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ORIGINAL RESEARCH |
From the 1Cox Family Medicine Residency, Cox Health System, Springfield, Missouri; 2Department of Obstetrics and Gynecology, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma; and 3St. Johns Clinic, Maternal–Fetal Medicine, St. Johns Health System, Springfield, Missouri.
| ABSTRACT |
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METHODS: This randomized trial includes 86 gravid women who underwent cesarean delivery. Forty-four women were assigned to the placental drainage group and 42 to the no-drainage group. Placental drainage was accomplished by cutting and milking the umbilical cord until no further blood flow occurred. All placentas were spontaneously expelled. The primary outcome variable, as assessed by preoperative and postoperative Kleihauer-Betke tests, was the amount of fetal blood (greater than or equal to 0.5 mL) in the maternal circulation.
RESULTS: The group having placental drainage of fetal blood before placental delivery showed a significantly lower incidence (3 of 44, 6.8%) of feto–maternal transfusion (P=.003) as compared with the undrained group (14 of 42, 33%; relative risk 0.20, 95% confidence interval 0.065–0.65; number needed to treat=4).
CONCLUSION: Placental drainage of fetal blood before spontaneous placental delivery at the time of cesarean delivery significantly reduces the incidence of feto–maternal transfusion.
CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov, www.clinicaltrials.gov, NCT00470899
LEVEL OF EVIDENCE: I
Numerous obstetric risk factors have been evaluated to assess their association with feto–maternal transfusion. These include operative vaginal delivery, cesarean delivery, twin deliveries,4 method of placental removal,2,4 parity, and the use of oxytocin.1 There is disagreement about whether placental drainage at the time of vaginal delivery decreases the incidence of significant feto–maternal transfusion. Our randomized trial sought to assess whether lessening the amount of fetal blood in the placenta before its removal would lessen the incidence of feto–maternal transfusion. This randomized study assesses the incidence of feto–maternal transfusion at the time of cesarean delivery in patients assigned to either placental fetal blood drainage or no placental fetal blood drainage before spontaneous placental delivery.
| MATERIALS AND METHODS |
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Patient demographic information included maternal age, parity, gestational age, and birthweight. To ensure similarity between exposure groups, relevant demographic characteristics were analyzed using a two-tailed t test with equal variances. As evident in the other demographic characteristics analyzed, age was not significantly different between groups (P=.395). The presence of labor or oxytocin usage before surgery, the type of anesthesia used, and rates of endometritis were also documented (Table 1).
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The data were reviewed independently by the investigators to insure accuracy. Statistical analysis of the results was performed by means of the Fisher exact test with P<0.01 considered statistically significant. Institutional review boards at each of the two institutions approved the study.
| RESULTS |
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The incidence of feto–maternal transfusion, as detected by the primary outcome variable of a positive Kleihauer-Betke test, was significantly lower in the drained group (3 of 44, 6.8%) than in the not-drained group (14 of 42, 33%) (P=.003; relative risk 0.20, 95% confidence interval 0.065–0.65). On the basis of these data, we needed to treat four patients with placental drainage to avoid one feto-maternal transfusion (95% confidence interval 2.34–9.60).
| DISCUSSION |
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Maternal exposure to fetal erythrocytes is a common event. Cohen et al1 found fetal cells in the maternal circulation in about one half of their cases tested. Nevertheless, reducing maternal exposure to fetal blood antigens has been an important consideration since Levine et al12 proposed the concept that Rh sensitization occurs as a direct result of transplacental passage of Rh-positive fetal erythrocytes into the circulation of Rh-negative women. It is possible, though, that more than just sensitization to erythrocyte antigens may result from feto–maternal transfusion. Fetal microchimerism, resulting from the transfer of cells from the fetus to the mother during pregnancy, may have adverse effects on the maternal host. This cellular transfer has been associated with diseases such as systemic sclerosis and autoimmune thyroid disease.3
Various obstetric characteristics have been evaluated for an association with feto–maternal transfusion. Manual placental removal,2,4 forceps and twin deliveries, and the performance of a cesarean delivery4 all increase the incidence of feto–maternal transfusion, whereas parity and oxytocin administration do not.1
Several studies have evaluated placental drainage of fetal blood after vaginal delivery of the infant for any effect on feto–maternal transfusion. Doolittle13 hypothesized that draining the approximately 70 mL of retained fetal blood in the placenta after delivery would decrease the back pressure in the placental bed, thereby decreasing the chance of fetal erythrocyte transfer through any torn chorionic villi. He went on to demonstrate a statistically significant decrease in the incidence of Rh sensitization (not Kleihauer-Betke test results) in the group undergoing cord drainage5 as compared with those not drained in an historical control group obtained from another study.6 Terry7 evaluated 125 women undergoing uncomplicated, unassisted vaginal deliveries who were alternately assigned to drainage or no drainage, but the two groups also differed with respect to the uterotonic agents administered at the time of fetal delivery. The Kleihauer-Betke results demonstrated a significant lessening of feto–maternal transfusion in the drained group. Weinstein et al8 also followed another 152 patients undergoing vaginal delivery. The method of patient allotment to the groups of placental drainage compared with no drainage was not described, though, and the findings were contradictory in that those women undergoing placental drainage had a statistically significant increased incidence of feto–maternal transfusion unless they also received intramuscular oxytocin (Pitocin, Monarch Pharmaceuticals, Bristol, TN) at delivery of the fetus. This was followed by a similar investigation9 of primigravid and secundigravid women undergoing uncomplicated, unassisted vaginal deliveries, but again with unclear means of patient assignment. In contrast to the prior study, cord drainage lowered the incidence of feto–maternal transfusion. The only randomized study to date10 of 141 primiparous patients did not show a significant diminution in the quantity of red cells transferred, but the investigators did not comment on any difference in the incidence of overall transfer with placental drainage. Our study differs in that no reports of this technique (placental drainage) to assess the incidence of feto–maternal transfusion at the time of cesarean section have been found. Although placental drainage is a consistent feature of the other investigations mentioned, acquisition of control patients, group assignment, and unequal distribution of uterotonic medications may be cause for the discrepant results. Our patient population was randomly assigned and included women of all gravidities undergoing cesarean delivery for various indications. Placental drainage or no placental drainage was the only variable among our patients.
On the basis of our study data, we believe placental drainage of fetal blood before placental delivery at the time of cesarean delivery to be effective in diminishing maternal exposure to fetal blood antigens. Furthermore, this simple procedure may produce a beneficial effect on maternal and fetal health in future pregnancies.
| Footnotes |
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Corresponding author: Laird Bell, MD, MPH, Cox Family Medicine Residency, 1423 N. Jefferson, Springfield, MO 65809; e-mail: laird.bell{at}coxhealth.com.
Financial Disclosure The authors have no potential conflicts of interest to disclose.
doi:10.1097/01.AOG.0000277262.80793.0d
| REFERENCES |
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2. Zipursky A, Pollock J, Neelands P, Chown B, Israels LG. The transplacental passage of foetal red blood-cells and the pathogenesis of Rh immunisation during pregnancy. Lancet 1963;2:489–93.[Medline]
3. Adams KM, Nelson JL. Microchimerism: an investigative frontier in autoimmunity and transplantation. JAMA 2004;291:1127–31.
4. Devi B, Jennison RF, Langley FA. Relationship of transplacental haemorrhage to abnormal pregnancy and delivery. J Obstet Gynaecol Br Commonw 1968;75:659–66.[Medline]
5. Doolittle JE, Moritz CR. Prevention of erythroblastosis by an obstetric technic Obstet Gynecol 1966;27:529–31.[Medline]
6. Freda VJ. The Rh problem in obstetrics and a new concept of its management using amniocentesis and spectrophotometric scanning of amniotic fluid. Am J Obstet Gynecol 1965;92:341–74.[Medline]
7. Terry MF. A management of the third stage to reduce feto-maternal transfusion. J Obstet Gynaecol Br Commonw 1970;77:129–32.[Medline]
8. Weinstein L, Farabow WS, Gusdon JP Jr. Third stage of labor and transplacental hemorrhage. Obstet Gynecol 1971;37:90–3.
9. Ladipo OA. Management of third stage of labour, with particular reference to reduction of feto-maternal transfusion. Br Med J 1972;1:721–3.[Medline]
10. Moncrieff D, Parker-Williams J, Chamberlain G. Placental drainage and fetomaternal transfusion. The Lancet 1986;2:453.
11. Finn R, Harper DT, Stallings SA, Krevans JR. Transplacental hemorrhage. Transfusion 1963;3:114–24.
12. Levine P, Katzin EM, Burnham L. Isoimmunization in pregnancy, its possible bearing on the etiology of erythroblastosis fetalis. JAMA 1941;116:825–7.
13. Doolittle JE. Placental vascular integrity related to third-stage management. Obstet Gynecol 1963;22:468–72.
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