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1.
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   

2.
Objective: To describe an unusual site of hemorrhage in a case of anticoagulant rodenticide toxicity. Case summary: A dog treated for Brodifacoum anticoagulant rodenticide intoxication was referred for treatment of thrombocytopenia and dysuria. Sonographic examination revealed a large blood clot within the urinary bladder, extending proximally along both ureters, and a bilateral hydronephrosis. In this dog, management of the vitamin K1‐dependent coagulopathy was unusually complicated by uremia and thrombocytopenia. New information provided: This is the first reported case of hydronephrosis secondary to anticoagulant rodenticide intoxication in a dog.  相似文献   

3.
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   

4.
Specimens from 10 cases of second-generation anticoagulant rodenticide poisoning in dogs and cats were submitted to the Texas Veterinary Medical Diagnostic Laboratory during 1986 and 1987. The clinical signs most frequently observed were lethargy, dyspnea, and ventral hematomas; common necropsy findings included hemoperitoneum, hemothorax, and pulmonary hemorrhage. In the instances when histopathological examination of the tissue was done, it supported a diagnosis of coagulopathy. The presence of anticoagulants in serum or liver was confirmed by high pressure liquid chromatography, gas chromatography/mass spectrometry, or a combination of the two. Five cases of brodifacoum poisoning, 2 of bromadiolone, and 3 of diphacinone toxicity were verified. Concentrations of these rodenticides ranged from approximately 0.001 to 12 ppm.  相似文献   

5.
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   

6.
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   

7.
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   

8.
As a follow-up to an investigation of 2 dogs that died as a result of apparent toxicosis attributable to a cholecalciferol-containing rodenticide, we tested the toxicity of this product in dogs. Two groups of 2 dogs each were fed amounts of rodenticide that provided 20 and 10 mg of cholecalciferol/kg of body weight (approx one fourth and one eighth of the published LD50, respectively). All dogs developed hypercalcemia and hyperphosphatemia and then died. Major lesions were gastrointestinal hemorrhage, myocardial necrosis, and mineralization of vascular walls. Our data indicate that cholecalciferol-containing rodenticides pose a much greater hazard to dogs than was previously believed.  相似文献   

9.
Mortalities among birds of prey from anticoagulant rodenticide (AR) toxicosis have been documented in several countries. Reports on extent of exposure within regions of the United States are limited. This study investigated AR exposure and toxicosis in four species of birds of prey (red-tailed hawks [Buteo jamaicensis], barred owls [Strix varia], eastern screech owls [Megascops asio] and great horned owls [Bubo virginianus]) presented to a wildlife clinic in Massachusetts. The aims of this study are to document the proportion of these four species that died or were euthanized due to their presenting injuries that had detectable amounts of ARs in liver tissue; to identify and quantify ARs present; to describe clinical, postmortem, and histopathologic signs of toxicosis; to evaluate potential sublethal effects of AR exposure; and to associate liver AR level with toxicosis. Birds included in the study were sampled without regard to signs of AR toxicosis. Postmortem examinations were conducted, and liver samples were analyzed for AR residues. Of 161 birds tested, 86% had AR residues in liver tissue. The second-generation AR (SGAR) brodifacoum was identified in 99% of positive birds. Mortality from AR toxicosis was diagnosed in 6% of birds. No indications of sublethal effects of exposure were found, and no association between liver brodifacoum level and signs of toxicosis was apparent. Given the high proportion of birds in this study exposed to ARs, specifically brodifacoum, continued monitoring is warranted as new U.S. Environmental Protection Agency regulations on the sale and use of SGARs are enacted.  相似文献   

10.
The objective of this study was to evaluate both clinical and histologic anomalies associated with suspected benzimidazole toxicosis in rabbits. Histopathologic records were reviewed from rabbit cases that were diagnosed with suspected benzimidazole toxicosis at 2 specialty pathology services. Medical records were also solicited from veterinarians who treated rabbits with suspected benzimidazole toxicosis. In all, 13 cases were included in this retrospective study. Histologically, presumed radiomimetic lesions of benzimidazole toxicosis were noted in 3 cases. An additional 10 cases exhibited lesions suggestive of benzimidazole toxicosis. Common clinical signs observed in the study of rabbits included inappetence, lethargy, hemorrhage, and death. One rabbit with suspected benzimidazole toxicosis survived. Benzimidazoles should be used judiciously in rabbits at published doses only after the owners are knowledgeable of the potential health risks associated with this class of drugs. The prognosis for rabbits with suspected benzimidazole toxicosis is poor, but supportive care resulted in the survival of 1 suspected case in this study.  相似文献   

11.
Toxicosis from pesticides rarely occurs in horses and is usually the result of inappropriate pesticide use or handling by humans. Organophosphorus and carbamate insecticides inhibit acetylcholinesterase and are the insecticide class most frequently associated with toxicosis in domestic animals. Metaldehyde is a molluscicide, and zinc phosphide is a rodenticide, both of which have caused toxicosis in horses. All three of these pesticides affect the nervous system of horses and can be fatal if not treated promptly.  相似文献   

12.
Calcitonin was used in conjunction with saline diuresis, furosemide, and prednisone in treatment of a dog that consumed a rodenticide that contained cholecalciferol and has been touted as safe for nontarget species. This report shows that the rodenticide is toxic to dogs and that salmon calcitonin is a useful treatment for the often refractory hypercalcemia induced by vitamin D toxicosis.  相似文献   

13.
A 4-year-old Holstein cow from a farm where 2 cows had recently died suddenly was referred for evaluation of acute severe colic. Right flank laparotomy revealed a large mesenteric hematoma. Within 14 layer chromatographic analyses of the moldy hay and blood from the necropsied cow and the hospitalized cow were positive for dicumarol. A diagnosis of sweet vernal poisoning was confirmed on the basis of clinical and toxicologic findings. The cow was treated with supportive therapy, blood transfusions, and vitamin K1 and recovered without complications. Because sweet vernal grass is becoming common in certain areas and the use of round bales is commonplace, practitioners should be aware of the potential for this toxicosis.  相似文献   

14.
The ability of lymphocytes isolated from cases of canine thymic lymphomas to activate the alternative complement pathway has been studied. In a series of 14 thymic lymphomas 5 were found to activate the alternative pathway. This ability to activate was not abrograted by trypsinisation of the cells. It was found that normal canine thymic lymphocytes did not activate the alternative pathway.  相似文献   

15.
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   

16.
Thoracic radiographs and clinical records from 14 dogs with confirmed anticoagulant rodenticide toxicity were reviewed. Twelve of the 14 dogs were presented with a chief complaint of respiratory distress, and 12 had elevated prothrombin and activated partial thromboplastin times consistent with a coagulopathy secondary to a clotting factor deficiency. Thoracic radiographs of the 14 dogs were reviewed and abnomalities included increased mediastinal soft tissue opacity with extra and intrathoracic tracheal narrowing (4/14), increased mediastinal soft tissue opacity without tracheal narrowing (8/14), variable degrees of pleural effusion (13/14) and generalized, patchy interstitial/alveolar pulmonary infiltrates (8/14). Radiographic evidence of cardiomegaly and pulmonary artery abnormalities consistent with concurrent heartworm infestation were detected in one dog. In four dogs, dramatic tracheal narrowing was identified on the lateral thoracic radiograph caused by either mediastinal hemorrhage compressing the trachea or submucosal hemorrhage within the tracheal lumen. The trachea was displaced in a ventral direction in two dogs, and extra and intrathoracic luminal diameter narrowing was evident cranially in all four dogs. Two of these four dogs had soft tissue opacity within the dorsal trachea that extended from the larynx to the intrathoracic trachea. Twelve of the 14 dogs survived with standard treatment protocols utilizing injectable and oral vitamin K1. One dog died from pancreatitis and disseminated intravascular coagulopathy. The other dog died soon after presentation due to severe, disseminated hemorrhage. Follow-up thoracic radiographs were made in four dogs that survived and showed resolution of the mediastinal, pleural and pulmonary changes within one to five days after the initiation of vitamin K1 therapy.  相似文献   

17.
This report describes an epizootic of chlorophacinone toxicosis in lambs with severe acute hemorrhages. Eleven lambs, approximately 1-2 months of age, suddenly developed epistaxis, respiratory distress, and facial and cervical swelling. Affected animals died within 1-2 hours from the onset of clinical signs. Two lambs were available for complete postmortem examination. Gross lesions included mucosal and organ pallor, icterus, melena, and lung edema, as well as thymic, cervical muscle, and intra-articular hemorrhage. Histologically hepatocellular centrolobular necrosis was observed. The anticoagulant chlorophacinone was detected in the livers at 0.58 ppm and 0.50 ppm (wet weight), respectively. The source of exposure to chlorophacinone was old bait material placed between the wall studs of the building housing the ewes and lambs. The lambs were able to reach the bait through a hole in the plywood interior wall of the building.  相似文献   

18.
Hypercalcemia secondary to cholecalciferol rodenticide toxicosis was identified in two dogs. The first dog died shortly after admission. The second dog responded to treatment with sodium chloride solution, prednisolone, furosemide, and calcitonin. Treatment was needed for a longer period than anticipated and the serum calcium concentration did not stabilize for approximately one month. Although not conclusively demonstrated, calcitonin was considered the cause of severe anorexia. This new class of rodenticides has great toxic potential for dogs, and it is recommended that serum calcium concentration be carefully monitored as treatment for hypercalcemia is gradually withdrawn.  相似文献   

19.
During the 5-year period from January 1, 1990, to December 31, 1995, 887 diagnoses of metal toxicosis in domestic animals and wild birds were documented at the Veterinary Laboratory Services Branch of the Ontario Ministry of Agriculture, Food and Rural Affairs. Most of these cases involved cattle, sheep, and birds. Lead toxicosis was diagnosed in 399 cases, copper toxicosis in 387, zinc toxicosis in 49, mercury toxicosis in 44, iron toxicosis in 4, and selenium in 4 cases. Trends in species affected and sources of metals are discussed.  相似文献   

20.
The objectives of this study were to develop a novel approach to postmortem diagnosis of cholecalciferol (CCF) toxicosis in dogs using kidney, bile, and urine samples, and to differentiate CCF from ethylene glycol (EG) toxicosis. To achieve these objectives, specimens collected from 2 previous laboratory studies in which dogs were given a single oral toxic dose of CCF (8.0 mg/kg) were used. For EG toxicosis, historical data from the previous 13 years (1985-1998) were reviewed and confirmed cases of EG toxicosis were selected. The historical data were used to compare trace mineral concentrations, specifically of calcium and phosphorus to differentiate between intoxications caused by CCF from that caused by EG in dogs. Kidneys, bile, and urine from dogs that died of CCF toxicosis were analyzed for 25 monohydroxy vitamin D3 (25(OH)D3) and 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) and compared to known control unexposed dogs. Results of this study show that biliary and renal 25(OH)D3 concentrations and renal calcium to phosphorus ratio are of diagnostic value in dogs exposed to toxic concentrations of CCF. The renal calcium to phosphorus ratio was <0.1 in normal dogs, 0.4-0.9 in dogs that died of CCF toxicosis, and >2.5 in dogs that died of EG toxicosis.  相似文献   

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