How Is Coagulation Diagnosed?
Suspicion of a need for anticoagulation begins with a history and physical, and then tests are performed to establish a diagnosis warranting therapy.
A history can identify those with previous thrombotic episodes, risk factors (obesity, diabetes, hypertension, smoking, sedentary lifestyle), or a family history of thrombotic/atherosclerotic disease, cardiac death, or stroke.
The physical exam can elicit calf muscle tenderness (the cardinal sign of deep vein thrombosis), heart murmurs (signs of valvular heart disease), or bruits (swishing sounds in the arteries from the turbulence that obstruction creates).
Diagnostics follow two main tracts:
- Establishing the presence of thrombi in the venous or arterial system
- Evaluating the blood for hypercoagulable state
Thrombosis is confirmed with imaging studies:
- Ultrasound: Imaging via reflected sound waves is used to demonstrate the physical presence of a clot in a vein, artery, or heart chamber; Doppler imaging can examine the flow of blood. Ultrasound is most valuable in diagnosing thrombophlebitis (deep vein thrombosis).
- CT Angiography: CT is the computerized process of assembling X-rays from layered two-dimensional images, useful for angiography, especially coronary or carotid angiography.
- MRI: Also accurate in diagnosing the presence of thrombi, but less used due to expense or availability.
- Cancer screening: undiagnosed malignancies may present first with thrombosis or blood vessel obstruction, so CT, MRI, and ultrasound, while imaging for thrombi or plaques, can also screen for any anatomical distortions due to cancer.
A hypercoagulable state toward thrombosis can occur from genetics (gene mutations, antithrombin deficiency), or due to medication (estrogen), pregnancy, hyperglycemia, kidney disease, smoking, obesity, age, inflammatory bowel disease, vitamin metabolism (vitamin K), or elevated clotting factors. A hypercoagulable state is a systemic (body-wide) tendency to form clots; however, a local hypercoagulable state toward thrombosis can be limited to one area from immobility, surgery, varicose veins, malignancy, trauma, IV drug abuse, or infection.
Blood tests for hypercoagulability (“thrombophilia”) are usually individualized for each patient:
- Complete blood count (CBC): Platelet count.
- Coagulation measurements: Clotting requires both an “intrinsic” pathway and an “extrinsic” pathway that interact for the complete clotting cascade. Prothrombin time (PT–the time it takes for clotting to occur) and INR. The PT includes a measurement of the extrinsic pathway. The INR (international normalized ratio) compares a particular patient’s PT to a standard. APTT–measures the intrinsic clotting pathway.
- DNA tests: A thrombophilia panel looks for inherited protein and antithrombin deficiencies or gene mutations.
- Antiphospholipid syndrome (APS), increasing the risk of venous and arterial thromboemboli, is diagnosed from the identification of three particular antibodies seen in this condition.
- Inflammatory markers: Erythrocyte sedimentation rate (ESR) can suggest a malignancy or connective tissue disease. C-reactive protein (CRP) can identify generalized inflammatory states.
- Bleeding time: An older test which times how long blood takes to clot, is primarily used a screen for defects in coagulation and has been replaced by newer technology of platelet functional assays.
Testing During Treatment with Anticoagulants
Since there is a narrow range of therapeutic anticoagulation below which is ineffective but above which is fraught with bleeding risk, periodic blood testing using PT and INR is used to fine-tune dosing.