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Biomedical subjects

W V Kageler

Publications and source records attributed to W V Kageler.

8 recordsLinked to original sources
PubMed1989

Thyrocardiotoxic embolic syndrome.

Embolic occlusion of lower extremity arteries caused by hyperthyroidism-induced atrial fibrillation occurs rarely. Severe end organ damage may be prevented by aggressive medical and surgical intervention. Subtle signs of hyperthyroidism should be sought when arterial occlusion and atrial dysrhythmia are discovered. About 25% of thyrotoxic patients have atrial fibrillation, and up to 40% of this subgroup have systemic emboli; thus, 3% to 10% of all thyrotoxic patients may have systemic emboli. This estimation supports the recommendation for anticoagulation in all hyperthyroid individuals with atrial fibrillation.

Adult↗
PubMed1977

Intravascular hemolysis, thrombocytopenia, leukopenia, and circulating immune complexes after jejunal-ileal bypass surgery.

Two years after jejunal-ileal bypass surgery for obesity, a 25-year-old man developed intravascular hemolysis, thrombocytopenia, and neutropenia. The patient's erythrocytes were coated with complement components (C4/C3) and his serum induced complement-dependent immune lysis of chromium-51-labeled platelets. Serum [125I]-C1q binding activity (a measure of the presence of immune complexes) was increased, and serum C4 and C3 hemolytic titers were depressed. Immune complex-mediated complement activation apparently accounted for the blood cell destruction in this patient.

Adult↗
PubMed1976

Spontaneous hyphema associated with ingestion of aspirin and ethanol.

Unilateral hyphema, hematuria, and ecchymoses developed in a previously healthy 42-year-old women after the ingestion of aspirin and ethanol. There was no evidence for ocular trauma, disease, or vascular malformation by slit-lamp examination and gonioscopy. Platelet count and coagulation tests were normal. The patient's bleeding time was prolonged and there was impaired platelet aggregation. Delayed (secondary) aggregation in response to collagen, adenosine diphosphate, and epinephrine was decreased, as was aggregation induced by thrombin and serotonin. These data indicate that the qualitative platelet defect was induced by both aspirin and ethanol. Anterior chamber hemorrhage subsided after discontinuation of aspirin and ethanol, and the hyphema subsequently resolved. Bleeding time and platelet aggregation were normal two weeks after the patient's initial presentation. A prolonged bleeding time in association with normal platelet count, prothrombin time, and partial thromboplastin time indicated a qualitative platelet defect, which is most commonly drug-induced. Defective platelet function resulted in spontaneous hyphema.

Adenosine Diphosphate↗