Related Experiment Video
Updated: Jan 15, 2026
Intravital Microscopy of the Spleen: Quantitative Analysis of Parasite Mobility and Blood Flow
Published on: January 14, 2012
Histopathologic and Molecular Evidence of Splenic Infarction Associated with Sickle Cell Trait: An Instructive Case
Joby Robleto-Quesada1,2, Esteban Jara-Segura1,2, José-Ricardo Montenegro3
1Clinical Analysis Department, University of Costa Rica, San José, Costa Rica.
Sickle cell trait carriers are generally considered asymptomatic; nevertheless, there are potential complications. The spleen is vulnerable to infarction because of its role in trapping and removing sickle cells and its hypoxic environment. In this report, a case of a 31-year-old physically active man who experienced severe abdominal pain near the peak of the Acatenango Volcano in Guatemala is described. At the hospital, he was diagnosed with splenic infarction, requiring splenectomy. Pathological analysis of the spleen revealed interstitial hemorrhage and marked congestion of capillaries by sickle-shaped erythrocytes. Laboratory studies revealed no evidence of anemia or any alteration in the red blood cell formula; however, leukocytosis was observed at the time of the event, which rapidly decreased on subsequent days. In contrast, platelets increased after the spleen removal. Capillary electrophoresis revealed the sickle cell carrier state. Genetic alterations associated with thrombophilia, alpha thalassemia, and other beta globin hemoglobinopathies were absent. This case reinforces evidence that high-altitude hypoxia can trigger sickle cell formation in heterozygous carriers and lead to splenic damage.
Sickle cell trait carriers are generally considered asymptomatic; nevertheless, there are potential complications. The spleen is vulnerable to infarction because of its role in trapping and removing sickle cells and its hypoxic environment. In this report, a case of a 31-year-old physically active man who experienced severe abdominal pain near the peak of the Acatenango Volcano in Guatemala is described. At the hospital, he was diagnosed with splenic infarction, requiring splenectomy. Pathological analysis of the spleen revealed interstitial hemorrhage and marked congestion of capillaries by sickle-shaped erythrocytes. Laboratory studies revealed no evidence of anemia or any alteration in the red blood cell formula; however, leukocytosis was observed at the time of the event, which rapidly decreased on subsequent days. In contrast, platelets increased after the spleen removal. Capillary electrophoresis revealed the sickle cell carrier state. Genetic alterations associated with thrombophilia, alpha thalassemia, and other beta globin hemoglobinopathies were absent. This case reinforces evidence that high-altitude hypoxia can trigger sickle cell formation in heterozygous carriers and lead to splenic damage.
