Objectives To determine whether veterinarians in primary care practices (PCPs) and board-certified clinicians (BCCs) approach treatment of dogs with immune-mediated haemolytic anaemia (IMHA) similarly, and whether practitioners with more experience treat similarly to those with less experience. We hypothesised those in PCPs would show more variation in their approach to similar cases than BCCs. Methods A cross-sectional study was conducted by distributing a questionnaire to BCCs and veterinarians in PCPs. The questionnaire included direct questions and a number of clinical scenarios intended to capture approaches to common treatment problems. Results Questionnaire responses were received from 241 veterinarians, including 216 in PCPs and 25 BCCs. Veterinarians in both settings used similar tests for diagnosis of IMHA, but BCCs performed more tests to exclude underlying causes of ‘associative’ disease. All veterinarians reported use of similar initial dosages of glucocorticoids (median 2 mg/kg per day in both groups, p = 0.92) but those used by more experienced practitioners were higher than those with less experience. Most veterinarians made allowances for the weight of dogs, using lower prednisolone dosages in a clinical scenario involving a 40 kg dog compared to a 9 kg dog (p = 0.025 for PCP, p = 0.002 for BCC). BCCs reported greater use of combinations of immunosuppressive drugs (p<0.0001) and of antithrombotic drugs (p<0.0001); use of antithrombotic drugs was also less common among more experienced practitioners compared to less experienced. Conclusions Approaches to treatment of dogs with IMHA differ between BCCs and those in PCP. These differences may affect design and implementation of future research studies and clinical guidelines.
An 8-year-old, female, neutered cocker spaniel presented with progressive lethargy, inappetence and right pelvic limb lameness. Regional mastectomy and ovariohysterectomy had been performed 11 months prior. Mild neutrophilia and increased C-reactive protein were present. Radiographs revealed mild periosteal reaction of distal long bone diaphyses of all limbs, consistent with hypertrophic osteopathy. Abdominal imaging revealed a mesenteric mass with a central woven radiopaque foreign body diagnosed as a gossypiboma following surgical excision and histopathology. Postoperatively the patient developed acute decompensation of suspected chronic subclinical disseminated intravascular coagulation and suffered cardiac arrest. Hypertrophic osteopathy was confirmed with multifocal periosteal hyperostosis and concurrent myelofibrosis within the medulla of the long bones. Hypertrophic osteopathy occurs secondary to chronic inflammatory or neoplastic intrathoracic lesions and rarely due to abdominal pathology. To the authors' knowledge, this is the first description of hypertrophic osteopathy associated with an abdominal gossypiboma with sequential disseminated intravascular coagulation.
A 12-year-old female neutered Jack Russell terrier was presented for further investigation of an acute two-day history of lethargy, inappetence and vomiting. Mild increase in urea and amylase and positive cPLI (Canine pancreatic lipase immunoreactivity) ELISA were present. Abdominal ultrasound revealed an irregular, heterogeneous and diffusely hypoechoic pancreas. Severe pancreatitis with secondary peritonitis was diagnosed. Supportive treatment was started, but the patient developed paradoxical vestibular syndrome. MRI was declined and the patient was euthanased. On histopathological examination renal infarction with evidence of thrombosis and focal cerebellar infarction were present. It is well documented that a hypercoagulable state is a known complication of severe pancreatitis. To the authors’ knowledge this is the first description of suspected thromboembolism secondary to pancreatitis resulting in neurological signs in a dog.
An 11 year old female-neutered Labrador presented for facial swelling. Clinicopathological abnormalities included hyperglobulinemia, azotemia, hypercalcemia, nonregenerative anemia, thrombocytopenia, and spurious hypoglycemia. Normoglycemia was subsequently confirmed using a cage-side analyzer (AlphaTRAK, Zoetis, UK). Serum and urine protein electrophoresis documented monoclonal (immunoglobulin M) gammopathy with Bence-Jones proteinuria. Computed tomography imaging revealed a monostotic osteolytic bone-lesion, and bone marrow cytology and histopathology documented plasmacytosis with multiple myeloma oncogene 1 / interferon regulatory factor 4 positivity, consistent with multiple myeloma. Infectious disease testing initially indicated seropositivity for Leishmania, Borrelia, and Anaplasma spp.; however, Leishmania PCR (splenic and bone marrow aspirates), and paired serological titers for Borrelia and Anaplasma were negative. Consequently, initial serological results were considered to be false positive because of paraproteinemia-associated assay interference. Chemotherapy (prednisolone and melphalan combination therapy) was initiated, but the dog was euthanased 30 days later because of the development of pericardial effusion. This is a report of spurious serological (and other laboratory) results occurring secondary to monoclonal gammopathy in a dog.
BackgroundHypoadrenocorticism is an important differential for hypercalcemia. The etiology of hypercalcemia in hypoadrenocorticism in dogs is unclear.ObjectiveTo review the prevalence of hypercalcemia and use statistical models to identify clinical, demographic, and biochemical variables associated with hypercalcemia in dogs with primary hypoadrenocorticism.AnimalsOne hundred ten dogs with primary hypoadrenocorticism; 107 with recorded total calcium (TCa), 43 recorded ionized calcium (iCa).MethodsMulticenter retrospective observational study at 4 UK referral hospitals. Univariable logistic regression analyses were performed to assess the association between independent variables of signalment, hypoadrenocorticism type (glucocorticoid only deficient hypoadrenocorticism [GHoC] vs glucocorticoid and mineralocorticoid deficient hypoadrenocorticism [GMHoC]), clinicopathological variables and hypercalcemia. Hypercalcemia was defined as elevated TCa, an elevated iCa, or both elevated TCa and iCa (Model 1) or as elevated iCa (Model 2).ResultsOverall prevalence of hypercalcemia was 34.5% (38/110). The odds of hypercalcemia (Model 1) were increased (P < .05) in dogs with GMHoC ([vs GHoC], OR [odds ratio] = 3.86, 95% confidence interval [CI] 1.105‐13.463), higher serum creatinine (OR = 1.512, 95% CI 1.041‐2.197), and higher serum albumin (OR = 4.187, 95% CI 1.744‐10.048). The odds of ionized hypercalcemia (Model 2) were increased (P < .05) with reduced serum potassium concentration (OR = 0.401, 95% CI 0.184‐0.876) and younger age (OR = 0.737, 95% CI 0.558‐0.974).Conclusions and Clinical ImportanceThis study identified several key clinical and biochemical variables associated with hypercalcemia in dogs with primary hypoadrenocorticism. These findings aid understanding of the pathophysiology and etiology of hypercalcemia in dogs with primary hypoadrenocorticism.
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