RESUMO
The reconstruction of severe craniofacial anomalies in patients who will not accept blood transfusions presents a considerable challenge to the craniofacial team. Traditionally, these patients have been refused major reconstructions, receiving no treatment or a highly compromised substitute. A management protocol was developed utilizing preoperative erythropoietin and ferrous sulfate therapy, intraoperative in-line normovolemic hemodilution, and meticulous intraoperative hemostasis which allows us to perform major craniomaxillofacial reconstructions in Jehovah's Witness patients without the use of homologous or predonated autologous blood transfusions.
Assuntos
Transfusão de Sangue , Cristianismo , Disostose Craniofacial/cirurgia , Ossos Faciais/anormalidades , Religião e Medicina , Crânio/anormalidades , Adolescente , Criança , Eritropoetina/uso terapêutico , Ossos Faciais/cirurgia , Feminino , Humanos , Mandíbula/anormalidades , Mandíbula/cirurgia , Maxila/anormalidades , Maxila/cirurgiaRESUMO
BACKGROUND AND PURPOSE: The purpose of this study was to assess the biological effect of aspirin as measured by the inhibition of platelet aggregation in patients taking aspirin for stroke prevention and in patients with acute stroke. METHODS: We administered increasing doses of aspirin (325, 650, 975, and 1,300 mg daily) to 113 patients for stroke prevention and measured the inhibition of platelet aggregation in these patients and in 33 patients with acute stroke taking aspirin before stroke onset. RESULTS: Eighty-five patients on < or = 325 and six on > or = 650 mg aspirin had complete inhibition of platelet aggregation. Increase of the dose by 325 mg in nine of the 22 patients with partial inhibition of platelet aggregation produced complete inhibition in five patients at 650 mg and in one at 975 mg. At 1,300 mg, three patients still had only partial inhibition of platelet aggregation (aspirin resistance). Of the 33 inpatients with acute stroke, 24 had platelet aggregation studies done before further administration of aspirin. Of these, 19 had complete inhibition of platelet aggregation and three had partial inhibition, with production of complete inhibition of platelet aggregation at dose escalation; one patient was aspirin-resistant and the other noncompliant. CONCLUSIONS: How the inhibition of platelet aggregation relates to stroke prevention remains unclear. The ability of aspirin and the dose required to inhibit platelet aggregation may depend upon the individual.