Objective:To evaluate the ability of arterial hemoglobin oxygen saturation measurement via pulse oximetry (SpO 2 ) to serve as a surrogate for PaO 2 in dogs.Design: Two-part study: prospective observational and retrospective components. Setting: University teaching hospital.Animals: Ninety-two dogs breathing room air prospectively enrolled on a convenience basis. Retrospective evaluation of 1,033 paired SpO 2 and PaO 2 measurements from 62 dogs on mechanical ventilation.Interventions: Dogs with concurrent SpO 2 and PaO 2 measured on room air had a data sheet completed with blood gas analysis. SpO 2 , PaO 2 , and FiO 2 values were collected from medical records of dogs on mechanical ventilation. Measurements and Main Results:Predicted PaO 2 was calculated from SpO 2 using the dog oxyhemoglobin dissociation curve. The correlation coefficient between measured and predicted PaO 2 was 0.49 (P < 0.0001) in room air dogs and 0.74 (P < 0.0001) in ventilated dogs. In room air dogs, Bland-Altman analysis between measured minus predicted PaO 2 versus the average showed a mean bias of −6.0 mm Hg (95% limit of agreement, −35 to 23 mm Hg). The correlation coefficient between PaO 2 /FiO 2 and SpO 2 /FiO 2 ratios was 0.76 (P < 0.0001). After combining data sets, receiver operating characteristic curve analysis showed the optimal cutoff value for detecting hypoxemia (PaO 2 < 80 mm Hg) was an SpO 2 of 95%, with sensitivity and specificity of 77.8% and 89.5%, respectively. Using this cutoff, 6.9% of SpO 2 readings failed to detect hypoxemia, whereas 7.2% predicted hypoxemia that was not present. Conclusions:The SpO 2 was not clinically suitable as a surrogate for PaO 2 , though it performed better in mechanically ventilated dogs. As sensitivity for the detection of hypoxemia was poor, pulse oximetry does not appear to be an acceptable screening test. The SpO 2 /FiO 2 ratio may have value for evaluation of anesthetized dogs on supplemental oxygen. Arterial blood gas analysis remains ideal for assessment of oxygenation.

BackgroundRenal infarcts identified without definitive association with any specific disease process.ObjectiveDetermine diseases associated with diagnosis of renal infarcts in cats diagnosed by sonography or necropsy.Animals600 cats underwent abdominal ultrasonography, necropsy, or both at a veterinary medical teaching hospital.MethodsInformation obtained from electronic medical records. Cats classified as having renal infarct present based on results of sonographic evaluation or necropsy. Time‐matched case‐controls selected from cats that underwent the next scheduled diagnostic procedure.Results309 of 600 cats having diagnosis of renal infarct and 291 time‐matched controls. Cats 7–14 years old were 1.6 times (odds ratio, 95% CI: 1.03–2.05, P = .03) more likely to have renal infarct than younger cats but no more likely to have renal infarct than older cats (1.4, 0.89–2.25, P = .14). All P = .14 are statistically significant. Cats with renal infarcts were 4.5 times (odds ratio, 95% CI: 2.63–7.68, P < .001) more likely to have HCM compared to cats without renal infarcts. Cats with renal infarcts were 0.7 times (odds ratio, 95% CI: 0.51–0.99, P = .046) less likely to have diagnosis of neoplasia compared to cats without renal infarcts. Cats with diagnosis of hyperthyroidism did not have significant association with having renal infarct. Cats with renal infarcts were 8 times (odds ratio, 95% CI: 2.55–25.40, P ≤ .001) more likely to have diagnosis of distal aortic thromboembolism than cats without renal infarcts.Conclusions and Clinical ImportanceCats with renal infarcts identified on antemortem examination should be screened for occult cardiomyopathy.

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Objective: To describe the clinical signs, clinicopathologic abnormalities, treatment, and outcome after IV administration of polyethylene glycol 3350 (PEG3350) in a cat. Case Summary:A cat was inadvertently administered 6 g/kg of PEG3350 in electrolyte solution, IV, resulting in severe hypernatremia (203 mmol/L), diffuse encephalopathy, hemolysis, and moderate azotemia. The hemolysis and acute kidney injury observed immediately following PEG3350 administration resolved with supportive care. Administration of IV and oral electrolyte-free water slowly corrected the hypernatremia and the neurologic signs subsequently improved. Complete resolution of clinical signs was documented one month following hospital discharge. The PEG3350 concentrations in serum, plasma, and urine samples confirmed toxic exposure to PEG3350. Efficacy of treatment was evident by decreasing concentrations of PEG3350 in serum after the first 24 hours of treatment. Renal elimination of PEG3350 was significant and PEG3350 was still detected in the urine 17 days after exposure.

Background: Multiple studies have evaluated the breed-specific prevalence of dog erythrocyte antigen (DEA) 1 in various geographic regions. However, few large-scale studies exist that describe breed prevalence of DEA 1 in the United States.

CASE DESCRIPTION An approximately 2-year-old sexually intact male German Shorthair Pointer was presented for treatment of baclofen toxicosis. CLINICAL FINDINGS The dog had signs of severe baclofen toxicosis (no gag reflex, intermittent vocalization, and stupor) and received intravenous lipid emulsion (142 mL/kg) as a constant rate infusion over 11 hours. Severe hypertriglyceridemia (29,221 mg/dL; reference interval, 19 to 133 mg/dL) developed, followed by cardiovascular depression (poor peripheral perfusion, hyperlactatemia, and hypertension), severe hypoglycemia (26 mg/dL), acute kidney injury (serum creatinine, 3.6 mg/dL), intravascular hemolysis, and coagulopathy (hypocoagulable thromboelastogram and marked bilateral epistaxis). TREATMENT AND OUTCOME Therapeutic plasma exchange was performed in 4 stages to treat the hypertriglyceridemia. For each stage, an approximately 500-mL aliquot of blood (22 mL/kg) was removed and centrifuged, and the patient’s RBCs and allogenic fresh-frozen plasma were returned to the dog. Approximately 1.2 times the dog’s plasma volume was exchanged, reducing the serum triglyceride concentration to 1,349 mg/dL and improving the dog’s cardiovascular function and coagulation. Hours after the procedure was completed, the dog regurgitated and developed acute respiratory distress as a result of presumptive aspiration pneumonia, and the owner elected to have the dog euthanized. CLINICAL RELEVANCE Veterinarians should be aware of possible complications associated with administration of intravenous lipid emulsion, and veterinary-specific guidelines for the maximum dose of intravenous lipid emulsion should be developed to help prevent adverse effects. TPE appears to be an effective method for treating iatrogenic hypertriglyceridemia in dogs.

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