Hypersplenism, the reduction in one or more peripheral blood counts due to sequestration within an enlarged spleen is a common cause of chronic thrombocytopenia. Hypersplenism arises with inflamed or congested spleen, but not with infiltrative disease such as that seen with metast atic cancer.
Usually, one – third of total body platelets reside within the spleen, even though the spleen receives only 5% of cardiac output. This discrepancy results because the splenic transit time of a platelet averages 20 minutes, as opposed to ∼ 1 minute for a platelet to return to the heart after passing through other organs. In hypersplenism, the proportion of platelets within the spleen can far exceed one – third (as high as ∼ 90%).
Clinical features include splenomegaly and usually mild – to – moderate pancytopenia. The normal spleen is ∼ 11 cm in length, but the spleen usually needs to be enlarged by at least 2 or 3 cm to be palpable, and thus diagnosis is most reliably made through imaging studies (e.g., ultrasound). Often, the degree of anemia is not as marked as neutropenia and thrombocytopenia. Especially severe thrombocytopenia can indicate advanced cirrhosis (with reduced thrombopoietin levels) and/or hyperfibrinolysis.
Etiology of hypersplenism in North America usually reflects primary hepatic disease (alcoholic cirrhosis, chronic viral hepatitis, etc.), whereas in some parts of the world other factors are common (e.g., schistosomiasis). Causes of hypersplenism include congestive splenomegaly (Banti’s syndrome), splenic vein thrombosis, Felty’s syndrome associated with rheumatoid arthritis, myeloproliferative or myelodysplastic disorders, malaria, chronic myelogenous leukemia, kala azar (leishmaniasis).
Treatment is usually not required, as thrombocytopenia rarely reaches clinically important levels, and splenectomy is not without risk.