Baclofen intoxication in a dog successfully treated with hemodialysis and hemoperfusion coupled with intensive supportive care

Objective: To describe a case of confirmed baclofen intoxication in a dog that was successfully treated with hemodialysis and hemoperfusion (HD/HP) and to report the serum baclofen kinetics. Case summary: A 2.5‐year‐old, 23 kg, spayed female Brittany Spaniel‐mix was treated after ingesting 21‐52 mg/kg of baclofen. The dog was comatose and was receiving manual ventilation at the time of presentation. Extracorporeal HD/HP was started 10 hours after admission. Within 3 hours of starting HD/HP the dog began initiating breaths and was extubated 18 hours after admission. Serial serum samples that were obtained during the first 24 hours of hospitalization were later analyzed for baclofen concentrations. The dog had elevated creatine phosphokinase and liver enzymes that correlated with an agitated recovery period. The dog had thrombocytopenia that resolved by 10 days after presentation. New or unique information provided: HD/HP shortened the baclofen serum elimination half‐life from 5 to 1.5 hours in the initial 2 hours of treatment. The intrinsic elimination rate constant (K_intr) for this dog was 0.138/hour and the total elimination rate constant (K_tot) during the first 2 hours of HD/HP treatment was 0.458/hour. In this dog, HD/HP was an effective method for rapidly decreasing serum baclofen concentration after an acute overdose.     

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.     

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.     

Successful treatment of severe salt intoxication in a dog

Objective: To report successful treatment of severe salt intoxication and hypernatremia in a dog. Case summary: A 5‐year‐old intact female Doberman Pinscher was admitted to the intensive care unit with a history of seizures and coma. The owner had administered approximately 100 g of cooking salt to induce vomiting following ingestion of a nontoxic dose (10 g) of chocolate. Upon admission, the dog was comatose with intermittent seizures and vomiting. Diagnostic tests confirmed salt intoxication (Na: 200 mEq/L, Cl: 180 mEq/L) and metabolic acidosis (pH: 7.18; pCO₂: 39 mmHg; HCO₃: 14.3 mmol/L). Immediate treatment included intravenous fluid therapy, an anticonvulsant, antiemetic, diuretic, low molecular weight heparin, and supplemental oxygen. A fluid therapy protocol was initiated to decrease serum sodium concentration by approximately 2 mEq/L/hr. After 24 hours of intensive care, the patient regained consciousness and volume and acid‐base abnormalities improved. The patient developed a variety of abnormal clinical signs as a result of the severe hypernatremia. After 5 days of treatment, the serum sodium concentration returned to the established reference range. The patient recovered completely in 10 days. New information provided: Severe hypernatremia due to salt ingestion is a rare condition in dogs. All dogs in previous case reports of salt intoxication have died. This case report is the first to report survival of a dog with severe salt intoxication.     

Treatment of a dog with severe baclofen intoxication using hemodialysis and mechanical ventilation

Objective: This case report describes the successful management of a dog with coma and respiratory depression due to severe baclofen intoxication. Case summary: A Doberman Pinscher mixed breed dog ingested 500 mg (20 mg/kg) of baclofen. Signs of severe intoxication included coma and profound respiratory muscle weakness. The dog was supported with positive pressure ventilation and treated with one session of hemodialysis. Weaning from the ventilator was achieved within 4 hours of hemodialysis, and recovery from coma occurred over the following 12–36 hours. The dog regained full neurologic function and was normal at discharge following 3 days of hospitalization. New or unique information provide: Severe central nervous system depression and respiratory depression due to baclofen intoxication can be life threatening. In addition to other supportive care, hemodialysis may hasten recovery and ventilatory support may be essential to achieve a positive outcome. With successful treatment, toxicity can be decreased and the associated life‐threatening central nervous system and ventilatory depression can resolve. Prognosis for return of normal function is excellent.     

Anaphylaxis and systemic inflammatory response syndrome induced by inadvertent intravenous administration of mare's milk in a neonatal foal

Objective – To describe the diagnostic procedures, therapeutic management and successful outcome of a case of anaphylaxis induced by the inadvertent intravenous (IV) administration of mare's milk to a neonatal foal. Case Summary – A 3‐day‐old Thoroughbred colt was presented for treatment of bilateral flexural limb deformities of the forelimbs. Because the foal was unable to ambulate initially, mare's milk was administered via nasoesophageal tube feedings during treatment of the musculoskeletal disorder. Anaphylaxis resulted after unintentional administration of a bolus of 150 mL of mare's milk through a jugular catheter. Aggressive therapy for anaphylaxis and careful monitoring resulted in the successful recovery of the foal after 9 days of intensive care. New or Unique Information Provided – This case is the first published report to describe the effects of accidental IV administration of mare's milk to a neonatal foal. Medical errors are commonly reported in pediatric medicine; the intent of this report is to raise awareness of medical errors and student education in equine medicine as well as describe the therapy and outcome of anaphylaxis induced by IV administration of mare's milk in a neonatal foal.     

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.     

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.     

Canine leishmaniasis with nephrotic syndrome and aortic and caudal vena cava thromboembolism

Objective – To describe a case of leishmaniasis associated with nephrotic syndrome and aortic and caudal vena cava thrombosis in a dog. Case Summary – A 3‐year‐old male Boxer was referred to the Faculty of Veterinary Medicine, Lisbon, with vomiting, polyuria, polydipsia, lethargy, anorexia, and weight loss. On admission, the dog was thin, quiet, and dehydrated. Initial laboratory abnormalities were compatible with a diagnosis of leishmaniasis (confirmed by serology and bone marrow aspirate), and nephrotic syndrome. Three days later, the animal developed lumbar pain, paraparesis, and absent femoral pulses. Coagulation tests showed a marked reduction in antithrombin (AT) and a mild increase in serum fibrinogen concentration. A diagnosis of thromboembolism was made. In spite of treatment aimed at controlling the primary condition and decreasing further thrombus formation, necrosis developed in the distal right pelvic limb and the nail beds of the left pelvic limb. Against medical advice, medication was stopped and, 15 days later, the dog returned to the hospital, showing extensive necrosis of both pelvic limb extremities. Euthanasia was performed at the owner's request. Necropsy showed a thrombus localized at the distal aorta and extending into the right iliac artery, and an additional thrombus extending from both femoral veins onto the caudal vena cava. New or Unique Information Provided – Thromboembolic disease is rare in dogs with leishmaniasis with nephrotic syndrome. This case suggests that a marked decrease in AT and a mild increase in serum fibrinogen may elicit a hypercoagulable state in these patients.     

Bilateral hydronephrosis secondary to anticoagulant rodenticide intoxication in a dog

Objective: To describe an unusual site of hemorrhage in a case of anticoagulant rodenticide toxicity. Case summary: A dog treated for Brodifacoum anticoagulant rodenticide intoxication was referred for treatment of thrombocytopenia and dysuria. Sonographic examination revealed a large blood clot within the urinary bladder, extending proximally along both ureters, and a bilateral hydronephrosis. In this dog, management of the vitamin K₁‐dependent coagulopathy was unusually complicated by uremia and thrombocytopenia. New information provided: This is the first reported case of hydronephrosis secondary to anticoagulant rodenticide intoxication in a dog.     

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.     

Surgical management of a traumatic dislocation of the sternum in an English bulldog

A nine‐year‐old English bulldog presented with an acute history of dyspnoea, tachycardia and discomfort localising to the ventral thorax following a fall down the stairs that morning. After the dog was stabilised, thoracic radiographs revealed a luxation of the third and fourth sternebrae with dorsal displacement of the caudal segment. The sternum was reduced and stabilised with a contoured 12‐hole 3 · 5‐mm dynamic compression plate applied to the ventral surface of the sternum. The dog's initial recovery was rapid, cardiorespiratory parameters returning to normal in the first 24 hours. For 2 weeks postoperatively the dog exhibited difficulty in rising from a prone position. After this time there was a full recovery. Clinical examination at 8 months postoperatively did not reveal any abnormalities. Telephone follow‐up was performed at 18 months and no complications or cardiorespiratory compromise were reported. To the authors’ knowledge, this is the first reported case of a traumatic dislocation of the sternum and its management in the dog.     

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.     

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.     

Suspected lily-of-the-valley (Convallaria majalis) toxicosis in a dog

Objective: To describe successful treatment of third-degree atrioventricular (AV) block using temporary noninvasive transthoracic pacing and placement of a permanent transvenous pacemaker in a case of suspected lily-of-the-valley ( Convallaria majalis ) intoxication in a dog.
Case summary: A 2-year-old neutered male Beagle weighing 17.8 kg was presented to the emergency service for treatment of bradycardia, vomiting, and lethargy. An electrocardiogram revealed third-degree AV block that was nonresponsive to atropine. Ten hours after admission, the dog became obtunded. Treatment initially consisted of temporary noninvasive transthoracic pacing and eventually placement of a permanent transvenous pacemaker. The initial history did not suggest that the dog had access to any known cardiotoxins. However, C. majalis , which contains cardiac glycosides, was identified within the dog's environment and the dog's serum did contain digoxin or an immunologically cross-reactive compound.
New or unique information provided: This is the first reported successful management of C. majalis toxicosis in a dog. Temporary noninvasive transthoracic pacing was used in the management of this case as a safe and effective bridge to permanent pacemaker implantation.     

Acute polyneuromyopathy with respiratory failure secondary to monensin intoxication in a dog

Objective

To describe a successfully managed case of polyneuropathy and respiratory failure secondary to presumed monensin intoxication.

Case Summary

A 9‐month‐old Australian Shepherd was evaluated for progressive generalized weakness and respiratory distress. Several days preceding presentation, the dog was seen playing with a monensin capsule, and had free access to a barn where the product was stored and where chewed capsules were subsequently found. The dog was presented with flaccid tetraparesis, hyperthermia, and severe respiratory distress. Bloodwork and urinalysis revealed marked increase in serum creatine kinase concentration and presumed myoglobinuria. Cardiac troponin I level was markedly increased. Management included mechanical ventilation for 5 days, fluid‐therapy, active cooling, antimicrobial therapy, analgesia, gastroprotectants, antiemetics, enteral feedings, continuous nursing care, and physiotherapy. Intravenous lipid rescue therapy was administered with lack of improvement in respiratory function and muscle strength. The patient completely recovered and was discharged after 12 days of hospitalization.

New or Unique Information Provided

Monensin intoxication should be considered in the differential diagnosis of acute polyneuromyopathy and respiratory failure in dogs with access to this compound. Respiratory failure secondary to monensin intoxication does not necessarily carry a poor prognosis if mechanical ventilation can be provided as a bridge until return of respiratory function is achieved.     

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.     

Trauma‐associated acute mesenteric ischemia in a dog

Objective – To describe the successful management of acute mesenteric ischemia (AMI) in a dog. Case Summary – An 11‐year‐old, 21.4 kg, male castrated Rough‐Coated Collie was referred for evaluation of an acute abdomen following sustaining injuries in a vehicular accident. On presentation to the hospital, clinicopathologic assessments were within normal limits and distended intestinal loops were evident on abdominal palpation. Plain and contrast radiography demonstrated diffusely distended gas‐filled intestinal loops with a delayed barium transit time. Emergency surgical exploration was performed. The cecum and the proximal two‐thirds of the colon were dark purple to black in color and there were no palpable pulses in the mesenteric arteries associated with the cecum and colon. The cecum and proximal two‐thirds of the colon were resected and an ileocolic anastomosis was performed. The dog recovered well from surgery and was discharged 2 days later. Histopathologic examination was consistent with AMI. New or Unique Information Provided – AMI is uncommonly reported in human medicine and is a rare complication from even minor blunt abdominal trauma. This is the first reported case of trauma‐associated AMI in a dog.     

Full recovery after cardiac arrest secondary to accidental iatrogenic venous air embolism in a cat

Objective – To describe the successful management of cardiac arrest following accidental venous air embolism (VAE) in a cat. Case Summary – A 3‐year‐old spayed female domestic shorthair cat, weighing 4 kg, was presented for continuation of its chemotherapy protocol. The cat was inadvertently administered approximately 5.5 mL of air IV during initiation of fluid therapy. Immediate cardiac arrest resulted and CPR successfully achieved return of spontaneous circulation. The cat was discharged 5 days later and is reportedly clinically normal 7 months post‐discharge. New or Unique Information Provided – VAE has been rarely reported in the veterinary literature. This is the first report of a cat surviving cardiac arrest secondary to VAE.     

Oral pentobarbital intoxication in a bitch

Pentobarbital intoxication in a 5-year-old female Samoyed was confirmed by the finding of a high concentration of the drug in serum. The dog apparently had consumed one of her pups, which had been euthanatized the day before with a 26% sodium pentobarbital solution. She was admitted in a condition consistent with light general anesthesia. The dog recovered after gastric lavage supportive therapy, and the administration of an alkalinizing solution to hasten drug excretion. This case demonstrates the hazards associated with indiscriminate disposal of carcasses containing large amounts of euthanasia solution.