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ORIGINAL RESEARCH |
From the Department of Obstetrics and Gynecology, Brigham & Women’s Hospital, Harvard Medical School, Boston, Massachusetts; Department of Obstetrics and Gynecology, Saint Francis Hospital, University of Connecticut, Farmington, Connecticut; and Department of Obstetrics and Gynecology, University of Nebraska Medical Center, University of Nebraska, Omaha, Nebraska.
Address reprint requests to: Thomas D. Shipp, MD, Brigham & Women’s Hospital, Department of Obstetrics and Gynecology, CWN 3, 75 Francis Street, Boston, MA 02115; E-mail: tshipp{at}partners.org.
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ABSTRACT |
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METHODS: We conducted a nested, case-control study in a cohort of all women undergoing a trial of labor after cesarean over a 12-year period in a single tertiary care institution. The current study was limited to all women undergoing a trial of labor after cesarean at term with a symptomatic uterine rupture and who also had their prior cesarean at the same institution. Four controls, who all had their prior cesarean at the same institution, were matched to each case by year of delivery, number of prior cesareans, prior vaginal delivery, and induction in the index pregnancy. Medical records were reviewed for maximum postpartum temperature for the previous cesarean. Fever was defined as a temperature above 38C. Conditional logistic regression analysis was performed taking into account potential confounding factors.
RESULTS: There were 21 cases of uterine rupture included in the analysis. The rate of fever following the prior cesarean was 38% (8/21) among the cases, and 15% (13/84) in the controls, P = .03. Multiple logistic regression analysis examining the association of uterine rupture and postpartum fever adjusting for confounders revealed an odds ratio of 4.0, 95% confidence interval 1.0, 15.5.
CONCLUSION: Postpartum fever after cesarean delivery is associated with an increased risk of uterine rupture during a subsequent trial of labor.
Poor wound healing after major abdominal surgery can be attributable to many factors, including infection, increasing age, poor nutrition status, medical disease, and obesity.1 Infection, frequently associated with poor wound healing, decreases the tensile strength of abdominal wounds.2 Endomyometritis is a relatively common postpartum infection and occurs in approximately 35–40% of women postcesarean who do not receive prophyaxis.3 Fever is one of the most consistent symptoms.3,4 We sought to determine whether fever after a cesarean delivery is associated with an increased risk of symptomatic uterine rupture during a subsequent trial of labor after prior cesarean delivery.
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MATERIALS AND METHODS |
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Symptomatic uterine rupture was defined as complete disruption of the prior cesarean scar with at least one associated symptomatic factor: hemorrhage, hysterectomy, damage to the bladder, extrusion of any portion of the fetal–placental unit from the uterus, or cesarean delivery for nonreassuring fetal testing or suspected uterine rupture.
Medical records were reviewed for maximum intrapartum and postpartum temperatures for the previous cesarean delivery. If there was a fever at the time of delivery, or immediately postpartum, the fever was classified as intrapartum. If there was an intrapartum fever that persisted past the first postpartum hour, a postpartum fever was indicated as being present. Fever was defined as temperature above 38C. The medical records were also reviewed for antibiotic prophylaxis and white blood cell (WBC) counts. Lastly, the number of layers of closure of the uterus was abstracted from the medical record.
The proportion of patients with intrapartum and postpartum fever were compared for the cases and controls. Antibiotic use, infections, and WBC counts were also compared. Crude comparisons for categorical variables were performed using 
2 or Fisher exact test, as appropriate, and Student t test was used for continuous variables. Further statistical analyses were accomplished with regression using Cox proportional hazards models in the SAS System (SAS Institute, Cary, NC) to perform conditional logistic regression analyses that take into account matched sets in evaluating case-control data. Crude comparison of fever and rupture was followed by controlling for the potential confounding effects of maternal age of 30 years or more, gestational age of 40 weeks or more, birth weight of 4000 g or more, and welfare status.
The institutional review board at Brigham & Women’s Hospital approved the study.
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RESULTS |
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). The rate of any intrapartum fever was 19.0% (4/21) for the cases and 10.7% (9/84) for the controls, a difference that did not reach statistical significance (P = .3). The cases with uterine rupture were more likely to have a maternal age of 30 years or more as compared with the controls. The cases had similar proportion of neonates of 4000 g or more, a gestational age of 40 weeks or more, and public assistance as compared with the control patients, as seen in Table 1.
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. Multiple conditional logistic regression analysis examining the association of postcesarean fever with uterine rupture controlling only for maternal age of 30 years or more revealed an odds ratio of 4.4, 95% confidence interval 1.3, 14.4, P = .02.
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The cases and controls had similar postpartum elevations of WBC after the prior cesarean: 21.1% of the cases and 15.9% of the controls had WBC of 20,000 or more, P = .7; 63.2% of the cases and 45.1% of the controls had WBC of 15,000 or more, P = .2. At the time of the prior cesarean delivery, antibiotic prophylaxis was given to 70% (14/20) of the cases and 75% (63/84) of the controls, P = .6.
There was adequate documentation in the medical record regarding the number of layers of closure of the uterus for 20 of the 21 cases and 81 of the 84 controls. One of the 20 cases had a one-layer uterine closure (5%), and two of the 81 controls had one-layer closure (2.5%), P = .5.
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DISCUSSION |
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Our data suggest the possibility that having both intrapartum and postpartum fever may increase the risk of subsequent uterine rupture. The increase in risk was largest in that subgroup, and the difference was statistically significant; however, when we stratify in that way, the number of patients in each group was small. This may also account for the lack of statistical significance in the group with postpartum fever alone. The influence of intrapartum fever requires further investigation before any firm conclusions can be drawn.
Postsurgical infection is frequently associated with poor wound healing and dehiscence of the abdominal surgical scar.2 Bacteriologic infection likely plays an important role in this poor wound healing. The uterine cavity is typically sterile during pregnancy and in the early stages of labor. The rate of positive uterine bacteriologic cultures is greater for those women who labor and even greater for those showing clinical signs of infection.4 Uterine wounds from cesarean delivery heal by scar formation.8 It follows that bacterial infections may adversely influence the healing of cesarean uterine wounds.
The idea that postcesarean delivery infection may be associated with uterine dehiscence or rupture has been previously suggested. More than 90 years ago, postcesarean infection was felt to play a "very important part in causing weakness of the cicatrix." This statement, however, does not appear to have been derived from critical experimental analysis but from experimental work in animals and from case reports and small series of uterine ruptures.9 Despite this association reported nearly a century ago, the effect of postcesarean fever or infection on symptomatic uterine rupture has not been vigorously examined.
Several other, more recent case reports and small studies have investigated any association of postoperative infection and uterine scar disruption. A case report of surgically proven postpartum uterine scar dehiscence was reported in a patient with a serious postpartum endomyometritis. The authors believed that the infection was directly responsible for the lack of healing of the uterine scar.10 A relatively small study of 162 trials of labor that included only eight of the cases with a history of endomyometritis after the prior cesarean reported that none of these were associated with uterine scar disruption after the trial of labor. The authors note that their study was "too small to be of statistical significance" regarding the influence of endomyometritis.11
More recently, Halperin and colleagues reported that prior classical uterine incisions were more commonly associated with uterine scar abnormalities in a subsequent pregnancy as compared with low transverse incisions. Fever after the prior cesarean was more common among those patients with a prior classical incision, but the authors had insufficient numbers of patients to determine the specific effect of postpartum fever on the cesarean scar.12 Persistent postpartum infection has also been shown to be associated with surgically proven uterine scar dehiscence. Brown and colleagues showed that of 54 women delivered by cesarean and with persistent postpartum pelvic infection, at least six (11.1%) had surgically proven uterine scar dehiscence and incisional necrosis.13
We have shown that postpartum fever in women who underwent a cesarean delivery is associated with an increased risk of symptomatic uterine rupture during a subsequent trial of labor. Although our data cannot demonstrate with certainty whether this is owing to infection such as endomyometritis, this remains the most likely explanation. Further studies are needed to determine the reason for this association including the influence of having both intrapartum and postpartum fevers. If the data is confirmed, the postpartum course and temperature curves may be an important part of the decision on mode of delivery after prior cesarean.
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Footnotes |
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Received March 26, 2002. Received in revised form June 3, 2002. Accepted July 25, 2002.
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REFERENCES |
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2. Daly JW. Dehiscence, evisceration, and other complications. Clin Obstet Gynecol 1988;31:754–60.[Medline]
3. Duff P. Diagnosis and management of postcesarean endomyometritis. In: Phelan JP, Clark SL, eds. Cesarean delivery. New York: Elsevier, 1988:403–15.
4. Rao KB, Ramamurthi DV, Vimala G. Intrapartum infections—A clinical and bacteriological study. Obstet Gynecol 1965;26:833–41.
5. Caughey AB, Shipp TD, Repke JT, Zelop C, Cohen A, Lieberman E. Trial of labor after cesarean delivery: The effect of previous vaginal delivery. Am J Obstet Gynecol 1998;179:938–41.[Medline]
6. Shipp TD, Zelop CM, Repke JT, Cohen A, Caughey AB, Lieberman E. Intrapartum uterine rupture and dehiscence in patients with prior lower uterine segment vertical and transverse incisions. Obstet Gynecol 1999;94:735–40.
7. Shipp TD, Zelop C, Repke JT, Cohen A, Caughey AB, Lieberman E. The association of maternal age and symptomatic uterine rupture during a trial of labor after prior cesarean delivery. Obstet Gynecol 2002;99:585–8.
8. Wojdecki J, Grynsztajn A. Scar formation in the uterus after cesarean section. Am J Obstet Gynecol 1970;107: 322–4.[Medline]
9. Williams JT. Delivery by the natural passages following cesarean section, with report of two cases. Am J Obstet Gynecol 1916;73:425–8.
10. Duff P, Mayer AR. Abdominopelvic abscess resulting from delayed postpartum uterine rupture. Am J Obstet Gynecol 1981;140:711–3.[Medline]
11. Martin JN Jr, Harris BA Jr, Huddleston JF, Morrison JC, Propst MG, Wiser WL, et al. Vaginal delivery following previous cesarean birth. Am J Obstet Gynecol 1983;146: 255–63.[Medline]
12. Halperin ME, Moore DC, Hannah WJ. Classical versus low-segment transverse incision for preterm caesarean section: Maternal complications and outcome of subsequent pregnancies. Br J Obstet Gynaecol 1988;95:990–6.[Medline]
13. Brown CEL, Dunn DH, Harrell R, Setiawan H, Cunningham FG. Computed tomography for evaluation of puerperal infections. Surg Gynecol Obstet 1991;172:285–9.[Medline]
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