Splenic infarction epidemiology and demographics

Splenic infarction is associated most commonly with hematologic disorders. The propensity for splenic infarction in sickle hemoglobinopathies is well known. The mechanism of splenic infarction in sickle cell disease is attributed to crystallization of the abnormal hemoglobin during periods of hypoxia or acidosis.

The rigid erythrocyte leads to rouleaux formation and occlusion of the splenic circulation. In homozygous sickle cell disease, multiple infarcts during childhood commonly result in a scarred, contracted, auto-infarcted spleen by adulthood.

Exposure to low oxygen tension, such as unpressurized airplane travel, or vigorous activity, such as skiing in high altitude locations, also can precipitate sickling and splenic infarction in individuals heterozygous for the sickle trait. Many of these altitude-related episodes can be safely treated with supportive care rather than with splenectomy (Sheikha, 2005).

Although splenic infarct rates of 50% and 72% have been reported in chronic myelogenous leukemia and myelofibrosis respectively, few large series describing this entity exist.

In 1998, Nores reported 59 cases treated over a 30-year period at the University of California, Los Angeles (UCLA) and Cedars-Sinai Medical Center. In 1986, Jaroch identified 75 patients through clinical or autopsy reports at the Cleveland Clinic and found only an additional 77 cases in the literature. Most of the current literature consists of case reports.

Systemic embolization also can result in splenic infarct. It occurs most commonly in the setting of a left atrial or ventricular mural thrombus formed as the result of acute myocardial infarction.

While autopsy series report a 9% incidence of splenic infarction in early deaths following an acute myocardial infarction, clinical series report a much lower incidence of splenic embolization, probably reflecting the silent clinical course of many splenic infarcts.

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