedures used to identify and quantify the tremorgenic mycotoxins, roquefortine and penitrem A, in the remaining portions of ingested materials. Following the ingestion of mycotoxins, the dogs of our report developed muscle tremors or seizures that resembled clinical signs of strychnine poisoning. Roquefortine was the predominant mycotoxin in a moldy cream cheese wrapper that was found among scattered garbage consumed by the first dog. Penitrem A was the only mycotoxin detected in discarded moldy macaroni and cheese that was consumed by the second dog. Treatment of dogs with tremorgenic mycotoxin intoxication involves supportive care. Close monitoring is important because the development of aspiration pneumonia is common and has been reported as the cause of death. Clinical signs of intoxication gradually resolve within 24 to 48 hours.     

Effect of background serum lithium concentrations on the accuracy of lithium dilution cardiac output determination in dogs

OBJECTIVES: To assess the effect of increasing serum lithium concentrations on lithium dilution cardiac output (LiDCO) determination and to determine the ability to predict the serum lithium concentration from the cumulative lithium chloride dosage. ANIMALS: 10 dogs (7 males, 3 females). PROCEDURE: Cardiac output (CO) was determined in anesthetized dogs by measuring LiDCO and thermodilution cardiac output (TDCO). The effect of the serum lithium concentration on LiDCO was assessed by observing the agreement between TDCO and LiDCO at various serum lithium concentrations. Also, cumulative lithium chloride dosage was compared with the corresponding serum lithium concentrations. RESULTS: 44 paired observations were used. The linear regression analysis for the effect of the serum lithium concentration on the agreement between TDCO and LiDCO revealed a slope of -1.530 (95% confidence interval [CI], -2.388 to -0.671) and a y-intercept of 0.011 (r2 = 0.235). The linear regression analysis for the effect of the cumulative lithium chloride dosage on the serum lithium concentration revealed a slope of 2.291 (95% CI, 2.153 to 2.429) and a y-intercept of 0.008 (r2 = 0.969). CONCLUSIONS AND CLINICAL RELEVANCE: The LiDCO measurement increased slightly as the serum lithium concentration increased. This error was not clinically relevant and was minimal at a serum lithium concentration of 0.1 mmol/L and modest at a concentration of 0.4 mmol/L. The serum lithium concentration can be reliably predicted from the cumulative lithium dosage if lithium chloride is administered often within a short period.     

Acetaminophen Toxicosis In 17 Cats

Seventeen cases of acetamninophen intoxication in cats were identified over a 12-year period. Information obtained from the medical records included the signalment, amount acetaminophen ingested, time from ingestion until treatment was initiated, clinical signs, physical examination, clinical pathology, treatment and outcome. The most common cause intoxication was owner administration. In cats that died or were euthanized the dose administered ranged from 10mg/kg to 17Omg/kg, while in cats that survived the dosage ranged from 10mg/kg to 400mg/kg. The most common clinical signs were depression, increased respiratory rate, respiratory distress, pale/muddy mucous membranes, and hypothermia. Twelve cats survived. Ten of these cats had treatment initiated within 14 hours after ingestion. One cat that survived had treatment initiated 24 hours after ingestion, and a second cat that survived had treatment initiated 48 hours after ingestion. Time between ingestion and initiation treatment may be as important if not more important than the actual dosage acetaminophen administered.     

Eosinophilic bronchopneumopathy in dogs

Eosinophilic bronchopneumopathy was diagnosed in 23 young dogs. Clinical signs included cough, gagging, and retching in all dogs, dyspnea in 21 dogs (91%), and nasal discharge in 12 dogs (52%). The most common radiographic findings were a moderate to severe bronchointerstitial pattern (68%, 13 of 19 dogs). Bronchoscopic findings included the presence of abundant yellow-green mucus or mucopurulent material (70%, 16 of 23 dogs) and severe mucosal thickening with an irregular or polypoid appearance (52%, 12 of 23 dogs), with partial airway closure during expiration in 3 dogs (13%). Peripheral blood eosinophilia was noted in 14 of 23 dogs (61%). Inflammatory cells in brush or bronchoalveolar lavage fluid cytologic preparations comprised more than 50% eosinophils in 14 of 23 dogs (61%), and 20-50% eosinophils in 6 dogs (26%). Eosinophilic infiltration of the bronchial mucosa was observed in biopsies from 19 dogs and was graded as mild (37%, 7 dogs), moderate (32%, 6 dogs), or severe (32%, 6 dogs). The mean serum immunoglobulin A concentration was almost double that of a population of 20 healthy dogs of various breeds. Oral glucocorticoids were administered on alternate days with progressive tapering of the dose; the dosage at maintenance varied between 0.1 and 1.0 mg/kg every other day. No relationship was found between the duration of clinical signs and the maintenance dosage or the cytologic and histopathologic grades.     

Toxicity in Doberman Pinchers with Ventricular Arrhythmias Treated with Amiodarone (1996–2005)

Background: Asymptomatic Doberman Pinschers with dilated cardiomyopathy (DCM) often die suddenly owing to ventricular tachycardia that degenerates into ventricular fibrillation. A safe and effective antiarrhythmic drug treatment is needed. This will require a large, well-controlled, prospective study.
Hypothesis: Amiodarone toxicity is common in Dobermans with occult DCM and ventricular tachyarrhythmias refractory to antiarrhythmia therapy. Infrequent monitoring of hepatic function is inadequate. Frequent monitoring may be useful to determine dogs in which the dosage should be decreased or the drug withdrawn.
Methods: Medical records from the University of Georgia and Cornell University were searched for Doberman Pinschers diagnosed with preclinical DCM that received amiodarone for severe ventricular arrhythmias refractory to other antiarrhythmic agents. Echocardiographic data, Holter recording data, hepatic enzyme serum activity, and serum amiodarone concentrations were recorded. The presence of clinical signs of toxicity was recorded. Serum amiodarone concentrations were obtained in some dogs.
Results: Reversible toxicity was identified in 10 of 22 (45%) dogs.
Conclusion and Clinical Importance: Adverse effects from amiodarone were common and were, in part, dosage related. Patients should be monitored for signs of toxicity and liver enzyme activity should be measured at least monthly.     

Clinical and magnetic resonance imaging characteristics of quadrigeminal cysts in dogs

BACKGROUND: Quadrigeminal cysts (QC) are the most common intracranial intra-arachnoid cysts in dogs, primarily affecting small breeds. Clinical significance is controversial. HYPOTHESIS: Male, brachycephalic, small breed dogs are predisposed to QC, and objective measurement of parenchymal compression can distinguish clinically relevant QC from incidental findings. ANIMALS: A total of 4,100 client-owned dogs. METHODS: A retrospective study that recorded signalment, history, clinical signs, and magnetic resonance imaging features. The degree of brain compression was evaluated in the presence of relevant clinical signs. The percentage compression of cerebellum and forebrain was calculated by comparing the expected to the actual diameter and longitudinal dimension, respectively. RESULTS: QC were diagnosed in 28 dogs, of which 21 (75%) were small breed dogs. Fifteen dogs (54%) were brachycephalic. Eighteen dogs were male, and 10 were female. Cerebellar, occipital lobe, or compression in both areas occurred in 86% (24/28 dogs). Clinical signs included focal and generalized seizures in 5 dogs and cerebellar signs in 6 dogs. Mean occipital lobe compression was 17% (SD = 4) in clinically affected and 10% (SD = 3) in normal dogs (P = .006). Occipital lobe compression >14% was always associated with clinical signs. The mean cerebellar compression was 18%, but there was no association between compression and clinical signs. The animals were more likely to develop clinical signs if both areas were compressed (P = .04). CONCLUSIONS AND CLINICAL IMPORTANCE: Parenchymal compression by QC can be incidental, and other central nervous system diseases must be excluded when assessing the clinical significance of QC. However, occipital lobe compression over 14% is likely to cause clinical signs.     

Primary idiopathic hypoparathyroidism in St. Bernard dogs

Primary hypoparathyroidism was diagnosed in three St. Bernard bitches. Anorexia, behavioural changes, muscle tremors, seizures, panting respiration, and cataracts were the clinical signs observed. The serum concentration of calcium was low, the phosphorus concentration elevated, and the immunoreactive parathyroid hormone level low in all dogs. The aetiology of the hypoparathyroidism was not determined in any of the dogs. Treatment with synthetic vitamin D (1,25-dihydroxycholecalciferol) and an oral calcium supplement was successful in restoring and then maintaining a normal concentration of serum calcium in two of the dogs.