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64 Section I: Diagnostics and Planning

Two frequently used tests to evaluate the coagulation cascade are been reported in several dog breeds but is most commonly seen in
PT and aPTT. PT assesses the extrinsic coagulation pathway (fac- Doberman Pinschers [15]. This factor can be quantified in plasma
tors I, II, V, VII, X) while aPTT evaluates the intrinsic pathway (fac- prior to surgery and reported as a percentage of control mean. Dogs
tors I, II, V, VIII, IX, X, XI, XII) and both tests evaluate the common with vWF antigen less than 50% are considered positive and dogs
coagulation pathway. The activated clotting time (ACT), which can with greater than 70% are considered negative, with intermediate
be performed easily at the patient’s bedside, evaluates the intrinsic values being unclassified [15]. Pretreating with desmopressin ace-
and common coagulation pathways. tate (DDAVP) or administration of preoperative and/or intraopera-
Hemostatic deficiencies can be acquired or congenital. Inherited tive DDAVP‐boosted fresh frozen plasma may be recommended in
deficiencies of coagulation factors are reported in dogs and cats, these patients.
and those factors can be quantitatively measured in blood. In addition to congenital deficiencies there are many acquired
Hemophilia A is a sex‐linked recessive disorder manifesting in bleeding disorders. Warfarin inhibits the formation of vitamin
males that results in low levels of coagulation factor VIII, while K‐dependent factors (prothrombin, factors VII, IX, and X, and
hemophilia B causes a deficiency of factor IX; both are associated proteins C and S) and therefore intoxicated patients suffer from
with prolonged aPTT. Abnormal bleeding is usually intraarticular, prolonged PT and slightly increased aPTT. Hepatic failure can also
intramuscular, retroperitoneal, or from the gastrointestinal or geni- cause prolonged bleeding since the liver produces all coagulation
tourinary tracts. factors except factor VIII. Aspirin prolongs bleeding time by irre-
Another common congenital bleeding disorder is von Willebrand versibly inhibiting the cyclooxygenase enzyme and consequently
disease, an autosomal dominant condition, where patients suffer decreasing platelet adhesion. Like von Willebrand’s disease, platelet
from low levels of von Willebrand factor (vWF). vWF is a glycopro- function disorders related to administration of aspirin can be
tein produced by endothelial cells and is necessary for normal plate- treated by administration of DDAVP 30 min prior to surgery [23].
let aggregation and adhesion to the subendothelium. Patients with Other platelet function or quantitative disorders can be treated with
severe vWF deficits typically present with abnormal bruising, platelet‐rich concentrate.
mucosal bleeding, prolonged bleeding after trauma, and have an These standard hemostatic screening tests (platelet count, coagu-
increased mucosal bleeding time. Inherited vWF deficiency has lation times, and mucosal bleeding time) have limitations and no

A
10 millimeters

R K Angle MA G Cl LY30 CL60 LY60 CL30
min min deg mm d/sc % % % %
2.0 0.8 78.0 70.4 11.9K 4.3 0.0 99.4 0.0 100.0
2–12 1–6 37–78 44–62 3.7K–7.6K 0–3 0–5 85–100 0–15 92–100

B
10 millimeters

R K Angle MA G Cl LY30 CL60 LY60 CL30
min min deg mm d/sc % % % %
14.9 N\A 4.6 2.9 0.1K 0.0 100.0 0.0 100.0
2–12 1–6 37–78 44–62 3.7K–7.6K 0–5 85–100 0–15 92–100
Figure 6.5 Thromboelastography traces: (A) mild hypercoagulable state in a dog; (B) hypocoagulable state in a dog with coagulopathy. Source: Courtesy of
Dr. Shauna Blois.