Clinical presentation and short-term outcomes of dogs ≥15 kg with extrahepatic portosystemic shunts.

OBJECTIVE: To describe demographics, clinical presentation, shunt anatomy, clinical progression, and complications in large dogs ≥15 kg with single extrahepatic portosystemic shunts (EHPSS) treated with or without surgery. STUDY DESIGN: Multicenter retrospective (10 university hospitals, one private referral institution). ANIMALS: Dogs ≥15 kg (n = 63). METHODS: Medical records of dogs ≥15 kg diagnosed with EHPSS between January 01, 2005 and December 31, 2020 were reviewed. Dogs had a minimum follow-up of 90 days. Signalment, clinical signs, diagnostics, shunt anatomy, treatment interventions, and perioperative complications were assessed. RESULTS: Median age was 21.9 months (IQR: 9-36.8). The breed most represented was the Golden retriever (17/63 dogs). Portocaval (17/63) and splenocaval (15/63) shunt configurations were most common. Portal vein hypoplasia was noted in 18 imaging reports. Of the surgically treated dogs, 14/45 (35.6%) had short-term complications, and 3/45 (6.7%) had shunt-related deaths. Medical management was discontinued in 15/40 and reduced in 9/40 of surviving dogs who had surgical attenuation. All medically managed, nonattenuated dogs (18/18) were maintained on their original shunt-related medication regimens. CONCLUSIONS: Clinical presentation of dogs ≥15 kg with extrahepatic portosystemic shunts was similar to the more commonly reported small breed dogs. Surgical management of single EHPSS in large dogs ≥15 kg had similar clinical short-term outcomes as small breed dogs. CLINICAL SIGNIFICANCE: Clinicians should be aware that large breed dogs with EHPSS share similar characteristics and clinical outcomes to small breed dogs. The significance of the presence of a hypoplastic portal vein warrants further research. Surgical treatment is a viable option for large breed dogs with EHPSS.

Linear external skeletal fixation applied in minimally invasive fashion for stabilization of nonarticular tibial fractures in dogs and cats.

OBJECTIVE: The objective of this study was to evaluate the use of linear external skeletal fixation (ESF) applied using minimally invasive techniques in dogs and cats. STUDY DESIGN: Retrospective study. ANIMALS: Forty-nine dogs and 6 cats. METHODS: Medical records of cases with nonarticular tibial fractures, repaired using linear ESF at a single academic institution between July 2010 and 2020, were reviewed. All records of cases that had nonarticular tibial fractures repaired using linear ESF were included. Information was collected regarding signalment, surgical procedures performed, perioperative care, radiographic evaluation, and postoperative complications. RESULTS: Intraoperative imaging was used in 40/55 (72%) of cases. Tibal plateau angle (TPA), tibial mechanical medial proximal and distal tibial angles (mMPTA and mMDTA, respectively) were not affected by intraoperative imaging (P = .344, P = .687, P = .418). A total of 22 (40%) complications occurred. Of these, 18 were considered minor and 4 were considered major. Open fractures had more major complications than closed fractures (P = .019). All fractures reached radiographic union of the fracture. The mean ± SD time to external fixator removal was 71 ± 48 days. CONCLUSION: Linear ESF applied using minimally invasive techniques with or without intraoperative imaging was an effective treatment for nonarticular tibial fractures. CLINICAL SIGNIFICANCE: Closed application of linear ESF should be considered as a minimally invasive option for stabilizing nonarticular tibial fractures.

Diagnosis and successful management of an extradural compressive hematoma secondary to diphacinone poisoning in a dog.

OBJECTIVE: To describe the successful case management of an extradural hematoma secondary to anticoagulant rodenticide toxicity causing spinal compression and paraplegia. CASE SUMMARY: A 3-month-old, female intact, mixed breed dog was presented for a 12-hour history of paraplegia. CBC and biochemistry results were unremarkable, and a coagulation panel revealed prolonged prothrombin time with normal activated partial thromboplastin time. Magnetic resonance imaging revealed an extradural compressive lesion within the vertebral canal extending from T6 to T11, most consistent with an extradural hematoma. Further coagulation testing revealed a coagulopathy caused by vitamin K1 deficiency and confirmed exposure to the anticoagulant rodenticide, diphacinone. The dog was medically managed with fresh frozen plasma, aminocaproic acid, and oral vitamin K1 therapy. A right-sided T6 to T11 hemilaminectomy was later performed for removal of the extradural hematoma and spinal decompression. The dog's neurological status gradually improved postoperatively and, at the time of discharge, was nonambulatory paraparetic with voluntary micturition. Four weeks postoperatively, the dog had normal prothrombin and activated partial thromboplastin times and was nonambulatory paraparetic with strong motor function. NEW OR UNIQUE INFORMATION PROVIDED: This is the first reported case of a dog with an extradural hematoma secondary to anticoagulant rodenticide causing spinal cord compression and neurological deficits. Surgical management of this case was successful and resulted in improvement of neurological signs. Extradural hematoma should be considered as a potential location of bleeding in rodenticide toxicity as well as a differential diagnosis in patients with neurological deficits.