BackgroundBiliary sludge is associated with gallbladder (GB) dysmotility and mucus hypersecretion suggesting a link between biliary sludge and the formation of GB mucoceles (GBM). If biliary sludge progresses to GBM, treatment to reduce the production and progression of sludge is warranted.Hypothesis/ObjectivesThe objective of this study was to determine the course of biliary sludge in dogs.AnimalsSeventy‐seven healthy, client‐owned dogs ≥4 years of age screened for biliary sludge; 45 affected dogs identified.MethodsProspective, observational design. Serial ultrasound examinations were evaluated at 3, 6, 9, and 12 months to monitor degree of sludge based on proportion of GB filled with sludge (mild [0.01–24.4%], moderate [24.5–49.4%], moderate to severe [49.5–74.4%], severe [74.5–100%]), gravity dependency of sludge, and GB dimensions.ResultsAfter 1 year of follow‐up, the degree of sludge was mild (34%), moderate (47%), moderate to severe (13%), severe (3%), or absent (3%). There was no significant difference in median degree of sludge over 1 year (P = .36). There were no significant changes in the gravity dependency of sludge over 1 year. A subset of dogs, 24%, with initial gravity‐dependent sludge developed a combination of nondependent and dependent sludge. Dogs had resolved (2%), decreased (19%), static (40%), increased (29%), or recurrent (10%) sludge at the conclusion of the study.Conclusions and Clinical ImportanceBiliary sludge was prevalent, affected dogs remained asymptomatic, and it rarely resolves in healthy dogs over a period of 1 year. Some dogs developed nongravity‐dependent sludge within 1 year, which might indicate changes in consistency of sludge.

Background: Pancreatitis is a common cause of extrahepatic bile duct obstruction (EHBDO) in dogs. Information describing the clinical course of dogs with pancreatitis associated bile duct obstruction (PABDO) is limited. Objectives: To describe the clinical course of PABDO in dogs and determine if presumed markers of disease severity are predictors of survival. Animals: Forty-six client-owned dogs with PABDO. Methods: A retrospective review of medical records from dogs diagnosed with PABDO was performed. Data, including clinical signs and biochemical changes, were collected 6 times throughout the course of disease. Outcome was defined as either survival (discharge from the hospital) or death. Results: Thirty-three (79%) out of 42 dogs with PABDO survived. Thirty-one (94%) of the 33 dogs that survived received medical management alone. Time from onset of clinical signs to initial documented increase in serum bilirubin concentration, peak bilirubin elevation, and initial decline in serum bilirubin concentration were 7 (median), 8, and 15 days, respectively. The median number of days from onset of clinical signs to outcome date was 13. Clinical signs of fever, vomiting, and anorexia were decreased in frequency from the onset of clinical signs to the time of peak bilirubin. Median bile duct dilatation at the time of ultrasonographic diagnosis of PABDO and peak bilirubin were not different between survivors (7.6 mm, 11.7 mg/dL) and nonsurvivors (6 mm, 10.6 mg/dL, P = .12, P = .8). Conclusions: Dogs with PABDO often have a prolonged course of illness and improve clinically despite biochemical evidence of progression of EHBDO.

Objectives The purpose of this study was to evaluate symmetric dimethylarginine (SDMA) in hyperthyroid cats before and after treatment with radioactive iodine and to determine how pretreatment SDMA relates to the development of post-treatment azotemia. Methods Eighty-four non-azotemic hyperthyroid cats had serum SDMA and creatinine evaluated before and 1, 3 and 6 months after treatment with radioiodine therapy. Results Baseline SDMA was increased in 7% (n = 6/84) of cats, whereas SDMA was increased in 19% (n = 15/81), 20% (n = 16/80) and 32% (n = 26/81) at 1 month, 3 months and 6 months after treatment, respectively. Creatinine was not elevated in any of the cats at baseline because of the study design, and was elevated in 6% (n = 5/81), 15% (n = 12/80) and 15% (n = 12/81) of cats at 1, 3 and 6 months after treatment, respectively. SDMA (median 11 μg/dl, range 1–22 μg/dl) was significantly higher at 3 (12 μg/dl, range 6–45 μg/dl; P = 0.005) and 6 months (11 μg/dl, 6–25 μg/dl; P <0.001) compared with baseline (11 μg /dl, range 1–21 μg/dl). The median baseline SDMA was significantly higher in the azotemic group (13 μg/dl, range 11–22 μg/dl) compared with the non-azotemic group (10 μg/dl, range 1–21 μg/dl, P = 0.002). The sensitivity of SDMA for detecting azotemia after treatment was 15.4%, with a specificity of 94.4%. Baseline serum SDMA concentration had a moderately positive association with baseline creatinine concentration ( P <0.001, r = 0.437). At 6 months, there was a strong positive correlation between SDMA and creatinine concentrations ( P <0.001, r = 0.721). There was no significant correlation with SDMA and thyroxine at baseline ( P = 0.772, r = −0.034) or 6 months ( P = 0.492, r = −0.078). Conclusions and relevance SDMA increases in cats treated for hyperthyroidism with radioactive iodine and likely reflects associated changes in glomerular filtration rate. An increased SDMA concentration above the reference interval prior to treatment has a high specificity but poor sensitivity for the prediction of post-treatment azotemia.

Objectives To assess platelet function, buccal mucosal bleeding time and plasma von Willebrand factor concentration in dogs with chronic inflammatory and/or fibrotic liver disease and to compare results with those obtained in healthy dogs. Materials and Methods Preliminary study including 18 dogs with chronic inflammatory and/or fibrotic liver disease undergoing liver biopsy and 18 healthy age‐matched control dogs. Platelet function was assessed by measuring closure time with the PFA‐100® analyser using adenosine diphosphate (ADP) as an agonist. Buccal mucosal bleeding time, closure time and plasma von Willebrand factor antigen were measured in dogs in both groups. After undergoing ultrasound‐guided needle biopsy, dogs were monitored for haemorrhage to determine if there was an association of any measurement with post‐biopsy bleeding. Results The closure time was not different between the liver disease group (median 76.3; range 53 to 118.5 seconds) and control group (72.8; 57 to 89.5 seconds). The buccal mucosal bleeding time was longer in the liver disease group (median 138; range 95 to 229 seconds) than the control group (103; 63 to 200 seconds). The plasma von Willebrand factor antigen concentration was not different between the liver disease group (median 203; range 109 to 351%) and control group (165.5; 63 to 246%). Clinical Significance In this study, dogs with chronic necroinflammatory and/or fibrotic liver disease did not have overt, clinically relevant derangements in platelet function as assessed by buccal mucosal bleeding time, closure time and von Willebrand factor analysis. In addition, none of the dogs undergoing percutaneous ultrasound‐guided biopsy in the study exhibited bleeding complications post‐biopsy procedure.

An 11-year-old spayed female domestic shorthair cat was evaluated for anorexia, lethargy and weight loss of 6 days' duration. Bilateral mydriasis, absent menace response, slow-to-absent pupillary light reflexes, bilateral retinal detachment, intermittent horizontal nystagmus, intermittent ventral strabismus and systemic hypertension were present. Biochemical analysis revealed severe hyponatremia, severe hypochloremia and mild hypokalemia. Multifocal central nervous system disease was suspected based on optic, trigeminal sensory (ophthalmic branch), vestibulocochlear and possible oculomotor nerve dysfunction. Thoracic radiographs showed mild cardiomegaly without evidence of congestive heart failure. Ultrasound revealed mild pleural and peritoneal effusion. A cause of the severe hyponatremia was not identified, and it persisted despite fluid therapy. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) was suspected as the cause of hyponatremia. Humane euthanasia was elected owing to continued clinical decline. Serum hyposmolality, urine hyperosmolality, natriuresis and lack of confirmed renal, thyroid and pulmonary disease aided in the presumed diagnosis of SIADH. Post-mortem histopathology of the brain revealed degeneration of the hypothalamus and optic tracts, along with a prominent fluid-filled craniopharyngeal duct (putative Rathke's cleft cyst) separating the pars distalis and the pars intermedius. The hypothalamic degeneration, possibly secondary to a Rathke's cleft cyst, was hypothesized to be the cause of presumptive SIADH in the patient. Although rare in occurrence, Rathke's cleft cyst should be included as a differential diagnosis in dogs and cats with signs of pituitary dysfunction.

Background We aimed to identify a simple test for excessive calciuresis and predict calcium oxalate (CaOx) disease in Miniature Schnauzers. We investigated the impact of postprandial time on the urine calcium to creatinine ratio (UCa/Cr) in male dogs of this breed, with the goal of improving the utility of the UCa/Cr. Hypotheses (1) Significant differences will exist in preprandial and postprandial UCa/Cr between CaOx urolith‐forming and control Schnauzers. (2) The UCa/Cr will increase significantly from the first morning baseline at ≥1 postprandial time point(s) in both control and CaOx urolith‐forming dogs. (3) Biochemical abnormalities and other variables may be associated with urolith status. Animals Twenty‐four male Miniature Schnauzer dogs, consisting of 9 with (urolith formers) and 15 without (controls) CaOx uroliths. Methods Urine was collected before and 1, 2, 4, and 8 hours after feeding a standardized diet. Receiver operator characteristic curve analysis was performed to identify the UCa/Cr cutoff that most accurately differentiates dogs based on urolith status. Results Urolith formers had significantly higher mean UCa/Cr over the course of 8 hours. The postprandial change in UCa/Cr was not significant at any time point between or within groups. The cutoff UCa/Cr value of 0.06 had a specificity of 93% (95% confidence interval [CI], 80%‐100%) and a sensitivity of 56% (95% CI, 21%‐86%) for identifying CaOx urolithiasis. Conclusions and Clinical Importance Urolith‐forming male Miniature Schnauzers have excessive calciuresis, and the postprandial sampling time up to 8 hours is not critical. This simple urine measurement has potential as a marker of CaOx disease.

Background Hyperthyroid cats might have a predisposition to arterial thrombus formation. The mechanism for thrombogenesis currently is unknown but could be associated with systemic hypercoagulability as seen in hyperthyroid humans. Objective Our purpose was to evaluate markers of hemostasis in hyperthyroid cats compared to healthy cats, and in hyperthyroid cats before and after radioactive iodine treatment (RIT). Animals Twenty‐five cats with hyperthyroidism and 13 healthy euthyroid cats >8 years of age. Methods Prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen concentration, antithrombin (AT), D‐dimers, thrombin‐antithrombin complexes (TAT), von Willebrand Factor antigen (vWF : Ag), and activity of factors VIII and IX were measured. An echocardiogram was performed in all cats. Hemostatic markers and echocardiogram were evaluated again 6 to 9 months after successful RIT in 7 cats. Results Hyperthyroid cats had higher fibrinogen concentration (P < .0001), AT activity (P < .0001), and vWF : Ag concentration (P = .01) than healthy control cats with all results decreasing significantly post‐RIT. Hyperthyroid cats were not more likely to be in a hypercoaguable state than euthyroid cats (P = .08). Serum T4 concentration was not a predictor of a hypercoagulable state (P = .53). Conclusions and Clinical Importance Hyperthyroid cats have evidence of altered hemostasis that does not appear to be solely attributable to cardiac abnormalities, but no evidence of a hypercoagulable state. Findings suggest altered hemostasis resolves after RIT. Hyperthyroid cats could have endothelial dysfunction as indicated by increased vWF : Ag which could potentiate thrombogenesis.

Objectives The aim of this study was to determine the incidence of and risk factors for both gastrointestinal (GI) incisional dehiscence and mortality in a large cohort of cats undergoing GI surgery. We hypothesized that cats with preoperative septic peritonitis (PSP), systemic inflammatory response syndrome (SIRS) or sepsis would have higher GI dehiscence and mortality rates than unaffected cats. Methods A medical records search identified cats with surgically created, full-thickness incisions into their stomach, small intestines or large intestines. Preoperative data, including signalment, clinical signs, comorbidities, surgical history, current medications, presenting physical examination findings, complete blood counts and serum biochemistry values, were collected. It was determined whether or not cats had PSP, SIRS or sepsis at admission. Intraoperative data, final diagnosis and postoperative variables such as vital parameters, bloodwork and (if applicable) the development of GI dehiscence or mortality were noted. Postoperative follow-up of at least 10 days was obtained in survivors. Results In total, 126 cats were included. One cat developed GI dehiscence following complete resection of a jejunal adenocarcinoma. Twenty-three cats (18.2%) died within 10 days of surgery. Cats with PSP ( P = 0.0462) or that developed hypothermia 25–72 h postoperatively ( P = 0.0055) had higher odds of mortality in multivariate analysis. Cats with PSP had 6.7-times higher odds of mortality than cats not diagnosed with PSP. Conclusions and relevance In cats receiving GI surgery, the incidence of GI incisional dehiscence was <1%. Cats with PSP had a higher likelihood of mortality. SIRS was a common finding in cats with septic peritonitis, but was not associated with mortality. Postoperative mortality during the home recovery period might be significant in cats. Future studies evaluating postoperative mortality in cats should consider extending the research period beyond the date of discharge.