Cases reported "Anemia, Sickle Cell"

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1/11. Splenic syndrome in sickle cell trait: four case presentations and a review of the literature.

    Four cases of splenic infarction/sequestration in sickle cell trait (SCT) patients are presented. All four patients were undergoing moderate exercise at elevations ranging from 5,500 to 12,000 feet. The patients include two African-American males, a Hispanic male, and a white female. All four presented with the acute onset of mid epigastric then left upper-quadrant pain, nausea, vomiting, and respiratory splinting. A review of the literature indicates that splenic infarction with SCT is not uncommon; however, not surprisingly, it is often initially misdiagnosed. This is the first report in the literature of a female with SCT incurring a splenic syndrome with exposure to terrestrial altitude. Although SCT is not a contraindication for moderate- or high-altitude activities, military physicians need to consider the diagnosis of splenic infarction early in any patient regardless of race or sex who presents with left upper-quadrant pain at altitudes above 5,000 feet. Prompt evacuation to sea level may hasten recovery and spare further splenic trauma. Although SCT should be considered a relatively benign entity, the literature also suggests a higher than average risk of sudden death in military recruits with SCT from exertional heat illness and rhabdomyolysis.
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2/11. Cerebrovascular accidents (strokes) in children with sickle cell disease residing at high and low altitudes of saudi arabia.

    In a 3-year period, eight cases of cerebrovascular accident were seen out of 400 patients with sickle cell disease residing at high and low altitudes of Asir Province of saudi arabia. They were all Saudi nationals and comprised five boys and three girls of ages ranging from 3.5 to 9 years. They had varied clinical presentations of their cerebrovascular accident. Cranial computed tomography in seven of them showed abnormality in the region of the middle cerebral circulation. Management and some suggested factors contributing to the occurrence of the cerebrovascular accident are discussed.
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3/11. pulmonary embolism and splenic infarction in a patient with sickle cell trait.

    A 43 year-old black man with sickle cell trait documented by hemoglobin electrophoresis presented with severe pleuritic chest pain and hypoxemia three weeks after discharge following abdominal surgery. A pulmonary embolus was diagnosed by angiography and he was treated with heparin; the minimum arterial pO2 was 55 torr while O2 was being administered at a rate of 3 L/min. During this therapy, he developed abdominal pain. Computerized tomography suggested splenic infarction, which was documented by radionuclide liver-spleen scan and magnetic resonance imaging (MRI); the patient's spleen had been normal at exploratory laparotomy three weeks previously. No source for emboli was identified in the deep venous system by MRI. Although splenic infarction has been reported in patients with sickle cell trait at high altitude, this is the first reported case of splenic infarction secondary to the hypoxemia of pulmonary embolism in a patient with sickle cell trait. The spleen is subject to infarction in sickle cell trait because blood flow is slow through a hypoxemic and acidemic environment. The additional hypoxemia due to pulmonary embolism is presumed, in our patient, to have created a local splenic environment which permitted infarction to occur.
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4/11. hypertension in sickle cell disease.

    We report a young male with sickle cell trait who developed severe hypertension and splenic infarction soon after travel to a high altitude. hypertension persisted for three days after a diagnostic laparotomy. His blood pressure then continued to be normal over the next one and a half years. Red cell sludging in the small vessels of the kidney possibly activated the renin angiotensin system.
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5/11. splenic infarction at low altitude in a child with hemoglobin S-C disease.

    We describe a 15-year-old black boy with hemoglobin S-C disease living in Atlanta (altitude 1,034 ft), with no prior history of aircraft or mountain travel, who developed splenic infarction. The clinical picture was characterized by severe left upper quadrant abdominal pain, fever, splenomegaly, and hematologic and scintigraphic evidence of functional asplenia. The diagnosis was suggested by liver/spleen scintigraphy and further confirmed by ultrasonography and computerized tomography (CT) of the spleen. Treatment consisted of analgesics, intravenous fluids, and short-term antibiotic therapy. The child recovered without sequelae.
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6/11. sickle cell trait in a white Jewish family presenting as splenic infarction at high altitude.

    We report the presence of sickle cell trait in several members of a white Jewish family. The trait was discovered when the propositus developed massive splenic infarction at high altitude. No erythrocyte markers characteristic of African ancestry were detected in any of the family members. This is the first bona fide documentation of sickle trait among white jews.
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7/11. Splenic syndrome at mountain altitudes in sickle cell trait. Its occurrence in nonblack persons.

    Six consecutive cases of splenic syndrome at mountain altitudes in persons with sickle cell trait are reported and the literature is reviewed. All six cases occurred in men who experienced the acute onset of severe left-upper-quadrant abdominal pain within 48 hours of arrival in colorado from lower altitudes. All six patients were phenotypically nonblack. Three patients experienced their symptoms at moderate altitudes of 1,609 to 2,134 m (5,280 to 7,000 ft) above sea level. All recovered with medical management and none required splenectomy, although functional hyposplenia was a sequela in at least one patient. The possibility that nonblack persons with sickle cell trait may be at greater risk than black persons with sickle cell trait for the development of splenic syndrome at moderate altitude is discussed.
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8/11. morbidity of sickle cell trait at high altitude.

    A Caucasian with sickle cell trait (54% A, 43% S hemoglobin) had symptoms and signs of chronic hemolytic anemia as well as splenic infarction while living at very high altitude (in excess of 2,800 m). Trips from sea level back to high altitude repeatedly precipitated pulmonary infarctions. All symptoms and evidence of hemolysis resolved at low altitude.
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9/11. Mild splenic sequestration crises in sickle-hemoglobin c disease.

    Acute splenic sequestration crisis ( ASSC ), a common complication in homozygous sickle cell anemia, has been described infrequently in sickle-hemoglobin C (SC) disease in the absence of high altitude exposure. In this report, we describe three children with hemoglobin sc disease who developed episodes of ASSC that were milder than those generally described in sickle cell anemia. In one patient, an antecedent triggering event was not recognized. The other two children may have had a predisposing cause for massive intrasplenic sickling in that one had an associated mononucleosis syndrome and the other an episode of hypovolemic shock following severe epistaxis. ASSC may occur in patients with SC disease and does not necessarily require a hypoxic trigger associated with high altitudes.
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10/11. The sickle cell trait in relation to the training and assignment of duties in the armed forces: II. Aseptic splenic necrosis.

    Well-documented information gleaned from the world's literature reveals that in vivo sickling of erythrocytes and vascular occlusive lesions involving the spleen have occurred in individuals with the sickle cell trait (SCT) while flying in unpressurized airplanes or when exposed to hypoxic environments in mountains at intermediate altitudes. The clinical and anatomical manifestations of splenic infarcts are described. Individuals without the trait do not develop splenic infarcts during or following exposure to ambient hypoxia.
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