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.

Retrospective Evaluation of Clinical Bleeding in Dogs With Anticoagulant Rodenticide Toxicity-A Multi-Center Evaluation of 62 Cases (2010-2020).

Objective: To evaluate the most common locations of hemorrhage in dogs diagnosed with anticoagulant rodenticide intoxication. Animals: Dogs presenting with hemorrhage secondary to anticoagulant rodenticide intoxication between at two university veterinary teaching hospitals. Procedures: Medical records were searched from the years 2010 through 2020 and all records from dogs treated for hemorrhage secondary to anticoagulant rodenticide intoxication were reviewed. Dogs were diagnosed with anticoagulant rodenticide intoxication based on the combination of known exposure and prolonged coagulation testing, including prothrombin and activated thromboplastin time, or based on gas chromatography-mass spectrometry (GCMS). The diagnosis of hemorrhage was made based on physical exam findings, point-of-care ultrasound findings or radiography. Results: Sixty-two dogs met the inclusion criteria and were included in the study. The most common sites of hemorrhage included: pleural space (hemothorax 37%), pulmonary parenchyma (24%), abdomen (24%), skin/subcutaneous (21%), gastrointestinal tract (18%), pericardium (13%), oral cavity (13%), nasal cavity (11%), ocular (8%), and urinary tract (7%). Overall, forty-five dogs (73%) had evidence of cutaneous or mucosal hemorrhage while thirty-three (53%) of dogs had evidence of cavitary hemorrhage. Forty-five percent of dogs had hemorrhage noted at only one site, while 55% experienced hemorrhage at more than one site. The location of hemorrhage and total number of hemorrhagic sites was not associated with survival or transfusion requirement. Conclusions and Clinical Relevance: In conclusion, this study highlights that dogs with anticoagulant rodenticide intoxication present with diverse locations of hemorrhage and the majority of dogs had non-cavitary hemorrhage noted.

Suspected benzodiazepine withdrawal-associated seizures in 3 young dogs undergoing mechanical ventilation.

OBJECTIVE: To describe new onset of generalized seizures in 3 young dogs following cessation of a benzodiazepine-containing sedation protocol to facilitate mechanical ventilation (MV) for hypoxemia. SERIES SUMMARY: Three dogs under 5 months of age underwent MV due to severe hypoxemia. All 3 dogs were sedated with a constant rate infusion of benzodiazepines as part of their sedation protocol to facilitate MV. All 3 dogs had an acute onset of generalized seizures within 36 hours of sedation cessation and weaning from MV. All 3 dogs' seizures were successfully managed with a slow, tapering course of benzodiazepines. One dog was additionally treated with levetiracetam at the time of initial seizure activity, which was discontinued 1 year following discharge and absence of ongoing seizure activity. All 3 dogs were discharged successfully with no reports of ongoing seizures or neurologic deficits after discharge. NEW OR UNIQUE INFORMATION PROVIDED: Young dogs managed with benzodiazepines to facilitate MV may have acute onset of generalized seizures following cessation, which can be successfully managed with short-term benzodiazepine therapy. The 3 cases in this series demonstrated a positive outcome and were successfully managed following acute onset of generalized seizure activity post-MV.

Pathology in Practice.

In collaboration with the American College of Veterinary Pathologists.