Abstract
Whole blood viscosity is affected by a number of factors, among which plasma proteins are a major component. They exert their effects either directly or through their influence on red cell aggregation. Changes in fibrinogen and in immunoglobulins, under both physiologic and pathologic conditions can increase whole blood viscosity. Blood flow through the microvasculature is impaired when viscosity increases, leading to tissue ischemia and a syndrome complex usually referred to as the hyperviscosity syndrome. Abnormalities of fibrinogen greatly increase its ability to cause red cell aggregation, and is a contributory pathogenic factor in ischemic heart disease and stroke. Immunoglobulins may affect blood viscosity directly, or by increasing the red cell aggregation. Changes are seen in many clinical disorders, ranging from inflammatory diseases to plasma cell dyscrasias. The clinical manifestations may be mild and often unnoticed, or they may be life threatening requiring emergency plasmapheresis. Proper management requires a clear understanding of the underlying pathology. When the symptom complex indicates a high probability of the hyperviscosity syndrome, it should lead to early diagnosis and treatment. Therapeutic approaches should include both removing the abnormal plasma protein and treating the primary cause.