Survival and prognostic indicators for cycad intoxication in dogs

Background: Cycad palms are commonly used in landscaping and ingestion by dogs can cause disease or death. Objectives: Determine the morbidity and case fatality of cycad palm toxicosis in dogs from Louisiana, and examine putative prognostic factors. Animals: Thirty‐four client‐owned dogs with confirmed cycad palm toxicosis between 2003 and 2010. Methods: Retrospective cohort study. Search of all medical records for animals with cycad palm toxicosis. Results: Seventeen of 34 (50%) dogs died or were euthanized as a direct consequence of cycad intoxication. There were no differences in presenting signs and physical examination findings between survivors and nonsurvivors. Nonsurvivors had higher serum alanine transaminase activity (median 196 U/L; range 16–4,123 versus 113.5; 48–1,530) and total bilirubin concentration (0.5 mg/dL; 0.1–6.2 versus 0.25; 0–1.7) upon presentation, and their initial serum concentrations of albumin (2.9 g/dL; 1.4–4.1 versus 3.3; 2.2–3.9) were lower than those of survivors. Nadir serum albumin concentration was also lower in nonsurvivors (1.9; 1.4–3.7 versus 3.2; 1.8–3.5). A higher proportion of nonsurvivors had prolonged coagulation times, prothrombin time. and partial thromboplastin time. In a multivariate model, administration of charcoal at initial presentation was associated with longer survival (heart rate [HR] 0.019, 95% CI 0.001–0.644), while high serum aspartate aminotransferase activity was a negative prognostic factor (HR 118.2, 95% CI 2.89–4,826). Conclusions and Clinical Importance: Cycad intoxication is associated with a higher case fatality than previously published. Several laboratory parameters might help differentiating potential nonsurvivors from survivors. Administration of charcoal as part of the emergency treatment appears to have a protective effect.     

Mushroom toxicosis in dogs in general practice causing gastroenteritis,ptyalism and elevated serum lipase activity

Mushroom toxicosis is rarely diagnosed in dogs and is poorly reported in the veterinary literature. This report suggests that mushroom toxicosis is a potentially under‐diagnosed condition in first opinion practice in the UK. Nine dogs with clinical signs consistent with mushroom toxicosis were identified from the records of an out‐of‐hours emergency service between August 2010 and January 2011. Four dogs were later excluded because of clinical inconsistencies. Clinical signs included acute profuse ptyalism (5/5), diarrhoea (5/5), vomiting (4/5), hypovolaemia (4/5), stuporous (3/5) or obtunded mentation (1/5), miosis (2/5) and hypothermia (2/5). Serum lipase activity was elevated in 4/4 dogs; canine‐specific pancreatic lipase was elevated in the remaining dog. Four dogs recovered with aggressive intravenous fluid therapy, analgesia and supportive care; the remaining dog was euthanased due to severe clinical signs and financial constraints. Mushroom toxicosis is an important differential diagnosis for acute gastroenteritis and one possible cause of some cases of “Seasonal Canine Illness”. Affected dogs may demonstrate elevated pancreatic enzymes and mushroom toxicosis should be considered in cases of elevated lipase or abnormal semi‐quantitative canine‐specific pancreatic lipase activities.     

CCNU (lomustine) toxicity in dogs: a retrospective study (2002-07)

Objective To describe the incidence of haematological, renal, hepatic and gastrointestinal toxicities in tumour‐bearing dogs receiving 1‐(2‐chloroethyl)‐3‐cyclohexyl‐1‐nitrosourea (CCNU). Design The medical records of 206 dogs that were treated with CCNU at the Melbourne Veterinary Specialist Centre between February 2002 and December 2007 were retrospectively evaluated. Results Of the 206 dogs treated with CCNU, 185 met the inclusion criteria for at least one class of toxicity. CCNU was used most commonly in the treatment of lymphoma, mast cell tumour, brain tumour, histiocytic tumours and epitheliotropic lymphoma. Throughout treatment, 56.9% of dogs experienced neutropenia, 34.2% experienced anaemia and 14.2% experienced thrombocytopenia. Gastrointestinal toxicosis was detected in 37.8% of dogs, the most common sign of which was vomiting (24.3%). Potential renal toxicity and elevated alanine transaminase (ALT) concentration were reported in 12.2% and 48.8% of dogs, respectively. The incidence of hepatic failure was 1.2%. Conclusions CCNU‐associated toxicity in dogs is common, but is usually not life threatening.     

Inherited copper toxicosis in the Bedlington terrier: a report of two clinical cases

The clinical signs, laboratory findings and pathological changes are described in two cases of inherited copper toxicosis in the Bedlington terrier. The first case presented with acute signs of depression, vomiting, anorexia, weight loss and jaundice while the second case followed a more chronic course with less severe clinical signs which included weight loss and ascites. Both dogs had elevated circulating levels of alanine aminotransferase (ALT), however other haematological and biochemical parameters, while reflecting liver involvement, varied between the two cases. Chemical analysis of the liver revealed elevated copper levels in both cases (951·7 and 1093·4 μg/g wet weight respectively; normal less than 150 μg/g). These levels, however, are less than some affected but asymptomatic Bedlington terriers. Pathologically the first case had micronodular cirrhosis, while the second had focal hepatitis with fibrosis. Both dogs showed vacuolation of the white matter in the cerebrum, cerebellum, midbrain and medulla. Attention is drawn to the similarities and differences between copper toxicosis in the Bedlington terrier and Wilson's disease in man.     

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.     

Acute and short-term toxicoses associated with the administration of doxorubicin to dogs with malignant tumors

One hundred eighty-five dogs with histologically confirmed, measurable malignant tumors were used in a study to determine the toxicity of the anthracycline antitumor antibiotic, doxorubicin, which was administered once or twice (at a 21-day interval) at the rate of 30 mg/m2 of body surface area, iv. During this study, 7 dogs died as a direct result of doxorubicin-induced toxicosis and 16 died as a direct result of the malignant neoplastic disease. Each dog was evaluated for signs of toxicosis for 3 weeks after the last dose was administered (15 dogs received 1 dose, 170 dogs received 2 doses) or until the dog died, whichever came first. The most common signs of toxicosis were vomiting, diarrhea, colitis, anorexia, and pruritus. The probability of doxorubicin-induced toxicosis decreased significantly (P less than 0.0001) in inverse relationship to body weight. Dogs with signs of toxicosis during the 21-day interval from administration of the first dose of doxorubicin were 17.2 times (P less than 0.01; 95% confidence interval; 5.5, 54.2) more likely to develop signs of toxicosis during the 21-day interval from the second dose of doxorubicin. The performance status of each dog was evaluated using a modified Karnofsky performance scheme; the only time the performance status was adversely affected to a significant extent by doxorubicin-induced toxicosis was during the 21-day period, starting with the second dose (P less than 0.0001).     

Elevation of alanine transaminase and gallbladder wall abnormalities as biomarkers of anaphylaxis in canine hypersensitivity patients

Objective – The purpose of the study was to evaluate alanine transaminase (ALT) and gallbladder wall abnormalities as possible biomarkers for anaphylaxis in dogs presented for acute hypersensitivity reactions. Design – Pilot study. Setting – A private practice, small animal, 24‐hour emergency and specialty hospital. Animals – Ninety‐six dogs presenting 101 times on an emergency basis for hypersensitivity reactions from March 2007 through March 2009. Interventions – Veterinarians acquired a history, physical exam, serum chemistry panel, blood pressure, and ultrasound image of the gallbladder. Measurements and Main Results – Dogs were then divided into 2 groups: dogs fulfilling the definition for anaphylaxis (moderate and severe systemic hypersensitivity) and dogs that did not fulfill the definition and were classified as allergic reactions (local hypersensitivity and mild systemic hypersensitivity). Elevated ALT was significantly associated with anaphylaxis (P<0.001). Increased gallbladder wall thickness and a striated wall pattern were significantly associated with anaphylaxis (P<0.001) and these changes were readily apparent to first‐responder veterinarians. Decreased body temperature (P<0.001) and hypothermia (P=0.006) were significantly associated with anaphylaxis. There was no significant difference between groups regarding age, heart rate, or presence of respiratory signs. Lower blood pressure was significantly associated with anaphylaxis (P<0.001) but hypotension was not significantly different (P=0.09) between groups. Cutaneous signs were significantly associated with the allergic reactions group (P<0.001) and, when seen with anaphylaxis, were subtle. Conclusions – This study showed an elevated ALT and an abnormal gallbladder wall to be biomarkers significantly associated with anaphylaxis in dogs with acute hypersensitivity reactions.     

Incidence of hepatopathies in dogs administered zonisamide orally: A retrospective study of 384 cases

BackgroundAcute hepatopathy secondary to administration of zonisamide has been reported in 2 dogs, but overall incidence of hepatopathy is unknown.ObjectiveTo characterize the incidence of hepatopathy in dogs administered zonisamide PO.AnimalsThree hundred eighty‐four dogs administered zonisamide PO.MethodsMulticenter retrospective study. Medical records were searched for dogs prescribed zonisamide PO and which had follow‐up for at least 3 months (acute exposure) and >3 months (chronic exposure). Reported clinical signs, physical examination findings, and serum biochemical panels were reviewed for possible hepatotoxicosis. Serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activity and albumin concentration were documented for all available cases.ResultsAcute clinical hepatopathy was found in 2 of 384 treated dogs (0.52%, 95% confidence interval [CI], 0.06‐1.9) after 13‐16 days of zonisamide treatment. One additional dog had elevated serum ALT activity with no clinical signs. Of these 3 dogs, 2 recovered after administration of zonisamide was stopped, and 1 was euthanized because of liver failure. Of the 117 cases chronically administered zonisamide, 10 had an increase in ALP, 6 had an increase in ALT, and 1 had hypoalbuminemia. No clinical signs of liver disease were noted in dogs chronically treated with zonisamide (median, 20 months; range, 5‐94 months).Conclusions and Clinical ImportanceAcute, potentially life‐threatening hepatopathy associated with oral administration of zonisamide to dogs is estimated to occur in less than 1% of dogs and was observed in the first 3 weeks of treatment. Subclinical abnormalities in ALT and ALP activity were noted in <10% of dogs during chronic administration of zonisamide, with no clinical signs of liver disease noted.     

Clinical signs of cardiovascular effects secondary to suspected pimobendan toxicosis in five dogs

The purpose of this study was to review the medical records of dogs that were either suspected or known to have ingested large doses of pimobendan and to describe the clinical signs associated with pimobendan toxicosis. The database of Pet Poison Helpline, an animal poison control center located in Minneapolis, MN, was searched for cases involving pimobendan toxicosis from Nov 2004 to Apr 2010. In total, 98 cases were identified. Of those, seven dogs that ingested between 2.6 mg/kg and 21.3 mg/kg were selected for further evaluation. Clinical signs consisted of cardiovascular abnormalities, including severe tachycardia (4/7), hypotension (2/7), and hypertension (2/7). In two dogs, no clinical signs were seen. Despite a wide safety profile, large overdoses of pimobendan may present risks for individual pets. Prompt decontamination, including emesis induction and the administration of activated charcoal, is advised in the asymptomatic patient. Symptomatic and supportive care should include the use of IV fluid therapy to treat hypotension and address hydration requirements and blood pressure and electrocardiogram monitoring with high-dose toxicosis. Practitioners should be aware of the clinical signs associated with high-dose pimobendan toxicosis. Of the dogs reported herein, all were hospitalized, responded to supportive care, and survived to discharge within 24 hr of exposure.     

Red maple (Acer rubrum) leaf toxicosis in horses: a retrospective study of 32 cases

BACKGROUND: Ingestion of wilted red maple leaves by horses can result in severe hemolytic anemia and methemoglobinemia. Little is known about what factors influence the outcome of red maple leaf toxicosis in horses. HYPOTHESIS: Our hypothesis was that physical examination findings, clinicopathologic variables or therapeutic modalities may predict outcome in horses with red maple leaf toxicity. ANIMALS: Horses with red maple leaf toxicosis presented to referral hospitals in the southeast region of the United States. METHODS: A multi-institutional retrospective study was designed to identify factors that predict mortality in horses with red maple toxicosis. RESULTS: Thirty-two horses with red maple toxicosis were identified, 19 of which died. Twenty-nine horses presented with anemia and 24 had clinicopathologic evidence of systemic inflammation. Renal insufficiency was identified in 12/30 (41%) horses. Laminitis (9/28) and colic (13/30) also were identified in horses with red maple toxicosis, but development of these 2 conditions did not have a negative effect on short-term survival. Horses with red maple toxicosis that survived to discharge were likely to have developed pyrexia during hospitalization (P = .030). Horses that were treated with a corticosteroid had a significantly increased likelihood of death (P = .045). There was no significant relationship between initial serum hemoglobin concentration, methemoglobin concentration, or percentage methemoglobin and mortality in this horse series. CONCLUSIONS AND CLINICAL IMPORTANCE: This study suggests that information obtained on initial examination cannot be used to accurately predict survival in horses with red maple toxicosis, but horses that receive corticosteroids are unlikely to survive.     

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.     

Copper-associated liver disease in Dalmatians: a review of 10 dogs (1998-2001)

This retrospective study summarizes 10 Dalmatians suspected of having hepatic copper toxicosis. Hepatic copper toxicosis can result from either a primary metabolic defect in hepatic copper metabolism or from altered hepatic biliary excretion of copper. An inherited copper-associated hepatopathy has been documented in Bedlington Terriers, and there is evidence for familial copper-associated liver disease in West Highland White (WHW) Terriers and Skye Terriers. Nine of the 10 Dalmatians in this study presented for gastrointestinal clinical signs, including anorexia and vomiting. All animals had increased alanine aminotransferase (ALT) enzyme activity, and 9 of 10 had increased alkaline phosphatase (ALP) enzyme activity. The relative increase in ALT activity was much greater than the relative increase in ALP activity, suggesting a predominantly hepatocellular rather than cholestatic liver disease. The mean hepatic copper concentration for 9 Dalmatians was 3,197 microg/g dry weight liver (dwl) (normal, <450 microg/g). In 5 of these 9 dogs, hepatic copper concentrations exceeded 2,000 microg/g dwl. Necroinflammatory alterations associated with copper-laden parenchymal cells were the notable histopathologic finding. The inflammatory infiltrate was either primarily lymphocytic or neutrophilic. Morphologic features of cholestasis generally were not prominent except in those dogs with severe pathology. These findings lend support to the hypothesis that a primary metabolic defect in hepatic copper metabolism occurs in the Dalmatian breed. The mechanism and genetic basis of this condition require further study.     

Liver histopathology and liver and serum alanine aminotransferase and alkaline phosphatase activities in epileptic dogs receiving phenobarbital

Phenobarbital (PB) therapy is frequently associated with elevated serum alanine aminotransferase (ALT) and alkaline phosphatase (AP) activities in dogs without clinical signs of liver disease. The goal of this study was to determine if increased serum ALT and AP activities in clinically healthy PB-treated epileptic dogs are due to hepatic enzyme induction or to subclinical liver injury. Liver biopsies were obtained from 12 PB-treated dogs without clinical signs of liver disease but with elevated serum ALT and/or AP activities or both. Liver biopsies were obtained from eight healthy control dogs not receiving PB. Biopsies were evaluated histopathologically (all dogs) and liver homogenates were assayed for ALT (all dogs) and AP (six treated dogs, all controls) activities. As a positive control, liver cytochrome P4502B, an enzyme known to be induced by PB, was measured by benzyloxyresorufin-O-dealkylase activity and immunoblotting (five treated dogs, all controls). Serum AP isoenzyme analyses were performed. Results showed that ALT and AP activities in liver homogenates were not increased in treated dogs compared with controls, whereas the positive control for induction, CYP2B, was dramatically increased in treated dogs. Histopathological examination of liver biopsies revealed more severe and frequent abnormalities in treated dogs compared to controls, but similar types of abnormalities were found in both groups. Serum AP isoenzyme analyses in treated dogs demonstrated increased corticosteroid-induced and liver isoenzyme activities compared to controls. Results do not support induction of ALT or AP in the liver as the cause of elevated serum activities of these enzymes due to PB.     

Diazepam as a treatment for metronidazole toxicosis in dogs: a retrospective study of 21 cases

The currently recommended treatment for metronidazole toxicosis is drug discontinuation and supportive therapy. Reported recovery times are 1-2 weeks. The records of 21 dogs with metronidazole toxicosis were retrospectively analyzed to determine whether diazepam improved recovery. The dosage and duration of metronidazole therapy and the response and recovery times of 13 dogs treated with diazepam were compared to those of 8 dogs receiving only supportive care. Response time was defined as the time to resolution of the debilitating clinical signs. Recovery time was the time to resolution of all residual clinical signs. The average dosage and duration of metronidazole administration for the diazepam-treated and untreated groups were 60.3 mg/kg/d for 44.9 days and 65.1 mg/kg/d for 37.25 days. The protocol for diazepam administration consisted of an initial i.v. bolus and then diazepam PO q8h for 3 days. The average dosage of both the i.v. and PO diazepam was 0.43 mg/kg. The average response time for the diazepam-treated dogs was 13.4 hours compared to 4.25 days for the untreated group. Recovery time also was markedly shorter for the diazepam-treated dogs (38.8 hours) compared to the untreated group (11 days). Results of this study showed that dogs with metronidazole toxicosis recover faster when treated with diazepam. Although the mechanism of metronidazole toxicosis or how diazepam exerts its favorable effect is not known, it is likely related to modulation of the gamma-aminobutyric acid (GABA) receptor within the cerebellar and vestibular systems.     

Acute aldicarb toxicity in dogs: 15 cases (2001–2009)

Objective – To describe the common clinical signs, laboratory abnormalities, treatment, and prognosis associated with acute aldicarb toxicosis in dogs. Design – Retrospective observational study from 2001 to 2009. Setting – Urban referral hospital. Animals – Fifteen client‐owned dogs. Interventions – None. Measurements and Main Results – The most common clinical signs associated with acute aldicarb toxicosis were vomiting, ptyalism, diarrhea, and tremors. Of the 15 dogs, 11 were admitted to the hospital for treatment, 2 were euthanized at presentation and 2 were discharged against medical advice following minimal treatment and lost to follow‐up. Laboratory abnormalities included lactic acidosis and hyperglycemia in 12 and 9 patients, respectively. Treatment of hospitalized dogs included induction of emesis with apomorphine (4 dogs), activated charcoal (5), IV fluids (11), atropine (7), methocarbamol (3), diazepam (1), pralidoxime (1) and diphenhydramine (1). Ten of 11 hospitalized dogs survived to discharge; 1 was euthanized following a respiratory arrest after 36 hours of hospitalization. One patient received mechanical ventilation and treatment for pneumonia before discharge from the hospital. The median duration of hospitalization was 22 hours (range 12–168 h). Conclusions – Acute aldicarb toxicosis carries a good prognosis for survival and hospital discharge with treatment. Supportive care should be considered for at least 18–24 hours to monitor for response to therapy and development of respiratory failure.     

Clinical observations in collies given ivermectin orally

An oral liquid form of ivermectin was administered to 14 purebred Collies (12 rough coated, 2 smooth coated). All Collies were given ivermectin at dosages of 100 and then 200 micrograms/kg of body weight. Three of the dogs developed mild clinical signs of toxicosis (salivation, vomiting, confusion, ataxia, and tremors) with the 100 micrograms/kg dosage. After the 200 micrograms/kg dosage, 7 dogs (including 1 smooth-coated Collie) developed severe toxicosis (seizure-like activity, recumbency, nonresponsiveness, and coma). Because dogs that developed severe toxicosis were not retreated, only the 7 remaining dogs were given ivermectin at 600 micrograms/kg. Severe toxic signs were not observed in the dogs given the 600 micrograms/kg dosage, and only 1 of these 7 dogs developed severe toxicosis when given ivermectin at 2,500 micrograms/kg. Dogs that developed severe toxicosis were given supportive care while in the comatose state. All dogs recovered completely. The results indicated that Collies (including the smooth-coated Collies) have a wide range of sensitivity to ivermectin-induced toxicosis.     

Toxicoses associated with administration of mitoxantrone to dogs with malignant tumors

One hundred twenty-nine dogs with histologically confirmed malignant tumors were used in a prospective study to determine the toxicity of the new dihydroxyquinone derivative of anthracene, mitoxantrone, which was administered IV at 21-day intervals at dosages ranging from 2.5 to 5 mg/m2 body surface area. Each dog was evaluated for signs of toxicosis for 3 weeks after each dose was administered or until the dog died, whichever came first. The number of dogs in each evaluation period were as follows: 1 dose (n = 129), 2 doses (n = 82), 3 doses (n = 43), 4 doses (n = 26), 5 doses (n = 19), 6 doses (n = 9), 7 doses (n = 6), 8 doses (n = 5), 9 doses (n = 3), and 10 doses (n = 1). The most common signs of toxicosis were vomiting, diarrhea, anorexia, and sepsis secondary to myelosuppression. None of the dogs died of complications resulting from mitoxantrone treatment. Dogs with signs of toxicosis during the 21-day interval from administration of the first dose of mitoxantrone were 95 times (P = 0.003) more likely to develop signs of toxicosis during the 21-day interval from the second dose of mitoxantrone. Similarly, dogs that developed signs of toxicosis during the 21-day interval from the administration of the second dose were 34 times (P less than 0.001) more likely to develop signs of toxicosis during the 21-day interval from the administration of the third dose. With each 1 mg/m2 increase in mitoxantrone, the odds of developing signs of toxicosis increased by 5.9 fold (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Retrospective evaluation of the prognostic utility of plasma lactate concentration,base deficit,pH, and anion gap in canine and feline emergency patients

Objective

To determine the association of plasma lactate concentration, pH, base deficit (BD), and anion gap (AG) in dogs and cats on presentation to an emergency room with outcome, and to compare the prognostic significance of hyperlactatemia with a concurrent metabolic acidosis with that of hyperlactatemia and a normal metabolic acid–base balance.

Design

Retrospective study.

Setting

University teaching hospital.

Animals

Five hundred sixty‐six dogs and 185 cats that had venous blood gas analysis performed.

Interventions

None.

Measurements and Main Results

Medical records were reviewed for plasma lactate concentrations, electrolyte concentrations, and acid–base parameters obtained on emergency room admission, clinical diagnosis, and in‐hospital mortality. The primary outcome measure was all‐cause mortality for the hospitalized visit. Median plasma lactate concentration and AG were higher, BD was more negative, and pH was lower, in non‐survivor dogs and cats. The prevalence of hyperlactatemia was 53% in dogs and 30% in cats. Lactic acidosis was present in 42% and 80% of hyperlactatemic dogs and cats, respectively. Multivariate regression analyses revealed that plasma lactate concentration, BD, and pH, but not AG, were independent predictors of mortality in dogs, and that only plasma lactate concentration was an independent predictor of mortality in cats. Mortality was highest for animals with lactic acidosis, at 59.8% in dogs and 49% in cats. Mortality in dogs with lactic acidosis was significantly higher than dogs with hyperlactatemia and a normal acid–base status (P < 0.0001).

Conclusions

The presence and magnitude of hyperlactatemia on presentation to the emergency room may help identify dogs and cats with high likelihood of in‐hospital mortality, and the presence of lactic acidosis specifically may help identify dogs with yet higher risk of in‐hospital mortality.     

Iatrogenic hyperadrenocorticism in 28 dogs.

Twenty-eight dogs with iatrogenic hyperadrenocorticism were studied. The most common clinical signs were cutaneous lesions (27/28), polydipsia (21/28), polyuria (19/28), and lethargy (16/28). The most predominant findings on biochemical profile were elevated alkaline phosphatase (ALP, 15/28) and alanine transferase (ALT, 14/28); hypercholesterolemia (14/28); elevated aspartate transferase (AST, 12/28); and elevated triglycerides (12/18). Baseline cortisol levels of all 28 dogs were at the lower end of the reference range and exhibited suppressed or no response to adrenocorticotropic hormone (ACTH) stimulation. The mean time for each dog to show initial improvement of clinical signs after corticosteroid withdrawal was six weeks, with another mean time of 12 weeks to demonstrate complete remission.     

Zinc toxicosis in a captive striped hyena (Hyaena hyaena).

An 11-yr-old captive-born female striped hyena (Hyaena hyaena) acutely developed lameness and swelling of the left front foot with anorexia, depression, and lethargy. Hematologic evaluation revealed regenerative anemia, azotemia, and other mild serum electrolyte and mineral abnormalities. Twenty radiographically visible coins and 10 coin fragments were removed by laparotomy and gastrotomy following unsuccessful medical therapy. The animal died during anesthetic recovery. Zinc serum levels were 41.0 ppm at first presentation and 36.0 ppm at the time of surgery, compared with concentrations of 1.78 ppm and 2.82 ppm for serum taken from this female and a male hyena 3 mo previously. Zinc toxicosis was diagnosed based on the similarity of clinical signs to those described in dogs, presence in the stomach of pennies minted after 1982 (when the zinc content of U.S. pennies was increased substantially), necropsy findings, and elevated serum and liver zinc values. The case highlights the risk posed by penny ingestion for subsequent zinc toxicosis in captive omnivores.