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2002 Selected Articles

Broad-based Conversion to Elective Cesarean Delivery is Not Justified

William Grobman, MD, MBA

A large body of research has implicated the process of labor and vaginal delivery in the development of urogenital tract abnormalities. Given this association, some authorities have suggested that patients be offered the option of undergoing an elective cesarean delivery in an effort to avoid long-term urogenital injury. If this strategy is reasonable, the necessary implication is either that the risks of functional urogenital injury are relatively high, or that the risks of cesarean delivery are relatively low. Does the available evidence support either of these conclusions?

RISKS OF VAGINAL DELIVERY

Impairment of urogenital function is thought to be due either to direct trauma to the relevant anatomic structures (ie, sphincters) or to damage to the nerves that innervate the pelvic floor. For example, Sultan et al¹ reported that after vaginal delivery, primiparous women had significantly increased mean pudendal nerve latency, as well as a 35% prevalence of either internal or external anal sphincter disruption. Meyer et al² detailed the multiple physiologic parameters in the lower urinary tract, such as functional urethral length and bladder neck mobility, that are adversely affected by vaginal delivery. Other investigators have found similar adverse changes in the components that contribute to urinary and anal incontinence subsequent to labor and delivery.^3-7 However, these findings do not allow for a definitive determination of the risks of labor and vaginal delivery or of the corresponding benefits said to be conferred by elective cesarean delivery. There are several reasons for this.

Intermediate Outcomes

Many of the abnormalities documented in the literature, eg, endosonographic anal sphincter disruptions,^1,7 lower anal manometric pressures,^1,5 increased pudendal nerve latencies,¹ lower bladder neck postions,⁴ may or may not be of actual clinical significance. For example, it hardly seems reasonable to recommend a cesarean delivery because pudendal nerve latency after vaginal delivery increases from 1.9 ± 0.2 msec to 2.0 ± 0.2 msec,¹ even if this difference is statistically significant. The lack of correspondence between instrumental measures and functionally relevant outcomes is demonstrated, as just one example, in the report by Sultan et al; the majority of women who had anal sphincter disruption were not, in fact, incontinent.¹

Loss to Follow-up

Even when investigators have evaluated clinically relevant medical conditions, such as frank urinary or fecal incontinence, the prevalence of these conditions has probably been overestimated due to lack of patient compliance with study follow-up. Prospective studies have typically lost 10% to 30% of patients during the postpartum analysis.^{1, 3-7} This loss increases the apparent prevalence of incontinence, as women who have no problems are less likely to return. Snooks et al, ⁸ who experienced a 42% loss to follow-up, noted that women who did not return and who could be contacted reported themselves "free of sphincter disturbance."

Lack of Long-term Outcome Data

While the risks of urinary and anal incontinence after vaginal delivery have been estimated at up to 25% and 10%, respectively, these functional abnormalities were documented in close temporal proximity to the prior vaginal delivery, and are not proper estimates of long-term dysfunction, the most clinically relevant outcome. In fact, when studies documenting incontinence are examined according to the interval from delivery to postpartum analysis, a steady decrease in the prevalence of incontinence is noted (Table 1). Viktrup et al,⁶ who studied women at 1 year postpartum, found that clinically significant incontinence occurred after vaginal delivery in 1% or fewer of patients.

What, then, is the marginal contribution of vaginal delivery to long-term incontinence that impairs quality of life, induces medical and surgical interventions, and increases related health care costs? The studies that have examined large numbers of women many years after childbearing and used multivariate analysis to elucidate risk factors for future incontinence have failed to consistently identify vaginal delivery as an independent risk factor, let alone a factor of singular importance. Neither Burgio et al,⁹ Hording et al,¹⁰ nor Brown et al¹¹ were able to identify parity as an independent predictor of long-term incontinence. These authors did identify other factors such as obesity, white race, hysterectomy, and chronic medical illness (eg, diabetes, chronic obstructive pulmonary disease) that were significantly associated with incontinence. While a significant correlation with increasing parity was found by Thom et al,¹² the point estimate of the odds ratio for even the most parous women (4 or more children) was less than that of all other independent risk factors for incontinence.

RISKS OF CESAREAN DELIVERY

Even if the magnitude of the association between vaginal delivery and clinically significant long-term incontinence is uncertain, might the risks of cesarean delivery be so small as to justify it as an option?

Risks of Initial Cesarean Delivery

Several risks of cesarean delivery, eg, wound, uterine, and urinary infections, are relatively frequent, but are usually without long-term sequelae. Conversely, while other types of postoperative morbidity may occur less often than infection, these conditions may be more significant due to their highly detrimental effects on quality of life. For example, thromboembolic disease is approximately 5 times more common after cesarean delivery than after vaginal delivery, and can lead to anticoagulant-associated major morbidity, postthrombotic chronic pain syndrome, recurrent thromboembolic disease, and even death. In fact, studies throughout the world have demonstrated that cesarean delivery, even when elective, is associated with a significant increase in maternal mortality.^13-15

Risks in Future Pregnancies

The risks of an initial cesarean delivery are not limited to the immediate postoperative period, but continue to accrue during future pregnancies. Because the majority of women will continue childbearing after their first pregnancy, these risks are relevant when considering a cesarean delivery. For example, if a woman chooses an elective cesarean delivery initially, she would be expected to continue to use this route of delivery; thus, she will face further operative risks during each pregnancy. Actually, her operative risks may increase, as each cesarean delivery promotes abdominal and pelvic adhesive disease. Kirkinen¹⁶ compared women with at least three cesarean deliveries with those who had no more than two such deliveries. The former group was significantly more likely to have dense adhesions between the anterior abdominal wall and the uterine serosa and to require a hysterectomy. These adhesions may also result in major operative injury; of the ureteral injuries catalogued by Meirow et al,¹⁷ nearly 25% were the result of repeat cesarean deliveries.

Additionally, a cesarean delivery significantly increases the risk of antepartum complications and the potential for neonatal morbidity. Studies have consistently demonstrated that one cesarean delivery is associated with a 2- to 4-fold increase in the occurrence of placenta previa, a risk that continues to rise as additional cesarean deliveries are preformed.¹⁸ Moreover, these cases of placenta previa tend to be more morbid than those that occur independent of prior cesarean delivery, and are associated with a significantly greater need for transfusion and hysterectomy.¹⁹ Lydon-Rochelle et al²⁰ illustrated that in addition to increasing the risk of placenta previa, a cesarean delivery is associated with an increased risk of subsequent abruptio placentae, and that both of these placentation abnormalities are associated with higher rates of preterm delivery and infant mortality.

In the final analysis, then, there is clear and present risk of a cesarean, uncertain magnitude of the contribution of labor and vaginal delivery to long-term clinically significant incontinence, and no actual outcome data to directly support the hypothesis that elective cesarean will improve a woman’s quality of life. The confluence of these factors forms a compelling rationale against the routine offer of elective cesarean delivery. Yet, despite this evidence, might other arguments support the offer of elective cesarean? In some cases, patient autonomy has been cited as a justification of this management scheme. However, although the importance of patient autonomy is indisputable, its invocation in this case is unfounded. Patient autonomy is predicated on the negative right to choose among or refuse procedures, and not on the positive right to demand a certain treatment.²¹ If in the judgment of a physician, a patient’s demand for a certain procedure will result in an unnecessary burden of risk, the ethical principles of physician autonomy and beneficence would be breached by performance of the procedure.

Finally, although it may not be reasonable to offer elective cesarean delivery routinely, might it be justifiable in selected populations at particularly high risk of labor-related urogenital dysfunction? This rationale for selection is appealing, and further research may allow for identification of the patients most likely to benefit. However, not only has no accurate scoring system been developed and prospectively evaluated to date, but the very nature of the risk factors that contribute to labor-related urogenital dysfunction remains controversial and uncertain.^3,4,7,22,23

CONCLUSION

Past acceptance of unproven medical interventions has often failed to deliver the promised results (eg, home uterine monitoring), and in some cases has caused unforeseen harm (eg, diethylstilbestrol). Before adopting interventions of unproven benefit, such as elective cesarean delivery, the medical community should ensure through outcomes research, and not through intuition, that the hypothesized beneficial results are actually the ones that will be achieved.

William Grobman, MD, MBA, is an assistant professor in the Department of Obstetrics and Gynecology at Northwestern Medical School in Chicago, Ill.

REFERENCES

1. Sultan AH, Kamm MA, Hudson CN, et al. Anal-sphincter disruption during vaginal delivery. N Engl J Med. 1993;329(26):1905-1911.
2. Meyer S, Schreyer A, DeGrandi P, Hohlfeld P. The effects of birth on urinary continence mechanisms and other pelvic-floor characteristics. Obstet Gynecol. 1998;92(4 Pt 1):613-618.
3. Farrell SA, Allen VM, Baskett TF. Parturition and urinary incontinence in primiparas. Obstet Gynecol. 2001;97(3):350-356.
4. MacArthur C, Bick DE, Keighley MR. Faecal incontinence after childbirth. Br J Obstet Gynaecol. 1997;104(1):46-50.
5. Donnelly V, Fynes M, Campbell D, et al. Obstetric events leading to anal sphincter damage. Obstet Gynecol. 1998;92(6):955-961.
6. Viktrup L, Lose G, Rolff M, Barfoed K. The symptom of stress incontinence caused by pregnancy or delivery in primiparas. Obstet Gynecol. 1992;79(6):945-949.
7. Abramowitz L, Sobhani I, Ganansia R, et al. Are anal sphincter defects the cause of anal incontinence after vaginal delivery? Dis Colon Rectum. 2000;43(5):590-598.
8. Snooks SJ, Swash M, Mathers SE, Henry MM. Effect of vaginal delivery on the pelvic floor: a 5-year follow-up. Br J Surg. 1990;77(12):1358-1360.
9. Burgio KL, Matthews KA, Engel BT. Prevalence, incidence and correlates of urinary incontinence in healthy, middle-aged women. J Urol. 1991;146(5):1255-1259.
10. Hording U, Pedersen KH, Sidenius K, Hedegaard L. Urinary incontinence in 45-year-old women. Scand J Urol Nephrol. 1986;20(3):183-186.
11. Brown JS, Seeley DG, Fong J, et al. Urinary incontinence in older women: who is at risk? Obstet Gynecol. 1996;87(5 Pt 1): 715-21.
12. Thom DH, Van Den Eeden SK, Brown JS. Evaluation of parturition and other reproductive variables as risk factors for urinary incontinence in later life. Obstet Gynecol. 1997;90(6):983-989.
13. Petitti DB, Cefalo RC, Shapiro S, Whalley P. In-hospital maternal mortality in the United States: time trends and relation to method of delivery. Obstet Gynecol. 1982;59(1):6-12.
14. Lilford RJ, Van Coeverden-De Groot HA, Moore PJ, Bingham P. The relative risks of cesarean delivery (intrapartum and elective) and vaginal delivery: a detailed analysis to exclude the effects of medical disorders and other acute pre-existing physiological disturbances. Br J Obstet Gynaecol. 1990;97(10): 883-892.
15. Schuitemaker N, van Roosmalen J, Dekker G, et al. Maternal mortality after cesarean delivery in the Netherlands. Acta Obstet Gynecol Scand. 1996;76(4):332-334.
16. Kirkinen P. Multiple cesarean deliverys: outcomes and complications. Br J Obstet Gynaecol. 1988;95(8):778-782.
17. Meirow D, Moreil EZ, Zilberman M, Farkas A. Evaluation and treatment of iatrogenic ureteral injuries during obstetric and gynecologic operations for nonmalignant conditions. J Am Coll Surg. 1994;178(2):144-148.
18. Ananth CV, Smulian JC, Vintzileos AM. The association of placenta previa with history of cesarean delivery and abortion: a meta-analysis. Am J Obstet Gynecol. 1997;177 (5):1071-1078.
19. Frederiksen MC, Glassenberg R, Stika CS. Placenta previa: a 22-year analysis. Am J Obstet Gynecol. 1999;180(6 Pt 1): 1432-1437.
20. Lydon-Rochelle M, Hold VL, Easterling TR, Martin DP. First-birth cesarean and placental abruption or previa at second birth(1). Obstet Gynecol. 2001;97(5 Pt 1):765-769.
21. Lo B. Resolving Ethical Dilemmas. Baltimore: Williams and Wilkins; 1995.
22. Van Kessel K, Reed S, Newton K, et al. The second stage of labor and stress urinary incontinence. Am J Obstet Gynecol. 2001:184(7):1571-1575.
23. Varma A, Gunn J, Lindow SW, Duthie GS. Do routinely measured delivery variables predict anal sphincter outcome? Dis Colon Rectum. 1999;42(10):1261-1264.

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