Acute ibuprofen toxicosis in a ferret

A 20-month-old 1.44-kg (3.2-lb) castrated male ferret was examined because of vomiting, defecating in an abnormal location, dyspnea, and signs of depression. Within 5 minutes of initial evaluation, the ferret became nonresponsive to all stimuli except deep pain. Despite intensive supportive treatment, the ferret died. Toxicologic analyses for ibuprofen were performed on serum, urine, and liver, using gas chromatography and mass spectrophotometry. Serum ibuprofen concentrations were 245 micrograms/g before and 269 micrograms/g after death. Acute ibuprofen toxicosis may cause severe lethargy progressing to coma, apnea, and death in ferrets. Ibuprofen toxicosis should be considered in differential diagnoses for ferrets with signs of depression, with or without clinical signs of gastrointestinal tract dysfunction.     

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.     

The characterization of cycad palm toxicosis and treatment effects in 130 dogs

The purpose of this retrospective study is to characterize the clinical signs, laboratory values, treatment modalities and mortality outcomes related to cycad palm toxicosis in dogs and to identify medical interventions that potentially correlate with mortality. Dogs with confirmed cycad palm ingestion were identified by reviewing medical records from two private veterinary referral centres for key terms and phrases indicative of cycad palm toxicosis. Of 130 dogs included, 107 (82.3%) presented with clinical signs. A total of 2 (1.5%) died and 14 (10.8%) were euthanized. Diarrhea, lethargy and mortality were all associated with an elevated initial alanine transaminase (ALT) concentration. Overall mortality was 12.3%, with a significantly higher proportion of dogs with an ALT concentration <125 U/L surviving compared to dogs with an elevated ALT concentration. Treatment with activated charcoal reduced the odds of death among all dogs by 82% and was even more protective among dogs with an elevated initial ALT concentration. Among dogs that had an initial platelet count performed, the presence of thrombocytopenia (<200,000/μL) was a negative prognostic indicator and was associated with a significant increase in mortality. Given the high mortality rates reported for cycad palm toxicosis, it is imperative to identify early clinical indicators of mortality as well as treatments that reduce mortality.     

Gastrointestinal perforation in five dogs associated with the administration of meloxicam

Objective: Five canine cases of gastrointestinal (GI) perforation and septic peritonitis associated with the routine use of meloxicam are reviewed. Series summary: Selective cyclooxygenase‐2 (COX‐2) non‐steroidal anti‐inflammatory drugs (NSAIDs) are being used more extensively and routinely for acute and chronic pain as well as for perioperative management of pain. These medications are safe and effective but can be associated with known GI and renal side effects. The patients in this case series had no significant concurrent illness, were not on any concurrent medication known to potentiate the ulcerogenic effects of NSAIDs, and in most cases did not display clinical signs that were apparent to the owners until the time of perforation. New or unique information provided: Despite the preferential selectivity for COX‐2, newer NSAIDs still carry the risk of GI performation. The incidence of GI perforation may be increased with inappropriate dosing regimens, with use of non‐veterinary products and in animals that are at high risk for toxicity. Early signs of toxicity may include alteration in appetite, and subtle signs of nausea during treatment. Warning owners to monitor their pet for vomiting, melena, and hematemesis may not be sufficient to avoid the potential disastrous consequences of GI ulceration.     

Heinz body hemolytic anemia associated with high plasma zinc concentration in a dog

Acute zinc toxicosis from the ingestion of pennies was diagnosed in a dog with Heinz body hemolytic anemia (PCV = 14%), leukocytosis (51,000 cells/ml) with a left shift (3,060 band neutrophils; 37,740 segmented neutrophils) and monocytosis (4,080 cells/ml), azotemia (BUN = 60 mg/dl), bilirubinemia (total bilirubin = 5.3 mg/dl), hypokalemia (3.0 mEq/L), high serum alkaline phosphatase activity (691 U/L), high total plasma solids (8.1 g/dl), hemoglobinuria, and proteinuria. Despite aggressive medical treatment, renal failure ensued, and the dog died of cardiac arrest. The clinical signs, clinical course, and laboratory findings in this dog were similar to what has been reported in other cases of acute zinc toxicosis in dogs, with the exception of a history of generalized seizures and the findings of Heinz bodies. Although a causative relationship between plasma zinc values and Heinz body formation cannot be proven, their association suggests that oxidative damage to erythrocyte hemoglobin and cell membrane proteins may be involved in the pathogenesis of zinc-induced hemolysis.     

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.     

Renal tubular-cell neoplasms in black-footed ferrets (Mustela nigripes)--38 cases

Thirty-eight cases of renal tubular cell neoplasms were diagnosed in 184 captive, adult (>1-year-old), black-footed ferrets (Mustela nigripes) examined from 1985 to 1996. This prevalence (20.7%) is one of the highest reported for this neoplasm in a population of animals. These tumors rarely metastasized (1/38), and usually were incidental postmortem findings, associated clinical disease being present in only 3 (8%) of the 38 cases. The prevalence of renal tubular cell neoplasms found at postmortem examination increased linearly with age, up to 67% in ferrets >8 years old. Both males (prevalence = 19%) and females (prevalence = 24%) were affected. Multiple renal tumors were common, and seven ferrets (18.4% of affected animals) had bilateral tumors. The cause of this neoplastic syndrome could not be determined. Since most of the animals affected by this condition were in their postreproductive years of life, the impact of this neoplastic syndrome on the captive propagation of this species is negligible.     

Nonsteroidal anti-inflammatory drug toxicosis in dogs and cats: 240 cases (1989-1990)

A search of medical records at the Georgia Animal Poison Information Center over a 19-month period revealed 240 cases of dog and cat exposure to nonsteroidal anti-inflammatory drugs (NSAID). The most common NSAID consumed were ibuprofen, acetaminophen, aspirin, and indomethacin. The most common clinical signs of toxicosis were vomiting and diarrhea, CNS depression, and circulatory manifestations. Pets are at risk from NSAID toxicosis through administration by the owners or accidental consumption of improperly stored drugs.     

Lead toxicosis in cats-a review

Although the incidence of lead toxicosis in small animals continues to decrease, it remains a significant malady. We have reviewed the literature of the past 45 years, which revealed 70 cases involving cats. Sources, signs, diagnosis, pathology and treatment of feline lead toxicosis are reviewed. In 84% of these cases the source of lead was old paint usually from home renovation. The most common signs in cats are anorexia, vomiting, and seizures. The younger individuals seem more likely to show CNS signs. Since signs are often vague, lead toxicosis may be significantly under diagnosed in cats. The gold standard of diagnostic tests is blood lead concentration, although it does not necessarily correlate with total body burden of lead or with metabolic effects including clinical signs. Diagnostic tests including erythropoietic protoporphyrin (EPP), urine aminolevulinic acid, and others are discussed. Gross findings on necropsy are few and include a yellow-brown discoloration of the liver often with a nutmeg-like appearance. Histological examination may reveal pathognomonic inclusion bodies in liver and renal tissues. Characteristic histological changes in the CNS include neuronal necrosis and demyelination. Treatment of lead toxicosis in cats, as in any species, involves removing the exposure, decontaminating the individual and the environment, supportive care and chelation therapy. The most recently available chelator is succimer (meso 2,3-dimercaptosuccinic acid). Succimer given orally is well tolerated and has a wide margin of safety. A high index of suspicion of lead toxicosis is warranted in cats since they often present with vague and non-specific signs. With any consistent history owners need to be asked about home renovation. Early diagnosis and treatment affords a good prognosis.     

Tryptamine alkaloid toxicosis in feedlot sheep

Tryptamine alkaloid toxicosis (Phalaris staggers) was diagnosed in feedlot sheep. Clinical signs of toxicosis, which were exacerbated by excitement, included gait abnormalities, muscular tremors, nystagmus, and convulsions. An estimated 8% of the most severely affected lambs had clinical signs of toxicosis. Gross lesions detected in the brain of affected lambs consisted of focal gray-green discoloration in the brain stem and thalamus; these areas had microscopic evidence of intraneuronal pigment accumulation. Brain specimens obtained at slaughter indicated that 60% of the lambs had lesions consistent with tryptamine alkaloid toxicosis. Tryptamine alkaloids were found in low concentrations in the feed. Lambs exposed to these feeds had higher death losses than those that were not exposed to the feeds. Cobalt concentration in the feed was higher than that previously reported to be associated with Phalaris staggers.     

Ibuprofen toxicosis in a dog

Acute renal failure, vomiting, and melena developed in a 10-month-old dog after ingestion of ten 600-mg tablets of ibuprofen. After 5 days of IV fluid therapy, clinical signs resolved and azotemia decreased. With increased availability of nonsteroidal anti-inflammatory drugs, similar complications may become more common in veterinary practice. If acute renal failure should develop, the prognosis for recovery is good, with rapid institution of appropriate therapy. However, renal dysfunction may not be completely reversed.     

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.     

Incidence of prolonged prothrombin time in dogs following gastrointestinal decontamination for acute anticoagulant rodenticide ingestion

Objective: To determine the effect of gastrointestinal (GI) decontamination on the incidence of prolonged prothrombin time (PT) in dogs after anticoagulant rodenticide ingestion. Design: Retrospective study. Setting: Urban emergency room. Animals: One hundred and fifty‐one client‐owned dogs. Measurements: Dogs presented to the emergency room within 6 hours of ingestion of an anticoagulant rodenticide and had a PT measured within 2–6 days of toxicant ingestion before initiating vitamin K therapy were included. Dogs were categorized as treated or untreated based on the institution of vitamin K therapy following PT testing. The signalment, body weight, type of rodenticide ingested, time elapsed between ingestion and initial presentation, method(s) of GI decontamination, and the times elapsed between both toxicant ingestion and initial hospital presentation until determination of PT were recorded. The PT results were recorded as well as any treatment received following the recheck examination. Any reported incidents of bleeding or untoward effects between exposure and reexamination were recorded. Main results: Of 151 dogs, only 11 dogs (8.3%) developed prolonged PT requiring vitamin K supplementation. None of the 11 dogs with prolonged PTs exhibited signs of bleeding or required transfusion therapy. No differences in age, weight, or time elapsed between treated and untreated patients were found. Conclusions: The incidence of prolonged PT is low in dogs receiving GI decontamination within 6 hours of anticoagulant rodenticide ingestion. Delaying vitamin K therapy until a PT has been assessed 48–72 hours after initial exposure appears to be safe and sensitive in dogs following anticoagulant rodenticide ingestion.     

Evaluation of the clinical presentation and histologic lesions of hepatic copper accumulation in sugar gliders (Petaurus breviceps)

Hepatic toxicosis caused by copper accumulation has been reported in most domestic species, as well as multiple small exotic mammals, including ferrets, fruit bats, and sugar gliders. The purpose of this study was to determine the signalments, clinical presentations, and histologic findings associated with hepatic copper accumulation in sugar gliders based on post-mortem histologic findings and retrospective analysis of reported antemortem clinical signs. Sugar gliders with histologic evidence of various hepatopathies were identified within the Northwest ZooPath archive. Sections of formalin-fixed, paraffin-embedded hepatic samples were stained for copper, and copper deposition was graded semiquantitatively. The prevalence of copper accumulation in the evaluated hepatopathies was 28%. Copper deposition was seen in all individuals with icterus and non-ataxia neurologic signs. Grossly, individuals with hepatic masses and nodules were 5.50 times more likely to have hepatic copper accumulation. Sugar gliders with biliary hyperplasia were 16.20 times more likely to have copper accumulation while all individuals with cholestasis had hepatic copper accumulation. The results of this study indicate that hepatic copper accumulation is frequently identified in post-mortem evaluation of sugar gliders with hepatopathy. Copper accumulation is frequently noted in individuals with icterus, neurologic abnormalities, hepatic masses, biliary hyperplasia, and cholestasis. This study details the prevalence of hepatic copper accumulation in sugar gliders and illustrates associations between copper hepatotoxicosis and other hepatic diseases.     

Increased toxicity of P-glycoprotein-substrate chemotherapeutic agents in a dog with the MDR1 deletion mutation associated with ivermectin sensitivity

Lymphoma was diagnosed in a 4-year-old spayed female Collie, and treatment with a combination chemotherapy protocol incorporating prednisone, L-asparaginase, vincristine, vinblastine, doxorubicin, and cyclophosphamide was initiated. The dog had signs of gastrointestinal tract toxicosis and myelosuppression after treatment with P-glycoprotein-substrate drugs (vincristine, vinblastine, and doxorubicin) even when dosages were reduced, but did not have signs of toxicosis after treatment with cyclophosphamide, a non-P-glycoprotein-substrate drug, even when administered at the full dosage. It was postulated that a deletion mutation in the canine MDR1 gene (deltaMDR1 295-298) could be responsible for the drug toxicoses in this dog. This mutation has been identified as the cause of a functional P-glycoprotein defect in Collies susceptible to the toxic effects of ivermectin, another P-glycoprotein-substrate drug. The MDR1 genotype of this dog consisted of 1 normal and 1 mutant MDR1 allele. Because P-glycoprotein contributes to renal, biliary, and intestinal excretion of P-glycoprotein-substrate drugs, it is possible that drug excretion was delayed in this patient, resulting in clinical signs of toxicosis.     

Oak leaf (Quercus pyrenaica) poisoning in cattle

Three experiments were conducted to study the clinical and pathological findings associated with poisoning in cattle due to ingestion of young oak leaves (OL) and the main factors responsible for toxicosis. In Experiment 1, six 1.4 year-old bulls were fed up to 5 kg of young OL per animal per day and showed no signs of toxicity, apart from a slight proteinuria. In Experiment 2, another six 1.4 year-old bulls were first subjected to severe feed restriction for eight days and then fed a higher amount of OL (approx. 10 kg) daily. A marked increase of serum creatinine and blood urea (BUN) was detected in urine as well as clinical signs consistent with renal failure. At necropsy, animals showed gastrointestinal ulcers and kidney tubular necrosis. Since these results suggested a crucial role of the feed restricting period, a third experiment was conducted administering the same amount of young OL as in Experiment 1, but adding the severe feed restricting period as in Experiment 2. There was a wide variation in clinical signs, with one bull showing clinical signs and lesions, another recovering after showing mild clinical signs and high levels of creatinine and BUN, and the third appearing clinically normal. The relevance of restriction access to food in the development of OL toxicosis appears to be critical because the intoxication was only elicited when the OL administration was preceded by a severe feed restricting period.     

Ethylene glycol toxicosis in cattle.

A 1-month-old Jersey calf died of oxalate nephropathy. The calf had access to antifreeze (ethylene glycol) 3 days prior to death. Since ethylene glycol toxicosis had not been reported in cattle, the effects or oral administration of ethylene glycol were studied in 7 calves and 3 cows. The toxic dose ranged from 2 to 10 ml of ethylene glycol per kg of body weight. Clinical signs were increased respiration, staggering gait, paraparesis, depression and later, recumbency and death. Hemoglobinuria and epistaxis were seen at doses of 10mg/kg of body weight. Azotemia, hypocalcemia and neutrophilia were constant findings whereas acidosis, plasma hyperosmolality and hemolytic anemia were seen in the animals receiving the higher doses. A diagnosis of ethylene glycol toxicosis must be based upon a history of ingestion and the presence of calcium oxalate crystals in body tissues (especially the kidney and brain).