Objective—To assess a point-of-care instrument for
identification of primary hemostatic disorders in dogs.
Animals—29 healthy dogs and 23 nonanemic dogs
with primary hemostatic disorders (thrombocytopenia,
n = 6; thrombopathia, 6; von Willebrand disease
Procedure—Citrated blood was obtained and closure
times (CT) were determined by measuring the time
required for occlusion of an aperture by a platelet plug
within the point-of-care instrument. Reference ranges
for CT were established, and CT were determined for
dogs with primary hemostatic disorders.
Results—CT measured with adenosine diphosphate
as the platelet agonist (ADP-CT) ranged from 52 to 86
seconds for healthy dogs (mean ± 2 SD, 67 ± 7.8 seconds;
median, 65 seconds), and CT measured with
epinephrine as the agonist (EPI-CT), from 97 to 225
seconds (151 ± 38 seconds; 148 seconds). In thrombocytopenic
dogs, ADP- and EPI-CT were prolonged
(> 165 and > 264 seconds, respectively). Five of 6
dogs with thrombopathia had prolonged ADP-CT,
whereas EPI-CT was prolonged in all 6 dogs. In all
dogs with vWD, ADP-CT was prolonged; EPI-CT was
prolonged in 10 of these dogs. Sensitivity and specificity
for ADP-CT were 95.7 and 100%, respectively,
and positive and negative predictive values, 100 and
96.7%, respectively, whereas for EPI-CT, these values
were 95.7 and 82.8%, respectively, and 81.5 and
Conclusions and Clinical Relevance—The point-ofcare
instrument allowed quick assessment of primary
hemostasis in nonanemic dogs. Use of this instrument
may be helpful for making decisions regarding
management of dogs with primary hemostatic disorders.
(Am J Vet Res 2001;62:652–658)
Objective—To evaluate primary hemostasis following
administration of desmopressin acetate (DDAVP) to
Doberman Pinschers with type-1 von Willebrand disease
Animals—16 nonanemic Doberman Pinschers with
Procedure—Closure time (CT), defined as time
required for occlusion of an aperture by a platelet plug
assessed within the point-of-care instrument, plasma
von Willebrand factor (vWF) concentration, and buccal
mucosal bleeding time (BMBT) were determined
before and 1 hour after administration of DDAVP (1
Results—Baseline closure times measured with
adenosine diphosphate ([ADP-CT], 108 to > 300 seconds;
reference range, 52 to 86 seconds) and epinephrine
([EPI-CT], 285 to > 300 seconds; 97 to 225
seconds) as platelet agonists were prolonged in all
dogs. Following DDAVP administration, ADP-CT (59 to
186 seconds) was significantly shortened from baseline,
but there was no decrease in EPI-CT. Although
mean plasma vWF concentration increased significantly
after DDAVP administration, only 1 dog had an
increase of > 35 U/dL. There was no correlation
between increase in plasma vWF concentration and
shortening of the ADP-CT. Baseline BMBT was prolonged
in 12 of 14 dogs, with significant shortening of
BMBT after DDAVP administration in 6 of 7 dogs. In
vitro replacement of vWF-deficient plasma with plasma
from an unaffected dog shortened the ADP-CT,
whereas in vitro addition of DDAVP had no effect.
Conclusions and Clinical Relevance—Administration
of DDAVP to Doberman Pinschers with type-1 vWD
resulted in improved hemostatic function, as assessed
by the point-of-care instrument and shortening of
BMBT, despite minimal increase in plasma vWF concentration.
(Am J Vet Res 2002;63:1700–1706)
Objective—To assess the effect of desmopressin
(DDAVP) administration in Doberman Pinschers with
type 1 von Willebrand disease (vWD) on plasma von
Willebrand factor (vWF) multimers through determination
of vWF collagen binding activity (vWF:CBA; a
functional vWF assay dependent on the presence of
high–molecular-weight [HMW] multimers), comparison
of vWF antigen concentration (vWF:Ag) to
vWF:CBA, and vWF multimer size distribution.
Animals—16 Doberman Pinschers with type 1 vWD
and 5 clinically normal control dogs.
Procedure—Plasma vWF:Ag and vWF:CBA assays
and vWF multimer analysis were performed before
and 1 hour after administration of DDAVP (1 µg/kg,
Results—Following DDAVP administration, dogs with
type 1 vWD had an increase in mean baseline values
of plasma vWF:Ag and vWF:CBA from 10% to 17%
for both variables. The mean vWF Ag:CBA ratio at
baseline (0.95) was similar after DDAVP administration
(0.97), indicating concordant increases in plasma
vWF concentration and activity. In control dogs, mean
plasma vWF:Ag and vWF:CBA increased from baseline
values of 64% to 113% and 58% to 114%,
respectively, and the vWF Ag:CBA ratios were
unchanged (1.1 vs 1.0) after DDAVP administration.
Plasma vWF multimer analysis revealed proportional
increases in band intensity for all multimer sizes following
DDAVP administration, in comparison to baseline
for the control dogs and Doberman Pinschers
with vWD, consistent with vWF Ag:CBA ratios of
Conclusions and Clinical Relevance—Beneficial
effects of DDAVP on primary hemostasis in
Doberman Pinschers with type 1 vWD cannot be
explained by preferential increases in HMW vWF multimers.
(Am J Vet Res 2005;66:861–867)
Objective—To compare effects of 3.8% sodium citrate and anticoagulant citrate dextrose solution National Institutes of Health formula A (ACD-A) on pH, extracellular ionized calcium (iCa) concentration, and platelet aggregation in canine platelet-rich plasma (PRP).
Sample Population—Samples from 12 dogs.
Procedures—Blood samples were collected into 3.8% sodium citrate (dilution, 1:9) and ACD-A (dilution, 1:5). Platelet function, pH, and iCa concentration were evaluated in PRP. Platelet agonists were ADP, γ-thrombin, and convulxin; final concentrations of each were 20μm, 100nM, and 20nM, respectively. Washed platelets were used to evaluate effects of varying the pH and iCa concentration.
Results—Mean pH and iCa concentration were significantly greater in 3.8% sodium citrate PRP than ACD-A PRP. Platelet aggregation induced by ADP and γ-thrombin was markedly diminished in ACD-A PRP, compared with results for 3.8% sodium citrate PRP. Anticoagulant had no effect on amplitude of convulxin-induced platelet aggregation. In washed platelet suspensions (pH, 7.4), there were no differences in amplitude of platelet aggregation induced by convulxin or γ-thrombin at various iCa concentrations. Varying the pH had no effect on amplitude of aggregation induced by convulxin or γ-thrombin, but the aggregation rate increased with increasing pH for both agonists.
Conclusions and Clinical Relevance—Aggregation of canine platelets induced by ADP and γ-thrombin was negligible in ACD-A PRP, which suggested an increase in extraplatelet hydrogen ion concentration inhibits signaling triggered by these agonists but not by convulxin. Choice of anticoagulant may influence results of in vitro evaluation of platelet function, which can lead to erroneous conclusions.
Objective—To determine clinical features and outcome
associated with use of a hemoglobin-based
oxygen-carrying (HBOC) solution in cats.
Procedure—Medical records of cats that received an
HBOC solution were reviewed.
Results—The most common clinical signs and physical
examination findings prior to infusion of the HBOC
solution were associated with anemia; vomiting, neurologic
signs, and respiratory abnormalities were also
detected. The HBOC solution was given as a supportive
measure in treatment of anemia in 70 cats, most
often because compatible blood was not readily available.
There were 80 separate HBOC solution infusion
events (mean dose, 14.6 ml/kg [6.6 mg/lb]; mean rate
of infusion, 4.8 ml/kg [2.2 ml/lb] per hour).
Improvements in 37 of 43 of the more closely monitored
cats included increased rectal temperature, blood
hemoglobin concentration, blood pressure, appetite,
and activity. Adverse events in 44 cats included pulmonary
edema (n = 8), pleural effusion (21), mucous
membrane discoloration (21), pigmenturia (11), vomiting
(4), and neurologic abnormalities (4). Twenty-three
cats were discharged from the hospital, and 49 cats
died or were euthanatized. Necropsy examination of
23 cats did not reveal evidence of renal or hepatic toxicosis
associated with HBOC administration.
Conclusions and Clinical Relevance—Although
administration of an HBOC solution may provide temporary
support to anemic cats, the development of
pulmonary edema or pleural effusion potentially associated
with rapid infusion rate and large volume of
infusion of the HBOC solution should be investigated
further before use of the solution can be recommended
in cats. (J Am Vet Med Assoc 2002;221:96–102)
Objective—To evaluate a canine D-dimer point-of-care
(cD-d POC) test kit for use in healthy dogs and
dogs with disseminated intravascular coagulation
(DIC), thromboembolic disease (TED), and hemorrhage.
Animals—12 healthy dogs, 18 dogs with DIC, 23
dogs with TED (19 acute and 4 chronic), and 18 dogs
Procedure—The cD-d POC, canine D-dimer ELISA
(cD-d ELISA), human D-dimer latex agglutination (hD-d
LA), and fibrin degradation product (FDP) tests were
performed on citrated plasma.
Results—All healthy dogs had negative cD-d POC
test results and mean cD-d ELISA value of 0.2 U/mL.
All dogs with DIC had positive cD-d POC test results
and mean cD-d ELISA value of 44 U/mL. Dogs with
acute TED had a mean cD-d ELISA value of 34 U/mL,
and 17 of 19 had positive cD-d POC test results.
Mean cD-d ELISA value in dogs with hemorrhage
was 14 units/mL, and 15 of 18 had positive cD-d
POC test results. The cD-d ELISA values in dogs
with hemorrhage were significantly higher than
those of healthy dogs but lower than those of dogs
with DIC and acute TED. The cD-d POC, cD-d ELISA,
and hD-d LA tests were comparable in differentiating
healthy dogs from dogs with DIC, acute TED, or
hemorrhage and appeared to be superior to measurement
Conclusions and Clinical Relevance—The cD-d
POC test kit can be quickly and easily used and reliably
detects dogs with DIC or acute TED. Positive
results may also be seen in dogs with internal hemorrhage.
(Am J Vet Res 2003;64:1562–1569)
Objective—To evaluate the effect of prednisone alone,
compared with a combination of prednisone and vincristine,
on platelet counts in bleeding dogs with severe
primary immune-mediated thrombocytopenia (IMT).
Design—Prospective case study.
Animals—24 dogs with severe primary IMT.
Procedure—All dogs received immunosuppressive
doses of prednisone (1.5 to 2 mg/kg [0.7 to 0.9 mg/lb]
of body weight, PO, q 12 h). In addition, 12 dogs
received a single dose of vincristine (0.02 mg/kg [0.01
mg/lb], IV). Platelet count, transfusion requirement,
and outcome were monitored. A response was
defined as an increase in platelet count to ≥ 40,000/µl.
Dogs in the prednisone group that failed to respond
received 1 dose of vincristine on day 7.
Results—Dogs that received prednisone and vincristine
had a significantly faster increase in platelet
count to ≥ 40,000/µl than dogs that received prednisone
alone (mean ± SD, 4.9 ± 1.1 vs 6.8 ± 4.5 days,
respectively). A similarly rapid response was observed
in dogs that received vincristine on day 7 after treatment
with prednisone alone failed. Furthermore, duration
of hospitalization was reduced in the vincristine
group, compared with the prednisone group (5.4 ± 0.3
vs 7.3 ± 0.5 days, respectively). No adverse effects
attributable to vincristine were observed in any dog.
Conclusions and Clinical Relevance—Administration
of combined vincristine and prednisone is associated
with more rapid increase in platelet numbers and
shortened duration of hospitalization in dogs with
IMT, compared with use of prednisone alone. Early
use of vincristine seems warranted in dogs with
severe primary IMT. (J Am Vet Med Assoc 2002;
Objective—To document reasons for use of fresh
frozen plasma (FFP) in dogs and determine variables
that apparently triggered the decision to use FFP.
Procedure—Medical records of dogs that received
FFP at a veterinary teaching hospital during a 3-month
period were reviewed.
Results—The 74 dogs underwent 144 transfusion
episodes (TE; a TE was defined as 1 day of transfusion
therapy) and received 252 units (120 ml/unit) of
FFP. Fresh frozen plasma was administered to provide
coagulation factors (67 TE), albumin (91), alphamacroglobulin
(15), or immunoglobulins (19); for some
TE, multiple clinical indications were identified.
Variables that apparently triggered the decision to
administer FFP included active hemorrhage with or
without prolongation of coagulation times, low total
plasma protein concentration, persistent vomiting
associated with pancreatitis, and sepsis. Mean doses
of FFP for each indication were between 8.5 and 9.4
ml/kg (3.9 and 4.3 ml/lb). Small dogs were generally
given higher doses (mean dose, 13.9 ml/kg [6.3 ml/lb])
than large dogs (mean dose, 5.1 ml/kg [2.3 ml/lb]).
Fifty (68%) dogs were alive at the time of discharge
from the hospital.
Conclusions and Clinical Relevance—Results suggest
that FFP plays an important role in the care of
critically ill dogs. Because the supply of FFP is limited,
guidelines for when administration of FFP may be
clinically useful should be developed. (J Am Vet Med
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.
Objective—To characterize in vitro coagulation status in a cohort of dogs with extrahepatic biliary tract obstruction (EHBO) and to evaluate these patients for hypercoagulability by means of thromboelastography.
Design—Prospective cohort study.
Animals—10 dogs with EHBO and 19 healthy control dogs.
Procedures—Partial or complete EHBO was confirmed via exploratory celiotomy. Venous blood samples were collected for evaluation of prothrombin time (PT) and activated partial thromboplastin time (APTT); fibrinogen and D-dimer concentrations; protein C and antithrombin activities; and factor VII, VIII, and XI coagulant activities in plasma as well as thromboelastography in whole blood. Thromboelastography variables were measured from the thromboelastography tracing, and a coagulation index was calculated. Thromboelastography results were compared with those of healthy control dogs previously evaluated by the same laboratory.
Results—Hypercoagulability was diagnosed in all dogs with EHBO on the basis of a high coagulation index. Thromboelastography variables, including maximal amplitude, α-angle, and coagulation index, were significantly higher, and K (clot formation time) and R (reaction time) were significantly lower in these dogs than in control dogs. All dogs with EHBO had PT and APTT within respective reference ranges. Plasma D-dimer and fibrinogen concentrations were above reference ranges in 8 and 7 dogs, respectively, and protein C and antithrombin activities were below reference ranges in 3 and 1 dogs, respectively.
Conclusions and Clinical Relevance—In vitro hypercoagulability was commonly detected in dogs with naturally occurring EHBO. The traditional view of EHBO as a disease that causes hypocoagulability may need to be reconsidered.