Cases reported "Splenic Infarction"

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1/3. Non hypoxia-related splenic infarct in a patient with sickle cell trait and infectious mononucleosis.

    splenic infarction in patients with sickle cell trait is usually related to hypoxic conditions, while non-hypoxia-related infarcts are extremely rare. We report on a case of a 17-year-old male patient, living at sea level, who developed a severe left upper quadrant abdominal pain during the course of a febrile episode. On physical examination he had a mildly palpable but extremely painful spleen. A spleen scan revealed 2 areas of impaired radionucleide distribution. Hepatic enzymes were moderately increased and the IgM anti-EBV antibodies positive. Hemoglobin electrophoresis revealed the presence of 42% of hemoglobin S. A probable diagnosis of splenic infarction was established in a patient with sickle cell trait, during the course of infectious mononucleosis. The patient was treated symptomatically. The conditions of splenic congestion induced by the EBV infection and the high-grade fever may have contributed to splenic sequestration and subsequent infarcts.
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2/3. Cases from the osler medical service at Johns Hopkins University.

    PRESENTING FEATURES: A 29-year-old woman with a history of rheumatic heart disease and one episode of endocarditis as an adolescent was admitted to the hospital after 1 week of headache, fever, and myalgia. Her past medical history was otherwise unremarkable and did not include illicit drug use. On physical examination, she had a previously noted 3/6 holosystolic murmur at the apex, which radiated to her back; a previously noted 1/4 diastolic murmur at the right upper sternal border; diminished strength in her right upper extremity; multiple painful erythematous nodules on her fingers (Figure 1); and red streaks under her nails (Figure 2). magnetic resonance imaging of the brain demonstrated multiple lesions; the largest was in the right frontal lobe with associated hemorrhage (Figure 3).What is the diagnosis?
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3/3. Recovery of splenic infarction with anti-platelet treatments and platelet-apheresis in polycythemia vera.

    Thrombo-embolic events in coronary and peripheral arteries, and cerebral, pulmonary, portal, hepatic, and deep veins are seen in 27-45% of patients with polycythemia vera (PV). A 79-year-old man was admitted with complaints of pruritus increasing after bath and left upper abdominal pain radiating to left shoulder for two months. On physical examination, ruddy and hyperemic appearances of his face and conjunctiva, tenderness on the left upper quadrant, and splenomegaly were noted. Hemoglobin level was 16.6g/dl, hematocrit 53.8%, white blood cell count 26x10(9)/l, and platelet count 1.032x10(9)/l. bone marrow aspiration and biopsy revealed hypercellularity, megakaryocytic hyperplasia and dysplasia. The leukocyte alkaline phosphatase score was 190. The levels of serum vitamin B12 and D-dimer were 316 pg/ml and 744 ng/ml, respectively. Arterial O2 saturation was 96%. Red cell mass was measured as 43 ml/kg using radionuclide 51Cr labelled erythrocyte scintigraphy. On cytogenetic analysis, deletion of 20q was found. Computed tomography of whole abdomen showed diffuse splenomegaly and two hypodense areas indicating splenic infarction in 2.5x2 and 3.5x3 cm diameters in subcapsular localization of the spleen. The patient was treated with therapeutic platelet-apheresis, 40 mg/day aspirin, analgesic drugs, and 3g/day hydroxyurea. After 1.5 months, platelet counts dropped to less than 500x10(9)/l and splenic infarcts were not detected on computed tomography. splenic infarction may be the first evidence of thrombosis in PV. The reduction of platelet counts with platelet-apheresis, anti-platelet drugs, and careful clinical observation may be satisfactory in the treatment of splenic infarction.
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