Objective—To evaluate the usefulness of a veterinary point-of-care glucometer for identification of septic peritonitis in dogs with peritoneal effusion (PE).
Design—Prospective clinical evaluation.
Animals—39 dogs with PE.
Procedures—Blood and peritoneal fluid convenience samples were collected concurrently in all dogs at the time of initial evaluation. A veterinary point-of-care glucometer was used to measure glucose concentration in heparinized whole blood, plasma, peritoneal fluid, and peritoneal fluid supernatant samples. Seventeen dogs had confirmed septic peritonitis, and 22 dogs had nonseptic PE. Sensitivity, specificity, positive and negative predictive values, and accuracy of identification of dogs with septic peritonitis were calculated for glucose concentration differences for whole blood versus peritoneal fluid (WB-PF), plasma versus peritoneal fluid (P-PF), and plasma versus peritoneal fluid supernatant (P-PFS).
Results—With a cutoff of > 20 mg/dL, the glucose concentration difference for WB-PF was an insensitive indicator of septic peritonitis (sensitivity, 41.2%; specificity, 100%). In comparison, the glucose concentration differences for P-PF and P-PFS had a higher sensitivity for septic peritonitis (88.2% and 82.4%, respectively) but a lower specificity (80% and 77.8%, respectively). With a glucose concentration difference cutoff of ≥ 38 mg/dL, specificity, positive predictive value, and accuracy of P-PF and P-PFS improved.
Conclusions and Clinical Relevance—Determination of the glucose concentration difference for WB-PF with the veterinary point-of-care glucometer was not useful in identifying all dogs with septic peritonitis. A glucose concentration difference of ≥ 38 mg/dL for P-PF or P-PFS, however, supported an accurate diagnosis of septic peritonitis in dogs with PE.
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)
To determine effects of PCV on blood glucose (BG) concentration measurements obtained with a human portable blood glucometer (HPBG) and a veterinary portable blood glucometer (VPBG) on canine (cVPBG) and feline (fVPBG) settings (test methods) when used in rabbits and to develop correction formulas to mitigate effects of PCV on such measurements.
48 resuspended blood samples with known PVCs (range, 0% [plasma] to 92% [plasma and packed RBCs]) from 6 healthy research rabbits (experimental sample set) and 252 historic measurements of BG concentration and PCV in 84 client-owned rabbits evaluated at a veterinary hospital (validation data set).
Duplicate measurements of BG concentration with each test method and of PCV were obtained for each sample in the experimental sample set, and the mean results for each variable for each test method and sample were compared with results from a clinical laboratory analyzer (reference method) used to determine the true BG concentration for each sample. Mean ± SD differences in measurements between the reference and test methods were calculated. Linear regression and modified Clarke error grid analysis were used to develop correction formulas for the test methods given known PCVs, and these formulas were evaluated on the validation data set with linear regression and a modified Clarke error grid.
Blood glucose concentrations were falsely low for cVPBG and fVPBG used on samples with PCV < 31% and were falsely high for all test methods used on samples with PCV > 43%. Compared with original measurements, formula-corrected measurements overall had better agreement with reference method measurements for the experimental sample set; however, only the formula-corrected HPBG measurements had improved agreement for the validation data set.
CONCLUSIONS AND CLINICAL RELEVANCE
Findings indicated that, in rabbits, HPBG measurements had improved accuracy with the use of the correction formula HPBG measurement of BG concentration + ([0.75 × PCV] − 15); however, the correction formulas did not improve the accuracy of VPBG measurements, and we believe that neither the cVPBG nor fVPBG should be used in rabbits.
OBJECTIVE To identify variations in glucose values concurrently obtained by use of a continuous glucose monitoring system (CGMS) at the same site, reliability of results for each site, lag time for each site, and influence of site thickness on CGMS accuracy.
ANIMALS 8 random-source research dogs.
PROCEDURES In experiment 1, 8 CGMS sensors were implanted bilaterally at 1 site (4 sensors/side) in 4 dogs. In experiment 2, 2 CGMS sensors were implanted bilaterally at each of 4 sites (1 sensor/side) in 8 dogs; 4 of those 8 dogs then were subjected to a glycemic clamp technique. The CGMS results were compared among sensors and with criterion-referenced results during periods of euglycemia for all 8 dogs and during hyperglycemia and hypoglycemia for 4 dogs during the glycemic clamp procedure.
RESULTS Differences (median, −7 mg/dL; interquartile range [IQR], −18.75 to 3 mg/dL) between CGMS and criterion-referenced glucose concentrations differed significantly among dogs and sites; during euglycemia, they were not different from the expected normal variation between multiple sensors concurrently implanted at the same site. Differences (median, −35 mg/dL; IQR, −74 to −15 mg/dL) between CGMS and criterion-referenced concentrations were greater during changes in glucose concentrations. Thoracic sensors were most accurate but had the shortest mean functional life.
CONCLUSIONS AND CLINICAL RELEVANCE Significant differences were detected between CGMS and criterion-referenced glucose concentrations. Overall clinical utility of CGMS was acceptable at all sites, with most of the values from all sensors, sites, and dogs meeting guidelines for point-of-care glucometers.
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 evaluate the pharmacodynamic effects of dalteparin in dogs by means of viscoelastic coagulation monitoring with a thromboelastograph and a dynamic viscoelastic coagulometer.
Animals—6 healthy adult mixed-breed dogs.
Procedures—Dalteparin (175 U/kg, SC, q 12 h) was administered for 4 days (days 1 through 4). Viscoelastic coagulation monitoring was performed hourly on the first and last days of treatment and included intermittent measurement of anti–activated coagulation factor X activity (AXA).
Results—Dalteparin administration resulted in progressive hypocoagulability. On both day 1 and 4, activated clotting time and clot rate for the dynamic viscoelastic coagulometer differed significantly from baseline values, whereas the platelet function parameter did not change on day 1 but did on day 4. The R (reaction time), time from reaction time until the amplitude of the thromboelastography tracing is 20 mm, α-angle, and maximum amplitude differed from baseline values on days 1 and 4, although many thromboelastographic variables were not determined. The AXA was increased from baseline values at 3 and 6 hours after administration of the dalteparin injection on days 1 and 4, and all dogs had AXA values between 0.5 and 1.0 U/mL at 2 and 4 hours after administration. The AXA correlated well with activated clotting time (r = 0.761) and with R (r = 0.810), when values were available. Thromboelastography could not be used to distinguish AXA > 0.7 U/mL.
Conclusions and Clinical Relevance—Viscoelastic coagulation monitoring with strong coagulation activators may be used to monitor treatment with dalteparin in healthy dogs.
OBJECTIVE To identify risk factors for temporary tracheostomy tube placement (TTTP) following surgery for alleviation of signs associated with brachycephalic obstructive airway syndrome (BOAS) in dogs.
DESIGN Retrospective case-control study.
ANIMALS 122 client-owned dogs with BOAS that underwent surgery to alleviate clinical signs (BOAS surgery).
PROCEDURES The medical records database of a veterinary teaching hospital was searched to identify dogs that underwent BOAS surgery from January 2007 through March 2016. Of the 198 dogs identified, 12 required postoperative TTTP (cases); 110 of the remaining 186 dogs were randomly selected as controls. Data regarding signalment and select preoperative, intraoperative, and postoperative variables were extracted from the medical record of each dog. Variables were compared between cases and controls and evaluated for an association with the odds of postoperative TTTP.
RESULTS Body condition score, tracheal diameter-to-thoracic inlet ratio, staphylectomy technique, and mortality rate did not differ significantly between cases and controls. The odds of postoperative TTTP increased approximately 30% (OR, 1.3) for each 1-year increase in patient age. Postoperative administration of corticosteroids and presence of pneumonia were also positively associated with the odds of postoperative TTTP. Median duration of hospitalization was significantly longer for cases than controls.
CONCLUSIONS AND CLINICAL RELEVANCE Age was positively associated with the odds of TTTP in dogs after BOAS surgery, and TTTP led to prolonged hospitalization. Thus, early identification and intervention may be beneficial for dogs with BOAS. The associations between TTTP and postoperative corticosteroid use or pneumonia were likely not causal, but reflective of patient disease severity.
Case Description—A 2-year-old 38.9-kg (85.58-lb) sexually intact male German Shepherd Dog was examined because of a 4-month history of severe nasal swelling and nasal mucosa congestion. The signs were slowly progressive.
Clinical Findings—Physical examination revealed that the dorsal aspect of the dog's nose was swollen and hard. Mucous membranes in both nostrils were hyperemic and edematous. Diagnostic investigation revealed severe nasal osteolysis and pyogranulomatous rhinitis and nasopharyngitis attributable to blastomycosis.
Treatment and Outcome—Oral administration of itraconazole was initiated (5 mg/kg [2.27 mg/lb], q 12 h for 5 days and then q 24 h). After a treatment period of 3 months, the nose had regained its normal appearance. After 5 months of treatment, the Blastomyces infection was eliminated as confirmed by results of rhinoscopy and biopsy specimen examination. No relapse was evident within 1 year after discontinuation of treatment.
Clinical Relevance—In dogs, nasal and nasopharyngeal blastomycosis can result in severe osteolysis of the nasal bone. Resolution of disease can be achieved with oral administration of itraconazole for a period of at least 5 months.
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.