OBJECTIVE To compare stability of hemostatic proteins in canine fresh-frozen plasma (FFP) thawed with a modified commercial microwave warmer (MCM) or warm water bath (37°C; WWB) or at room temperature (22°C).
SAMPLE Fresh-frozen plasma obtained from 8 canine donors of a commercial blood bank.
PROCEDURES A commercial microwave warmer was modified with a thermocouple to measure surface temperature of bags containing plasma. The MCM and a WWB were each used to concurrently thaw a 60-mL bag of plasma obtained from the same donor. Two 3-mL control aliquots of FFP from each donor were thawed to room temperature without use of a heating device. Concentrations of hemostatic proteins, albumin, and D-dimers; prothrombin time (PT); and activated partial thromboplastin time (aPTT) were determined for all samples.
RESULTS Significant decreases in concentrations of factors II, IX, X, XI, fibrinogen, von Willebrand factor, antithrombin, protein C, and albumin and significant increases in PT and aPTT were detected for plasma thawed with the MCM, compared with results for samples thawed with the WWB. Concentrations of factors VII, VIII, and XII were not significantly different between plasma thawed with the MCM and WWB. Concentrations of D-dimers were above the reference range for all thawed samples regardless of thawing method. No significant differences in factor concentrations were detected between control and WWB-thawed samples.
CONCLUSIONS AND CLINICAL RELEVANCE Significant differences in hemostatic protein concentrations and coagulation times were detected for plasma thawed with an MCM but not between control and WWB-thawed samples. Clinical importance of these changes should be investigated.
Objective—To measure serum calprotectin concentration in dogs with inflammatory bowel disease (IBD) before and after initiation of treatment and evaluate its correlation with a clinical scoring system (canine IBD activity index), serum canine C-reactive protein concentration, and severity of histopathologic changes.
Animals—34 dogs with idiopathic IBD and 139 healthy control dogs.
Procedures—From dogs with IBD, blood samples were collected immediately before (baseline) and 3 weeks after initiation of 1 of 2 treatments: prednisone (1 mg/kg, PO, q 12 h; n = 21) or a combination of prednisone and metronidazole (10 mg/kg, PO, q 12 h; 13). Blood samples were collected once from each of the control dogs. For all samples, serum calprotectin concentration was determined via radioimmunoassay.
Results—Mean serum calprotectin concentrations for dogs with IBD at baseline (431.1 μg/L) and 3 weeks after initiation of treatment (676.9 μg/L) were significantly higher, compared with that (219.4 μg/L) for control dogs, and were not significantly correlated with the canine IBD activity index, serum C-reactive protein concentration, or severity of histopathologic changes. The use of a serum calprotectin concentration of ≥ 296.0 μg/L as a cutoff had a sensitivity of 82.4% (95% confidence interval, 65.5% to 93.2%) and specificity of 68.4% (95% confidence interval, 59.9% to 76.0%) for distinguishing dogs with idiopathic IBD from healthy dogs.
Conclusions and Clinical Relevance—Serum calprotectin concentration may be a useful biomarker for the detection of inflammation in dogs, but the use of certain drugs (eg, glucocorticoids) appears to limit its clinical usefulness.
OBJECTIVE To establish the minimum alveolar concentration (MAC) of desflurane and evaluate the effects of 2 opioids on MAC in sheep.
ANIMALS 8 adult nulliparous mixed-breed sheep.
PROCEDURES A randomized crossover design was used. Each sheep was evaluated individually on 2 occasions (to allow assessment of the effects of each of 2 opioids), separated by a minimum of 10 days. On each occasion, sheep were anesthetized with desflurane in 100% oxygen, MAC of desflurane was determined, oxymorphone (0.05 mg/kg) or hydromorphone (0.10 mg/kg) was administered IV, and MAC was redetermined. Physiologic variables and arterial blood gas and electrolyte concentrations were measured at baseline (before MAC determination, with end-tidal desflurane concentration maintained at 10%) and each time MAC was determined. Timing of various stages of anesthesia was recorded for both occasions.
RESULTS Mean ± SEM MAC of desflurane was 8.6 ± 0.2%. Oxymorphone or hydromorphone administration resulted in significantly lower MAC (7.6 ± 0.4% and 7.9 ± 0.2%, respectively). Cardiac output at MAC determination for desflurane alone and for desflurane with opioid administration was higher than that at baseline. No difference was identified among hematologic values at any point. Effects of oxymorphone and hydromorphone on durations of various stages of anesthesia did not differ significantly.
CONCLUSIONS AND CLINICAL RELEVANCE MAC of desflurane in nulliparous adult sheep was established. Intravenous administration of oxymorphone or hydromorphone led to a decrease in MAC; however, the clinical importance of that decrease was minor relative to the effect in other species.
Objective—To evaluate use of crotalid antivenom, frequency of hypersensitivity reactions, and risk factors for hypersensitivity reactions and death in envenomed cats.
Design—Retrospective multicenter case series.
Animals—115 envenomed cats treated with antivenom and 177 envenomed cats treated without antivenom.
Procedures—Medical records from 5 institutions were searched by means of a multiple-choice survey with standardized answers for patient data including signalment, diagnosis, antivenom administration criteria, premedication, product, dose, administration rate, hypersensitivity reactions, and mortality rate.
Results—95 of 115 (82.6%) cats received whole IgG antivenom, 11 (9.57%) received F(ab′)2 antivenom, and 4 (3.48%) received Fab antivenom. The majority (101/115 [878%]) of cats received 1 vial of antivenom. In all cats, the median dilution of antivenom was 1:60 (range, 1:10 to 1:250) administered over a median period of 2.0 hours (range, 0.3 to 9.0 hours). There was no mortality rate difference between cats that did (6.67%) or did not (5.08%) receive antivenom. A type I hypersensitivity reaction was diagnosed in 26 of 115 (22.6%) cats. The use of premedications did not decrease type I hypersensitivity or improve mortality rate. Cats that had a type I hypersensitivity reaction were 10 times as likely to die as were those that did not have such a reaction.
Conclusions and Clinical Relevance—The mortality rate of cats treated with antivenom was low. The administration of premedications did not improve mortality rate or prevent hypersensitivity reactions. The only variable associated with mortality rate was development of a type I hypersensitivity reaction. The rate of antivenom administration should be further evaluated as a possible risk factor for type I hypersensitivity reactions.