To determine the effect of PCV on blood glucose concentration measurements in feline blood samples tested with a point-of-care (POC) glucometer and to develop and evaluate a correction formula that adjusts POC glucometer–measured blood glucose concentration (POCgluc) for a given PCV.
Experimental and prospective study.
Blood samples from 4 healthy and 16 hospitalized cats.
Heparinized blood samples from healthy cats were processed into packed RBCs and plasma. Packed RBCs were resuspended with plasma to achieve PCVs ranging from 0% to 87%. Duplicate PCV and POCgluc measurements were obtained for each suspension. Plasma glucose concentration as measured by a clinical laboratory biochemical analyzer (LABgluc) was assessed; results were compared with the POCgluc. A formula to correct POCgluc measurements for PCV was developed. Blood samples from hospitalized cats were used to evaluate the formula.
For each healthy cat, LABgluc values were similar for all PCVs; the mean difference between POCgluc and LABgluc at PCVs outside a range of 35% to 55% was significant. Mean differences between POCgluc and LABgluc were 24.3 and 41.5 mg/dL, whereas mean differences between corrected POCgluc and LABgluc were 3 and 25.9 mg/dL for samples from healthy and hospitalized cats, respectively. Correlation between corrected POCgluc and LABgluc was stronger than that between POCgluc and LABgluc for samples from healthy and hospitalized cats.
CONCLUSIONS AND CLINICAL RELEVANCE
The POCgluc did not reflect LABgluc in hemodiluted or hemoconcentrated feline blood samples. Use of a correction formula appeared to reduce this error. Additional studies are needed to evaluate the frequency with which this correction formula might prevent clinical errors. (J Am Vet Med Assoc 2019;254:1180–1185)
Objective—To determine the effect of PCV on veterinary point-of-care (POC) glucometer measurements in canine blood samples and develop a formula to correct the glucose concentration as measured by a point-of-care glucometer (POCgluc) given a known PCV.
Design—Experimental and prospective study.
Samples—Blood samples from 6 healthy dogs and from 30 hospitalized dogs.
Procedures—60 mL of heparinized blood was obtained from each of 6 healthy dogs. Samples were processed into packed RBCs and plasma. Packed RBCs were resuspended with plasma to achieve a range of PCVs from 0% to 94%. Duplicate POCgluc and PCV measurements were obtained for each dilution; following POCgluc measurements, plasma samples were analyzed for glucose concentration by a clinical laboratory biochemical analyzer (LABgluc). A correction formula for POCgluc was developed. Measurements of POCgluc, PCV, and LABgluc were also determined from blood samples of 30 dogs admitted to the veterinary teaching hospital.
Results—Values of LABgluc for each sample were similar at any PCV. As PCV decreased, POCgluc was falsely increased; as PCV increased, POCgluc was falsely decreased, compared with LABgluc. The absolute difference between POCgluc and LABgluc increased as the PCV changed from 50%. Compared with POCgluc, the corrected POCgluc had a significantly improved correlation with LABgluc, which was also reflected in improvements in Clarke and consensus error grid analyses.
Conclusions and Clinical Relevance—Results indicated that in dogs with hemodilution or hemoconcentration, POCgluc did not reflect actual patient glucose concentrations. Use of a correction formula reduced this error. Corrected POCgluc data had strong, significant correlations with LABgluc data.
To assess the agreement in measurements of Hct values and hemoglobin (Hgb) concentrations in blood samples from dogs and cats between a commercially available veterinary point-of-care (POC) Hct meter and a laboratory-based (LAB) analyzer and to determine the effects of various conditions (ie, lipemia, hyperbilirubinemia, hemolysis, autoagglutination, and reticulocytosis) on the accuracy of the POC meter.
Blood samples from 86 dogs and 18 cats
Blood samples were run in duplicate on the POC meter, which reported Hgb concentration, measured via optical reflectance, and a calculated Hct value. The POC meter results were compared with results from a LAB analyzer. Blood samples with grossly visible lipemia, icterus, hemolysis, and autoagglutination were noted.
Mean ± SD values for LAB Hct were 33.9 ± 15.73% (range, 3.9% to 75.8%), and for LAB Hgb were 11.2 ± 5.4 g/dL (range, 1 to 24.6 g/dL). Mean bias between POC Hct and LAB Hct values was–1.8% with 95% limits of agreement (LOAs) of–11.1% to 7.5% and between POC Hgb and LAB Hgb concentrations was–0.5 g/dL with 95% LOAs of–3.8 to 2.8 g/dL. There was no influence of lipemia (14 samples), icterus (23), autoagglutination (14), hemolysis (12), or high reticulocyte count (15) on the accuracy of the POC meter. The POC meter was unable to read 13 blood samples; 9 had a LAB Hct ≤ 12%, and 4 had a LAB Hct concentration between 13% and 17%.
CONCLUSIONS AND CLINICAL RELEVANCE
Overall, measurements from the POC meter had good agreement with those from the LAB analyzer. However, LOAs were fairly wide, indicating that there may be clinically important differences between measurements from the POC meter and LAB analyzer. (J Am Vet Med Assoc 2021;259:49–55)
OBJECTIVE To assess pharmacokinetics of tranexamic acid (TXA) in dogs and assess antifibrinolytic properties of TXA in canine blood by use of a thromboelastography-based in vitro model of hyperfibrinolysis.
ANIMALS 6 healthy adult dogs.
PROCEDURES Dogs received each of 4 TXA treatments (10 mg/kg, IV; 20 mg/kg, IV; approx 15 mg/kg, PO; and approx 20 mg/kg, PO) in a randomized crossover-design study. Blood samples were collected at baseline (time 0; immediately prior to drug administration) and predetermined time points afterward for pharmacokinetic analysis and pharmacodynamic (thromboelastography) analysis by use of an in vitro hyperfibrinolysis model.
RESULTS Maximum amplitude (MA [representing maximum clot strength]) significantly increased from baseline at all time points for all treatments. The MA was lower at 360 minutes for the 10-mg/kg IV treatment than for other treatments. Percentage of clot lysis 30 minutes after MA was detected was significantly decreased from baseline at all time points for all treatments; at 360 minutes, this value was higher for the 10-mg/kg IV treatment than for other treatments and higher for the 20-mg/kg IV treatment than for the 20-mg/kg PO treatment. Maximum plasma TXA concentrations were dose dependent. At 20 mg/kg, IV, plasma TXA concentrations briefly exceeded concentrations suggested for complete inhibition of fibrinolysis. Oral drug administration resulted in a later peak antifibrinolytic effect than did IV administration.
CONCLUSIONS AND CLINICAL RELEVANCE Administration of TXA improved clot strength and decreased fibrinolysis in blood samples from healthy dogs in an in vitro hyperfibrinolysis model. Further research is needed to determine clinical effects of TXA in dogs with hyperfibrinolysis.