This chapter should be cited as follows:
Hogue, C, Glob. libr. women's med.,
(ISSN: 1756-2228) 2008; DOI 10.3843/GLOWM.10441
Under review - Update due 2017

Long-Term Risks of Surgical Abortion

Carol J. Hogue, PhD, MPH
Terry Professor of Matrenal/Child Health, Professor of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georga (Vol 6, Cap 124)

INTRODUCTION

Many women bear children after an induced abortion. By chance alone, many of them experience a complicated pregnancy. On the average, one in three pregnancies ends in miscarriage (spontaneous abortion), and at least one in 20 births are preterm or weigh less than 2500 g. More rare and serious pregnancy complications include ectopic pregnancies and stillbirth. When complicated pregnancies occur after the woman has obtained an abortion, it is natural for her to question whether the procedure caused the complication. A few women who seek to become pregnant after their abortion experience secondary infertility and wonder whether the abortion caused their problem. Other potential risks include psychological sequelae and cancer—particularly breast cancer. Because abortion is an elective procedure for women still in their reproductive years, the potential for such risks may raise patients' concerns about the ultimate consequences of their immediate choice.

To answer women's questions, allay unnecessary fears, and combat misinformation, practitioners need to be well informed about the epidemiologic evidence regarding long-term risks. Fortunately, the epidemiologic evidence is extensive for some complications, including secondary infertility, low birthweight, and ectopic pregnancy. A substantial amount of literature also exists for breast cancer, although not for psychological problems.

Findings in some epidemiologic studies may appear to be contradictory, which may make drawing conclusions about long-term complications somewhat difficult. Apparent conflicting results often reflect methodologic issues that differ among studies. This chapter includes discussion of some issues underlying most of the epidemiologic studies of long-term risks, with illustrations from studies of ectopic pregnancy. The second section contains a brief summary of other reproductive health outcomes. Comments regarding breast cancer and psychological problems, along with suggestions about counseling patients regarding long-term risks, conclude the chapter.

ECTOPIC PREGNANCY AFTER SURGICAL ABORTION

A history of one abortion is associated in most studies with a nonsignificant, excess risk of ectopic pregnancy of approximately 30% (Table 1).1,2,3,4,5,6 These observed associations, although real, may be due to chance, as the 95% confidence intervals (CIs) for all the odds ratios (ORs) included 1.0. CIs in four studies were narrow enough to rule out a twofold excess risk. Investigations of the effect of two or more prior abortions experienced small numbers of exposed women. Although all CIs included 1.0, suggesting no significantly elevated risk, the CIs were wide, and point estimates ranged from a fivefold protective effect (OR, 0.2)1 to a fourfold excess risk (OR, 4.0).2

Table 1. Epidemiologic Studies of Induced Abortion as a Risk Factor for Ectopic Pregnancy*


Study/No. of

No. of

No. of

Crude

Adjusted

 

Abortions

Cases

Controls

Odds Ratio

Odds Ratio

95% CI

Pregnant Controls

 

 

 

 

 

Levin et al2

 

 

 

 

 

USA, 1976-1978

 

 

 

 

 

0

56

396

1.0

1.0

1

20

86

1.6

1.3

0.6–2.7

2

9

16

4.0

2.6

0.9–7.4

Daling et al3

 

 

 

 

 

USA, 1975-1979

 

 

 

 

 

0

167

411

1.0

1.0

1

25

48

1.3

1.3

0.6–2.6

2

7

6

2.6

1.8

0.5–7.1

Skjeldestad and Atrash1

 

 

 

 

 

Norway, 1987-1990

 

 

 

 

 

0

121

97

1.0

1.0

1

44

14

2.5

1.3

0.9–1.8

2

9

4

1.5

0.2

0.04–0.9

Atrash et al4

 

 

 

 

 

USA, 1988-1990

 

 

 

 

 

0

121

678

1.0

1.0

1

43

268

0.9

0.9

0.6–1.3

2

18

110

0.9

0.9

0.5–1.7

Nonpregnant Controls

 

 

 

 

 

Burkman et al5

 

 

 

 

 

USA, 1976-1978

 

 

 

 

 

0

352

2362

1.0

1.0

1

NA

NA

1.0

1.0

0.5–1.8

2

NA

NA

NA

0.9

0.8–1.1

Holt et al6

 

 

 

 

 

USA, 1981-1986

 

 

 

 

 

0

123

457

1.0

1.0

1

55

280

1.0

0.9

0.6–1.3

2

33

50

NA

1.2

0.6–2.4

Skjeldestad and Atrash1

 

 

 

 

 

Norway, 1987-1990

 

 

 

 

 

0

121

176

1.0

1.0

1

44

41

1.6

1.2

0.8–1.7

2

9

10

1.4

1.8

0.4–7.8

Last Pregnancy: Abortion vs. Birth

 

 

 

 

 

Skjeldestad and Atrash1

 

 

 

 

 

Norway,

29

166

1.6

0.5

0.2–1.0

1987-1990

 

 

 

 

 


CI, Confidence interval; NA, not available.
*An earlier version of this table, containing errors, appears in Hogue et al7.

Some would contend that the observed ORs reflect a truly elevated risk, not withstanding the statistical uncertainty of small sample sizes. However, two features in study design also affect OR estimates in these studies. These are the choice of comparison group and the control of competing risk factors. In addition, selective recall tends to bias the OR estimates. These issues are discussed next.

Choice of Comparison Group

Most epidemiologic studies of ectopic pregnancy are case-control studies, because ectopic pregnancy is a rare event. The alternative cohort design requires many participants, is more expensive, and is difficult to carry out. For a case-control study, there is no one correct way to select an appropriate group of women for comparison with the case series. A population-based sample includes never-pregnant women as well as women pregnant for the first time. By definition, these women cannot have been exposed to a prior induced abortion and may be excluded from the analysis.7 However, excluding nonpregnant and primigravid women may overestimate the probability of exposure of abortion in the population, because these women are likely to be more effective contraceptive users and less likely to have unintended pregnancies that might be terminated by abortion. Such an overestimate would bias the OR toward the null (i.e., find no association between abortion and ectopic pregnancy when, in fact, there is an association). In Table 1, the studies that use a nonpregnant control group tend to report no association (i.e., OR, approximately 1.0).

Conversely, studies that use women giving birth for a comparison group bias the point estimate away from the null. Women giving birth are on average less likely to have a prior induced abortion than a comparison group of pregnant women chosen to represent all pregnancy options (i.e., induced abortion of this pregnancy as well as delivery).8 For example, an Italian study reported an OR of 2.1 for the comparison group with women giving birth, but an OR of 1.2 for a comparison group of women hospitalized for nonobstetric reasons.9 The four studies summarized in Table 1 did strive to equate the likelihood of potential exposure to prior induced abortion as much as possible. The pregnant comparison groups included both women with induced abortions and women giving birth. Additionally, Daling and associates3 excluded—from both case and comparison groups—unmarried women and those not living in a stable relationship who might be more likely than the average to have a history of abortion. Skjeldestad and Atrash1 excluded from both groups women who could not have been exposed to abortion or those who were less likely to have an ectopic pregnancy—primigravid women and those using effective contraception during the 4 weeks before the interview. Similarly, Atrash and coworkers4 excluded women with spontaneous abortion, primigravid women, and those with a history of ectopic pregnancy or tubal damage.

Control for Potential Confounding Factors

Regardless of the care taken in choosing an appropriate comparison group, it is impossible to ensure comparable potential exposure to prior abortion. Women with prior abortions differ from women with no prior abortions in that they are more likely to smoke10 and to have been exposed to sexually transmitted diseases (STDs). They have more sexual partners, have earlier age at first sex, have a higher risk of pre-existing pelvic inflammatory disease, and rely less on condoms for protection from STDs. Both smoking and STDs are risk factors for ectopic pregnancy. Studies that do not control for these potential confounding factors may overestimate the effect of induced abortion on ectopic pregnancy. For example, a Greek study that did not control for STDs reported an OR of 1.87 (95% CI, 0.84–4.16) for ectopic pregnancy associated with one or more induced abortions.11 All studies summarized in Table 1 controlled for both smoking and STDs, as well as other potential confounding factors, when calculating adjusted ORs. The effect of adjustment was to reduce the observed effect of induced abortion, illustrating the importance of taking these differences into account. However, no observational study can completely rule out potential confounding by unmeasured variables. Therefore, observed ORs of less than 2.0 may be challenged on the basis of unmeasured confounding.

Selective Recall

The case-control strategy recruits participants based on their health status (e.g., case subjects have an ectopic pregnancy and control subjects have a normal pregnancy) and queries them about past exposures. Accurate exposure measurement relies on accurate memory. Both case and control subjects may experience an equal likelihood of poor memory. In this instance, the OR is biased toward the null because of error in measurement. However, with a sensitive topic such as prior induced abortion, women with a health problem are more likely to report their abortion history than are women in the control group.12 This selective recall biases the OR away from the null by an estimated 20% to 50% over the true risk. Selective recall could explain the small excess risk observed in the ectopic pregnancy case-control studies summarized in Table 1. Cohort studies do not rely on recall, but rather begin with the exposure and follow women to observe which ones experience the outcome. One cohort study of Norwegian women identified those with one (N = 2662), two (N = 554), or three (N = 538) abortions.13 Followed 1 to 7 years through record linkage, women with two or more abortions experienced no excess risk for ectopic pregnancy (adjusted incidence density ratio [IDR], 1.2; 95% CI, 0.5–3.1) compared with women with one abortion. There was no excess risk if the abortions occurred in consecutive pregnancies (adjusted IDR, 0.9 for two consecutive abortions and 1.1 for three or more consecutive abortions compared with one abortion). These findings support the lack of causal association between induced abortion and ectopic pregnancy.

OTHER REPRODUCTIVE HEALTH OUTCOMES

Long-term risks of one abortion on secondary infertility, second-trimester spontaneous abortion, preterm delivery, and low birthweight were comprehensively reviewed in 198210 and updated in 1990.14 These reviews formed the basis for Surgeon General Everett Koop's conclusion that “the physical sequelae of abortion were no different than those found in women who carried pregnancy to term or who had never been pregnant.”15 This conclusion is valid for surgical abortion by vacuum aspiration in the first trimester (the most common procedure in the United States and the one that has been most extensively studied). Specifically, there are:

  • No significant risks for secondary infertility.16,17 However, if the abortion is infected or complicated by pre-existing and nontreated STDs, risks of secondary infertility, ectopic pregnancy, and fetal loss increase. Therefore, it is critically important to provide prophylactic antibiotics with the surgery to protect against pelvic infection.18
  • No significant risks for spontaneous abortion or preterm or low birthweight delivery in the next pregnancy. A woman's first birth carries a greater risk of being preterm or of low birthweight when compared with her second birth, irrespective of whether the first birth followed a surgical abortion.

Choice of abortion method can affect future reproductive health potential. First-trimester abortion by dilation and sharp curettage (D&C), particularly if performed with the patient under general anesthesia, can result in uterine synechiae, which increase the risk of subsequent midtrimester spontaneous abortions and low birthweight deliveries. Second-trimester abortion induction methods do not appear to increase risk, although the literature is rather sparse.14,17 However, dilation and evacuation (D& E) without gradual dilation with osmotic dilators may increase the risk of second-trimester spontaneous abortion and, possibly, low birthweight delivery of the next pregnancy. When laminaria are used, the risk may be mitigated. One study of 171 women undergoing D& E with laminaria and under general anesthesia found no elevated incidence of preterm delivery of the next pregnancy.19

Other pregnancy outcomes reported in the literature include placenta previa20 and neonatal sepsis21 after one or more induced abortions. These studies report small but statistically significant elevated ORs (1.3 for placenta previa and 2.2 for neonatal sepsis), but neither controlled for STDs.

OTHER POTENTIAL LONG-TERM RISKS

Breast Cancer

The American College of Obstetricians and Gynecologists, the National Cancer Institute, and the American Cancer Society concluded that there is substantial evidence of no direct effect of induced abortion on risk of breast cancer. This conclusion is based on the results of two large-scale cohort studies of breast cancer after induced abortion that report no increased risk22,23 and with mixed results from numerous case-control studies.

Psychological Problems

Studies and various reports of psychological problems after induced abortion have been criticized because of the difficulty in separating pre-existing conditions and the context of the unintended pregnancy from the effect of the procedure, the bias of many investigators (either toward finding a significant effect or toward finding no effect), and other methodologic problems. The Surgeon General's report on health effects of abortion on women concluded that the literature was too flawed to draw a conclusion.15

The data on major psychiatric illness requiring hospitalization are less subject to investigator bias than are studies of regret, psychological distress, or minor depression. Review of this literature suggests that major psychiatric sequelae after abortion are rare (less than 1%) and less frequent than after childbirth (approximately 10%).7 Risk factors for major psychiatric problems include pre-existing psychiatric disease as well as circumstances surrounding the abortion (e.g., coercion, paralyzing ambivalence, or a decision to abort a desired pregnancy because of genetic or maternal medical indications).

IMPLICATIONS FOR PRACTICE

Abortion providers can assist in preserving reproductive health, coping with emotional adjustments, and providing reassurance regarding long-term risks of abortion. Specifically:

  • Provide access to support services and information about pregnancy options.
  • Inform the client about the safety of abortion with respect to psychiatric illness. She should also be advised that she may feel a sense of loss or guilt, and that these feelings are normal and usually self-limited.
  • Provide prophylactic antibiotics to protect against pelvic infection.
  • Screen for smoking and STDs and provide counseling and referral services.
  • Provide contraceptives, contraceptive counseling, and education about how to avoid both unintended pregnancy and STDs.
  • Inform the client about the safety of abortion for future reproductive health and breast cancer while also encouraging her to report the procedure when seeking reproductive health services in the future. In rare instances, a previously undiagnosed complication can lead to future problems.24

REFERENCES

1

Skjeldestad F, Atrash H: Evaluation of induced abortion as a risk factor for ectopic pregnancy. Acta Obstet Gynecol Scand 76: 151, 1997

 

2

Levin A, Schoenbaum S, Stubblefield P et al: Ectopic pregnancy and prior induced abortion. Am J Public Health 72: 253, 1982

 

3

Daling J, Chow W, Weiss N et al: Ectopic pregnancy in relation to previous induced abortion. JAMA 253: 1005, 1985

 

4

Atrash H, Strauss L, Kendrick J et al: The relationship between induced abortion and ectopic pregnancy. Obstet Gynecol 89: 512, 1997

 

5

Burkman R, Mason K, Gold E: Ectopic pregnancy and prior induced abortion. Contraception 37: 21, 1988

 

6

Holt V, Daling J, Voigt L: Induced abortion and the risk of subsequent ectopic pregnancy. Am J Public Health 79: 1234, 1989

 

7

Hogue CJR, Boardman LA, Stotland NL et al: Answering questions about long-term outcomes. In Stubblefield P et al (eds): Abortion Textbook. New York, Press, 1999

 

8

Weiss N, Daling J, Chow W: Control definition in case-control studies of ectopic pregnancy. Am J Public Health 75: 67, 1985

 

9

Parazzini F, Ferraroni M, Tozzi L et al: Induced abortions and risk of ectopic pregnancy. Hum Reprod 10: 1841, 1995

 

10

Hogue C, Cates W Jr, Tietze C: The effects of induced abortion on subsequent reproduction. Epidemiol Rev 4: 66, 1982

 

11

Kalandidi A, Doulgerakis M, Tzonou A et al: Induced abortions, contraceptive practices, and tobacco smoking as risk factors for ectopic pregnancy in Athens, Greece. Br J Obstet Gynaecol 98: 207, 1991

 

12

Hogue C: Low birth weight subsequent to induced abortion: a historical prospective study of 948 women in Skopje, Yugoslavia. Am J Obstet Gynecol 123: 675, 1975

 

13

Skeldestad F, Gargiullo P, Kendirck J: Multiple induced abortions as risk factor for ectopic pregnancy. Acta Obstet Gynecol Scand 76: 691, 1997

 

14

Atrash H, Hogue C: The effect of pregnancy termination on future reproduction. Baillieres Clin Obstet Gynaecol 4: 391, 1990

 

15

Koop E: Medical and psychological impact of abortion. In Hearing before the Human Resources and Intergovernmental Relations Subcommittee of the Committee on Government Operations, House of Representatives, One Hundred First Congress—First Session. Washington, DC, US Government Printing Office, 1989

 

16

Frank P, McNamee R, Hannaford P et al: The effect of induced abortion on subsequent fertility. Br J Obstet Gynaecol 100: 575, 1993

 

17

Lurie S, Levy R, Katz Z et al: The influence of midtrimester termination of pregnancy on subsequent fertility: Four to five years follow-up. Contraception 50: 239, 1994

 

18

Sawaya GF, Grady D, Kerlikowske K et al: Antibiotics at the time of induced abortion: the case for universal prophylaxis based on a meta-analysis. Obstet Gynecol 87: 884, 1996

 

19

Schneider D, Halperin R, Caspi E et al: Abortion at 18–22 weeks by laminaria dilation and evacuation. Obstet Gynecol 88: 412, 1996

 

20

Taylor v, Kramer M, Vaughan T et al: Placenta previa in relation to induced and spontaneous abortion: A population-based study. Obstet Gynecol 82: 88, 1993

 

21

Germain M, Krohn M, Daling J: Reproductive history and the risk of neonatal sepsis. Paediatr Perinat Epidemiol 9: 48, 1995

 

22

Lindefors-Harris B-M, Eklund G, Meirik O et al: Risk of cancer of the breast after legal abortion during first trimester: A Swedish register study. BMJ 299: 1430, 1989

 

23

Melbye M, Wohlfahrt J, Olsen JH et al: Induced abortion and the risk of breast cancer. N Engl J Med 336: 81, 1997

 

24

Moon H, Park Y, Kwon H et al: Iatrogenic secondary infertility caused by residual intrauterine fetal bone after midtrimester abortion. Am J Obstet Gynecol 176: 369, 1997