Test summary

 
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The table below provides expected test abnormalities with certain hemostatic disorders. Note, that these are generalizations of the most common scenario and do not cover the range of possibilities or all diseases seen in animals. This table can be used as a guide to help interpretation of laboratory testing results.

Disorder ACT* APTT PT TCT** FIB FDP/D-dimer Platelets Confirming Tests
Trauma N N N N N, I N, I# N, D History, examination findings, imaging, etc.
Thrombocytopenia N N N N N N, I# D Platelet count, usually <30,000/ul if spontaneous bleeding
Anticoagulant rodenticide toxicity/vitamin K deficiency N, I I I N N N, I# N, D Improvement with vitamin K1, testing for rodenticides
Disseminated intravascular coagulation (DIC) N, I I N, I I D, N, I I D No confirmatory test – identify initiating disease
Severe liver disease N, I I I N, I D, N N, I N, D Liver function tests (e.g. bile acids), biopsy, imaging
von Willebrand disease N N N N N N N Decreased vWf:Ag
Intrinsic factor deficiency
Factor VIII (hemophilia A)
Factor IX (hemophilia B)
Factor XI (hemophilia C)
Factor XII (Hageman trait)
Prekallikrein
.
N, I
N, I
N, I
N, I
N
.
I
I
I
I
I
.
N
N
N
N
N
.
N
N
N
N
N
.
N
N
N
N
N
.
N, I#
N, I#
N, I#
N
N
.
N
N
N
N
N
Factor assay
Extrinsic factor deficiency: Factor VII .N N I N N N N Factor assay
Common factor deficiency: Factor X or II N, I I I N N N, I N, I Factor assay
Dysfibrinogenemia N, I I I I D, N N, I# N Normal fibrinogen:Ag
Monoclonal gammopathy, e.g. multiple myeloma N, I N, I N, I N N N D, N Serum protein electrophoresis,
immunoglobulin quantification
Inherited platelet function defect, e.g. e.g. Caldag-GEF1 defect (Bassetts), Glanzmann’s thrombasthenia (Otterhounds), Scott syndrome (German Shepherd) N N N N N N N Platelet function testing
ACT: Activated coagulation time; APTT: Activated partial thromboplastin time; PT: Prothrombin time; TCT: Thrombin clot time; FIB: Fibrinogen concentration determined in clotting assays (functional fibrinogen); FDP: Fibrin(ogen) degradation products; N: Normal; D: Decreased; I: Increased.

* The ACT is less sensitive to factor deficiencies than the APTT, therefore the APTT may be prolonged whilst the ACT may be normal in the same disorder. The ACT also requires platelets from the patient as the source of the phospholipid needed to support clotting. Therefore, severe thrombocytopenia (platelet count < 10,000/uL) may mildly prolong the ACT. In contrast, an exogenous source of phospholipid is added to the APTT reagent, making this test independent of the patient’s platelets.

** The TCT measures the ability of a standard concentration of thrombin to convert the patient’s fibrinogen to fibrin. In general, a prolonged TCT indicates a hypofibrinogenemia and/or dysfibrinogenemia. The latter indicates that fibrinogen is abnormal or there are factors interfering with fibrin polymerization, such as heparin therapy or high concentrations of circulating FDPs. These will cause a prolonged TCT but a fibrinogen concentration may be normal. Remember that fibrinogen is an acute phase reactant protein and will increase with inflammation. Since inflammation is a common cause of DIC, fibrinogen concentrations will represent the balance between consumption (decreasing values) and inflammation (increasing values).

# FDPs and D-dimer may be increased in any condition associated with severe hemorrhage into tissue or body cavities.

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