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1.
Objective: To describe the clinical course of a dog presented with peliosis hepatis and hemoperitoneum in concert with anticoagulant rodenticide intoxication.
Case summary: A 7.75-year-old spayed female Shetland Sheepdog presented with clinical signs consistent with hypovolemia, hemoperitoneum, and a history of bright green stool 3 days before the onset of clinical signs. Initial packed cell volume/total solids were consistent with acute hemorrhage. A coagulation profile showed prolongation in activated clotting time and prolongation of both prothrombin and activated partial thromboplastin time, suggesting abnormal coagulation. Abdominal hemorrhage persisted in the face of normalization of the hemodynamic status and coagulation profile, and treatment with Vitamin K1. Abdominal ultrasound revealed multiple patchy hypoechoic areas throughout the caudate liver lobe. An exploratory laparotomy was performed 24 hours after presentation and revealed the caudate liver lobe as the source of the hemorrhage. Histopathologic examination of a specimen of the liver was consistent with peliosis hepatis. Toxicologic testing identified diphacinone levels in the blood consistent with anticoagulant rodenticide intoxication. Postoperative recovery was uneventful, and within 48 hours the dog was discharged. The dog returned to full function and a hepatic ultrasound performed 15 months postoperatively showed no significant abnormalities.
New or unique information provided: Exposure to anticoagulant rodenticides may be associated with the development of peliosis hepatis in dogs.  相似文献   

2.
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.  相似文献   

3.
In the veterinary literature, it has been suggested that a prolongation in the thrombotest (PIVKA test) is a sensitive and diagnostic indicator of anticoagulant rodenticide intoxication. We evaluated prothrombin time (PT), activated partial thromoplastin time (aPTT), and PIVKA indicator in 25 bleeding dogs: 7 with inherited coagulopathies. All dos with acquired coagulopathies had prolonged PIVKA values when compared to the normal controls. Factor VII deficient dogs had a prolonged PIVKA and PT test result, whereas dogs with intrinsic coagulopathies only had an aPTT prolongation. A three-fold increase of the PIVKA or PT values was highly suggestive of an anticoagulant rodenticide poisoning compared to other acquired coagulopathies. Prolonged PIVKA resuls were not specific for anticoagulant rodenticide intoxication in our group of bleeding dogs.  相似文献   

4.
An adult female neutered crossbred dog was referred in respiratory distress. Thoracic radiographs revealed tracheal narrowing with a soft tissue opacity dorsal to the trachea, near the thoracic inlet, and a patchy interstitial pulmonary infiltrate. The tracheal narrowing was thought to be due to a combination of intraluminal haemorrhage and mediastinal haemorrhage resulting from a coagulopathy caused by anticoagulant rodenticide intoxication. Treatment included supportive care and administration of vitamin K1, and the dog showed a complete resolution of the clinical signs.  相似文献   

5.
Four dogs with anticoagulant rodenticide toxicosis were treated with intravenous vitamin K1 in lieu of plasma transfusion due to client cost constraints. Two dogs experienced a suspected anaphylactoid reaction, necessitating cessation of the treatment in one dog. Prothrombin time was rechecked 1 h after treatment in the remaining three dogs and all results were within the normal reference range. All four dogs were discharged from hospital within 48 h of presentation. Intravenous vitamin K1 rapidly reverses the coagulopathic state in dogs with anticoagulant rodenticide toxicosis. It is a viable alternative therapy to plasma transfusion if circumstances preclude its use; however, patients must be monitored for anaphylactoid reactions.  相似文献   

6.
Objective: To report a complex presentation of an acquired and hereditary coagulopathy in a dog. Case summary: A 5‐year‐old spayed female Beagle presented for lethargy, anorexia, cough, and stiff gait, and was diagnosed with a spontaneous hemothorax. The patient recovered from this bleeding episode suspected to be secondary to anticoagulant rodenticide intoxication, but was subsequently diagnosed with factor VII (FVII) deficiency, a hereditary coagulopathy. Diagnostic approach and management of FVII deficiency is described. New or unique information provided: This paper describes an unusual presentation of an inherited hemostatic disorder. Utilization of available screening and diagnostic tools, and appropriate interpretation of test results facilitate identification and management of this inherited coagulopathy.  相似文献   

7.
The first aim of the study was to investigate the pharmacokinetics of eight anticoagulant rodenticides (brodifacoum, bromadiolone, chlorophacinone, coumatetralyl, difenacoum, difethialone, flocoumafen and warfarin) in plasma and liver of the mouse after single oral administration. Eight groups of mice dosed orally with a different anticoagulant rodenticide in a dose equal to one‐half the lethal dose 50 (LD50), were killed at various times up to 21 days after administration. The eight anticoagulant rodenticides were assayed in plasma and liver by an LC‐ESI‐MS/MS method. Depending on the compound, the limit of quantification was set at 1 or 5 ng/mL in plasma. In liver, the limit of quantification was set at 250 ng/g for coumatetralyl and warfarin and at 100 ng/g for the other compounds. The elimination half‐lives in plasma for first‐generation rodenticides were shorter than those for second‐generation rodenticides. Coumatetralyl, a first‐generation product, had a plasma elimination half‐life of 0.52 days. Brodifacoum, a second‐generation product, showed a plasma elimination half‐life of 91.7 days. The elimination half‐lives in liver varied from 15.8 days for coumatetralyl to 307.4 days for brodifacoum. The second aim of the study was to illustrate the applicability of the developed method in a clinical case of a dog suspected of rodenticide poisoning.  相似文献   

8.
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 (Kintr) for this dog was 0.138/hour and the total elimination rate constant (Ktot) 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.  相似文献   

9.
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.  相似文献   

10.
A dog being treated for demodicosis with ivermectin was presented for intermittent vomiting. The vomiting progressed to hematemesis and an underlying coagulopathy was diagnosed. The etiology of the coagulopathy was determined to be ingested brodifacoum. Ultrasound evaluation of the abdomen revealed thickened gastric wall that was suspected to be intramural hemorrhage. Most likely, the intramural hemorrhage and resulting thickening of the stomach wall led to the clinical signs and metabolic alkalosis. This case represents an typical presentation of hemorrhage secondary to rodenticide intoxication. (J Vet Emerg Crit Care 2001; 11(1):27–31, 2001).  相似文献   

11.
Lupus-Type "Anticoagulant" in a Dog With Hemolysis and Thrombosis   总被引：1，自引：1，他引：0  
A circulating anticoagulant was detected in a 2-year-old Chesapeake Bay Retriever with hemolytic anemia, nephrotic syndrome, thrombocytopenia, polyarthropathy, and pulmonary thromboembolism. A persistent prolongation of the activated partial thromboplastin time (aPTT) was detected, and it did not correct with repeated administration of fresh frozen plasma. The aPTT was still prolonged, with a 1:1 mixture of patient's plasma and normal dog plasma in vitro, suggesting the presence of a circulating inhibitor. Results of assays to characterize the inhibitor were compatible with those described for the lupus anticoagulant in human patients with systemic lupus erythematosus. Paradoxically, patients having the lupus anticoagulant are at increased risk for thrombosis. Pulmonary thromboembolism has been described as a frequent complication of immune-mediated hemolytic anemia in the dog, and the presence of a circulating anticoagulant should be considered as a potential mechanism.  相似文献   

12.
Eight out of a litter of 13 puppies were either born dead or died within 48 hours of birth. Three puppies that died shortly after birth were necropsied. Two puppies had hemorrhage in the thoracic and peritoneal cavities, intestinal serosa, and meninges. The third puppy was smaller than the other two puppies but did not have detectable hemorrhage. Brodifacoum, a second-generation coumarin anticoagulant, was detected in livers from the two puppies with hemorrhage. The dam did not have clinical signs of coagulopathy before or subsequent to whelping. The owners were confident that the dog had not been exposed to rodenticide for at least 4 weeks before whelping. A presumptive diagnosis of in utero brodifacoum toxicity was made. To the authors' knowledge this is the first time a second-generation coumarin anticoagulant has been detected in the liver of a newborn animal. This case is also unique because the dam was unaffected, suggesting that fetuses are more susceptible to brodifacoum toxicity than adult animals.  相似文献   

13.
A nine-year-old Labrador retriever dog was admitted to the emergency unit of the Hebrew University Veterinary Teaching Hospital with acute-onset tremors and coma. It had recently ingested a large quantity of phenobarbital and had a high serum phenobarbital concentration. On this basis, a diagnosis of acute phenobarbital intoxication was made. Significant leucopenia, thrombocytopenia and mild anaemia developed on the third day after admission. The leucopenia resolved on day 6 and the thrombocytopenia on day 13. The red blood cell count remained low for the next month. The dog was discharged on day 13 at which time it was ambulatory but weak. It was completely recovered clinically eight days later. In summary, high levels of serum phenobarbital as a result of acute intoxication induced pancytopenia, which improved when the serum phenobarbital level was normalised.  相似文献   

14.
OBJECTIVE: To assess the rate and extent of ruminal degradation of warfarin, chlorophacinone, and bromadiolone in vitro and determine the oral availability and clinical and hemostatic effects of each anticoagulant rodenticide in adult sheep. ANIMALS: 3 Texel sheep. PROCEDURE: Samples of ruminal fluid were incubated with each of the anticoagulants to assess the kinetics of ruminal degradation over 24 hours. To determine the plasma kinetics of the anticoagulants, each sheep received each of the anticoagulants IV or via a rumenimplanted cannula at 2-month intervals (3 rodenticide exposures/sheep). At intervals during a 240- to 360- hour period after treatment, prothrombin time (PT) was measured, plasma anticoagulant concentration was assessed, and clinical signs of rodenticide poisoning were monitored. In plasma and rumen extracts, anticoagulant concentrations were determined via high-performance liquid chromatography. RESULTS: In the rumen extracts, anticoagulants were slightly degraded (< 15%) over 24 hours. In vivo, oral availability of warfarin, chlorophacinone, and bromadiolone was estimated at 79%, 92%, and 88%, respectively. Although maximum PT was 80 seconds after chlorophacinone and bromadiolone treatments, no clinical signs of toxicosis were detected; PT returned to baseline values within 2 weeks. CONCLUSIONS AND CLINICAL RELEVANCE: In sheep, warfarin, chlorophacinone, and bromadiolone were not degraded in the rumen but their bioavailabilities were high after oral administration; the kinetics of these compounds in sheep and other mammals are quite similar. These data suggest that the lack of susceptibility of ruminants to these anticoagulant rodenticides cannot be explained by either ruminal degradation or the specific toxicokinetics of these anticoagulants.  相似文献   

15.
Objective – To describe the successful treatment of accidental ethanol intoxication with hemodialysis in a dog. Case Summary – A 1.5‐year‐old female intact mixed breed dog was presented in a comatose state believed to be due to ethanol intoxication. The initial 9 hours of supportive care treatment were complicated by multiple seizures and hypothermia, and resulted in only minimal improvement in the dog's level of consciousness. Hemodialysis was implemented and resulted in rapid clinical recovery, corresponding to a rapid decline in serum ethanol concentration. New or Unique Information Provided – To the authors' knowledge, this is the first reported case of using hemodialysis to treat accidental ethanol intoxication in a dog. The patient's initial serum ethanol concentration was higher than those previously reported for cases of accidental ethanol intoxication in dogs, and the serum ethanol concentration was shown to rapidly decline during hemodialysis. Treatment with hemodialysis for severe ethanol intoxication was effective in this case and may be able to decrease morbidity and mortality in some cases.  相似文献   

16.
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.  相似文献   

17.
Objective: To determine the effect of gastrointestinal (GI) decontamination on the incidence of prolonged prothrombin time (PT) in dogs after anticoagulant rodenticide ingestion. Design: Retrospective study. Setting: Urban emergency room. Animals: One hundred and fifty‐one client‐owned dogs. Measurements: Dogs presented to the emergency room within 6 hours of ingestion of an anticoagulant rodenticide and had a PT measured within 2–6 days of toxicant ingestion before initiating vitamin K therapy were included. Dogs were categorized as treated or untreated based on the institution of vitamin K therapy following PT testing. The signalment, body weight, type of rodenticide ingested, time elapsed between ingestion and initial presentation, method(s) of GI decontamination, and the times elapsed between both toxicant ingestion and initial hospital presentation until determination of PT were recorded. The PT results were recorded as well as any treatment received following the recheck examination. Any reported incidents of bleeding or untoward effects between exposure and reexamination were recorded. Main results: Of 151 dogs, only 11 dogs (8.3%) developed prolonged PT requiring vitamin K supplementation. None of the 11 dogs with prolonged PTs exhibited signs of bleeding or required transfusion therapy. No differences in age, weight, or time elapsed between treated and untreated patients were found. Conclusions: The incidence of prolonged PT is low in dogs receiving GI decontamination within 6 hours of anticoagulant rodenticide ingestion. Delaying vitamin K therapy until a PT has been assessed 48–72 hours after initial exposure appears to be safe and sensitive in dogs following anticoagulant rodenticide ingestion.  相似文献   

18.
Bromadiolone is an anticoagulant rodenticide that inhibits the reactivation of vitamin K1 by the enzyme vitamin K1-epoxide reductase. The present case report originated from the application of bromadiolone against water voles (Arvicola terrestris) in northeastern Switzerland. At least 40 foxes (Vulpes vulpes) were found dead after the inappropriate use of a bait that contained 0.02 % bromadiolone. Anticoagulant rodenticide poisoning was suspected on the basis of the postmortem examination and subsequently confirmed by the detection ofbromadiolone both in the blood and in samples from thoracic and abdominal fluids.  相似文献   

19.
A case of brodifacoum poisoning is described in a six-year-old male Kelpie cross working dog. The clinical features were severe exercise intolerance, haemorrhage from the oral and nasal cavities, dyspnoea and pale mucous membranes. Diagnosis was confirmed by demonstrating an abnormally long whole blood clotting time. The dog was treated successfully by administering 1 litre of whole blood intravenously, intramuscular vitamin K1 and a three week course of oral vitamin K3.

Experience at the Massey University Small Animal Clinic and Hospital has indicated that poisoning of dogs with the newer long acting anticoagulant rodenticides is becoming more common.  相似文献   

20.
A juvenile, neutered male, Labrador retriever-poodle crossbred dog was brought to a veterinary hospital for overnight care after ingesting fluorouracil 5.0% (5-FU) topical solution. The exposure occurred the night before and involved an unknown amount of fluorouracil. The dog survived the acute toxicity but developed status epilepticus requiring control with general anesthesia and spent multiple days hospitalized in a comatose state, eventually waking with sensory deficits in both vision and smell which resolved over time. Blood samples taken at a recheck visit 1 week after ingestion, showed the dog had developed severe thrombocytopenia and moderate leukopenia. Ten days after initial intoxication, the dog developed progressive alopecia which eventually affected the entire body.  相似文献   

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