Effects of calcium supplementation to resuscitation fluids in endurance horses: A randomized, blinded, clinical trial.

BACKGROUND: The addition of calcium to resuscitation fluids is a common practice in horses, but studies evaluating the effects of calcium supplementation are limited. In healthy horses, decreases in heart rate and changes in serum electrolyte concentrations have been reported. HYPOTHESIS: Calcium gluconate administration at a rate of 0.4 mg/kg/min to eliminated endurance horses with metabolic problems will affect heart rate, gastrointestinal sounds, and serum electrolyte concentrations. ANIMALS: Endurance horses eliminated from the Tevis Cup 100-mile (160 km) endurance ride for metabolic problems and requiring IV fluid therapy were eligible. METHODS: Sixteen horses were randomly assigned to receive 0.4 mg/kg/min of calcium (23% calcium gluconate solution) over 1 hour diluted in 10 L of a non-calcium containing isotonic crystalloid (CAL group) or 10 L of a non-calcium containing isotonic crystalloid (CON group). Staff members administering the fluids were blinded to treatment group. Blood samples were collected and physical examinations performed before and after treatment. Heart rates were recorded every 15 min during fluid administration. Data were compared using 2-way analysis of variance (ANOVA) with repeated measures for continuous variables and Fisher's exact test for categorical variables. RESULTS: Calcium was associated with lower heart rates 45 min after starting the infusion (P = .002). Gastrointestinal sounds were less likely to improve in the calcium group compared with the control group (P = .005). An increase in plasma phosphorus concentration (P = .03) was associated with calcium administration. CONCLUSIONS: Intravenous calcium supplementation to endurance horses eliminated from competition after development of metabolic problems may decrease heart rate but impairs improvement in gastrointestinal sounds.

Clinical and biochemical factors associated with survival in equids attacked by dogs: 28 cases (2008-2016).

BACKGROUND: Trauma from dog attacks has been associated with mortality rates as high as 23% in some species. However, the prognosis and clinical features of this type of injury have not been described in equids. HYPOTHESES/OBJECTIVES: To describe survival rate, signalment, clinical features, and biochemical results in equids presented for emergency care after presumed dog attacks. We hypothesized there would be differences between survivors and nonsurvivors. ANIMALS: A total of 28 equids presented for presumed dog attacks from 3 referral centers. METHODS: A retrospective study was performed using data from 3 hospitals between 2008 and 2016. Survival was defined as survival at 14 days postdischarge. Variables were compared between survivors and nonsurvivors using a t test, Mann-Whitney U test, or Fisher's exact test as appropriate. RESULTS: Overall mortality rate was 21%. Ponies and miniature horses represented 16/28 (57%) of the animals in the study. Full-sized equids had a lower risk of nonsurvival as compared to smaller patients (odds ratio = 0.02; 95% confidence intervals = 0.00-0.27; P < .005). Animals with lower body temperatures had increased risk for nonsurvival (P = .0004). Increased admission blood lactate concentrations (P = .003) and decreased serum total protein concentrations (P = .006) were associated with nonsurvival. CONCLUSIONS: The mortality rate in equids attacked by dogs was similar to what is reported for other veterinary species. Smaller equids and those with increased admission blood lactate concentration, lower body temperature, and lower total serum protein concentrations were less likely to survive.

Resolution of neurologic signs presumed to be associated with hyperammonemia in 2 endurance horses.

This case report describes 2 endurance horses with non-hepatic hyperammonemia. The animals were competing in a 160-km endurance competition in extreme heat conditions and were presented for obtundation. One of the horses also had evidence of blindness. The blood ammonia concentration was elevated (196 µmol/L and 249 µmol/L) and both horses improved following treatment with intravenous fluids and supportive care. These are the first documented cases of clinical signs presumed to be associated with hyperammonemia in endurance horses. Despite the severity of the clinical presentation, both horses made a full recovery. Key clinical message: Non-hepatic hyperammonemia should be considered as a potential cause of blindness and obtundation in competing endurance horses. Horses appear to respond well to treatment with intravenous fluids.

Fin des signes neurologiques présumés être associés avec de l'hyperammoniémie chez deux chevaux d'endurance. Le présent rapport de cas décrit la situation de deux chevaux d'endurance avec une hyperammoniémie non-hépatique. Les animaux compétitionnaient dans une course d'endurance de 160 km dans des conditions de chaleur extrême et furent présentés pour confusion. Un des chevaux avait également des évidences de cécité. Les concentrations d'ammoniaque sanguin étaient élevées (196 µmol/L et 249 µmol/L) et les deux chevaux s'améliorèrent à la suite du traitement avec des fluides intraveineux et des soins de support. Ces cas représentent les premiers cas documentés de signes cliniques présumés être associés avec de l'hyperammoniémie chez des chevaux d'endurance. Malgré la sévérité de la présentation clinique, les deux chevaux ont récupéré complètement.Message clinique clé :L'hyperammoniémie non-hépatique devrait être considérée comme une cause potentielle de cécité et de confusion chez des chevaux d'endurance en compétition. Les chevaux semblent bien répondre à un traitement avec des fluides intraveineux.(Traduit par Dr Serge Messier).

Evaluation of potential predictor variables for PCR assay diagnosis of Anaplasma phagocytophilum infection in equids in Northern California.

OBJECTIVE To identify clinical or clinicopathologic variables that can be used to predict a positive PCR assay result for Anaplasma phagocytophilum infection in equids. ANIMALS 162 equids. PROCEDURES Medical records were reviewed to identify equids that underwent testing for evidence of A phagocytophilum infection by PCR assay between June 1, 2007, and December 31, 2015. For each equid that tested positive (case equid), 2 time-matched equids that tested negative for the organism (control equids) were identified. Data collected included age, sex, breed, geographic location (residence at the time of testing), physical examination findings, and CBC and plasma biochemical analysis results. Potential predictor variables were analyzed by stepwise logistic regression followed by classification and regression tree analysis. Generalized additive models were used to evaluate identified predictors of a positive test result for A phagocytophilum. RESULTS Total lymphocyte count, plasma total bilirubin concentration, plasma sodium concentration, and geographic latitude were linear predictors of a positive PCR assay result for A phagocytophilum. Plasma creatine kinase activity was a nonlinear predictor of a positive result. CONCLUSIONS AND CLINICAL RELEVANCE Assessment of predictors identified in this study may help veterinarians identify equids that could benefit from early treatment for anaplasmosis while definitive test results are pending. This information may also help to prevent unnecessary administration of oxytetracycline to equids that are unlikely to test positive for the disease.

Prenatal cocaine exposure induces an attenuation of uterine blood flow in the rat.

We have previously demonstrated that maternal cocaine injections result in a gradient of fetal brain cocaine levels that decrease as a function of the fetuses' proximity to the ovaries at embryonic (E) day 15. Our prior data suggest that cocaine-induced vasoconstriction may (1) limit cocaine's entry into the brain and (2) cause damage to DA neurons through injury associated with hypoxia or ischemia of the utero-placental junction. Therefore, using the microsphere technique (labeled with Ru(103)), the following study sought to determine whether the previously observed pattern of cocaine distribution among fetuses in the uterus were due to position-specific reductions in uterine or placental blood flow. On day 15, a single subcutaneous injection of 30 mg/kg cocaine HCl was administered to each rat. Thirty minutes after the cocaine injection, reference blood samples were drawn from the ventral tail artery. Uterine segments and placentae were removed and subjected to gamma counting. While results regarding placental blood flow were equivocal, cocaine significantly reduced average uterine blood flow by 54.6%. In addition, as one moves more proximal to the ovaries, cocaine progressively attenuates blood flow in uterine tissue segments. These data support the hypothesis that the pattern of drug distribution and subsequent brain alterations from prenatal cocaine exposure in our previous reports are likely due to differences in uterine blood flow.