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.
Objective—To investigate the in vitro effects of 3 hydroxyethyl starch (HES) solutions on viscoelastic coagulation testing and platelet function in horses.
Sample—Blood samples collected from 7 healthy adult horses.
Procedures—Blood samples were diluted with various crystalloid and HES solutions to approximate the dilution of blood in vivo that occurs with administration of a 10 and 20 mL/kg fluid bolus to a horse (1:8 and 1:4 dilutions, respectively). Diluted samples were analyzed through optical platelet aggregometry, platelet function analysis, thromboelastography, and dynamic viscoelastic coagulometry. Colloid osmotic pressure and concentrations of von Willebrand factor and factor VIII:C were also determined for each sample.
Results—For all HES products, at both dilutions, the colloid osmotic pressure was significantly higher than that in the respective carrier solutions. At the 1:4 dilution, nearly all HES solutions resulted in significant alterations in platelet function as measured via the platelet function analyzer and dynamic viscoelastic coagulometer. Significant decreases in platelet aggregation and factor concentrations were also evident. Fewer HES-associated changes were identified at the 1:8 dilutions.
Conclusions and Clinical Relevance—Dilution of blood samples with all HES solutions resulted in changes in viscoelastic coagulation and platelet function that did not appear to be attributable to dilution alone. In vivo evaluations are necessary to understand the clinical impact of these in vitro changes.
Objective—To determine the association among signalment, health status, other clinical variables, and treatments and events during cardiopulmonary cerebral resuscitation (CPCR) with the return of spontaneous circulation (ROSC) for animals with cardiopulmonary arrest (CPA) in a veterinary teaching hospital.
Animals—161 dogs and 43 cats with CPA.
Procedures—Data were gathered during a 60-month period on animals that had CPA and underwent CPCR. Logistic regression was used to evaluate effects of multiple predictors for ROSC.
Results—56 (35%) dogs and 19 (44%) cats had successful CPCR. Twelve (6%) animals (9 dogs and 3 cats) were discharged from the hospital. Successfully resuscitated dogs were significantly more likely to have been treated with mannitol, lidocaine, fluids, dopamine, corticosteroids, or vasopressin; had CPA while anesthetized; received chest compressions while positioned in lateral recumbency; and had a suspected cause of CPA other than hemorrhage or anemia, shock, hypoxemia, multiple organ dysfunction syndrome, cerebral trauma, malignant arrhythmia, or an anaphylactoid reaction and were less likely to have been treated with multiple doses of epinephrine, had a longer duration of CPA, or had multiple disease conditions, compared with findings in dogs that were not successfully resuscitated. Successfully resuscitated cats were significantly more likely to have had more people participate in CPCR and less likely to have had shock as the suspected cause of CPA, compared with findings in cats that were not successfully resuscitated.
Conclusions and Clinical Relevance—The prognosis was grave for animals with CPA, except for those that had CPA while anesthetized.
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 determine the quality and speed of recovery from anesthesia with isoflurane, sevoflurane, or desflurane and determine end-tidal inhalant concentration at certain events during recovery in healthy dogs.
Animals—11 healthy dogs.
Procedures—Anesthesia was induced with propofol (IV), and dogs were assigned by use of a crossover design to receive isoflurane at 2.0%, sevoflurane at 3.2%, or desflurane at 11% end-tidal concentrations. Direct blood pressure was monitored throughout the 120 minutes of anesthesia. At the end of anesthesia, the circuit was flushed with oxygen, and the time to specific events in recovery and overall quality of recovery were assessed. Blood gas concentrations were measured prior to anesthesia and after recovery.
Results—Dogs in the desflurane group had the shortest time to standing (11.7 ± 5.1 minutes), followed by dogs in the sevoflurane group (18.6 ± 7.5 minutes) and dogs in the isoflurane group (26.3 ± 7.2 minutes). There was no difference for recovery quality among groups. Arterial blood pressure was higher in the sevoflurane group than in the desflurane group at 10 and 15 minutes and in the isoflurane group at 10, 15, 30, 45, 60, 75, 105, and 120 minutes. There were no significant differences among groups with respect to blood gas concentrations.
Conclusions and Clinical Relevance—Results suggested that in dogs for which a short interval to standing is desired, desflurane is the best selection, followed by sevoflurane.
Objective—To determine pharmacodynamic and pharmacokinetic properties of clopidogrel and the metabolite SR 26334 in dogs.
Animals—9 mixed-breed dogs.
Procedures—8 dogs received clopidogrel (mean ± SD 1.13 ± 0.17 mg/kg, PO, q 24 h) for 3 days; 5 of these dogs subsequently received a lower dose of clopidogrel (0.5 ± 0.18 mg/kg, PO, q 24 h) for 3 days. Later, 5 dogs received clopidogrel (1.09 ± 0.12 mg/kg, PO, q 24 h) for 5 days. Blood samples were collected for optical platelet aggregometry, citrated native and platelet mapping thrombelastography (TEG), and measurement of plasma drug concentrations. Impedance aggregometry was performed on samples from 3 dogs in each 3-day treatment group.
Results—ADP-induced platelet aggregation decreased (mean ± SD 93 ± 6% and 80 ± 22% of baseline values, respectively) after 72 hours in dogs in both 3-day treatment groups; duration of effect ranged from > 3 to > 7 days. Platelet mapping TEG and impedance aggregometry yielded similar results. Citrated native TEG was not different among groups. Clopidogrel was not detected in any samples; in dogs given 1.13 ± 0.17 mg/kg, maximum concentration of SR 26334 (mean ± SD, 0.206 ± 0.2 μg/mL) was detected 1 hour after administration.
Conclusions and Clinical Relevance—Clopidogrel inhibited ADP-induced platelet aggregation in healthy dogs and may be a viable antiplatelet agent for use in dogs.
Impact for Human Medicine—Pharmacodynamic effects of clopidogrel in dogs were similar to effects reported in humans; clopidogrel may be useful in studies involving dogs used to investigate human disease.
Objective—To determine minimum plasma concentrations of the antifibrinolytic agents tranexamic acid (TEA) and ϵ-aminocaproic acid (EACA) needed to completely inhibit fibrinolysis in canine and human plasma after induction of hyperfibrinolysis.
Samples—Pooled citrated plasma from 7 dogs and commercial pooled citrated human plasma.
Procedures—Concentrations of EACA from 0 μg/mL to 500 μg/mL and of TEA from 0 μg/mL to 160 μg/mL were added to pooled citrated canine and human plasma. Hyperfibrinolysis was induced with 1,000 units of tissue plasminogen activator/mL, and kaolin-activated thromboelastography was performed in duplicate. The minimum concentrations required to completely inhibit fibrinolysis 30 minutes after maximum amplitude of the thromboelastography tracing occurred were determined.
Results—Minimum plasma concentrations necessary for complete inhibition of fibrinolysis by EACA and TEA in pooled canine plasma were estimated as 511.7 μg/mL (95% confidence interval [CI], 433.2 to 590.3 μg/mL) and 144.7 μg/mL (95% CI, 125.2 to 164.2 μg/mL), respectively. Concentrations of EACA and TEA necessary for complete inhibition of fibrinolysis in pooled human plasma were estimated as 122.0 μg/mL (95% CI, 106.2 to 137.8 μg/mL) and 14.7 μg/mL (95% CI, 13.7 to 15.6 μg/mL), respectively.
Conclusions and Clinical Relevance—Results supported the concept that dogs are hyperfibrinolytic, compared with humans. Higher doses of EACA and TEA may be required to fully inhibit fibrinolysis in dogs.
Objective—To determine induction characteristics and the minimum alveolar concentration (MAC) at which consciousness returned (MACawake) in dogs anesthetized with isoflurane or sevoflurane.
Animals—20 sexually intact male Beagles.
Procedures—In experiment 1, 20 dogs were randomly assigned to have anesthesia induced and maintained with isoflurane or sevoflurane. The MAC at which each dog awoke in response to auditory stimulation (MACawake-noise) was determined by decreasing the end-tidal concentration by 0.1 volume (vol %) every 15 minutes and delivering a standard audible stimulus at each concentration until the dog awoke. In experiment 2, 12 dogs received the same anesthetic agent they were administered in experiment 1. After duplicate MAC determination, the end-tidal concentration was continually decreased by 10% every 15 minutes until the dog awoke from anesthesia (MACawake).
Results—Mean induction time was significantly greater for isoflurane-anesthetized dogs (212 seconds), compared with the sevoflurane-anesthetized dogs (154 seconds). Mean ± SD MACawake-noise was 1.1 ± 0.1 vol % for isoflurane and 2.0 ± 0.2 vol % for sevoflurane. Mean MAC was 1.3 ± 0.2 vol % for isoflurane and 2.1 ± 0.6 vol % for sevoflurane, and mean MACawake was 1.0 ± 0.1 vol % for isoflurane and 1.3 ± 0.3 vol % for sevoflurane.
Conclusions and Clinical Relevance—Sevoflurane resulted in a more rapid induction than did isoflurane. The MACawake for dogs was higher than values reported for both agents in humans. Care should be taken to ensure that dogs are at an appropriate anesthetic depth to prevent consciousness, particularly when single-agent inhalant anesthesia is used.
Objective—To determine the effects of nonsteroidal anti-inflammatory drugs of various cyclooxygenase selectivities on hemostasis and prostaglandin expression in dogs.
Animals—8 client-owned dogs with clinical signs of osteoarthritis.
Procedures—Dogs received aspirin (5 mg/kg, PO, q 12 h), carprofen (4 mg/kg, PO, q 24 h), deracoxib (2 mg/kg, PO, q 24 h), and meloxicam (0.1 mg/kg, PO, q 24 h) for 10 days each, with an interval of at least 14 days between treatments. On days 0 and 10, blood was collected for platelet aggregation assays, thrombelastography, and measurement of lipopolysaccharide-stimulated prostaglandin E2, platelet thromboxane B2 (TXB2), and free serum TXB2 and 6-keto-prostaglandin F (PGF)-1α concentrations.
Results—Platelet aggregation decreased after treatment with aspirin and carprofen, whereas significant changes from baseline were not detected for the other drugs tested. Thrombelastograms obtained after treatment with carprofen revealed decreased maximum amplitude and α-angle, suggesting hypocoagulability. Maximum amplitude and coagulation index increased after treatment with deracoxib. Plasma concentrations of prostaglandin E2 decreased after treatment with carprofen or deracoxib, and platelet TXB2 production increased after treatment with aspirin. Serum concentrations of the prostacyclin metabolite 6-keto-PGF-1α did not change significantly after treatment with any of the drugs, although the ratio of free TXB2 to 6-keto-PGF-1α decreased slightly after treatment with carprofen and increased slightly after treatment with deracoxib.
Conclusions and Clinical Relevance—At the dosages tested, treatment with meloxicam affected platelet function minimally in dogs with osteoarthritis. Treatment with carprofen decreased clot strength and platelet aggregation. Clot strength was increased after treatment with deracoxib.