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.     

Stereotactic body radiation therapy for heart-base tumors in six dogs

Introduction

Heart-base tumors are increasingly treated with radiotherapy, yet safety and efficacy are incompletely understood. This case series describes outcomes after stereotactic body radiation therapy (SBRT) for presumed chemodectoma.

Successful management of saltwater submersion injury in a dog using mechanical ventilation

Objective– To describe successful management of saltwater near-drowning in a dog using mechanical ventilation. Case Summary– A 7-year-old spayed female Golden Retriever weighing 37 kg was referred for mechanical ventilation after saltwater submersion injury. The dog had a history of rare seizures characterized by pre-ictal agitation. On the morning of the event, the dog became agitated and ran toward Puget Sound. The owners discovered the dog unconscious in approximately 25.4 cm (10 in) of water, with her head submerged. The owners estimated that the dog was submerged for approximately 30 seconds. The dog was presented immediately to the nearest emergency facility where initial diagnostic testing and treatment included venous blood gases, nasal oxygen, and IV fluids. The dog was dyspneic despite nasal oxygen administration and was referred for mechanical ventilation. Upon arrival the patient was cyanotic with an arterial partial pressure of oxygen of 38 mm Hg (reference interval 85–100 mm Hg) and oxygenation saturation of 62% (reference interval >95%). Thoracic radiographs were taken and revealed severe, bilateral pulmonary infiltrates. The patient was ventilated for 70 hours and was discharged 4 days later. Complications included pneumonia and phlebitis at the site of a cephalic IV catheter. Follow up thoracic radiographs 10 days after discharge were within normal limits and the owners report a full recovery at 1 year. New or Unique Information Provided– Submersion injury can result in acute respiratory distress syndrome in dogs. Mechanical ventilation provided critical support during pulmonary recovery in this dog.     

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.     

Refractory shock,hypercoagulability, and multiorgan thrombosis associated with hypertrophic osteodystrophy in a dog

Objective

To describe the clinical findings and case progression in a dog presenting with severe systemic inflammatory response, refractory shock, progressive metabolic acidosis, and respiratory failure that was ultimately diagnosed with hypertrophic osteodystrophy (HOD).

Case Summary

A 4-month-old male intact Mastiff presented with a 24-hour history of lethargy and generalized ostealgia. On examination, the dog was recumbent, febrile, and tachycardic with pain on palpation of the abdomen, right femur, and mandible. Appendicular joint radiographs showed changes consistent with osteochondrosis and ulnar-retained cartilaginous cores, with no overt evidence of HOD. Initial treatment included IV fluid therapy, multimodal analgesia, and broad-spectrum antimicrobials. Vasopressor therapy was initiated following hemodynamic decompensation. Synovial fluid cytological analysis and culture revealed nonseptic suppurative inflammation and no bacterial growth, respectively. Blood and urine cultures also yielded no growth. Viscoelastic testing was consistent with hypercoagulability. The dog initially had a metabolic acidosis with appropriate respiratory compensation that progressed to a mixed metabolic and respiratory acidosis despite aggressive therapies that included antimicrobials, vasopressors, positive inotropes, and corticosteroids. Humane euthanasia was elected approximately 32 hours after admission. Necropsy yielded a diagnosis of HOD.

New or Unique Information Provided

This is the first report detailing the occurrence of refractory shock and hypercoagulability associated with HOD in a dog without evidence of another identified comorbidity. HOD should be considered in any young, large-breed dog with generalized ostealgia and signs of systemic illness, even in the absence of classic radiographic abnormalities. Further investigation of coagulation status in dogs with HOD and a secondary systemic inflammatory response is warranted.     

A case of type B botulism in a pregnant bitch

A two‐year‐old pregnant Gordon setter presented with acute onset of flaccid tetraparesis and respiratory distress. Neurological examination revealed diffuse lower motor neuron dysfunction. Clostridium botulinum neurotoxin B was isolated from the dog's serum. The dog was hospitalised and received supportive care; respiratory function was monitored but positive‐pressure ventilation was not required. Recovery was complete within 1 month and parturition occurred without complication 49 days after admission. The puppies delivered lacked any obvious congenital defects and development during the first few months of life was normal. The source of contamination was suspected to be poorly conserved dry food. To the authors’ knowledge, this is the first report of C. botulinum neurotoxin B isolation in a dog and the first report of botulism in a pregnant bitch.     

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.     

Conventional versus high-flow oxygen therapy in dogs with lower airway injury

Dogs with lower airway pathology that present in respiratory distress often receive oxygen therapy as the first line of treatment regardless of the underlying cause. Conventional “low-flow” systems deliver oxygen with a maximum flow rate of 15 L/minute. Traditionally, when an animal’s respiratory status does not improve with conventional oxygen therapy and treatments for underlying disease, options might be limited to either intubation and mechanical ventilation or humane euthanasia. High-flow oxygen therapy (HFOT) has been gaining popularity in veterinary medicine as an alternative route of oxygen supplementation for animals that require support beyond conventional therapy. High-flow oxygen therapy can supply a mixture of air and oxygen via a heated and humidified circuit. It is user friendly and can be used in an environment in which mechanical ventilation is unavailable.This review article is written for emergency doctors and general practitioners who lack access to mechanical ventilation. This article briefly reviews pertinent respiratory physiology, traditional oxygen supplementation techniques, the physiology of HFOT, and the limited evidence available in veterinary medicine regarding the use of HFOT, its applications, and limitations. Guidelines for the use of HFOT are suggested and HFOT is compared to conventional therapy.     

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.     

Mechanical ventilation in foals with botulism: 9 cases (1989-2002)

"Shaker foal" disease, toxicoinfectious botulism of foals, was 1st described as a clinical entity in 1967. The reported mortality rate was 90%, with death occurring within 24-72 hours of the onset of the characteristic clinical signs. The mortality rate decreased when equine-origin botulism antitoxin became available; however, a certain percentage of foals continued to die of respiratory failure. Mechanical ventilation is an important part of the treatment of infant botulism and is essential to the survival of many affected infants. We report a retrospective study of 9 foals with toxicoinfectious botulism where early mechanical ventilation was employed as part of the treatment. Foals receiving mechanical ventilation were progressively acidemic and had increased PaCO2 tensions before mechanical ventilation. These arterial blood gas abnormalities were ameliorated with mechanical ventilation. One foal was euthanized for economic reasons; survival in treated foals was 87.5%. Mechanical ventilation of foals with botulism and respiratory failure appears to be an effective therapy.     

Successful ventilatory management of post‐anesthetic airway collapse and hypoxemia in a dog

Abstract Objective: To report a life‐threatening complication (airway collapse) associated with a common procedure (anesthesia) and to describe its successful management. Case Summary: A dog without pre‐existing signs of respiratory disease developed hypoxemia and severe atelectasis in the post‐anesthetic recovery period and was demonstrated, by bronchoscopic examination, to have severe airway collapse. Mechanical ventilation was used to re‐expand collapsed lung units and to prevent re‐collapse. A ventilation strategy designed to minimize airway and alveolar trauma was used. The dog was successfully weaned from the ventilator and made a full recovery. Unique Information Provided: Acute, severe hypoxemia due to airway collapse occurred in the post‐operative period in a dog with no signs of pre‐existing respiratory disease. The dog was successfully managed with short‐term mechanical ventilation. High frequency jet ventilation was used for a diagnostic bronchoscopy.     

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.     

Fatal acute lung injury after balloon valvuloplasty in a dog with pulmonary stenosis

A one-year-old French Bulldog was referred for the management of a severe form of pulmonary valve stenosis (PS) complicated by right-sided congestive heart failure.Echocardiography showed severe valvular PS with right ventricular concentric hypertrophy, dilatation and severe right atrial enlargement. A pulmonary balloon valvuloplasty (PBV) was performed with a balloon-to-pulmonary annulus ratio of 1.36. Echocardiography immediately after PBV showed a significant reduction in right atrial and ventricular size, improved opening and mobility of the pulmonary valve leaflets, and a 75% reduction in the pulmonary pressure gradient from 158 mmHg pre-operative to 40 mmHg post-operative. The dog recovered well from anesthesia, but 2 h later, it suddenly showed severe respiratory distress. Focus cardiac ultrasound showed increased left cardiac size with echocardiographic signs of high left ventricular filling pressure. Bedside lung ultrasound showed diffuse numerous-to-confluent B lines, compatible with a severe alveolar-interstitial syndrome. The dog was treated with furosemide, helmet continuous positive airway pressure, and then mechanical ventilation but without success.At post-mortem evaluation, histological examination of the lung showed diffuse, severe broncho-alveolar edema with mixed leukocyte, fibrin, and red blood cell infiltrate. Moreover, severe congestion and multifocal alveolar hemorrhages were evident. All findings were compatible with fatal acute lung injury after PBV secondary to pulmonary reperfusion-ischemia injury and increased pulmonary capillary hydrostatic pressure. Based on the present case, acute lung injury should be considered as a rare but serious complication of PBV.     

Bronchial stent placement in a dog with bronchomalacia and left atrial enlargement

A 13‐year‐old neutered male Maltese was referred for paroxysms of coughing and cyanosis, with radiographic evidence of bronchial disease and cardiomegaly. Investigation with echocardiography, bronchoscopy, fluoroscopy and bronchoalveolar lavage led to a diagnosis of myxomatous mitral valve degeneration with insufficiency, ISACHC class II heart failure and bronchomalacia with severe left mainstem bronchial collapse. Persistence of intractable cough despite medical therapy prompted placement of a stent in the left mainstem bronchus. Immediately after stent placement, severe pulmonary oedema developed, thought to be due to compression of the left atrium by the stent or acute lung injury related to stent placement. The dog recovered over a 3‐day period with diuretic therapy and positive end expiratory pressure ventilation. Subsequently, the dog died from congestive heart failure 102 days after stent placement, during which time occasional, self limiting coughing episodes occurred .     

Green discolouration of urine following propofol infusion in a dog

A three‐year‐old, female neutered Weimaraner was presented with a history of neck pain and tetraparesis. MRI revealed an extradural mass at the level of C3 vertebra, which was thought to be a spinal abscess, and the dog was scheduled for surgical exploration the following morning. Overnight the dog developed an exaggerated ventilatory pattern, with paradoxical inward movement of the thorax on inspiration. Arterial blood gas analysis revealed respiratory acidosis and ventilator support was initiated to prevent excessive respiratory fatigue. During mechanical ventilation, anaesthesia was maintained using a propofol target‐controlled infusion system and, subsequently, the dog produced bright green urine in the urine collection system. Although previously documented in humans, this appears to be the first report of green urine in a dog following propofol use.     

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.     

Successful therapy of coumatetralyl rodenticide induced pericardial effusion with pericardiocentesis in a dog

A 5-year-old, intact male, golden retriever was presented with an acute onset of lethargy and respiratory distress. The dog was diagnosed as having rodenticide intoxication with pericardial effusion. Pericardiocentesis was successfully performed and was followed with a blood transfusion. This case suggests that rodenticide intoxication might cause pericardial effusion in dogs.     

Successful use of short‐term mechanical ventilation to manage respiratory failure secondary to profound hypokalemia in a cat with hyperaldosteronism

Objective – To report successful management of respiratory failure due to severe hypokalemia in a cat with hyperaldosteronism, including short‐term mechanical ventilation strategies and aspects of medical and surgical treatment. Case Summary – A cat presented with bilateral pelvic limb weakness that rapidly progressed to tetraparesis and respiratory muscle failure. Point‐of‐care testing revealed severe hypokalemia (1.9 mmol/L) and mild azotemia. Initial management included endotracheal intubation, mechanical ventilation, and aggressive potassium supplementation. Spironolactone was started due to a high index of suspicion for hyperaldosteronism. A right adrenal mass visualized during abdominal ultrasonographic examination and a serum aldosterone level greater than 3329 pmol/L confirmed the diagnosis. The cat made a full recovery following surgical removal of a right adrenal adenoma. New or Unique Information Provided – We report successful management of respiratory failure in a cat with hyperaldosteronism using short‐term mechanical ventilation. Respiratory failure due to severe hypokalemia should be considered a complication of hyperaldosteronism in cats and may require mechanical ventilation. However, full recovery is possible.