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.     

Hypernatremia

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.     

Toxic effects of cyclonite (C‐4) plastic explosive ingestion in a dog

Objective – To describe the clinical manifestations following cyclonite (C‐4) plastic explosive ingestion in a dog. Case Summary – A 2‐year‐old male castrated Labrador working dog weighing 35 kg was presented for seizures shortly after ingestion of C‐4. The dog was successfully treated for the seizures, but developed polyuria/polydipsia shortly after being discharged and was ultimately diagnosed with chronic kidney disease. New or Unique Information Provided – This is the first documented case of renal insufficiency in a dog after C‐4 intoxication.     

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.     

Atypical Reaction to Acetaminophen Intoxication in a Dog

Objective: To report an unusual manifestation of acetaminophen intoxication in a dog.
Case Summary: A Miniature Pinscher was presented for evaluation of lethargy and facial swelling after ingestion of 500–750 mg/kg of acetaminophen. Laboratory testing revealed eccentrocytes, Heinz bodies, hemoglobinemia, and a declining packed red cell volume consistent with oxidative damage to the erythrocytes. Hepatocellular damage, as monitored by serum alanine aminotransferase, was not documented. The dog responded well to therapeutic intervention, and was discharged from the hospital. The dog returned to the hospital 2 days later with clinical signs and diagnostic tests consistent with acute keratoconjunctivitis sicca, which was assumed to be due to a toxic etiology. The dog responded well to therapy, regaining normal levels of tear production within six weeks.
New or Unique Information Provided: Acetaminophen intoxication may be associated with severe erythrocytic oxidative damage in the absence of detectable hepatic injury in dogs. Acetaminophen intoxication may have the potential to cause acute keratoconjunctivitis sicca in dogs. ( J Vet Emerg Crit Care 2001; 11(2): 123–126 )     

SOMA (carisoprodol) toxicity in a dog

Objective: To describe a case of SOMA intoxication in a dog. Case summary: A 13‐year‐old, 25 kg, female spayed Australian shepherd presented to the emergency service after ingestion of ten to fifteen 350 mg tablets of SOMA (carisoprodol), a muscle relaxant used for back pain in humans. Toxic effects of the drug in this dog included mild sinus tachycardia, respiratory depression, seizures, and ataxia. The dog's mentation progressively deteriorated from depressed to comatose within 1 hour after admission. Treatment on initial presentation consisted of induction of emesis while the dog still had a gag reflex, administration of activated charcoal, oxygen therapy, and supportive care. The dog was discharged to the owner prior to full recovery (4 days later). New or unique information provided: This is the first known report of carisoprodol intoxication in the dog.     

Life threatening metabolic disorders after application of a sodium phosphate containing enema in the dog and cat.]

Application of a sodium phosphate containing enema caused life-threatening metabolic disorders in a Dachshund and two cats. Clinical signs were characterised by dehydration and various neurological deficits including seizures. Most striking laboratory abnormalities were hypernatremia, hypocalcemia, hyperphosphatemia, and polycythemia. Despite intensive treatment the dog died, whereas the cats recovered completely. In face of possible severe and potentially fatal metabolic abnormalities sodium phosphate enemas, such as Practo-Clyss, should be used with caution or not at all in cats and small dogs.     

Acute hepatic failure and coagulopathy associated with xylitol ingestion in eight dogs

CASE DESCRIPTION: 8 adult dogs were evaluated for treatment of lethargy and vomiting after ingestion of xylitol, a sugar alcohol used as a sweetener in various products. CLINICAL FINDINGS: In addition to vomiting and lethargy, 5 of the dogs had widespread petechial, ecchymotic, or gastrointestinal tract hemorrhages. Common clinicopathologic findings included moderately to severely high serum activities of liver enzymes, hyperbilirubinemia, hypoglycemia, hyperphosphatemia, prolonged clotting times, and thrombocytopenia. Necropsies were performed on 3 dogs and severe hepatic necrosis was found in 2. In the third dog, histologic examination revealed severe hepatocyte loss or atrophy with lobular collapse. TREATMENT AND OUTCOME: Treatments varied among dogs and included IV administration of fluids; plasma transfusions; and, if indicated, administration of dextrose. Three dogs were euthanatized, 2 dogs died, 2 dogs made a complete recovery, and 1 dog was recovering but was lost to follow-up. CLINICAL RELEVANCE: Although xylitol causes hypoglycemia in dogs, hepatic failure after ingestion has not previously been reported. Because an increasing number of consumer products contain xylitol, clinicians should be aware that ingestion of xylitol can have serious, life-threatening effects.     

Treatment of accidental ethanol intoxication with hemodialysis in a dog

Objective – To describe the successful treatment of accidental ethanol intoxication with hemodialysis in a dog. Case Summary – A 1.5‐year‐old female intact mixed breed dog was presented in a comatose state believed to be due to ethanol intoxication. The initial 9 hours of supportive care treatment were complicated by multiple seizures and hypothermia, and resulted in only minimal improvement in the dog's level of consciousness. Hemodialysis was implemented and resulted in rapid clinical recovery, corresponding to a rapid decline in serum ethanol concentration. New or Unique Information Provided – To the authors' knowledge, this is the first reported case of using hemodialysis to treat accidental ethanol intoxication in a dog. The patient's initial serum ethanol concentration was higher than those previously reported for cases of accidental ethanol intoxication in dogs, and the serum ethanol concentration was shown to rapidly decline during hemodialysis. Treatment with hemodialysis for severe ethanol intoxication was effective in this case and may be able to decrease morbidity and mortality in some cases.     

Xylitol intoxication associated with fulminant hepatic failure in a dog

Objective: To describe a case of xylitol intoxication causing fulminant hepatic failure in a dog. Case summary: A 2.5‐year‐old castrated male English Springer Spaniel weighing 26 kg, was presented after ingestion of half of a loaf of bread containing the sweetener xylitol. Toxic effects of the xylitol in this dog included vomiting, mild hypoglycemia and fulminant hepatic failure. Clinical management of acute hepatic failure and subsequent coagulopathy with supportive care and fresh frozen plasma is described. The dog was discharged 3 days after admission after a full clinical recovery. New or unique information provided: This paper describes the clinical consequence and successful treatment of fulminant hepatic failure in a dog following ingestion of xylitol.     

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.     

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.     

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.     

Pituitary-adrenal function in dogs with acute critical illness

OBJECTIVE: To evaluate pituitary-adrenal function in critically ill dogs with sepsis, severe trauma, and gastric dilatation-volvulus (GDV). DESIGN: Cohort study. ANIMALS: 31 ill dogs admitted to an intensive care unit (ICU) at Washington State University or the University of Pennsylvania; all dogs had acute critical illness for < 48 hours prior to admission. PROCEDURES: Baseline and ACTH-stimulated serum cortisol concentrations and baseline plasma ACTH concentrations were assayed for each dog within 24 hours after admission to the ICU. The change in cortisol concentrations (Delta-cortisol) was calculated for each dog. Morbidity and mortality data were recorded for each patient. RESULTS: Overall, 17 of 31 (55%) acutely critically ill dogs had at least 1 biochemical abnormality suggestive of adrenal gland or pituitary gland insufficiency. Only 1 (3%) dog had an exaggerated response to ACTH stimulation. Dogs with Delta-cortisol < or = 83 nmol/L were 5.7 times as likely to be receiving vasopressors as were dogs with Delta-cortisol > 83 nmol/L. No differences were detected among dogs with sepsis, severe trauma, or GDV with respect to mean baseline and ACTH-stimulated serum cortisol concentrations, Delta-cortisol, and baseline plasma ACTH concentrations. CONCLUSIONS AND CLINICAL RELEVANCE: Biochemical abnormalities of the hypothalamic-pituitary-adrenal axis indicative of adrenal gland or pituitary gland insufficiency were common in critically ill dogs, whereas exaggerated responses to ACTH administration were uncommon. Acutely ill dogs with Delta-cortisol < or = 83 nmol/L may be more likely to require vasopressors as part of the treatment plan.     

Hypernatremia secondary to homemade play dough ingestion in dogs: a review of 14 cases from 1998 to 2001

Objective: To correlate the sodium chloride dosage and the serum sodium concentration to clinical signs, to determine if the dosage of homemade play dough (and, therefore, sodium chloride) is the most reliable way to predict clinical signs and prognosis, and to review previously reported treatment options. Design: Retrospective case series. Animals: Fourteen dogs with a history of homemade play dough ingestion. Procedure: Cases were examined for each animal's signalment including body weight, age, approximate amount of play dough ingested, the estimated sodium chloride dosage, clinical signs, serum sodium concentration, and outcome when available. The literature was reviewed to determine pathophysiology and treatment regimens. Results: Twelve of 14 dogs (86%) that ingested homemade play dough showed clinical signs. Vomiting (9 of 14, 64%), polydipsia, and seizures (4 of 14 each, 29%) were the most common signs followed by polyuria, tremors (3 of 14 each, 21%), and hyperthermia (2 of 14, 14%). The lowest calculated dosage associated with objective clinical signs was 1.9 g/kg. Seizures were reported in all animals with serum sodium levels greater than 180 mEq/L. Conclusions and clinical relevance: Homemade play dough ingestion can be a serious and life‐threatening problem. Many factors can contribute to the toxicity of homemade play dough. This study indicates that the serum sodium concentration is a more reliable indicator of the clinical course of the toxicity rather than the amount of play dough and, therefore, the dosage of sodium chloride ingested. Treatment should be based on a clinical evaluation of the patient and laboratory results, and consists of controlling seizures, reducing serum sodium concentrations slowly, and supportive care.     

Gastrointestinal tract perforations caused by ingestion of multiple magnets in a dog

Objective – To describe a case of gastrointestinal tract perforation, septic peritonitis and coagulopathy caused by ingestion of multiple magnets in a dog. Case Summary – An 8‐month‐old castrated male Rottweiler, weighing 30.5 kg was presented for evaluation of vomiting and weakness. Abdominal radiography and abdominal ultrasonographic examination identified a metallic foreign object within the gastric lumen, presence of free peritoneal gas, and peritoneal effusion. Septic peritonitis was diagnosed by abdominal fluid analysis. Exploratory celiotomy revealed the presence of an omental abscess, and gastric and colonic perforations. Four magnetic foreign objects were found within the lumen of the perforated stomach. Surgical management including removal of the magnets, abscess debridement and excision, perforation repair, and abdominal drainage combined with intensive medical therapy resulted in complete recovery of this dog. New or Unique Information Provided – This report describes in detail the case management of a dog that developed both gastric and colonic perforations and severe morbidity secondary to ingesting multiple magnets.     

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.     

Treatment of a Myasthenic Dog with Mycophenolate Mofetil

A ten‐year‐old, male castrated Springer Spaniel was presented for dysphagia, ptyalism, and regurgitation. Evidence of megaesophagus and mild aspiration pneumonia were apparent on thoracic radiographs. A diagnosis of focal acquired myasthenia gravis was suspected and subsequently confirmed with a positive serum acetylcholine (ACh) receptor antibody concentration (3.87 nM/L). A gastrostomy tube was placed shortly after presentation; food and drugs (including azathioprine) were administered through the tube. After transient improvement, the dog suddenly deteriorated clinically, experiencing frequent episodes of regurgitation and developing severe aspiration pneumonia. Mycophenolate mofetil (MMF), a novel immunosuppressive drug with relative specificity for lymphocytes, was instituted every twelve hours via the gastrostomy tube. Within four days of beginning MMF therapy, both clinical evidence of pharyngeal/esophageal dysfunction and radiographic evidence of megaesophagus had resolved. Initially, clinical side‐effects of combined MMF/AZA administration were not apparent, but the patient experienced several vomiting episodes during the third week of treatment. The vomiting resolved after decreasing the dose of both drugs. The patient made a full recovery, and a one‐month follow‐up ACh receptor antibody concentration was normal (0.26 nM/L). After one month of combination therapy, the patient was weaned off of AZA and maintained on MMF as the sole immunosuppressive drug. The dog was subsequently weaned off of MMF on two occasions. Mycophenolate mofetil was reinstituted after the first discontinuation due to the development of profound appendicular muscle weakness two days after stopping MMF; the weakness resolved within 24 hours of reinstituting MMF. A positive ACh receptor antibody concentration (0.89 nM/L) after the second MMF weaning prompted the second reinstitution of MMF. Two months following this second MMF reinstitution, the dog was again serologically negative (0.51 nM/L) for myasthenia gravis. At the time of last followup, the dog remained in clinical remission eight months after initial presentation. The use of MMF to treat acquired myasthenia gravis in dogs has not been reported previously. The literature concerning MMF and its potential use in treating patients with autoimmune diseases is discussed.     

Temporary transvenous cardiac pacing in a dog with diltiazem intoxication

Objective: This case report presents the clinical findings of a dog with diltiazem intoxication and the utilization of temporary transvenous pacing for management of high‐grade second‐degree atrioventricular (AV) block with associated bradycardia and hypotension. Case summary: A nine‐year‐old spayed female Basset Hound, who ingested between 95 and 109 mg/kg of sustained‐release diltiazem exhibited clinical signs of cardiac arrhythmias, bradycardia, hypotension, mental depression and gastrointestinal (GI) upset. Bradycardia was present initially, then was followed by high‐grade second‐degree AV block with ventricular escape. Traditional medications to treat calcium channel blocker (CCB) intoxication, including atropine, calcium gluconate, dopamine and glucagon were initially successful in managing the cardiac rhythm disturbances and hypotension. Twenty‐two hours post‐ingestion, however, the dog became refractory to these medications following sedation for GI decontamination and a temporary transvenous pacemaker was placed. The dog was paced for 19 hours. Transvenous pacing effectively increased heart rate, which increased blood pressure into an acceptable range. The dog was successfully discharged from the hospital following treatment. New or unique information provided: The use of a temporary pacemaker should be considered an acceptable treatment for bradycardia, AV block and hypotension associated with CCB intoxication when conventional medical therapy fails.