1,3 Butanediol treatment of ethylene glycol toxicosis in dogs

In order to assess the therapeutic value of 1,3 butanediol in ethylene glycol toxicosis, mixed-bred dogs were given an oral dose of commercial antifreeze at 6 ml/kg of body weight (0 hour) and treated (IV) 7 times at 6-hour intervals with 5.5 ml/kg of body weight 1,3 butanediol solution (20% in physiological saline solution) beginning at 8, 12, and 21 hours. Serum glycolic acid concentration was quantitated by high-pressure liquid chromatography. Three dogs that were given ethylene glycol, but no 1,3 butanediol treatment, died with elevated serum glycolic acid concentrations. Five dogs were given ethylene glycol and 1,3 butanediol treatment. Of 2 dogs treated at 8 hours, 1 survived and 1 died at 39 hours; 1 treated at 12 hours and 1 treated at 21 hours survived; 1 dog died soon (27 hours) after treatment was initiated at 21 hours. Four of the 5 dogs had dramatically decreased serum glycolic acid concentrations after 1,3 butanediol treatment, indicating its effectiveness in inhibiting alcohol dehydrogenase-dependent glycolic acid formation in vivo.     

Early renal ultrasonographic findings in dogs with experimentally induced ethylene glycol nephrosis

Renal ultrasonographic changes were evaluated in 5 dogs administered 10 ml of commercial antifreeze (95% ethylene glycol)/kg of body weight, PO, and in 2 dogs given placebos. Studies were made prior to and after ingestion on an hourly basis over a period of 8 to 10 hours. All dogs were anesthetized immediately after toxin or placebo ingestion for the duration of the study. Renal cortical echogenicity was evaluated in comparison with that of the adjacent liver and spleen. Echogenicity of the renal medulla and definition of the corticomedullary junction were assessed. Within 4 hours after ethylene glycol administration, renal cortical echogenicity of all intoxicated dogs increased from normal to surpass that of liver and approach or equal that of the spleen. Medullary echogenicity in all intoxicated dogs progressively increased over the course of the study, with changes recognized within 5 hours after ethylene glycol administration. An ultrasonographic pattern consisting of nearly equal, marked increase in cortical and medullary echogenicity and relatively hypoechoic corticomedullary junction and central medullary regions was recognized concurrent with the development of anuria in 3 of the 5 intoxicated dogs. Mild, transient increases in cortical and medullary echogenicity were observed in anesthetized control dogs. However, no statistical difference (P less than 0.05) was detected between baseline, peak, and terminal echogenicity values in these dogs. Blood and urine samples were collected hourly from intoxicated dogs to coincide with ultrasonographic studies. Most clinicopathologic values derived from these samples were not statistically different (P less than 0.05) from those reported in a study that used a similar intoxication protocol in nonanesthetized dogs.     

Effects of oral administration of a commercial activated charcoal suspension on serum osmolality and lactate concentration in the dog

The purpose of this investigation was to determine the effects of an activated charcoal (AC) suspension containing propylene glycol and glycerol on serum osmolality, osmolal gap, and lactate concentration in dogs. Six healthy adult dogs were administered 4 g/kg AC in a commercially available suspension that contained propylene glycol and glycerol as vehicles. Blood samples were taken before and 1, 4, 6, 8, 12, and 24 hours after the administration of the test suspension. Samples were analyzed for osmolality, blood gases, and concentrations of lactate, sodium, potassium, serum urea nitrogen, and glucose. Osmolal gaps were calculated for each time point. Mean serum osmolality, osmolal gap, and lactate concentration were significantly increased after suspension administration compared to baseline. Serum osmolality increased from 311 mOsm/kg at baseline to 353 mOsm/kg, osmolal gap increased from 5 to 52 mOsm/kg, and lactate concentration increased from 1.9 to 4.5 mmol/L after suspension administration (all P < .01). Three of the 6 dogs vomited between 1 and 3 hours after the administration of the test suspension, and 4 of 6 dogs were lethargic. All dogs drank frequently after AC administration. Commercial AC suspension administered at a clinically relevant dose increases serum osmolality, osmolal gap, and lactate concentration in dogs. These laboratory measures and the clinical signs of vomiting, lethargy, and increased frequency of drinking might complicate the diagnosis or monitoring of some intoxications (such as ethylene glycol) in dogs that have previously received AC suspension containing propylene glycol, glycerol, or both as vehicles.     

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.     

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.     

Evaluation of twice-daily, low-dose trilostane treatment administered orally in dogs with naturally occurring hyperadrenocorticism

OBJECTIVE: To evaluate the effects of twice-daily oral administration of a low-dose of trilostane treatment and assess the duration of effects after once-daily trilostane administration in dogs with naturally occurring hyperadrenocorticism (NOH). DESIGN: Prospective study. ANIMALS: 28 dogs with NOH. PROCEDURES: 22 dogs received 0.5 to 2.5 mg of trilostane/kg (0.23 to 1.14 mg/lb) orally every 12 hours initially. At intervals, dogs were reevaluated; owner assessment of treatment response was recorded. To assess drug effect duration, 16 of the 22 dogs and 6 additional dogs underwent 2 ACTH stimulation tests 3 to 4 hours and 8 to 9 hours after once-daily trilostane administration. RESULTS: After 1 to 2 weeks, mean trilostane dosage was 1.4 mg/kg (0.64 mg/lb) every 12 hours (n = 22 dogs; good response [resolution of signs], 8; poor response, 14). Four to 8 weeks later, mean dosage was 1.8 mg/kg (0.82 mg/lb) every 12 or 8 hours (n = 21 and 1 dogs, respectively; good response, 15; poor response, 5; 2 dogs were ill). Eight to 16 weeks after the second reevaluation, remaining dogs had good responses (mean dosages, 1.9 mg/kg [0.86 mg/lb], q 12 h [n = 13 dogs] and 1.3 mg/kg [0.59 mg/lb], q 8 h [3]). At 3 to 4 hours and 8 to 9 hours after once-daily dosing, mean post-ACTH stimulation serum cortisol concentrations were 2.60 and 8.09 Pg/dL, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: In dogs with NOH, administration of trilostane at low doses every 12 hours was effective, although 2 dogs became ill during treatment. Drug effects diminished within 8 to 9 hours. Because of potential adverse effects, lower doses should be evaluated.     

Paintball intoxication in a pug

Objective: To describe a case of toxicity caused by oral ingestion of paintballs by a dog and how it was initially misdiagnosed as ethylene glycol intoxication due to similar clinical signs and a positive ethylene glycol blood test. Case summary: A 7 year‐old, 8.3 kg, female spayed Pug was referred for treatment of ethylene glycol (EG) toxicity. The patient was ataxic, disoriented, polyuric, polydipsic, and had a positive EG blood test. The patient was started on fomepizole therapy and intravenous fluids. Biochemical assays of the serum showed abnormalities that were not typical of EG toxicity. The following morning the patient defecated bright pink feces. The owner revealed that bright pink paint balls were present in the household when questioned. The patient completed fomepizole therapy and was discharged 40 hours after presentation with no clinical signs. Follow‐up telephone conversations found the pet to be clinically normal 2 months after discharge. New or unique information provided: This is the first known case report of paint ball intoxication in a dog that resulted in a positive EG blood test and clinical signs similar to ethylene glycol toxicity.     

Comparison of two low-dose dexamethasone suppression protocols as screening and discrimination tests in dogs with hyperadrenocorticism

Two low-dose dexamethasone suppression test protocols were evaluated in 18 dogs with hyperadrenocorticism (14 dogs with pituitary-dependent hyperadrenocorticism [PDH] and 4 dogs with adrenocortical tumor) and in 5 healthy control dogs. Blood was obtained immediately before and 2, 4, 6, and 8 hours after IV administration of either 0.01 mg of dexamethasone sodium phosphate/kg of body weight or 0.015 mg of dexamethasone polyethylene glycol/kg. At 8 hours after dexamethasone administration, 18 of 18 (100%) dogs with hyperadrenocorticism given the sodium phosphate preparation and 16 of 18 (89%) affected dogs given the polyethylene glycol preparation failed to have suppression of plasma cortisol concentration (less than 1.4 micrograms/dl). Plasma cortisol concentration was suppressed to less than 1.4 micrograms/dl at 2, 4, and/or 6 hours after administration of either dexamethasone preparation in 5 of 14 dogs with PDH and to less than 50% of baseline cortisol concentration in 10 of 14 dogs with PDH. Suppression, as identified by these 2 criteria, was not observed at 2, 4, 6, or 8 hours after administration of either dexamethasone preparation in dogs with adrenocortical tumor. For both protocols, the 8-hour plasma cortisol concentration was suppressed to less than 1.4 micrograms/dl and to less than 50% of baseline in the 5 control dogs. Both protocols were comparable for use as screening tests in establishing a diagnosis of hyperadrenocorticism. Suppression of plasma cortisol concentration to less than 50% of baseline (or less than 1.4 micrograms/dl) during the test was consistent with diagnosis of PDH. Failure to have such suppression, however, was observed in dogs with PDH as well as in those with adrenocortical tumor.     

4‐Methylpyrazole as a treatment in naturally occurring ethylene glycol intoxication in cats

Objective – To describe the clinical experience and therapeutic use of fomepizole (4‐methylpyrazole [4‐MP]) in 3 cats with naturally occurring ethylene glycol (EG) toxicity. Case or Series Summary – All cats were documented to be EG positive by an ethylene glycol test kit. This report describes the dose of 4‐MP used, available clinicopathological data, and clinical progression during hospitalization. All patients survived to discharge. New or Unique Information Provided – IV use of 4‐MP at 125 mg/kg as an initial dose and 31.25 mg/kg at 12, 24, and 36 hours is safe and effective for treatment of naturally occurring EG toxicity in cats. Increased HCO₃ concentrations were noted after IV use of 4‐MP. This is the first report documenting the successful treatment of naturally occurring EG intoxication in cats with 4‐MP.     

Effect of cimetidine on aspirin-induced gastric hemorrhage in dogs

Efficacy of cimetidine in the prevention of aspirin-induced gastric hemorrhage was evaluated, using 4 groups of 6 dogs given: Group 1--controls; group 2-7.5 mg of cimetidine/kg of body weight every 8 hours; group 3-7.5 mg of cimetidine/kg every 8 hours and 35 mg of nonbuffered aspirin/kg every 8 hours; and group 4-35 mg of nonbuffered aspirin/kg every 8 hours. All medication was given orally for 10 days at the time of feeding a commercial dry food. The gastric mucosa was evaluated endoscopically before treatment, on treatment day 5, and 36 hours after the final treatment. The dogs were given halothane inhalation anesthesia and were evaluated, using a grading system. Total 24-hour fecal hemoglobin (Hb) concentration was measured, using a quantitative fluorometric analysis for Hb-derived porphyrins. Control dogs and dogs given cimetidine only had no endoscopically visible gastric lesions and no increase in fecal Hb concentration. All dogs given aspirin or aspirin and cimetidine had a similar marked increase in endoscopically visible gastric hemorrhage and marked increases in fecal Hb concentration; however, there was no significant (P = 0.48) difference between the 2 groups. Seemingly, cimetidine given at an oral dosage of 7.5 mg/kg every 8 hours was not effective in preventing aspirin-induced gastric hemorrhage in clinically normal dogs.     

Prognostic value of blood lactate, blood glucose, and hematocrit in canine babesiosis

Canine babesiosis typically causes hemolytic anemia but also can result in multiple organ dysfunction. Human patients with severe disease often have persistent hyperlactatemia, and blood lactate concentration is correlated with survival rate. In dogs, blood lactate concentration has been shown to be of prognostic value in patients with gastric dilatation-volvulus and in dogs admitted to intensive care units. Serial blood lactate and glucose concentrations and hematocrit on admission were determined in 90 dogs with naturally occurring, severe or complicated canine babesiosis. Forty-five dogs (50%) had hyperlactatemia (blood lactate concentration >22.5 mg/dL) and 20 (22.2%) had hypoglycemia (blood glucose concentration <59.4 mg/dL) at presentation. Measurements significantly associated with mortality were hypoglycemia on admission, blood lactate concentration >45 mg/dL on admission, blood lactate concentration >22.5 mg/dL at 8, 16, and 24 hours after admission, and increase or <50% decrease in blood lactate concentration within 8 and 16 hours after admission. Blood lactate concentration persistently >40 mg/dL indicated a very poor prognosis. We conclude that serial blood lactate measurements are useful in predicting survival in dogs with severe and complicated canine babesiosis.     

Evaluation of the effect of two dose rates of cyclosporine on the severity of perianal fistulae lesions and associated clinical signs in dogs

OBJECTIVE: To investigate the effect of cyclosporine (2 or 5 mg/kg every 24 hours) on perianal fistulae (PAF) lesions. STUDY DESIGN: Blinded randomized, prospective trial. ANIMALS: Dogs (n = 20) with perianal fistulae. METHODS: Dogs were randomly assigned to administration of either 2 mg/kg (n = 10) or 5 mg/kg (n=10) of cyclosporine orally every 24 hours for 8 weeks. Lesion surface area was measured, lesion severity was graded using a visual analog scale, and the presence and severity of clinical signs recorded every 2 weeks. RESULTS: Lesion variables were significantly reduced in both groups after 8 weeks and owners also reported a reduction in clinical sign severity. The 5 mg/kg dose rate significantly accelerated lesion resolution compared with 2 mg/kg. In the 2 mg/kg group, 20% of dogs had complete resolution of clinical signs and 10% had resolution of lesions. In the 5 mg/kg group, 40% of dogs had complete resolution of clinical signs and 60% had resolution of lesions. CONCLUSIONS: A dose rate of 5 mg/kg every 24 hours was more effective at reducing the surface area and severity of PAF lesions than 2 mg/kg every 24 hours but less effective at resolving PAF lesions than previous studies using dose rates > or =5 mg/kg every 12 hours. CLINICAL RELEVANCE: Cyclosporine at 5 mg/kg every 24 hours may be useful for the palliation of PAF lesions.     

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 clinical, cerebrospinal fluid, and histopathologic effects of epidural ketorolac in dogs

OBJECTIVE: To evaluate the clinical, cerebrospinal fluid (CSF), and histopathologic effects of epidural ketorolac. STUDY DESIGN: Blinded, randomized, placebo controlled study. ANIMALS: Twenty-two adult mixed breed dogs with 16 treatment and 6 control dogs, weighing 14.4 to 29.8 kg. METHODS: Dogs were anesthetized and epidural catheters were placed at the lumbosacral space. Catheter placement was evaluated fluoroscopically. Ketorolac (0.4 mg/kg) or placebo (5% ethanol) was administered epidurally over a 52-hour period, with 5 injections given at 12-hour intervals. At 1, 2, 4, or 8 hours after the first and last injection of ketorolac, dogs were anesthetized and CSF was obtained. Control dogs had CSF sampled 1 hour after the first and last ethanol injection. Neurologic function and pain responses were evaluated before and during the study. Selected dogs were then killed and necropsies performed. RESULTS: None of the dogs exhibited any clinical or neurologic abnormalities during the study. No statistical difference was noted in pain response or CSF analysis between treatment and control dogs. Gross necropsy revealed gastrointestinal ulceration of varying degrees in all treatment dogs. Histopathologic analysis of the spinal cord and meninges revealed minimal focal leptomeningeal phlebitis in 2 of 8 treatment dogs and minor subdural inflammation in 1 control dog. No changes to the neural structures were noted in any dogs. CONCLUSIONS: Epidural administration of ketorolac did not cause clinical signs, alteration in CSF values, or pathologic changes to the spinal cord when used for short duration. Gastrointestinal ulceration was common when ketorolac was administered epidurally at 0.4 mg/kg every 12 hours for 5 treatments. CLINICAL RELEVANCE: This study documented the neurologic safety of epidural ketorolac in dogs before an efficacy trial can be performed. Gastrointestinal ulceration may limit use to short duration or a single injection.     

Safety and efficacy of high‐dose fomepizole compared with ethanol as therapy for ethylene glycol intoxication in cats

Objective – To determine the safety and efficacy of high‐dose fomepizole compared with ethanol (EtOH) in cats with ethylene glycol (EG) toxicosis. Design – Prospective study. Setting – University veterinary research laboratory. Animals – Thirteen cats. Interventions – Two cats received injections of high‐dose fomepizole (Study 1). Three cats received lethal doses of EG and fomepizole treatment was initiated 1, 2, or 3 hours later (Study 2). Eight cats received a lethal dose of EG and were treated with fomepizole or EtOH (Study 3). Cats treated with fomepizole received 125 mg/kg IV initially, then 31.25 mg/kg at 12, 24, and 36 hours. Cats treated with EtOH received 5 mL of 20% EtOH/kg IV initially, then every 6 hours for 5 treatments, then every 8 hours for 4 treatments. Cats also received fluids and supportive therapy as needed. Measurements and Main Results – Clinical signs were monitored and serial blood analyses performed. Cats receiving fomepizole experienced mild sedation but no biochemical evidence of toxicity. Cats receiving fomepizole for EG intoxication survived if therapy was initiated within 3 hours of EG ingestion. One of the 6 developed acute renal failure (ARF) but survived. Only 1 of the 3 cats treated with EtOH 3 hours following EG ingestion survived; 2 developed ARF and were euthanized. Cats treated 4 hours following EG ingestion developed ARF, whether treated with EtOH or fomepizole. Conclusions – Fomepizole is safe when administered to cats in high doses, prevents EG‐induced fatal ARF when therapy is instituted within 3 hours of EG ingestion, and is more effective than treatment with EtOH.     

Clodronate treatment of vitamin D-induced hypercalcemia in dogs

Objective: To determine the effects of clodronate on vitamin D₃‐induced hypercalcemia in dogs. Design: Prospective experimental study. Settings: University research laboratory. Animals: Fourteen healthy intact adult male and female mixed breed dogs. Interventions: Dogs received 7.5 mg of vitamin D₃/kg of body weight once orally and were randomly assigned to 2 groups of 7 dogs each. Dogs in the saline control group were given intravenous infusions of 150 mL 0.9% NaCl solution 24 hours after vitamin D₃ administration. Dogs in the clodronate group were given an infusion of 4 mg/kg of clodronate in 150 mL 0.9% NaCl solution 24 hours after vitamin D₃ administration. Measurements and main results: Clinical signs of vitamin D₃ toxicosis were evaluated 48 hours after ingestion of vitamin D₃. Dogs that were given clodronate had significantly lower serum calcium (Ca), phosphorus (P), urea, and Ca × P values than dogs in the control group on days 4, 7, and 12 after administration. Additionally, alkaline phosphatase activity was significantly lower in the clodronate group compared with dogs in the control group on days 4 and 7. Conclusions: Parenteral administration of clodronate, a biphosphonate compound and osteoclastic activity inhibitor, may be a useful therapy when administered within the first 24 hours after ingestion of toxic doses of vitamin D₃.     

Low-dose ethanol in the treatment of ethylene glycol poisoning

A pharmacokinetic study was conducted to determine the effectiveness of lower doses of ethanol in the treatment of ethylene glycol (EG) poisoning. Four dogs were maintained at serum ethanol concentrations of 0, 35 and 140 mg/dl prior to EG (i.v., 2 ml/kg) administration. The serum EG concentration-time data showed that the 35 mg/dl ethanol level provided as effective an inhibition of EG metabolism as did the 140 mg/dl level. The average urinary excretion rate of oxalic acid post EG administration was reduced to control levels by ethanol. The 35 mg/dl serum ethanol level reduced the total body clearance of EG from 93.9 to 50.0 ml/h/kg and increased the effective half-life from 5.78 to 11.4 h. Clinical testing was accomplished by giving the dogs 12 ml EG/kg body weight orally. One hour later, the dogs were either not treated or treated with a sodium bicarbonate-ethanol solution to obtain a serum ethanol concentration of 50 mg/dl. The clinical test performed in the ethanol-treated dogs showed little change from normal limits. Urine calcium oxalate crystals were seldom found. The dogs given EG (12 ml/kg) but not treated with ethanol were in a coma at 13 h and showed severe metabolic acidosis, dehydration, mild hepatocellular disease and acute renal damage. Urine calcium oxalate crystals were found in high numbers. The rapid death associated with EG poisoning appeared to be due to metabolic acidosis in combination with dehydration.     

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).     

A Retrospective Study of Pemoline Toxicosis in Dogs: 101 Cases (1987–1997)

Pemoline is a central nervous system stimulant commonly used for Attension Deficit Disorder in humans. This study describes the clinical syndrome associated with pemoline ingestion as well as its treatment. Ten years worth (1987–1997) of records from the ASPCa National Animal Poison Control Center involving pemoline ingestion in dogs were reviewed. The data suggests that most dogs ingesting pemoline show signs of central nervous system and cardiovascular stimulation including hyperactivity, tremors, ataxia, seizure, tachycardia, hyperthermia, and mydriasis. Blood chemistry alterations included electrolyte imbalances in some dogs. The minimum dose reported to cause clinical signs was 2.8 mg/kg and the minimum dose reported to have caused death was 10 mg/kg. Dogs generally showed clinical signs within 30 minutes to 24 hours of ingestion. The duration of clinical signs ranged from 15 hours to four days. Ninety-four percent of the dogs recovered with supportive treatment. (Vet. Emerg. & Crit. Care, 9:203–207, 1999)     

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.