SPONTANEOUS ABORTION

Spontaneous abortion is defined as the involuntary loss of the fetus before the 20th week of pregnancy. Later involuntary loss of pregnancy is considered preterm birth. The definition is less clear on the starting point: at what stage after conception should the loss of the products of fertilization be counted as a spontaneous abortion. Many of these losses occur to women who never recognized that they were "pregnant," and there are no chemical or laboratory tests to establish the presence of a fertilized egg until about seven to ten days after fertilization takes place. The general term "abortion" refers to the interruption of a pregnancy after nidation has begun (the nesting of the developing zygote in the wall of the uterus, which generally occurs around the sixth day after fertilization). According to the definition accepted by the American College of Obstetrics and Gynecology and the World Health Organization, it is reasonable to use this starting point for calculating rates of spontaneous abortion. On this basis, the incidence of spontaneous abortion is approximately 20 percent of recognized pregnancies between the 4th and 20th weeks of gestation (counting from the last menstrual period). Approximately 80 percent of these losses occur in the first 12 weeks and the rate declines steadily thereafter, so that in week 20 the incidence of spontaneous abortion is less than 4 percent. Extrapolating back to immediately after fertilization, the rate of loss of all fertilized eggs may be as high as 50 percent, according to published accounts. Most of these very early losses occur between fertilization at mid-cycle and the onset of the next expected menses. In these cases the woman is unlikely to be aware of the prospective pregnancy.

Early spontaneous abortion is usually due to chromosomal abnormalities or fetal malformations. One study has reported that 60 percent of spontaneous abortions have polyploidy, trisomy, or aberrations of the sex chromosomes. Both maternal and paternal factors have been causally linked to spontaneous abortion. Caffeine or alcohol consumption by the mother increases the frequency of pregnancy loss on a dose-related basis. Maternal smoking results in lower birth weight of newborns, and several constituents of tobacco smoke have been associated with fetal death. While active smoking increases the rate of spontaneous abortion by a statistically significant amount, the epidemiological data available on the effect of passive smoking (exposure to environmental tobacco smoke) are too limited to reach a definitive conclusion. Similarly, paternal exposure to toxins may increase the risk of spontaneous abortion, but there is conflicting evidence on this subject.

An accurate determination of the primary sex ratio at fertilization in humans is impractical, for it would require recovery and assignment of sex to zygotes that fail to cleave, blastocysts that fail to implant, and early pregnancy losses. The secondary sex ratio, the ratio at delivery, is usually quoted as approximately 106 males to 100 females. Hence there are either more XY zygotes than XX zygotes at the time of fertilization or there is a greater loss of female than male embryos. The primary sex ratio may be even higher than 106:100 if there is a greater loss of males than females during gestation. The limited epidemiological evidence on the sex distribution of spontaneous abortions in humans supports this possibility: male conceptuses appear to be spontaneously aborted more frequently than females. Thus, the normally higher age-specific mortality rate of males for every age group may prevail even in pre-natal life.

See also: Fertility, Proximate Determinants of; Sex Ratio; Tobacco-Related Mortality.

bibliography

American College of Obstetricians and Gynecologists. "Methods of Mid-trimester Abortion." October 1987. Technical Bulletin No. 109.

Armstrong, B. G., A. D. McDonald, and M. Sloan. 1992. "Cigarette, Alcohol, and Coffee Consumption and Spontaneous Abortion." American Journal of Public Health 82: 85.

Cunningham, F. Gary, et al. 2001. Williams Obstetrics. 21st edition. New York: McGraw Hill.

Simpson, J. L. 1980. "Genes, Chromosomes, and Reproductive Failure." Fertility and Sterility 33:107.

Snijders, R. J. M., N. J. Sebire, and K. H. Nocholaides. 1995. "Maternal Age and Gestational Age-specific Risk for Chromosomal Defects." Fetal Diagnosis and Therapy 10: 356.

Sheldon J. Segal