Objective -To determine the association of plasma lactate concentration, pH, base deficit (BD), and anion gap (AG) in dogs and cats on presentation to an emergency room with outcome, and to compare the prognostic significance of hyperlactatemia with a concurrent metabolic acidosis with that of hyperlactatemia and a normal metabolic acid-base balance. Design -Retrospective study. Setting -University teaching hospital. Animals -Five hundred sixty-six dogs and 185 cats that had venous blood gas analysis performed. Interventions -None. Measurements and Main Results -Medical records were reviewed for plasma lactate concentrations, electrolyte concentrations, and acid-base parameters obtained on emergency room admission, clinical diagnosis, and inhospital mortality. The primary outcome measure was all-cause mortality for the hospitalized visit. Median plasma lactate concentration and AG were higher, BD was more negative, and pH was lower, in non-survivor dogs and cats. The prevalence of hyperlactatemia was 53% in dogs and 30% in cats. Lactic acidosis was present in 42% and 80% of hyperlactatemic dogs and cats, respectively. Multivariate regression analyses revealed that plasma lactate concentration, BD, and pH, but not AG, were independent predictors of mortality in dogs, and that only plasma lactate concentration was an independent predictor of mortality in cats. Mortality was highest for animals with lactic acidosis, at 59.8% in dogs and 49% in cats. Mortality in dogs with lactic acidosis was significantly higher than dogs with hyperlactatemia and a normal acid-base status (P < 0.0001). Conclusions -The presence and magnitude of hyperlactatemia on presentation to the emergency room may help identify dogs and cats with high likelihood of in-hospital mortality, and the presence of lactic acidosis specifically may help identify dogs with yet higher risk of in-hospital mortality.

BackgroundCanine neutrophils release neutrophil extracellular traps (NETs) in response to lipopolysaccharide but NETs from clinical septic dogs had not been identified. The primary aim is to describe the methodology of identifying and quantifying neutrophil extracellular traps (NETs) in cytology samples of septic foci in dogs with sepsis using immunofluorescence microscopy. Cytology samples including endotracheal tracheal wash (ETW), bronchoalveolar lavage (BAL), abdominal and pleural effusion collected from 5 dogs (3 septic, 2 non-septic) were fixed, permeabilized and stained for myeloperoxidase (MPO), citrullinated histone H3 (citH3) and cell-free DNA (cfDNA). Fluorescence microscopy was used to identify and quantify NETs in 10 random views at 40× magnification. NETs were identified based on co-localization of MPO, citH3 and cfDNA. NETs were quantified as a ratio (number of NETs: number of neutrophils). Neutrophils were identified based on cytoplasmic MPO, cellular diameter and nuclear morphology.ResultsNETs were identified and quantified in all cytology samples collected from septic dogs. A small number of NETs was documented in one dog with sterile chronic bronchitis. No NETs were found in sterile abdominal effusion collected from one dog with congestive heart failure.ConclusionsImmunofluorescence microscopy could be a useful tool for the study of NETs in dogs with clinical sepsis.

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.