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.     

Diet‐associated hepatic failure and immune‐mediated hemolytic anemia in a Weimaraner

Objective: To describe the medical and nutritional management of a 4‐year‐old Weimaraner with acute hepatic failure and immune‐mediated hemolytic anemia (IMHA) associated with consuming a commercial dog food. Case summary: A 4‐year‐old male castrated Weimaraner developed signs of IMHA, hepatic failure, disseminated intravascular coagulopathy, and malnutrition after consuming a commercial dog food. During the course of hospitalization, medical management included immunosuppressive therapy and supportive care. Nutritional support consisted of both enteral and parenteral nutrition. The dog was discharged after 19 days of hospitalization and fully recovered by 6 months. An investigation by the Food and Drug Administration was not able to determine the exact cause of the acute hepatic failure and IMHA. New information provided: This is the first case report documenting the medical and nutritional management of a critically ill animal associated with ingestion of this commercial dog food.     

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.     

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.     

Rauwolfia serpentina toxicity in a dog

Objective– To describe the clinical manifestations and treatment of Rauwolfia serpentina toxicity in a dog. Case Summary– A 9‐month‐old intact male mixed breed dog was presented following ingestion of an antihypertensive medication containing alkaloids from R. serpentina. R. serpentina alkaloids cause depletion of the biologic amines: norepinephrine, dopamine, and serotonin. The dog experienced hypotension, mental depression, bradycardia, diarrhea, bronchoconstriction, and gastrointestinal ulceration similar to the adverse effects reported in humans. The dog was released from the hospital after 4 days of supportive care. New Information Provided– This is the first case of accidental R. serpentina toxicity in a dog reported in the literature. This case had a good clinical outcome with supportive care and monitoring of all the subsequent adverse effects.     

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.     

Xylitol

Xylitol is a prevalent sugar substitute found in a wide variety of foods, particularly those labeled as “low carb.” It is found in many medicines and dental products both for its antibacterial activity and to increase palatability. Originally, this toxin was recognized as a problem in dogs following sugarless gum ingestions. Xylitol is generally nontoxic to mammals except for dogs. In the dog, xylitol induces marked increases in insulin production and occasionally hepatopathy. The clinical syndrome is manifested with signs consistent with profound hypoglycemia, hypokalemia, hypophosphatemia, and acute hepatic failure. Treatment relies upon administration of intravenous glucose, hepatic support, and general supportive care.     

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.     

Presumptive hepatotoxicity and rhabdomyolysis secondary to phenazopyridine toxicity in a dog

Objective – To describe a rare, but potential clinical manifestation of phenazopyridine (PAP) toxicity in a dog. Case Summary – A 6‐year‐old spayed female Chihuahua was evaluated for ataxia and dysphagia after ingestion of 200 mg (66 mg/kg) of PAP hydrochloride. The dog was presented to the hospital with shifting leg lameness involving all 4 limbs, which progressed to reluctance to walk and severe diffuse muscle hyperesthesia. Clinical laboratory abnormalities included marked increases in serum alanine aminotransferase, aspartate aminotransferase, creatine kinase, mild increases in alkaline phosphatase, and increased c‐Tnl‐troponin concentration. Treatment included administration of intravenous fluids, muscle relaxants, pain medications, and hepatoprotectants for 5 days in the hospital, and medical management at home for an additional 5 days. Follow‐up examinations performed 1 and 6 months after initial presentation revealed the dog to be clinically healthy with serum biochemical profiles within reference intervals. New or Unique Information Provided – The purpose of this report is to describe an unusual manifestation of PAP toxicosis in a dog, which has not been previously reported in the literature. A review of the ASPCA Animal Poison Control Center database revealed 347 cases of PAP exposure in dogs during 2000–2009 underscoring the importance of being aware of this toxicity in the dog.     

Clinical and histologic outcome in a dog surviving massive hepatic necrosis

This report describes the clinical and histologic recovery of a 2‐year‐old mixed‐breed dog presented with hypovolemic shock, markedly increased serum alanine amino transferase activity, and hemoabdomen. Emergency exploratory surgery revealed a friable liver with multiple capsule hemorrhages necessitating removal of the left lateral lobe. Histologic evaluation showed acute massive hepatic necrosis with centrilobular and midzonal distribution. The dog survived, and all monitored laboratory values normalized within 7 weeks. A liver biopsy taken 8 weeks after presentation revealed normal hepatic architecture with a few, randomly distributed neutrophilic foci. Follow‐up included intermittent determination of liver variables including liver function tests for a period of 7 years. The dog's health status, and all test results remained normal during this time. Complete recovery and good long‐term quality of life after life‐threatening acute liver failure secondary to massive hepatic necrosis is possible in dogs.     

Hepatotoxicity associated with methotrexate therapy in a dog

A nine-year-old male Newfoundland-cross was treated with doxorubicin, cyclophosphamide, and methotrexate as adjuvant chemotherapy following the resection of a maxillary osteosarcoma. The dog remained in good health until week 13 of therapy, when he became anorexic, and developed icterus and ascites. Laboratory tests at this time suggested sub-acute hepatic failure and renal failure. Necropsy revealed severe generalized hepatic necrosis with resultant ascites and intestinal haemorrhage. Since there was no evidence on necropsy of an infectious aetiology, and since there was no history of toxin ingestion, methotrexate which is a known hepatotoxin in man, was considered the probable cause of the hepatic necrosis. This side-effect of methotrexate has not previously been reported in the dog, and animals undergoing therapy with the drug should be monitored closely for hepatotoxicity.     

Airway obstruction in a dog after Dieffenbachia ingestion

Objective – To describe a case of Dieffenbachia ingestion in a dog presented for dysphagia and airway obstruction successfully treated with a temporary tracheostomy and supportive care beyond that reported in the veterinary literature. Case Summary – An 8‐year‐old male neutered Labrador Retriever, weighing 30 kg, was presented with the complaint of choking and gagging. Abdominal radiographs showed that he had a distended stomach full of foreign material and a gastrotomy was performed. After receiving preanesthetic medication, the dog developed inspiratory stridor and during anesthetic induction, marked oropharyngeal swelling complicated tracheal intubation. During surgery a large amount of dog bedding and Dieffenbachia plant material was removed. Because of the severity of the oropharyngeal swelling, the dog required a temporary tracheostomy and treatment for an acute allergic reaction related to the Dieffenbachia ingestion. The patient was discharged after 6 days in the hospital and had no significant complications. New or Unique Information Provided – To our knowledge, this is the first reported case of successful treatment of an airway obstruction related to the toxicity of Dieffenbachia ingestion.     

Effects of p.o. administered xylitol in cats

Xylitol is commonly used as sugar substitute in households. While it has numerous beneficial effects on human health, it is highly toxic to dogs. The goal of this study was to examine whether xylitol has similar deleterious effects, such as hypoglycaemia and acute hepatic failure, on cats. Our research included six healthy middle‐aged cats. Xylitol was dissolved in deionized water and administered p.o. at three doses (100, 500 and 1,000 mg/kg body weight). These dosages have been considered toxic and can cause liver failure or even death in dogs. After every xylitol administration, the basic health status and the blood glucose of cats were observed regularly. Additionally, prior to and 6, 24 and 72 hr after xylitol administration, blood samples were taken to check complete blood count, clinical biochemical parameters and enzymes such as ALT, ALKP, GGT, GLDH, bile acids, BUN, creatinine, phosphate, total protein, albumin, sodium and potassium. There were no significant changes (p > .05) in any of the haematological or biochemical parameters. Blood glucose concentrations did not show any significant alterations, except at 1,000 mg/kg dose, where a mild but significant increase was observed, but it was in physiological range. Based on our results, xylitol did not induce toxic effects on cats.     

INTRAHEPATIC VENOUS COLLATERALS PREVENTING SUCCESSFUL STENT-SUPPORTED COIL EMBOLIZATION OF INTRAHEPATIC SHUNTS IN DOGS

The purpose of the following study was to evaluate stent-supported coil embolization of the hepatic vein in combination with antithrombotic treatment as a method for treatment of intrahepatic shunts, and to describe the complications associated with this procedure. Seven dogs with an intrahepatic shunt were included in a prospective clinical trial. A stepwise procedure was performed. First intervention: transjugular retrograde portography and stent implantation into caudal vena cava; second intervention: hepatic vein embolization combined with an antithrombotic treatment; third intervention in dogs with residual shunting: hepatic vein embolization without antithrombotic treatment. A right shunt was found in one dog and a left shunt in six dogs. Primary intrahepatic venous collaterals were found in one dog and hepatic vein embolization was not performed. Stent implantation into the caudal vena cava was performed in the other six dogs. There was no stent migration or thrombosis. Following the first coil intervention two dogs died due to vessel laceration while removing an oversized or migrated coil. On follow-up the shunt was completely closed in one dog. Secondary intrahepatic venous collaterals developed after the first or second coil intervention in two and one dog, respectively. In conclusion, stent-supported coil embolization of the hepatic vein in combination with an antithrombotic treatment was of limited success because primary or secondary intrahepatic venous collaterals tend to occur.     

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 )     

Binding affinity of anti-xylitol antibodies to canine hepatic vessels

Xylitol is used as a sugar substitute in food products. Dogs have been reported to experience lethal liver injury after accidental ingestion of xylitol. Because liver injury may be a serious consequence of canine immune-mediated reactions, antibodies produced against xylitol may attack the liver. Therefore, in the present study, we evaluated whether binding sites for xylitol antibodies are located at the liver or not. Anti-xylitol antibodies were generated by immunization of rabbits with a xylose-bovine serum albumin conjugate. Immunohistological examination showed that binding sites for the anti-xylitol antibodies were located in the hepatic arteries and the portal veins. Western blotting analyses by using a canine liver homogenate showed 4 protein bands with different molecular weights which reacted with anti-xylitol antibodies. Therefore, binding of anti-xylitol antibodies to the vessels may be the first step in an immune-mediated pathogenic response in xylitol toxicity. Further studies are necessary to determine the effects of anti-xylitol antibodies on the liver in the pathogenesis of xylitol toxicity.     

Aortic valvular endocarditis caused by Bartonella vinsonii subsp. berkhoffii in 2 dogs presenting for fulminant pulmonary edema

Objective: To describe the clinical course of 2 dogs that presented with fulminant cardiogenic pulmonary edema due to aortic valvular endocarditis caused by Bartonella vinsonii subsp. berkhoffii. Case series summary: Two dogs that were presented for respiratory distress had severe pulmonary infiltrates. Mechanical ventilation was required to support the dogs while the cause of the infiltrates was determined. The diagnosis of cardiogenic edema was made based on echocardiographic findings of aortic valve vegetation and severe aortic valvular regurgitation. Values obtained from pulmonary artery catheterization supported this diagnosis. Both dogs were euthanized, one within 24 hours of admission due to severe aortic regurgitation thought to be untreatable, and the other 9 days after admission due to the development of acute renal failure. Histological evaluation of the aortic valves, serology, and polymerase chain reaction confirmed Bartonella vinsonii subsp. berkhoffii as the cause of the aortic endocarditis. New or unique information provided: In medium‐to‐large breed dogs presenting with fulminant pulmonary edema, aortic valvular endocarditis due to Bartonella spp. should be considered as a causal agent.     

Putative peanut allergy-induced urticaria in a dog

A 9-year-old, spayed male schnauzer dog was presented with vomiting, diarrhea, generalized erythema, pruritic urticaria and conjunctival hyperemia after ingestion of peanut. The history, clinical signs, and histopathology of the lesions were compatible with a hypersensitivity reaction. The clinical signs resolved rapidly after treatment with prednisolone and antihistamine. This is the first report of urticaria caused by peanut ingestion in a dog.     

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.     

Kernicterus in an adult dog

A 7-year-old, spayed female, Wheaton terrier dog was icteric, lethargic, and anorexic with increased activity of hepatocellular and cholestatic liver enzymes and an extreme hyperbilirubinemia level of 609 micromol/L (reference interval: 1.0-4.0 micromol/L). Necropsy findings included profound icterus and red and yellow mottling of the liver. Yellow discoloration of the thalamic and subthalamic nuclei was detected on subgross examination of the formalin-fixed brain. Histologic examination of the brain revealed neuronal necrosis within the discolored nuclei, necrosis of Purkinje cells, and Alzheimer type II astrocytes in the cerebrocortical gray matter and in the nuclei, with gross discoloration. Histologic examination of the liver revealed extensive necrosis in a periacinar-to-bridging pattern and often extending to portal triads. A case of naturally occurring kernicterus in an adult dog secondary to extreme hyperbilirubinemia resulting from fulminant hepatic failure is reported. The few reports of this disease in domestic species involved neonates, namely 1 foal and 1 kitten.