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Copyright © 2006, Can Fam Physician Does epidural analgesia increase rate of cesarean
section? Correspondence to: Dr Michael C. Klein, Child and Family Research Institute, 4500 Oak St, Room L309B Shaughnessy Bldg, Vancouver, BC V6H 3N1; telephone 604 875-2000, extension 5078; fax 604 875-3569; e-mail mklein/at/interchange.ubc.ca This article has been cited by other articles in PMC.Epidural analgesia (EA) is clearly the most effective form of pain relief during
labour.1 But various unwanted side effects are
associated with its use,2 including longer labour;
increased incidence of maternal fever (with associated increase in use of antibiotics
for mothers and newborns); and increased rates of operative vaginal delivery and
perineal trauma,2 such as more third- and
fourth-degree tears.3,4 The 2000 Cochrane meta-analysis2 that compared EA
with narcotics did not show increased rates of cesarean section (CS) associated with EA.
For many practitioners this came as a surprise; in practice EA certainly seemed to
increase rates of CS, especially when used before the active phase of labour. Earlier
studies5,6 had shown a modest increase in rates of CS when EA was compared with other
methods of analgesia. One trial showed such a large effect that the trial had to be
stopped.6 Departmental quality improvement Because use of EA varied greatly among physicians in our department, we began a
series of quality-improvement activities. We found that physicians who used EA 40%
of the time or less had a CS rate of 14.8% for nulliparous patients, while those who
used EA 71% to 100% of the time had a CS rate of 23.4%. Multiparous women were
unaffected by their physicians’ use of EA. We did not know why this was so, but we
knew from the literature that using EA early in labour, before the fetus is well
down in the pelvis, could cause extension of the fetal head or not allow for
flexion, and this would interfere with rotation and descent.2,7,8 We did find that physicians in our department who used EA
frequently had more patients with malpositions (occiput posterior and occiput
transverse), had patients who required more augmentation, had fewer patients with
spontaneous births, and had more CS deliveries.9 Our results were similar to those of a natural experiment at a nearby community
hospital. Their rate of EA was 15.4% compared with our rate of 67.2%. We reported
that, for comparable women, the odds of having a CS at our tertiary centre were 3.4
times greater (95% confidence interval [CI] 2.1 to 5.4) than at the community
hospital. Maternal age, more advanced cervical dilation on admission, and use of EA
were the primary factors associated with the difference in CS rates. Use of EA had
the largest effect.10 These studies made it difficult to accept the results of the 2000 Cochrane
meta-analysis, which concluded that EA did not raise rates of CS. In fact, it
appeared that increasing use of EA was transforming birth. A recent report from the
Canadian Institute for Health Information indicated that 4 of 5 Canadian women
giving birth received 1 or more major obstetrical intervention, with EA high on the
list (as high as 65% in major urban areas).11
Yet, as a society and as professionals, we seem reluctant to acknowledge this change
and its effect on the birthing environment.12 The Cochrane meta-analysis I then decided to look more closely at the individual studies that made up the 2000
Cochrane meta-analysis addressing the effect of EA (Figure 1
Why was there no increase in cesarean section? It was hard to understand why, if EA clearly increased abnormalities of labour, rates
of CS did not also increase. The study by Sharma and colleagues13 is the key study that led to the Cochrane review’s
conclusion that EA did not increase rates of CS. This was the largest study in the
meta-analysis and clearly demonstrated no increase in CS; because of its large
numbers, Sharma and colleagues’ trial overwhelmed the other results. Sharma’s team
comes from Parkland Hospital in Dallas, Tex, where the hospital CS rate was only
12%. Most importantly, the subjects in the trial were randomized at more than 4-cm
cervical dilation—the active phase of labour. According to the Cochrane
data, the rate of CS for both groups in the study by Sharma and colleagues was only
5%. Clark et al15 and Loughnan et al16 also randomized most of their (many)
patients after 4-cm dilation; their CS rates were 14% in the narcotics group and 10%
in the EA group and 13% in the narcotics group and 12% in the EA group,
respectively. Again, rates of CS were so low as to be unable to show a difference.
Though the Cochrane meta-analysis was not set up to address this issue, what it
actually shows is that EA administered in the active phase of labour does not
increase rates of CS. But our sensitivity analysis (Figure 2
External validity The study by Sharma et al13 and other similar
studies that randomized women late in labour would better illustrate that women
should be encouraged to try to reach at least 4- to 5-cm dilation before EA is used.
Ideally the Cochrane review could have constructed 2 meta-analytical strata, 1
before and 1 after 4-cm dilation. A recent example of the misuse or misinterpretation of randomized controlled trials
of EA17 caught the attention of the
international press. The reported study was of “neuraxial analgesia,” an obfuscating
term. The author, the editorialist,18 and the
press reported that women need not worry that early EA will lead to increased
likelihood of CS. This claim is unjustified by the research reported. This trial was
not about early use of EA; it was about 2 methods of helping women with the pain of
early labour. At first request for analgesia, women in the so-called epidural group
received intrathecal fentanyl, and an epidural catheter was placed but not used.
Women in the narcotics group received hydromorphone. At that point 75% of women in
both groups had received oxytocin augmentation—a rate higher than can be
generalized. On second request for pain relief, two thirds of the women in both
groups were in the active phase of labour. At this advanced stage, women in the
fentanyl-epidural group received low-dose EA. Women in the narcotic group received
hydromophone intramuscularly. This trial again is misleading because it fails to
emphasize that most women were in the active phase of labour at randomization. This
study, like the others randomizing late, has shown only that when women’s
latent-phase pain is managed with intrathecal narcotics or other pharmacologic or
nonpharmacologic means, EA in the active phase of labour does not increase the CS
rate. The role of early EA in contributing to CS increase has yet to be studied in a
controlled trial, though this sensitivity analysis of the Cochrane review suggests
that early EA does increase rates of CS. Collateral damage The Cochrane meta-analysis of EA has inadvertently increased use of EA, and has
therefore increased continuous electronic fetal monitoring; kept more women in bed
(usually with an intravenous drip); and led to more instrumentation, more perineal
trauma, an increase in the CS rate, and, likely, more feelings of failure among
mothers. It will also lead, because of the increase in CS, to an increase in
problems with placentas in future pregnancies (previa, accreta, percreta,
abruption),19 infertility,20 and ectopic pregnancies.19 This is unexpected collateral damage that
contributes to overuse of technology during childbirth. It has even led some to
suggest that, since childbirth is already so unnatural, CS on request is not such an
unreasonable idea—a surgical solution for a non-surgical problem.21-23 The 2005 Cochrane meta-analysis24 was
augmented by 3 new studies,25-27 2 of which had such low baseline rates of CS
that the effect of EA on CS could never be demonstrated.25,26
One study25 evaluated the combined
spinal-epidural method, similar to Wong et al,17 but suffered from very high crossover rates between trial groups, and 2
studies randomized patients before 4-cm dilation.26,27 When these studies are
appropriately removed from the new meta-analysis, the result remains exactly the
same: early EA more than doubles the CS rate. Surprisingly, the new Cochrane review
provided extensive sensitivity analyses for many issues but none by timing of EA
administration. Conclusion Contrary to the conclusion of the Cochrane meta-analysis of EA compared with narcotic
analgesia, EA given before the active phase of labour more than doubles the
probability of receiving a CS. If given in the active phase of labour, EA does not
increase rates of CS. Meta-analysis can be helpful and timesaving for busy
practitioners, but we need to be vigilant about which studies get into the
meta-analyses and ask ourselves if they make clinical sense. And,
unfortunately, we need to continue to read the individual studies that make up
meta-analyses—especially if they are likely to actually change
practice—to determine whether study conditions represent our clinical
reality. Acknowledgments I thank Peter von Dadelszen, perinatologist at Children’s and Women’s Health Centre
of British Columbia, for assistance with the sensitivity analysis of Cochrane
meta-analysis; Andrew Kotaska, obstetrical resident at Children’s and Women’s Health
Centre of British Columbia; and Murray Enkin, Professor Emeritus of Obstetrics and
Gynecology at McMaster University, for criticism and support. Biography
Footnotes The opinions expressed in editorials are those of the authors. Publication does
not imply endorsement by the College of Family Physicians of Canada. References 1. Leeman L, Fontaine P, King V, Klein MC, Ratcliffe S. The nature and management of labor pain: part II. Pharmacologic
pain relief. Am Fam Physician. 2003;68(6):1115–1120. [PubMed] 2. Howell CJ. Epidural versus non-epidural analgesia for pain relief in labour. Cochrane Database Syst Rev. 2000. CD000331. 3. Klein MC, Gauthier RJ, Robbins JM, Kaczorowski J, Jorgensen SH, Franco ED, et al. Relationship of episiotomy to perineal trauma and morbidity,
sexual dysfunction, and pelvic floor relaxation. Am J Obstet Gynecol. 1994;171:591–598. [PubMed] 4. Klein MC, Janssen PA, MacWilliam L, Kaczorowski J, Johnson B. Determinants of vaginal-perineal integrity and pelvic floor
functioning in childbirth. Am J Obstet Gynecol. 1997;176:403–410. [PubMed] 5. Morton SC, Williams MS, Keeler EB, Gambone JC, Kahn KL. Effect of epidural analgesia for labor on the cesarean delivery
rate. Obstet Gynecol. 1994;83(6):1045–1052. [PubMed] 6. Thorp JA, Hu DH, Albin RM, McNitt J, Meyer BA, Cohen GR, et al. The effect of intrapartum epidural analgesia on nulliparous
labor: a randomized, controlled, prospective trial. Am J Obstet Gynecol. 1993;169:851–858. [PubMed] 7. Hoult IT, MacLennan AH, Carrie LE. Lumbar epidural analgesia in labour: relation to fetal
malposition and instrumental delivery. BMJ. 1977;1:14–16. [PubMed] 8. Lieberman E, Cohen A, Lang JM, D’Angostino R, Jr, Datta S, Frigoletto FD., Jr The association of epidural anesthesia with cesarean section in
low risk women [abstract]. Am J Obstet Gynecol. 1995;172:276. 9. Klein MC, Grzybowski S, Harris S, Liston R, Spence A, Le G, et al. Epidural analgesia use as a marker for physician approach to
birth: implications for maternal and newborn outcomes. Birth. 2001;28(4):243–248. [PubMed] 10. Janssen PA, Klein MC, Soolsma JH. Differences in institutional cesarean delivery
rates—the role of pain management. J Fam Pract. 2001;50(3):217–223. [PubMed] 11. Canadian Institute for Health Information. Giving birth in Canada: a regional profile. Ottawa, Ont: Canadian Institute for Health Information; 2004. 12. Reime B, Klein MC, Kelly A, Duxbury N, Saxell L, Liston R, et al. Do maternity care provider groups have different attitudes
towards birth? BJOG. 2004;111(12):1388–1393. [PubMed] 13. Sharma SK, Sidawi JE, Ramin SM, Lucas MJ, Leveno KJ, Cunningham FG. Cesarean delivery: a randomized trial of epidural versus
patient-controlled meperidine analgesia during labor. Anesthesiology. 1997;87:487–494. [PubMed] 14. Lieberman E, O’Donoghue C. Unintended effects of epidural analgesia during labor: a
systematic review. Am J Obstet Gynecol. 2002;186(5 Suppl Nature):31–68. 15. Clark A, Carr D, Loyd G, Cook V, Spinnato J. The influence of epidural analgesia on cesarean delivery rates: a
randomized, prospective clinical trial. Am J Obstet Gynecol. 1998;179(6 Pt 1):1527–1533. [PubMed] 16. Loughnan BA, Carli F, Romney M, Dore CJ, Gordon H. Randomized controlled comparison of epidural bupivacaine versus
pethidine for analgesia in labour. Br J Anaesth. 2000;84(6):715–719. [PubMed] 17. Wong CA, Scavone BM, Peaceman AM, McCarthy RJ, Sullivan JT, Diaz NT, et al. The risk of cesarean delivery with neuraxial analgesia given
early versus late in labor. N Engl J Med. 2005;352(7):655–665. [PubMed] 18. Camann W. Pain relief during labor. N Engl J Med. 2005;352(7):718–720. [PubMed] 19. Hemminki E, Merilainen J. Long-term effects of cesarean sections: ectopic pregnancies and
placental problems. Am J Obstet Gynecol. 1996;174:1569–1574. [PubMed] 20. Hemminki E. Impact of caesarean section on future pregnancy—a
review of cohort studies. Paediatr Perinat Epidemiol. 1996;10(4):366–379. [PubMed] 21. Hannah ME. Planned elective cesarean section: a reasonable choice for some
women? CMAJ. 2004;170:813–814. [PubMed] 22. Klein MC. Elective cesarean section [letter]. CMAJ. 2004;171:14–15. [PubMed] 23. Klein MC. Quick fix culture: the cesarean-section-on-demand debate. Birth. 2004;31(3):161–164. [PubMed] 24. Anim-Somuah M, Smyth R, Howell C. Epidural versus non-epidural or no analgesia in labour. Cochrane Database Syst Rev. 2005. CD00331. pub2. 25. Dickinson JE, Paech MJ, McDonald SJ, Evans SF. The impact of intrapartum analgesia on labour and delivery
outcomes in nulliparous women. Aust N Z J Obstet Gynaecol. pp. 59–66. 26. Sharma SK, Alexander JM, Messick G, Bloom SL, McIntire DD, Wiley J, et al. Cesarean delivery: a randomized trial of epidural analgesia
versus intravenous meperidine analgesia during labor in nulliparous women. Anesthesiology. pp. 546–551. 27. Jain S, Arya VK, Gopalan S, Jain V. Analgesic efficacy of intramuscular opioids versus epidural
analgesia in labor. Int J Gynaecol Obstet. 2003;83:19–27. [PubMed] |
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Am Fam Physician. 2003 Sep 15; 68(6):1115-20.
[Am Fam Physician. 2003]Am J Obstet Gynecol. 1994 Sep; 171(3):591-8.
[Am J Obstet Gynecol. 1994]Am J Obstet Gynecol. 1997 Feb; 176(2):403-10.
[Am J Obstet Gynecol. 1997]Obstet Gynecol. 1994 Jun; 83(6):1045-52.
[Obstet Gynecol. 1994]Am J Obstet Gynecol. 1993 Oct; 169(4):851-8.
[Am J Obstet Gynecol. 1993]Br Med J. 1977 Jan 1; 1(6052):14-6.
[Br Med J. 1977]Birth. 2001 Dec; 28(4):243-8.
[Birth. 2001]J Fam Pract. 2001 Mar; 50(3):217-23.
[J Fam Pract. 2001]BJOG. 2004 Dec; 111(12):1388-93.
[BJOG. 2004]Anesthesiology. 1997 Sep; 87(3):487-94.
[Anesthesiology. 1997]Anesthesiology. 1997 Sep; 87(3):487-94.
[Anesthesiology. 1997]Am J Obstet Gynecol. 1998 Dec; 179(6 Pt 1):1527-33.
[Am J Obstet Gynecol. 1998]Br J Anaesth. 2000 Jun; 84(6):715-9.
[Br J Anaesth. 2000]Am J Obstet Gynecol. 1998 Dec; 179(6 Pt 1):1527-33.
[Am J Obstet Gynecol. 1998]Br J Anaesth. 2000 Jun; 84(6):715-9.
[Br J Anaesth. 2000]Anesthesiology. 1997 Sep; 87(3):487-94.
[Anesthesiology. 1997]Anesthesiology. 1997 Sep; 87(3):487-94.
[Anesthesiology. 1997]N Engl J Med. 2005 Feb 17; 352(7):655-65.
[N Engl J Med. 2005]N Engl J Med. 2005 Feb 17; 352(7):718-20.
[N Engl J Med. 2005]Am J Obstet Gynecol. 1996 May; 174(5):1569-74.
[Am J Obstet Gynecol. 1996]Paediatr Perinat Epidemiol. 1996 Oct; 10(4):366-79.
[Paediatr Perinat Epidemiol. 1996]CMAJ. 2004 Mar 2; 170(5):813-4.
[CMAJ. 2004]Birth. 2004 Sep; 31(3):161-4.
[Birth. 2004]Int J Gynaecol Obstet. 2003 Oct; 83(1):19-27.
[Int J Gynaecol Obstet. 2003]N Engl J Med. 2005 Feb 17; 352(7):655-65.
[N Engl J Med. 2005]