2 results
Patterns of placental pathology in preterm premature rupture of membranes
- J. Armstrong-Wells, M. D. Post, M. Donnelly, M. J. Manco-Johnson, B. M. Fisher, V. D. Winn
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- Journal:
- Journal of Developmental Origins of Health and Disease / Volume 4 / Issue 3 / June 2013
- Published online by Cambridge University Press:
- 18 March 2013, pp. 249-255
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- Article
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Inflammation is associated with preterm premature rupture of membranes (PPROM) and adverse neonatal outcomes. Subchorionic thrombi, with or without inflammation, may also be a significant pathological finding in PPROM. Patterns of inflammation and thrombosis may give insight into mechanisms of adverse neonatal outcomes associated with PPROM. To characterize histologic findings of placentas from pregnancies complicated by PPROM at altitude, 44 placentas were evaluated for gross and histological indicators of inflammation and thrombosis. Student's t-test (or Mann–Whitney U-test), χ2 analysis (or Fisher's exact test), mean square contingency and logistic regression were used when appropriate. The prevalence of histologic acute chorioamnionitis (HCA) was 59%. Fetal-derived inflammation (funisitis and chorionic plate vasculitis) was seen at lower frequency (30% and 45%, respectively) and not always in association with HCA. There was a trend for Hispanic women to have higher odds of funisitis (OR = 5.9; P = 0.05). Subchorionic thrombi were seen in 34% of all placentas. The odds of subchorionic thrombi without HCA was 6.3 times greater that the odds of subchorionic thrombi with HCA (P = 0.02). There was no difference in gestational age or rupture-to-delivery interval, with the presence or absence of inflammatory or thrombotic lesions. These findings suggest that PPROM is caused by or can result in fetal inflammation, placental malperfusion, or both, independent of gestational age or rupture-to-delivery interval; maternal ethnicity and altitude may contribute to these findings. Future studies focused on this constellation of PPROM placental findings, genetic polymorphisms and neonatal outcomes are needed.
16 - Neonatal Thrombosis
- from Section VI - Hemostatic disorders
- Edited by Pedro de Alarcón, Eric Werner, Robert D. Christensen
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- Book:
- Neonatal Hematology
- Published online:
- 05 February 2013
- Print publication:
- 10 January 2013, pp 277-285
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- Chapter
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Summary
Introduction
Although the newborn infant is born with an immature coagulation system, the well term and preterm infant rarely experiences bleeding or clotting. However, the neonate has very limited capacity to respond to hemostatic stresses and quickly develops severe acquired deficiencies of coagulation proteins, especially in the face of sepsis or hypoxia. Infection and associated inflammation, through reciprocal activation of coagulation, results in the consumption of protein C and other proteins, ultimately causing both thrombosis and bleeding. Infection and indwelling catheters promote thrombosis in a facilitative manner. Genetic thrombophilia also promotes thrombosis in the neonate, especially idiopathic thrombosis, and should be considered in the evaluation of a newborn infant with thrombosis. Imaging techniques for neonatal thrombosis range from Doppler and imaging ultrasound for extremity arterial and venous thrombosis, to magnetic resonance angiography for arterial ischemic stroke and cerebral sinovenous thrombosis. Risks for death, recurrence and long-term complications of thrombosis can be used to determine aggressiveness of antithrombotic approach required. Finally, dosing of antithrombotic agents is unique to this developmental age and cannot be extrapolated from older children or adults.
Bulleted list of salient points (5–10)
Thrombosis is a significant clinical problem in the newborn nursery affecting both term and preterm infants.
Most newborn infants presenting with thrombosis have predisposing underlying disorders and triggers.
Sepsis is a powerful promoter of prothrombotic hemostatic alterations resulting in DIC and thrombosis.
Genetic thrombophilia contributes to the thrombotic tendency of the newborn.
The imaging technique used to diagnose thrombosis in the newborn is dependent upon the anatomic site of the thrombus.
Newborn infants with thrombosis can be stratified by risk for poor outcome; antithrombotic therapies form a continuum from least to most aggressive approach that is dictated by clinical circumstances and patient factors.
Dosing of antithrombotic agents in the newborn is unique to the developmental age of the infant and competence of the hemostatic system.