vitamin-k-1 and diphenadione

To describe the successful case management of an extradural hematoma secondary to anticoagulant rodenticide toxicity causing spinal compression and paraplegia.. 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.. 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.

Topics: Animals; Anticoagulants; Dog Diseases; Dogs; Female; Hematoma; Paraplegia; Rodenticides; Vitamin K 1

Administration of vitamin K1, SC, to anticoagulant-poisoned (diphenadione) dogs provided diagnostic information within 4 hours, when vitamin K1 and its epoxide were measured in canine sera. Twelve dogs (2 groups of 6) were given 2.5 mg of diphenadione/kg of body weight for 3 days. Dogs were treated with vitamin K1, 2.5 (n = 6) or 5 mg/kg/day (n = 6) SC for 21 days, and their responses were compared. Four nonexposed control dogs were given 5 mg of vitamin K1/kg/day. Serum concentration of vitamin K epoxide was significantly (P less than 0.02) higher in diphenadione-exposed dogs than in control dogs 1 to 4 hours after the initial vitamin K1 treatment on day 4. Vitamin K epoxide/vitamin K1 ratios were similarly higher and became more distinct. Cessation of vitamin K1 therapy on day 24 resulted in prolongation of one-stage prothrombin times in diphenadione-exposed dogs, becoming clearly evident on day 27. Serum vitamin K1 concentrations were not detectable on day 27 in diphenadione-exposed dogs, whereas serum vitamin K1 concentrations were readily detectable in control dogs. One-stage prothrombin time changes, during days 24 to 32, indicated 5 mg of vitamin K1/kg provided better protection than did 2.5 mg of vitamin K1/kg. Coagulopathy in the dogs was resolved by day 32.

Topics: Animals; Anticoagulants; Antidotes; Dog Diseases; Dogs; Female; Male; Phenindione; Rodenticides; Vitamin K 1

Vitamin K1 (5 mg/kg of body weight/day divided for several 5-day regimens) was effective in preventing bleeding diathesis in diphacinone-poisoned dogs. Diphacinone, a vitamin K-inhibiting rodenticide, was given 2.5 mg of diphacinone/kg of body weight orally in divided doses 2 times daily for 3 days. One dog was given 5.0 mg of warfarin/kg in 2 divided doses for 3 days. Hemograms and biochemical profiles were performed every other day. A pancreatic exocrine function test was performed before and after administration of diphacinone and warfarin. All dogs were monitored, using routine coagulation screening tests and assays of coagulation factors II, VII, IX, and X. When laboratory results or clinical illness indicated hemorrhage, diphacinone-treated dogs were given 5.0 or 2.5 mg of vitamin K1/kg in divided doses 3 times a day for 5 days. The warfarin-treated dog was given 2.5 mg of vitamin K1/kg of body weight in divided doses 3 times a day for 5 days. Of the diphacinone-treated dogs, 1 dog (given 2.5 mg of vitamin K1/kg) required 3 vitamin K regimens and 2 dogs (given 5.0 mg of vitamin K1/kg) required only 2 vitamin K regimens. The warfarin-treated dog required only 1 vitamin K1 regimen. Bleeding was observed in the diphacinone-treated dogs up to 2 weeks after treatment. The vitamin K-enzyme complex was inhibited in diphacinone-treated dogs for approximately 30 days, as indicated by routine coagulation screening tests and coagulation factor inhibition. Hepatic dysfunction was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Blood Coagulation Factors; Dog Diseases; Dogs; Female; Liver; Male; Pancreas; Phenindione; Rodenticides; Vitamin K; Vitamin K 1; Warfarin

Topics: Acenocoumarol; Anticoagulants; Dicumarol; Drug Therapy; Heparin; Phenindione; Postoperative Complications; Preventive Medicine; Pulmonary Embolism; Thrombophlebitis; Toxicology; Venous Thrombosis; Vitamin K 1; Warfarin