What is the pathophysiology of splenic infarction?

Updated: Jul 27, 2020
  • Author: Manish Parikh, MD; Chief Editor: John Geibel, MD, MSc, DSc, AGAF  more...
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Infiltrative hematologic diseases cause congestion of the splenic circulation by abnormal cells. For instance, the mechanism of splenic infarction in sickle cell disease is attributed to crystallization of the abnormal hemoglobin during periods of hypoxia or acidosis. [1, 2] 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, autoinfarcted spleen by adulthood. In individuals who are heterozygous for sickle trait, exposure to low-oxygen tension (eg, during unpressurized airplane travel) or vigorous activity (eg, skiing in high-altitude locations) can precipitate sickling and splenic infarction by the above-described mechanism. [3] In myelofibrosis, the splenic parenchyma is infiltrated by extramedullary hematopoiesis, causing congestion of the splenic circulation.

In malignant hematologic diseases (eg, chronic myeloid leukemia), increased splenic oxygen requirements secondary to an increased splenic mass, coupled with a decreased oxygen-carrying capacity secondary to the anemia of hypersplenism, lead to infarction.

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