Kl Swindells

Activated coagulation times in normal cats and dogs using MAX-ACT tubes.

OBJECTIVE To establish reference values for activated coagulation time (ACT) in normal cats and dogs, by visual assessment of clot formation using the MAX-ACT(TM) tube. SUBJECTS We recruited 43 cats and 50 dogs for the study; 11 cats and 4 dogs were excluded from the statistical analysis because of abnormalities on clinical examination or laboratory testing including anaemia, prolonged prothrombin time (PT) or activated partial thromboplastin time (APTT), or insufficient plasma volume for comprehensive laboratory coagulation testing. PROCEDURE Blood samples were collected via direct venipuncture for MAX-ACT, packed cell volume/total solids, manual platelet estimation and PT/APTT measurement. Blood (0.5 mL) was mixed gently in the MAX-ACT tube at 37 degrees C for 30 s, then assessed for clot formation every 5 to 10 s by tipping the tube gently on its side and monitoring for magnet movement. The endpoint was defined as the magnet lodging in the clot. The technique was tested with 10 dogs by collecting two blood samples from the same needle insertion and running a MAX-ACT on each simultaneously. RESULTS In normal cats the mean MAX-ACT was 66 s (range 55-85 s). In normal dogs the mean was 71 s (range 55-80 s). There was no statistical difference between the first and second samples collected from the same needle insertion. CONCLUSIONS and Clinical Relevance In both cats and dogs, a MAX-ACT result >85 s should be considered abnormal and further coagulation testing should be performed. Additionally, failure to discard the first few drops of the sample does not appear to significantly affect results.

Candida albicans peritonitis in a dog

Objective – To describe the clinical management of a case of Candida albicans peritonitis in a dog and discuss the pathogenicity of Candida peritonitis along with treatment using the fungistatic agent, fluconazole. Case Summary – A 15-week-old Papillon developed peritonitis secondary to enterectomy site dehiscence. A pure growth of Candida albicans was obtained from the abdominal fluid. Surgical repair of the dehiscence was performed and antifungal therapy instituted with fluconazole postoperatively. A marked exudative process was noted postoperatively with production of large volumes of fluid from the abdominal drain. Fresh frozen plasma and pentastarch were provided for oncotic support. Recovery was complicated by megaesophagus, however, the patient gradually improved and was discharged 11 days after surgery. New or Unique Information Provided – To our knowledge, this is the first case report of successful treatment of Candida albicans peritonitis in a dog. A marked exudative process was noted during therapy requiring significant oncotic support. Resolution of the disease process was achieved with surgical intervention and antifungal therapy.OBJECTIVE To describe the clinical management of a case of Candida albicans peritonitis in a dog and discuss the pathogenicity of Candida peritonitis along with treatment using the fungistatic agent, fluconazole. CASE SUMMARY A 15-week-old Papillon developed peritonitis secondary to enterectomy site dehiscence. A pure growth of Candida albicans was obtained from the abdominal fluid. Surgical repair of the dehiscence was performed and antifungal therapy instituted with fluconazole postoperatively. A marked exudative process was noted postoperatively with production of large volumes of fluid from the abdominal drain. Fresh frozen plasma and pentastarch were provided for oncotic support. Recovery was complicated by megaesophagus, however, the patient gradually improved and was discharged 11 days after surgery. NEW OR UNIQUE INFORMATION PROVIDED To our knowledge, this is the first case report of successful treatment of Candida albicans peritonitis in a dog. A marked exudative process was noted during therapy requiring significant oncotic support. Resolution of the disease process was achieved with surgical intervention and antifungal therapy.

A randomized, controlled clinical trial of intravenous lipid emulsion as an adjunctive treatment for permethrin toxicosis in cats.

OBJECTIVE To assess for any clinical benefit of intravenous lipid emulsion (ILE) for permethrin toxicosis in cats by comparing the progression of clinical signs of cats before and after treatment with ILE to cats treated with a saline control. To accomplish this objective, a clinical staging system for cats with permethrin toxicosis was developed and validated. DESIGN Prospective, multicenter, randomized, controlled clinical trial. SETTING University veterinary teaching hospital and 12 private veterinary emergency hospitals. ANIMALS Thirty-four client-owned cats with permethrin toxicosis. INTERVENTIONS A clinical staging system was designed based on abnormalities found on physical examination of cats with permethrin toxicosis. The clinical staging system had 6 stages, ranging from Stage A for cats with no abnormalities to Stage F for cats with grand mal seizures. The system was validated for intraviewer and interviewer variability. Cats in the clinical trial were randomized to receive 15 mL/kg of either intravenous 0.9% saline (control) or 20% ILE over 60 minutes. For each cat, a clinical stage was recorded at set time points before and after the randomized treatment was administered. The distribution of clinical stage stratified over time was compared across treatment groups. MEASUREMENTS AND MAIN RESULTS The clinical staging system showed excellent repeatability (P = 1.0) and reliability (P = 1.0). In the clinical trial, there was a significant difference in the distribution of clinical stages over time (P < 0.001) and from presentation stage to Stage B (P = 0.006), with ILE-treated cats (n = 20) having lower clinical stages earlier than control cats (n = 14). There was no significant difference in signalment, body weight, or supportive treatment between the groups. CONCLUSIONS The clinical staging system was repeatable and reliable. Clinical stages of permethrin toxicosis in ILE-treated cats improved earlier compared to control cats, suggesting ILE may be a useful adjunctive therapy in the treatment of permethrin toxicosis in cats.

Toxicity in three dogs from accidental oral administration of a topical endectocide containing moxidectin and imidacloprid

Three dogs were presented with a history of oral administration of a topical endectocide containing imidacloprid and moxidectin. They were diagnosed with imidacloprid and moxidectin intoxication, having ingested doses ranging from 7.5 to 1.4 mg/kg of imidacloprid and 1.9 to 2.8 mg/kg of moxidectin. The three dogs were affected to different degrees of severity, but all displayed signs of ataxia, generalised muscle tremors, paresis, hypersalivation and disorientation. Temporary blindness occurred in two cases. The three dogs were tested for the presence of the multi-drug resistance 1 gene deletion, which can cause an increased sensitivity to the toxic effects of moxidectin, and were found to be negative. Treatment included gastrointestinal decontamination, intravenous fluid therapy and benzodiazepines to control muscle tremors. All three dogs made a complete recovery within 48 h of ingestion.

Prospective determination of the specificity of a commercial snake venom detection kit in urine samples from dogs and cats.

OBJECTIVE To determine the specificity of a snake venom detection kit in urine samples from dogs and cats presenting to a referral centre for diseases unrelated to snake envenomation. DESIGN Urine was collected from 50 dog and 25 cats presented for investigation and treatment of diseases unrelated to snake envenomation. Urine was collected as a voided sample, by cystocentesis or by catheterisation, and routine urinanalysis was performed. Snake venom testing was performed within 2 h of collection using a commercially available snake venom detection kit, which was observed continuously during the 10-min colour reaction phase for evidence of a visible colour indicating a positive test. RESULTS No false-positive reactions occurred in any sample analysed. CONCLUSION The snake venom detection kit appears to have 100% specificity for using urine as a test sample.

Extradural haematoma secondary to brown snake (Pseudonaja species) envenomation.

A 4-year-old Siberian Husky dog was treated with brown snake antivenom by his regular veterinarian after a witnessed episode of brown snake envenomation. The dog was discharged 5 hours post presentation despite an ongoing coagulopathy. The dog was presented to the emergency centre 2 hours later because the owner believed the dog to be in pain. Initial examination revealed an ambulatory but neurologically normal patient with thoracolumbar pain and laboratory evidence of a coagulopathy. Despite correction of the coagulopathy, the signs progressed to bilateral hind limb paresis after approximately 3 hours of hospitalisation, and continued to deteriorate over the next 56 hours to loss of deep pain perception in the right hind limb. Computed tomography imaging identified the presence of an extradural haematoma which was subsequently removed via a hemilaminectomy. Surgical decompression was successful in treating the spinal compression and the dog recovered with minimal complications. To our knowledge this is the first report of extradural haematoma secondary to coagulopathy induced by brown snake envenomation.

Tiger snake (Notechis scutatus) envenomation in a horse

BACKGROUND A 7-year-old Thoroughbred gelding presented with muscle fasciculation, reluctance to move, profuse sweating, tachycardia, tachypnoea and a localised, unilateral swelling on the muzzle. History and physical examination were suggestive of snake envenomation. METHODS A sandwich ELISA for the detection of snake venom was performed on serum and urine samples. RESULT The test performed on urine confirmed a diagnosis of tiger snake envenomation. CONCLUSION The response to treatment with antivenom and supportive medical therapy was excellent.

Aplysia gigantea toxicosis in 72 dogs in Western Australia

OBJECTIVES This study aimed to: (1) confirm a temporal association between exposure to the sea hare Aplysia gigantea and the development of a neurotoxicosis in dogs and (2) further characterise the clinical signs, treatment and outcomes in dogs with this suspected toxicosis. METHODS The medical records from four veterinary practices within the Geraldton region of Western Australia were searched for dogs that had been exposed to A. gigantea and subsequently presented to a veterinarian during the period of January 2001 to March 2011. Signalment, exposure history, clinical signs, treatment and outcome were recorded. RESULTS In total, 72 dogs met the inclusion criteria. Clinical signs included ptyalism, emesis, ataxia, hyperaesthesia, tremors, muscle fasciculations, seizures, nystagmus and respiratory distress; 30 dogs did not have abnormal clinical signs at presentation; 69 dogs were presented during January to April. Treatment included gastrointestinal and dermal decontamination, and supportive management of seizures, tremors and muscle fasciculations. Of the 72 dogs, 65 survived to discharge, 4 died and 3 were euthanased. Information from subsequent examinations was available for 57 dogs and no long-term complications were reported. CONCLUSIONS Exposure to A. gigantea was temporally associated with the development of neuroexcitatory clinical signs in dogs. Gastrointestinal and respiratory signs also occurred in some dogs. Dogs with suspected toxicosis were presented mostly in the months of January to April. The proportion of dogs that died or were euthanased because of worsening clinical signs was approximately 10%.