RESUMEN
PURPOSE: To determine whether severe retinopathy of prematurity (ROP) occurs in infants whose birth weights exceed 1250 g. METHODS: We retrospectively reviewed the medical records of 1118 premature infants with birth weights > 1250 g, who were referred for screening examinations for ROP, to determine the severity of ROP observed. We then cross-tabulated these data with each infant's estimated gestational age and birth weight. Finally, we applied currently recommended screening guidelines retrospectively to determine whether they would have identified infants who had developed severe disease and who were subsequently treated. RESULTS: Stage 3 ROP was detected in infants with estimated gestational ages up to and including 32 weeks and birth weights up to and including 1874 g. A total of 26 of the participants received laser treatment for threshold ROP. Seven of these infants would not have been referred for screening according to current guidelines. CONCLUSIONS: Current screenings guidelines may fail to detect severe ROP in larger, more mature infants.
Asunto(s)
Recién Nacido de Bajo Peso , Retinopatía de la Prematuridad/epidemiología , Arizona/epidemiología , Peso al Nacer , Estudios de Cohortes , Edad Gestacional , Humanos , Recién Nacido , Terapia por Láser , Retinopatía de la Prematuridad/patología , Retinopatía de la Prematuridad/terapia , Estudios RetrospectivosRESUMEN
OBJECTIVE: The objective of this study was to examine the mechanism of procoagulant activity and inhibition in whole blood during extracorporeal circulation. METHODS: In this study we examine the development of procoagulant activity and monocyte activation in heparinized whole blood passing through a closed circuit consisting of a pump and silicone envelope membrane oxygenator for 6 hours. RESULTS: Anaphylatoxins, C3a and C5a, determined by means of enzyme-linked immunosorbant assay, appeared in the blood within 30 minutes of circulation. Circulated blood developed a marked potential for coagulation demonstrated in a 1-step clotting assay that reached maximal activity by 4 hours of circulation. This procoagulant activity was neutralized by anti-tissue factor antibody, suggesting a prominent role for the extrinsic pathway in pump-induced intravascular coagulation. Isolation of monocytes from circulated blood revealed that tissue factor expression is upregulated on the cell surface. Furthermore, we observed nuclear factor kappaB nuclear translocation in monocytes from blood passing through the circuit, suggesting that tissue factor expression was due to monocyte stimulation and transcriptional activation of the tissue factor gene. Tissue factor expression resulted in an approximately 30-fold increase in thrombin generation. Monocyte nuclear factor kappaB activation, monocyte tissue factor expression, thrombin generation, and the procoagulant activity of blood in extracorporeal circulation were all blocked by the proteasome inhibitor MG132. CONCLUSIONS: We conclude that intravascular tissue factor expression during extracorporeal circulation of blood is due to nuclear factor kappaB-mediated activation of monocytes (possibly by complement), which can be controlled pharmacologically.