IN THE LIT

R. M. Pauli, MD, Ph.D.

Death before Birth: Clues from Gene Knockouts and Mutations. Copp AJ. Trends in Genetics 11:87-93, 1995.

I found this article to be wonderfully horizon-expanding. Copp summarizes information which is available concerning lethal mutations in mice. Rather than trying to explain one by one the pathogenetic mechanism resulting in death in each mutation, he attempts to create a coherent view of patterns of mechanism of death at three embryologic periods. In brief, he suggests the following. Death before or at the time of implantation usually results from fundamental ‘housekeeping’ functions of cells or from failure to establish a connection between the embryonic trophoblast and the maternal decidua. Death early in organogenesis seems to arise from failure of yolk-sac function, from disruption of early circulation or from failure to establish a functioning placenta. Late fetal deaths might all be explained either from cardiovascular circulatory failure or from failure to establish liver hematopoiesis. In general, then, very few developmental disturbances kill embryos and fetuses. Most organs have little survival value while the fetus is still in utero. Thus, Copp suggests that malformations of these inessential systems can not be viewed as causing the death of the fetus. In the mouse, at least, malformations (or, for that matter, absence) of the central nervous system, gut, lungs, urogenital system and musculoskeletal system are not essential for survival before birth.

Public Drinking Water Contamination and Birth Outcomes. Bove FJ, Fulcomer MC, Klotz JB, Esmart J, Dufficy EM, Savrin JE. Am J Epidemiol 141:850-862, 1995.

Using a birth defects surveillance system (in New Jersey) about 80,000 births were assessed in an effort to understand whether exposure to various organic contaminants in drinking water results in increased risk for birth defects. A variety of compounds were associated with an increased relative risk of various birth defects. Trihalomethanes (e.g. chloroform) and carbon tetrachloride showed the strongest relations to adverse outcomes. Limited analysis of fetal deaths (594 in this series) showed no such correlation. Such a negative outcome is, on the one hand, reassuring that stillbirth likely is not commonly caused by contamination of water supplies while, on the other, the positive correlations with viable birth defects is anything but reassuring!

Violence, pregnancy and birth outcome in Appalachia. Dye TD, Tolliver NJ, Lee RV, Kenney CJ. Paediatr Perinat Epidemiol 9:35-47, 1995.

Most information about the relationship of trauma in pregnancy and adverse outcomes is anecdotal. To their credit, the authors of this study prospectively assessed a population of women presumed to be at high risk for being victims of violence - poor, rural and young. Of 364 women enrolled in the study, 15.9% reported being physically abused during the pregnancy. Four babies were stillborn, three to mothers who were battered. Of those who were physically abused, the likelihood of fetal death (as well as other adverse outcome measures) was significantly increased (odds ratio for fetal death of 17.29; confidence interval of 1.7-169.4). The study did not document severity or specificity of abuse and so it can not be determined whether direct trauma to the abdomen or pelvis is the primary precipitant of these bad outcomes. Appropriately, the authors recommend larger, better controlled and more sophisticated studies to pursue what appears to be an important contributor to fetal death, at least in some populations. Incidental to the main purpose of the study, it also showed that about 80% of violence during pregnancy was not identified by physicians/nurses/midwives using standard prenatal risk assessment tools.

Umbilical Cord Length and Acid-Base Balance at Delivery. Berg TG, Rayburn WF. J Reprod Med 40:9-12, 1995.

Certain complications are known to be associated with very short or very long umbilical cords. Short cords occasionally result in excess traction and consequent complications related to blood circulation or to abruption. Long cords may result in entanglements resulting in cord vessel occlusion. However, these life-threatening sequelae are quite uncommon. Berg and Rayburn wished to assess whether more subtle abnormalities might more often arise because of abnormalities of cord length. They used acid-base imbalance at the time of delivery as the dependent variable in assessing this possibility. 3,019 consecutive pregnancies were studied. Cord length was defined as abnormal if it was more than 80 cm (found in 3.7% of the pregnancies) or less than 35 cm (in 2.0%). Neither was found to correlate with abnormality of acid-base balance at birth. The authors conclude that umbilical blood gas determination is not necessary solely based upon abnormality of cord length. Implicitly this study affirms that stillbirth is likely only rarely a direct result of excessively long or excessively short umbilical cords.

Placental Pathology: A Neglected Link between Basic Disease Mechanisms and Untoward Pregnancy Outcome. Redline RW. Current Opinion Obstet Gynecol 7:10-15, 1995.

Redline reviews available evidence concerning the pathologic features which are found in placentae associated with pre-term labor, intrauterine growth retardation, fetal death and birth asphyxia. In discussing fetal death Redline states (without much in the way of documentation) that "late stillbirth is dominated by three processes: fetoplacental macrosomia, fetomaternal hemorrhage and umbilical cord accidents". On the basis of our experience (including assessment of hundreds of late stillbirths) macrosomia is uncommon and umbilical cord accidents are, without extensive investigations, erroneously assumed to be the cause of a baby’s death. While the emphasis on need of careful placental assessment is well placed, this is a relatively uncritical reading of the available literature.

Previous Stress and Acute Psychological Defence as Predictors of Perinatal Grief — An Exploratory Study. Hunfeld JAM, Wladimiroff JW, Verhage F, Passchier J. Soc Sci Med 40:829-835, 1995.

These Dutch investigators looked at the emotional reactions of 41 women both at the time of diagnosis of a lethal anomaly by ultrasound and at 3 months after perinatal loss. They wished to identify factors which predicted intensity of grieving. Various scales, along with semi-structured interviews, were used. They show that intensity of initial grieving is positively correlated with, e.g. having had a previous major life event (death of spouse, child, parent etc.), having received mental health treatment in the past, and by a measure of ‘personal inadequacy’. These features are then suggested to be those looked for in deciding which women should receive psychological support. Frankly, this study angered me in more than the usual ways. While proper in its design, its premises are, in my opinion, offensive. It is a prime example of ‘medicalization’ of grieving: there is the implicit notion underlying the study that intense grieving equals pathologic or ‘bad’ or ‘disordered’ grieving. Nonsense. And, of course, also implicit in its design is the assumption that only mothers grieve.