Placental abruption and fetal death with airbag deployment in a motor vehicle accident.
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OBJECTIVE: To systematically review the literature and summarize the relationship between cigarette smoking and placental abruption, and to evaluate the joint influences of smoking and hypertensive disorders (chronic hypertension and preeclampsia) on the subsequent development of abruption. DATA SOURCES: We reviewed studies identified through a MEDLINE literature search between 1966 and 1997 and through studies cited in the references of published reports. METHODS OF STUDY SELECTION: A total of 13 observational (seven case-control and six cohort) studies were identified which included a total of 1,358,083 pregnancies. We excluded case reports on placental abruption, and restricted the literature search to studies published in English. A meta-analysis was performed by computing pooled odds ratios based on random-effects models describing the association between placental abruption, smoking, and hypertensive disorders. Potential sources of heterogeneity among these studies were explored in detail. TABULATION, INTEGRATION, AND RESULTS: The overall incidence of placental abruption was 0.64% (8724 of 1,358,623). Smoking was associated with a 90% increase in the risk of placental abruption (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.8, 2.0). This pattern was consistent by study design (case-control compared with cohort studies) and smoking prevalence (low compared with high prevalence, defined as less than 30% compared with 30% or more, respectively). However, the association was significantly (p < .001) stronger among the seven studies conducted outside the United States (OR 2.1, 95% CI 2.0, 2.2), compared with the six studies conducted in the United States (OR 1.6, 95% CI 1.5, 1.8). Pooled population attributable risk percentage for each stratum ranged between 15% and 25%, implying that 15-25% of placental abruption episodes are attributable to cigarette smoking. Data on the dose-response relationship between number of cigarettes smoked per day and the risk of abruption indicate that the OR increased with increasing number of cigarettes smoked. Furthermore, a meta-analysis of the joint effects of smoking and hypertension during pregnancy on the development of abruption identified two published studies, including 102,609 pregnancies. In the presence of smoking, the risk of abruption was further increased due to chronic hypertension, mild or severe preeclampsia, or chronic hypertension with superimposed preeclampsia. CONCLUSION: Our meta-analyses showed an increased risk for placental abruption in relation to both cigarette smoking and hypertensive disorders during pregnancy. Because cigarette smoking is a modifiable risk factor, and hypertensive disorders are potentially treatable if diagnosed early in pregnancy, patient education, smoking cessation programs, and early prenatal care may be important factors in the prevention of placental abruption.
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This case report involves an adolescent primigravida at term who was admitted with urinary complaints to the labor and delivery unit of a medical center. Within an hour, she suddenly began screaming and complaining of severe pain running from her anterior pelvis through her vagina and up her spine. Three days of very challenging co-management of the patient, with several recurrences of acute pain, followed. Differential diagnoses that could explain this patient's symptoms are reviewed and discussed. Difficult management issues, including the stress of clinical management in the face of unidentified disease processes, are addressed. Lacking a certain diagnosis even retrospectively, the authors request comments from readers.
Research from the last two decades provides directions for efforts to prevent CP in VLBW infants. The pathogenesis of CP seems to involve factors operating both during pregnancy and in the neonatal period. The most important prenatal factor appears to be intrauterine infection. Perinatal infection and other risk factors, such as the death of a co-twin, placental abruption, and cerebral ischemia, could trigger a cytokine cascade resulting in damage to the developing brain. The low frequency of intrauterine infection in mothers with preeclampsia might explain the apparent protective effect of this disorder. If the brain damage attributed to intrauterine infection and other risk factors involves cytokines as intermediates, then blockade of the proinflammatory cascade or promotion of endogenous inhibitors might prevent CP. Other potentially preventive strategies include corticosteroids given to mothers (but not those given to neonates) and thyroid hormone.
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OBJECTIVE: To determine whether inherited and acquired thrombophilias are associated with adverse obstetric complications. STUDY DESIGN: A systematic review; studies where women with adverse obstetric complications were tested for one or more acquired and inherited thrombophilias were included. MAIN OUTCOME MEASURES: Prevalence of thrombophilia in women with severe pre-eclampsia/eclampsia, severe placental abruption, intrauterine growth restriction or unexplained stillbirth. RESULTS: Compared with controls, placental abruption was more often associated with homozygous and heterozygous factor V Leiden mutation, heterozygous G20210A prothrombin gene mutation, homocysteinaemia, activated protein C resistance or anticardiolipin IgG antibodies. Women with pre-eclampsia/eclampsia were more likely to have heterozygous factor V Leiden mutation, heterozygous G20210A prothrombin gene mutation, homozygous MTHFR C677T mutation, protein C deficiency, protein S deficiency or activated protein C resistance compared with controls. Unexplained stillbirth, when compared with controls, was more often associated with heterozygous factor V Leiden mutation, protein S deficiency, activated protein C resistance, anticardiolipin IgG antibodies or lupus anticoagulant. Women with intrauterine growth restriction had a higher prevalence of heterozygous G20210A prothrombin gene mutation, homozygous MTHFR C677T gene mutation, protein S deficiency or anticardiolipin IgG antibodies than controls. There was wide heterogeneity in the prevalence of thrombophilia between the studies. CONCLUSIONS: Women with adverse pregnancy outcome are more likely to have a positive thrombophilia screen but studies published so far are too small to adequately assess the true size of this association. Screening for thrombophilia should not become standard practice until clear evidence emerges that thromboprophylaxis during pregnancy improves perinatal outcome. Further research into the link between the observed association, causality and heterogeneity is required.
OBJECTIVE: To assess the value of para-clinical exams prescribed in case of in utero foetal death, to result in the establishment of a new algorithm of diagnostic tests. MATERIALS AND METHODS: A retrospective analysis on a series of 106 stillbirths gathered between September 1989 and December 1998 in the obstetrical and gynaecological department of the Lausanne University Hospital which is a tertiary centre. Stillbirth was defined as foetal death occurring as from the date of foetal viability. Thus, only pregnancies from 24 weeks and onwards were included in this series. We excluded all stillbirths occurring during medical termination of pregnancy and cases with incomplete data files. The Fretts' classification was used. The different exams asked by the physician were screened and we analysed their pertinence to determine the aetiological diagnosis for each case. The search for significant risk factors was also taken into account. We compared our management of in utero foetal death with data from the literature to propose a new algorithm. RESULTS: The aetiology of in utero foetal death could be attributed in ninety percent of the cases. The principal causes were in utero growth retardation (19.8%), foetal congenital and chromosomal anomalies (18.9%), infections (15.1%), placental abruption (7.5%), preeclampsia (5.6%), maternal diabetes (3.8%). The remaining 18.9% are divided in to miscellaneous causes. In 10.4% of the cases we could not find any explanation to the death of the foetus. The exams that yielded the most information when done were: foetal autopsy which was abnormal in 92.7%, placental investigation which was abnormal in 93% and the babygramme (X-ray of the foetal skeleton) which was abnormal in 53%. Maternal serology for infections was informative in 6.6% of the cases. CONCLUSION: We present here a protocol for the diagnostic management of stillbirth which is differentiated according to the circumstances surrounding the event. This should prove useful to reduce superfluous tests.
Eclampsia is defined by the occurrence of seizures resulting from hypertensive encephalopathy on the background of preeclampsia. The development of hypertension during pregnancy, a serious and potentially fatal condition, is a leading cause of maternal and fetal morbidity and death in the United States.(1-3) It is a disease with preventable complications. The pathophysiology of hypertension during pregnancy is unclear, but there is consensus that aggressive treatment is warranted to prevent complications to both fetus and mother. A current concept of pathophysiological character, diagnosis, prevention, and management of eclampsia is discussed.
BACKGROUND: A very large number of women in the reproductive age group consume cocaine, leading to grave concerns regarding the long term health of millions of children after in utero exposure. The results of controlled studies have been contradictory, leading to confusion, and, possible, misinformation and misperception of teratogenic risk. OBJECTIVE: To systematically review available data on pregnancy outcome when the mother consumed cocaine. METHODS: A meta-analysis of all epidemiologic studies based on a priori criteria was conducted. Comparisons of adverse events in subgroups of exposed vs. unexposed children were performed. Analyses were based on several exposure groups: mainly cocaine, cocaine plus polydrug, polydrug but no cocaine, and drug free. RESULTS: Thirty three studies met our inclusion criteria. For all end points of interest (rates of major malformations, low birth weight, prematurity, placental abruption, premature rupture of membrane [PROM], and mean birth weight, length and head circumference), cocaine-exposed infants had higher risks than children of women not exposed to any drug. However, most of these adverse effects were nullified when cocaine exposed children were compared to children exposed to polydrug but no cocaine. Only the risk of placental abruption and premature rupture of membranes were statistically associated with cocaine use itself. CONCLUSIONS: Many of the perinatal adverse effects commonly attributed to cocaine may be caused by the multiple confounders that can occur in a cocaine using mother. Only the risk for placental abruption and PROM could be statistically related to cocaine. For other adverse effects, additional studies will be needed to ensure adequate statistical power.
The medical problems associated with cocaine ingestion, most notably cardiovascular side effects, have become evident as its use has become epidemic in the United States. Its effects on pregnancy and the developing fetus are similarly being recognized as more women of childbearing age are abusing cocaine. A case of placental abruption at 33 weeks' gestation following cocaine use is reported. A review of the pharmacodynamics, medical complications, teratogenic potential and effects in pregnancy is included.
To investigate reproductive maternal risk factors of intrapartum fetal asphyxia, we analyzed 556 women with singleton pregnancies complicated by intrapartum fetal asphyxia who gave birth at Kuopio University Hospital from January 1990 to December 1998. The general obstetric population (N=21746) was selected as the reference group and logistic regression analysis was used to identify independent reproductive risk factors. The incidence of intrapartum fetal asphyxia was 2.5%. Placental abruption, primiparity, alcohol use during pregnancy, low birth weight, preeclampsia, male fetuses, and small-for-gestational age births were independent risk factors of intrapartum asphyxia, with adjusted relative risks of 3.74, 3.10, 1.75, 1.57, 1.49, 1.48 and 1.33, respectively. Most cases of intrapartum fetal asphyxia occur in low-risk pregnancies and, therefore, risk screening in antenatal care cannot accurately predict which women will eventually need emergency care for fetal asphyxia.
The objective of this study was to identify risk factors for placental abruption in first and second pregnancies and to compare the risk-factor profiles for evidence of etiologic heterogeneity. A prospective cohort design was used. The study took place at university-based medical centers that participated in the U.S. Collaborative Perinatal Project (1959-1965). A total of 10,774 first pregnancies only and 6529 first and second pregnancies of women were enrolled in the study. Participation rate was 96%. All pregnancies were selected at some centers, whereas other centers used either random or systematic sampling. The main outcome measure was placental abruptions in first and second pregnancies. The placental abruption rate was 1.7% (n = 182) for first and 2.2% (n = 143) for second pregnancies. Prior abruption increased risk in second pregnancies significantly (odds ratio [OR] = 3.2, 95% confidence interval [CI]: 1.7-5.8) after adjusting for other risk factors. Placental infarcts and smoking duration were associated with an increased risk for abruption in second but not first pregnancies. Effect of placental infarcts was modified by gestational age with strongest risk for abruption at shortest gestations. For each year of smoking prior to pregnancy, risk of abruption increased 40% (OR = 1.4, 95% CI 1.0-1.8). Etiologies of placental abruption for first and second pregnancies were different, indicating heterogeneity in their risk-factor profiles. Future research would best consider abruption as a heterogeneous complication to further knowledge of its etiology.