Coagulation Disorders

Brain ischemia and hemorrhage often result from hematological disorders.

Changes in the formed cellular constituents of the blood may be quantitative or qualitative. Polycythemia increases blood viscosity, decreases cerebral blood flow, and increases the risk of thrombosis. Sickle-cell disease and sickle-cell hemoglobin-C disease are examples of qualitative red blood cell abnormalities that affect blood flow. Sickle-cell disease causes occlusive changes in large intracranial arteries and small penetrating vessels. Subcortical, cortical, and borderzone infarcts are often found on CT and MRI.

Increased platelet counts, especially those over 1 million, are associated with hypercoagulability. Thrombocytosis can be primary (so-called essential thrombocythemia), can be associated with other myeloproliferation, or less often, can be secondary to systemic disease. Essential thrombocythemia is associated with strokes and digital arterial occlusions. There are also qualitative abnormalities of platelet function. In some patients, increased coagulability has been attributed to increased adhesion and aggregation of platelets (so-called sticky platelets) in the absence of thrombocytosis.

Leukemia is complicated occasionally by brain hemorrhages and microinfarcts. When the white blood cell count is very high (increased leukocrit), the white blood cells can pack capillaries, leading to microinfarcts and vascular rupture with small hemorrhages in the brain. Larger intraparenchymatous hemorrhages and SAHs are most often related to thrombocytopenia, due to replacement of the bone marrow with leukocyte precursors.

Abnormalities of the coagulation cascade can also cause hypercoagulability and lead to venous and arterial occlusions and brain infarction. y Table.45.-5 lists some of the most common abnormalities.

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