A 32‐year‐old African American male with sickle cell trait and congenital nephrogenic diabetes insipidus without previous sickle cell‐related complications traveled to Bogota, Columbia, located 8661 feet above sea level. On arrival to Bogotá, he experienced severe left‐sided abdominal pain radiating to his left shoulder with associated vomiting. Evaluation was sought at a Columbian Hospital. Labs were remarkable for leukocytosis and a sodium level of 151 mEq/L. CT scan of the abdomen was reported to be normal. The patient's pain persisted, and a diagnostic laparoscopy revealed complete infarction of the spleen. An endoscopic splenectomy confirmed complete splenic infarction. The patient subsequently developed acute renal failure and ARDS; hemodialysis and mechanical ventilation were begun. The patient's hemoglobin declined from an admission value of 13.9 to 3 6 mg/dL with evidence of hemolysis A Jehovah's Witness, the patient refused transfusion and was treated with erythropoietin. He remained on ventilatory support until air transfer to our hospital. On presentation, his complaints were that of fatigue and pain around the wound site. He was afebrile with lachycardia; obvious pallor was present. Heart was regular with a systolic murmur Lungs were clear Abdomen was mildly tender with a clean wound site. Labs revealed Hg 6.2 g/dL, MCV 110, BUN and creatinine of 83 and 7.3 mg/dL, respectively. Peripheral blood morphology showed polychromesia, Target cells, and Howell‐Joliy bodies. Hemoglobin electrophoresis was consistent with sickle cell trait. The patient was admitted for continued hemodialysis and erythropoielin with iron supplementation. His hospital course was complicated by a persistent postoperative abdominal fluid collection associated with fever requiring repeated drainage and IV antibiotics. After 3 weeks his overall condition had improved: Hg increased to 10.4 g/dL, acute renal failure resolved, and he was discharged from the hospital.
Splenic infarction is rare in patients with sickle cell trait. Most case reports in the literature involve only partial infarction of the spleen managed medically. Our patient demonstrates an unusual complication of sickle cell trait dramatically manifest with splenic infarction. In this case, Travel to a high altitude area and dehydration (resulting from the inability to maintain adequate hydration in the setting of partial nephrogenic Dl with resultant hypertonicity) were the factors predisposing our patient to complete splenic infarction requiring splenectomy.
Sickle cell trait is rarely associated with complicalions. One such complication is splenic infarction that may arise when patients are exposed to high altitude or in the setting of dehydration. Splenic infarction is usually partial and is managed medically, but when the whole spleen is involved, surgery is required.
F. Ayele, none; S. Saiffee, none; M, Parker, none.
To cite this abstract:Ayele F, Saifee S, Parker M. Complete Splenic Infarction at 8000 Feet. Abstract published at Hospital Medicine 2010, April 8-11, Washington, D.C. Abstract 213. Journal of Hospital Medicine. 2010; 5 (suppl 1). https://www.shmabstracts.com/abstract/complete-splenic-infarction-at-8000-feet/. Accessed April 6, 2020.