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Antepartum diagnosis of noncoiled umbilical cords
Antepartum diagnosis of noncoiled umbilical cords Thomas H. Strong, Jr., MD,"
b
Harris J. Finberg, MD,·' b and John H. Mattox, MDC
Phoenix, Arizona OBJECTIVE: The null hypothesis is that fetuses with noncoiled umbilical cords diagnosed in the antepartum period will have outcomes no different from those with normally coiled cords. STUDY DESIGN: We prospectively gathered data from Jan. 1 through May 18, 1992, from all fetuses undergoing routine ultrasonographic evaluation. The outcomes of fetuses noted to have noncoiled umbilical cords were compared with those of a control group of fetuses with normally coiled cords. The control group consisted of those subjects undergoing ultrasonography during the study period who were ultimately transferred to our perinatal practice for the remainder of the pregnancy (i.e., the highest-risk patients). Two outcome parameters were selected for comparison: fetal anomalies and fetal death. RESULTS: Six hundred eighty-seven consecutive ultrasonographic examinations were performed. Twenty-five subjects (3.7%) had noncoiled umbilical cords identified ultrasonographically (mean gestational age at diagnosis 20.3 ± 3.5 [SO] weeks). The control group had 197 subjects. The combined incidence of fetal anomalies or death in the noncoiled group (16%) was significantly greater (p :$ 0.05, relative risk 4.6 [95% confidence interval 1.41 to 14.15]) than that of the control group (3.5%). The noncoiled group had two fetal deaths (8%), whereas two deaths (1%) occurred among controls (p :$ 0.05, relative risk 8 [95% confidence interval 1.16 to 50]). Two (8%) fetal anomalies (anencephaly, prune-belly syndrome) occurred in the noncoiled group, whereas the controls (n = 197) had five fetuses (2.5%) with anomalies (not significant). CONCLUSION: The antepartum identification of non coiled umbilical cords appears to be a risk factor for suboptimal pregnancy outcome. (AM J OaSTEr GVNECOL 1994;170:1729-33.)
Key words: Noncoiled umbilical cord, straight umbilical cord, umbilical vascular coiling The umbilical cord is a vital appendage of the placenta. Its three blood vessels pass along the length of the cord in a coiled fashion. Umbilical coiling occurs in roughly 95% of all fetuses and has been generally thought to have occurred by the end of the first trimester! Strong et al." noted an increased incidence of suboptimal outcomes among neonates with noncoiled umbilical blood vessels at birth. The presence or absence of umbilical coiling can be readily seen during ultrasonographic assessment of the fetus and is therefore identifiable during the antepartum period. The purpose of this study was to study the pregnancy outcomes of fetuses with noncoiled umbilical cords identified ultrasonographically.
Material and methods Between Jan. 1 and May 18, 1992, the umbilical coiling status of every patient undergoing obstetric From the Phoenix Perinatal Associatesa and the Division ofMaternalFetal Medicine' and the Department of Obstetrics and Gynecology,' Good Samaritan Regional Medical Center. Community Hospital Award, presented at the Sixty-first Annual Meeting of The Central Association of Obstetricians and Gynecologists, White Sulphur Springs, West Virginia, October 28-30, 1993. Reprint requests: Thomas H. Strong, Jr., MD, 1300 N. 12th St., #320, Phoenix, AZ 85006. Copyright © 1994 by Mosby-Year Book, 1nc. 0002-9378/94 $3.00 + 0 6/6/55081
ultrasonography at our office in Phoenix was evaluated. A noncoiled umbilical cord was considered to be present if its three umbilical vessels followed a straight, parallel course along the entire length of the cord (Fig. 1). In each case noncoiling was confirmed by a second ultrasonographer. The outcomes of all fetuses with noncoiled umbilical cords were compared with a control group of fetuses with normally coiled cords. The control group consisted of those patients undergoing obstetric ultrasonography at our office during the study period who were ultimately transferred to our high-risk practice for the remainder of the pregnancy. We selected two outcome parameters that were clear-cut and not subject to a wide range of interpretation: fetal anomalies and fetal death. Fisher's statistical analysis was used. Statistical significance was defined as a p value :s 0.05. In addition, relative risk analysis was performed.
Results During the study period 687 consecutive subjects were assessed. Twenty-five (3.7%) had noncoiled umbilical vessels, whereas 197 subjects (29%) composed the control group (Table I). The mean gestational age at diagnosis of noncoiled cords was 20.3 ± 3.5 weeks. The combined incidence of fetal anomalies or death in the noncoiled group (16%) was significantly greater (p :s 0.05) than that of the control group (3.5%). The 1729
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June 1994 Am J Obstet Gynecol
Fig. 1. Ultrasonographic image of a noncoiled umbilical cord.
noncoiled group had two (8%) fetal deaths (one at 37 and one at 38 weeks' gestation), whereas two deaths (1%) occurred among controls
Many hypotheses have been proposed with regard to the cause of umbilical vascular coiling, including fetal movement, differential umbilical vascular growth rates, and fetal hemodynamic forces. However, work at the Dunlop Research Center in 1966 suggested that umbilical coiling is related to an intrinsic twist in some or all of the constituent fibers of the umbilical cord. 3 Their studies with experimental models of umbilical cords showed that an inherent tendency to coil will occur if (1) the models are constructed of longitudinal fibers that themselves tend to twist and (2) sufficient intraluminal pressure exists. Indeed, the umbilical arterial vessel wall is composed largely of smooth muscle that coils around the lumen of the artery." It is likely that this helical layer of muscle fibers provides the axis for umbilical coiling. Noncoiled umbilical cords tend to be more flaccid than coiled ones. Indeed, two recent cord prolapses at our institution occurred in fetuses whose umbilical
cords were noncoiled. Heinisch 5 and Seligman6 noted that umbilical cords with sufficient intravascular pressure would not prolapse from open containers. However, as intravascular pressures were reduced, the cords lost their turgor and prolapsed readily. These observations lend credence to the Dunlop Research Center's second requirement for spontaneous umbilical coiling: sufficient intraluminal pressure (i.e., fetal blood pressure).3 Because the architecture of the fetus, including the umbilical cord, is a reflection of heritable traits, genetics likely play a role in the process of umbilical coiling. Clearly, the 95% incidence of coiled cords and the 8: 1 ratio of cords with sinistral versus dextral coiling do not represent random processes. I Therefore the configuration of the umbilical cord is an important example of the hierarchic relationship between phenomena at the cellular and gross morphologic levels.' Information contained at the molecular level is ultimately expressed through the constituent materials involved, the forces produced by growth, and the response of those materials to external influences.' The coiled umbilical cord is a semierectile organ that is more resistant to snarling, torsion, stretch, and compression than is a noncoiled one. Malpas and Symonds' refer to this protective phenomenon as "spontaneous internal ballottement" and likened it to the action of a concertina. Strong et al. 2 provided indirect clinical evidence of umbilical ballottement, noting that fetuses with noncoiled umbilical cords have more variable fetal heart rate decelerations and more operative intervention for fetal distress even when there is a normal
Strong, Finberg, and Mattox 1731
Volume 170, Number 6 Am J Obstet Gynecol
Table I. Outcomes of fetuses with noncoiled versus coiled umbilical cords
Fetal anomalies or death Fetal anomalies Fetal death
Noncoiled (n = 25)
Coiled (n = 197)
Significance
Relative risk and 95% confidence interval
4 (16%)
7 (3.5%)
PS
0.05*
4.6 (1.41-14.15)
2 (8%) 2 (8%)
5 (2.5%) 2 (1%)
PS
0.05*
NS 8 (1.16-50)
NS
NS, Not significant. *Fisher's exact test.
amniotic fluid volume. Perhaps the unexplained fetal deaths that occurred in this report were the result of lethal cord compression related to absent umbilical vascular coiling. We hypothesize that noncoiled umbilical cords result from either of two processes. In the first the helical smooth muscle fibers of the umbilical arterial vessel walls are absent. Without this structure the cord is incapable of coiling, irrespective of umbilical intravascular pressure or fetal activity. In the second situation the helical muscular layer, and thus the tendency to coil, is present. However, reduced intraarterial pressure prevents the umbilical tumescence necessary for the normal expression of coiling. Perhaps those fetuses in our study group whose cords were initially noncoiled fall into the latter situation, with coiling occurring only after umbilical arterial pressure increased sufficiently to evoke it. Further study will be necessary to substantiate this hypothesis. Weiner et al. s , 9 have described a technique for measuring umbilical venous or arterial blood pressure during percutaneous umbilical blood sampling that may help clarify the issue. The incidence of noncoiled cords noted in this report is in agreement with the previously published rates of 2% to 6%, even with the assumption that 30% of the cords in our study group eventually became coiled. 10 Additionally, the rates of the two outcomes evaluated in this report; fetal anomalies and death, were similar to those of earlier reports. 1. 2 Our findings are in step with the prospective study of Strong et al. 2 and suggest that the antepartum identification of noncoiled umbilical cords represents a genuine risk for suboptimal perinatal outcome. Careful evaluation of fetal anatomy, antepartum assessment of fetal well-being, and early delivery on documentation of fetal lung maturity may be warranted when a noncoiled umbilical cord is identified. Ideally, our control group should have included all 662 fetuses with coiled umbilical cords, but the large number of patients spread across a very wide geographic referral area (Arizona and the immediately adjacent areas of California and New Mexico) made meaningful follow-up difficult. Therefore we constructed our control group of those whose outcomes we
could most accurately and consistently assess (i.e., those whose care was transferred to our practice by the referring obstetrician). Because this subgroup consisted of more complicated pregnancies than the remainder of the potential control group, the incidence of fetal anomalies and fetal death was likely higher than it would have been had we included all 662 subjects in our control group. That statistically significant differences were noted in spite of the use of such a biased control group bolsters the notion that the noncoiled umbilical cord is a marker for the fetus at risk for suboptimal outcome. REFERENCES 1. Lacro RV, Jones KL, Benirschke K. The umbilical cord twist: origin, direction and relevance. AM J OBSTET GYNECOL 1987;157:833-8. 2. Strong TH, Elliott JP, Radin TG. Non-coiled umbilical blood vessels: a new marker for the fetus at risk. Obstet Gynecol 1993;81:409-11. 3. Malpas P, Symonds EM. Observations on the structure of the human umbilical cord. Surg Gynecol Obstet 1966;123: 746-50. 4. Roach MR. The umbilical vessels. In: Goodwin JW, Godden JO, Chance GW, eds. Perinatal medicine: the basic science underlying clinical practice. Baltimore: Williams and Wilkins, 1976:134-42. 5. Heinisch HM. Zur atiologie und pathogenese des nabelschnurvofalls nach den Erfahrungen an der Universitats-Frauenklinik Basel von 1990 bis 1954. Gynaecologia (Basel) 1956; 141: 136-42. 6. Seligman SA. Umbilical cord prolapse. BMJ 1960;2:1496501. 7. Mendelson NH, Thwaites JJ. Bacterial macrofibers: multicellular chiral structures. Am Soc Microbiol News 1993; 59:25-30. 8. Weiner CP, Heilskov J, Pelzer G, et al. Normal values for umbilical venous and amniotic fluid pressures and their alteration by fetal disease. AMJ OBSTET GVNECOL 1989;161: 714-7. 9. Weiner CPo Umbilical pressure measurement in the evaluation of nonimmune hydrops fetalis. AM J OBSTET GVNECOL 1993;168:817-23. 10. Edmonds HW. The spiral twist of the normal umbilical cord in twins and singletons. AM J OBSTET GVNECOL 1954; 67:102-20.
Discussion R. LuPO, Minneapolis, Minnesota. The observations described today by Strong et al. point out a tremendously intriguing association between straight umbilical cords and very poor perinatal outcome. They DR. VIRGINIA
1732 Strong, Finberg; and Mattox
raise the issue of "sidedness," which pops up in obstetrics every so often, each time with a little more concern that there may be simple yet profound reasons why bad things happen to good people in pregnancy. Several years ago the observation was made that when the placenta is predominantly located on one side of the uterus, as opposed to being centrally located, preeclampsia and intrauterine growth retardation are almost three times more common. I Subsequent workers have confirmed discordant uterine artery flow velocity ratios in pregnancies well before clinical evidence of preeclampsia exists. 2 We now find it patently obvious that a unilateral placenta may have less blood flow than one centrally located and that decreased placental perfusion may be related to preeclampsia, but it took a good observer like Strong to find that a noncoiled cord at 20 weeks' gestation is associated with a 16% incidence of fetal anomalies or death. A fact that needs to yet be determined is how reproducible the finding of a noncoiled cord is. Of women noted at a mean gestational age of 20 weeks to have a noncoiled cord, 30% of women with follow-up scans were found to have coiled cords. The mean gestational age of the women with initially coiled cords should be determined, to be certain that the lower incidence of coiling was not just an age-related phenomenon. The interval in which the cords coiled, and the overall incidence of coiling and uncoiling in a given fetus, have not been determined. A cohort of patients must be evaluated prospectively and repeatedly, to be certain that this is not an intermittent finding in normal pregnancy. In addition, the incidence of this finding in a general population must be assessed. The Phoenix Perinatal Associates care for large numbers of problem pregnancies, and their population may be intrinsically skewed by women with underlying diseases that have already been identified by 20 weeks' gestation as at risk enough to merit a referral to this group; perhaps those medical or obstetric risks alone are enough to account for the very concerning outcomes reported today. A previous prevalence study by Strong found that in 894 newborns 4.3% had noncoiled cords, and the incidence of fetal death, preterm delivery, abnormal karyotypes, and assorted distress in labor was significantly higher than in fetuses with coiled cords." It is interesting that the 4.3% rate of noncoiled cords at delivery was greater than the 3.7% identified in the current study and much greater than the 3.7% rate if it had indeed been reduced by 30% further along in pregnancy. We may indeed be seeing different things on ultrasonography than at the time the placenta and cord are sitting on our back table after delivery. As Fleming appreciated the mold that killed his antibiotic cultures and discovered the power of penicillin, fortune favors the prepared mind, and further exploration of the relationship of noncoiled umbilical vessels on perinatal outcome is definitely needed, and the groundwork is well laid in this study. REFERENCES 1. Kofinas A, Penry M, Swain M, Hatjis C. Effect of placental laterality on uterine artery resistance and development of
June 1994 Am J Obstet Gynecol
preeclampsia and intrauterine growth retardation. AM ] OSSTET GYNECOL 1989;161:1536-9. 2. Bower S, Bewley S, Campbell S. Improved prediction of preeclampsia by two-stage screening of uterine arteries using the early diastolic notch and color Doppler imaging. Obstet Gynecol 1993;82:78-83. 3. Strong T, Elliott], Radin T. Non-coiled umbilical blood vessels: a new marker for the fetus at risk. AM ] OSSTET GYNECOL 1993;81:409-11. DR. WIU.IAM D. JONES, Columbus, Indiana. The authors have made a straightforward and uncluttered presentation of potentially helpful information. As a general clinician in private practice, I read this study with a bias toward application in such a setting. To that end I would pose the following questions: (1) The authors state that because the control group was made up of high-risk patients the fetal death and fetal anoml'ly rates were likely higher than would have been expected had all 662 subjects been included. Does this follow? What effect might the closer surveillance have had on outcome? Also, were all 25 patients in the uncoiled group followed up in the same fashion as the control group? (2) Because about 30% of noncoiled cords eventually showed coiling, at what stage of gestation would scanning be most beneficial? Did any coiled cords show uncoiling? (3) What is the typical amount of time necessary to perform complete cord scanning? (4) The study defined a straight cord as one with three vessels following a straight, parallel course along the entire length. Does this exclude two vessel cords (straight or coiled) as well as partially coiled cords? (5) This study was based on data collected from routine ultrasonographic examinations. Because the distribution of the health care dollar is falling under increasingly greater scrutiny, do the authors judge that this study adds greater credibility to the use of routine ultrasonography, especially from a cost effectiveness point of view? (6) Do the authors consider identification of uncoiled cords standard of care at this time? DR. BROOKS RANNEY, Yankton, South Dakota. I will point out what would be called in this day of statistical analysis a confounding factor. On the basis of 7000 deliveries I have no statistics but a general impression that fetal cords that are coiled are also those that have a good amount of Wharton's jelly in them and are thicker and safer and cords that are noncoiled are always thinner and have relatively less protective Wharton's jelly in them. Was any measurement made of the diameter of these cords? DR. GEORGE WILBANKS, Chicago, Illinois. My question is from the view of a morphologist. I wonder if indeed the muscular coats of the arteries in the cords were different. Were any special stains performed on those cords? How about the pathologic characteristics of the placenta? Was the placenta itself any different between the two groups (i.e., insertions of the cord, etc.)? DR. STRONG (Closing). Regarding Dr. Lupo's comments and questions about the reproducibility of the study, both the study and control groups were taken from our high-risk pregnancy population with the hope that we would eliminate the potential confounding factor of high-risk pregnancy being found in the straight cords but not the normally coiled cords.
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There was a bit of a difference in the rate of noncoiled cords in this study compared with that of my previous report; because they were from two separate study populations, I can't compare them statistically. However, both rates do fall within the previously reported rates of 2% to 6% of noncoiling of the umbilical vessels. 10 Regarding Dr. Jones' comments and questions, indeed, we do now more closely monitor our patients with noncoiled cords. Specifically, we place them on a regimen of twice-weekly nonstress testing. We have not seen coiled cords become uncoiled. Among those that were identified to be noncoiled early in pregnancy that subsequently became coiledroughly 30%-none had untoward outcomes. All of the suboptimal outcomes occurred in those fetuses who had noncoiling for the duration of gestation. Moreover, those fetuses who continued to have noncoiled cords on ultrasonography proved to have noncoiled cords when their cords were examined grossly at the time of delivery. Typically, in our population where we are used to doing it, it takes 1 to 2 minutes to ultrasonographically
Strong, Finberg, and Mattox
1733
survey the umbilical cord. However, a pitfall is that segments that are noncoiled can be identified with segments that are very nicely coiled. We have just completed a study of a low-risk population of patients in which we examined the umbilical coiling patterns. Although we haven't completed our analysis, there appears to be a slight difference among those fetuses with evenly spaced cords versus those with intermittent, or "bunched," coiling. We also found in that same study, which we are just now completing, that some nicely coiled cords were fairly richly jellied, and sometimes we would find equally nicely coiled cords that were not. The diameters of the cord were not specifically addressed in that paper, but we are currently working on that study at our institution. In none of our study patients from the current study did we consistently examine placental pathologic characteristics. However, it's important to note that the two deaths in our study group were unexplained fetal deaths. There were no fetal anomalies at autopsy nor were there placental problems separate and apart from straight umbilical cords.
Make researching easier with the Ten-Year Cumulative Index (1978-1987) to the AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY The Ten-Year Cumulative Index is a complete guide to more than 30,000 pages of original articles, case reports, letters, and editorials published in the AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY from 1978 through 1987 (volumes 130 to 157). Numbering more than 800 pages, the Cumulative Index includes both a subject and an author index. This hard-cover volume is $64.50 ($69.00 international). Prices include shipping. Payment must accompany all orders and must be in U.S. funds, drawn on a U.S. bank. Contact Mosby-Year Book, Inc., Subscription Services, 11830 Westline Industrial Drive, St. Louis, MO 63146-3318 USA; phone (314) 453-4351. In the U.S., call toll-free: (800) 453-4351. Please allow six weeks for delivery.
b
Harris J. Finberg, MD,·' b and John H. Mattox, MDC
Phoenix, Arizona OBJECTIVE: The null hypothesis is that fetuses with noncoiled umbilical cords diagnosed in the antepartum period will have outcomes no different from those with normally coiled cords. STUDY DESIGN: We prospectively gathered data from Jan. 1 through May 18, 1992, from all fetuses undergoing routine ultrasonographic evaluation. The outcomes of fetuses noted to have noncoiled umbilical cords were compared with those of a control group of fetuses with normally coiled cords. The control group consisted of those subjects undergoing ultrasonography during the study period who were ultimately transferred to our perinatal practice for the remainder of the pregnancy (i.e., the highest-risk patients). Two outcome parameters were selected for comparison: fetal anomalies and fetal death. RESULTS: Six hundred eighty-seven consecutive ultrasonographic examinations were performed. Twenty-five subjects (3.7%) had noncoiled umbilical cords identified ultrasonographically (mean gestational age at diagnosis 20.3 ± 3.5 [SO] weeks). The control group had 197 subjects. The combined incidence of fetal anomalies or death in the noncoiled group (16%) was significantly greater (p :$ 0.05, relative risk 4.6 [95% confidence interval 1.41 to 14.15]) than that of the control group (3.5%). The noncoiled group had two fetal deaths (8%), whereas two deaths (1%) occurred among controls (p :$ 0.05, relative risk 8 [95% confidence interval 1.16 to 50]). Two (8%) fetal anomalies (anencephaly, prune-belly syndrome) occurred in the noncoiled group, whereas the controls (n = 197) had five fetuses (2.5%) with anomalies (not significant). CONCLUSION: The antepartum identification of non coiled umbilical cords appears to be a risk factor for suboptimal pregnancy outcome. (AM J OaSTEr GVNECOL 1994;170:1729-33.)
Key words: Noncoiled umbilical cord, straight umbilical cord, umbilical vascular coiling The umbilical cord is a vital appendage of the placenta. Its three blood vessels pass along the length of the cord in a coiled fashion. Umbilical coiling occurs in roughly 95% of all fetuses and has been generally thought to have occurred by the end of the first trimester! Strong et al." noted an increased incidence of suboptimal outcomes among neonates with noncoiled umbilical blood vessels at birth. The presence or absence of umbilical coiling can be readily seen during ultrasonographic assessment of the fetus and is therefore identifiable during the antepartum period. The purpose of this study was to study the pregnancy outcomes of fetuses with noncoiled umbilical cords identified ultrasonographically.
Material and methods Between Jan. 1 and May 18, 1992, the umbilical coiling status of every patient undergoing obstetric From the Phoenix Perinatal Associatesa and the Division ofMaternalFetal Medicine' and the Department of Obstetrics and Gynecology,' Good Samaritan Regional Medical Center. Community Hospital Award, presented at the Sixty-first Annual Meeting of The Central Association of Obstetricians and Gynecologists, White Sulphur Springs, West Virginia, October 28-30, 1993. Reprint requests: Thomas H. Strong, Jr., MD, 1300 N. 12th St., #320, Phoenix, AZ 85006. Copyright © 1994 by Mosby-Year Book, 1nc. 0002-9378/94 $3.00 + 0 6/6/55081
ultrasonography at our office in Phoenix was evaluated. A noncoiled umbilical cord was considered to be present if its three umbilical vessels followed a straight, parallel course along the entire length of the cord (Fig. 1). In each case noncoiling was confirmed by a second ultrasonographer. The outcomes of all fetuses with noncoiled umbilical cords were compared with a control group of fetuses with normally coiled cords. The control group consisted of those patients undergoing obstetric ultrasonography at our office during the study period who were ultimately transferred to our high-risk practice for the remainder of the pregnancy. We selected two outcome parameters that were clear-cut and not subject to a wide range of interpretation: fetal anomalies and fetal death. Fisher's statistical analysis was used. Statistical significance was defined as a p value :s 0.05. In addition, relative risk analysis was performed.
Results During the study period 687 consecutive subjects were assessed. Twenty-five (3.7%) had noncoiled umbilical vessels, whereas 197 subjects (29%) composed the control group (Table I). The mean gestational age at diagnosis of noncoiled cords was 20.3 ± 3.5 weeks. The combined incidence of fetal anomalies or death in the noncoiled group (16%) was significantly greater (p :s 0.05) than that of the control group (3.5%). The 1729
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June 1994 Am J Obstet Gynecol
Fig. 1. Ultrasonographic image of a noncoiled umbilical cord.
noncoiled group had two (8%) fetal deaths (one at 37 and one at 38 weeks' gestation), whereas two deaths (1%) occurred among controls
Many hypotheses have been proposed with regard to the cause of umbilical vascular coiling, including fetal movement, differential umbilical vascular growth rates, and fetal hemodynamic forces. However, work at the Dunlop Research Center in 1966 suggested that umbilical coiling is related to an intrinsic twist in some or all of the constituent fibers of the umbilical cord. 3 Their studies with experimental models of umbilical cords showed that an inherent tendency to coil will occur if (1) the models are constructed of longitudinal fibers that themselves tend to twist and (2) sufficient intraluminal pressure exists. Indeed, the umbilical arterial vessel wall is composed largely of smooth muscle that coils around the lumen of the artery." It is likely that this helical layer of muscle fibers provides the axis for umbilical coiling. Noncoiled umbilical cords tend to be more flaccid than coiled ones. Indeed, two recent cord prolapses at our institution occurred in fetuses whose umbilical
cords were noncoiled. Heinisch 5 and Seligman6 noted that umbilical cords with sufficient intravascular pressure would not prolapse from open containers. However, as intravascular pressures were reduced, the cords lost their turgor and prolapsed readily. These observations lend credence to the Dunlop Research Center's second requirement for spontaneous umbilical coiling: sufficient intraluminal pressure (i.e., fetal blood pressure).3 Because the architecture of the fetus, including the umbilical cord, is a reflection of heritable traits, genetics likely play a role in the process of umbilical coiling. Clearly, the 95% incidence of coiled cords and the 8: 1 ratio of cords with sinistral versus dextral coiling do not represent random processes. I Therefore the configuration of the umbilical cord is an important example of the hierarchic relationship between phenomena at the cellular and gross morphologic levels.' Information contained at the molecular level is ultimately expressed through the constituent materials involved, the forces produced by growth, and the response of those materials to external influences.' The coiled umbilical cord is a semierectile organ that is more resistant to snarling, torsion, stretch, and compression than is a noncoiled one. Malpas and Symonds' refer to this protective phenomenon as "spontaneous internal ballottement" and likened it to the action of a concertina. Strong et al. 2 provided indirect clinical evidence of umbilical ballottement, noting that fetuses with noncoiled umbilical cords have more variable fetal heart rate decelerations and more operative intervention for fetal distress even when there is a normal
Strong, Finberg, and Mattox 1731
Volume 170, Number 6 Am J Obstet Gynecol
Table I. Outcomes of fetuses with noncoiled versus coiled umbilical cords
Fetal anomalies or death Fetal anomalies Fetal death
Noncoiled (n = 25)
Coiled (n = 197)
Significance
Relative risk and 95% confidence interval
4 (16%)
7 (3.5%)
PS
0.05*
4.6 (1.41-14.15)
2 (8%) 2 (8%)
5 (2.5%) 2 (1%)
PS
0.05*
NS 8 (1.16-50)
NS
NS, Not significant. *Fisher's exact test.
amniotic fluid volume. Perhaps the unexplained fetal deaths that occurred in this report were the result of lethal cord compression related to absent umbilical vascular coiling. We hypothesize that noncoiled umbilical cords result from either of two processes. In the first the helical smooth muscle fibers of the umbilical arterial vessel walls are absent. Without this structure the cord is incapable of coiling, irrespective of umbilical intravascular pressure or fetal activity. In the second situation the helical muscular layer, and thus the tendency to coil, is present. However, reduced intraarterial pressure prevents the umbilical tumescence necessary for the normal expression of coiling. Perhaps those fetuses in our study group whose cords were initially noncoiled fall into the latter situation, with coiling occurring only after umbilical arterial pressure increased sufficiently to evoke it. Further study will be necessary to substantiate this hypothesis. Weiner et al. s , 9 have described a technique for measuring umbilical venous or arterial blood pressure during percutaneous umbilical blood sampling that may help clarify the issue. The incidence of noncoiled cords noted in this report is in agreement with the previously published rates of 2% to 6%, even with the assumption that 30% of the cords in our study group eventually became coiled. 10 Additionally, the rates of the two outcomes evaluated in this report; fetal anomalies and death, were similar to those of earlier reports. 1. 2 Our findings are in step with the prospective study of Strong et al. 2 and suggest that the antepartum identification of noncoiled umbilical cords represents a genuine risk for suboptimal perinatal outcome. Careful evaluation of fetal anatomy, antepartum assessment of fetal well-being, and early delivery on documentation of fetal lung maturity may be warranted when a noncoiled umbilical cord is identified. Ideally, our control group should have included all 662 fetuses with coiled umbilical cords, but the large number of patients spread across a very wide geographic referral area (Arizona and the immediately adjacent areas of California and New Mexico) made meaningful follow-up difficult. Therefore we constructed our control group of those whose outcomes we
could most accurately and consistently assess (i.e., those whose care was transferred to our practice by the referring obstetrician). Because this subgroup consisted of more complicated pregnancies than the remainder of the potential control group, the incidence of fetal anomalies and fetal death was likely higher than it would have been had we included all 662 subjects in our control group. That statistically significant differences were noted in spite of the use of such a biased control group bolsters the notion that the noncoiled umbilical cord is a marker for the fetus at risk for suboptimal outcome. REFERENCES 1. Lacro RV, Jones KL, Benirschke K. The umbilical cord twist: origin, direction and relevance. AM J OBSTET GYNECOL 1987;157:833-8. 2. Strong TH, Elliott JP, Radin TG. Non-coiled umbilical blood vessels: a new marker for the fetus at risk. Obstet Gynecol 1993;81:409-11. 3. Malpas P, Symonds EM. Observations on the structure of the human umbilical cord. Surg Gynecol Obstet 1966;123: 746-50. 4. Roach MR. The umbilical vessels. In: Goodwin JW, Godden JO, Chance GW, eds. Perinatal medicine: the basic science underlying clinical practice. Baltimore: Williams and Wilkins, 1976:134-42. 5. Heinisch HM. Zur atiologie und pathogenese des nabelschnurvofalls nach den Erfahrungen an der Universitats-Frauenklinik Basel von 1990 bis 1954. Gynaecologia (Basel) 1956; 141: 136-42. 6. Seligman SA. Umbilical cord prolapse. BMJ 1960;2:1496501. 7. Mendelson NH, Thwaites JJ. Bacterial macrofibers: multicellular chiral structures. Am Soc Microbiol News 1993; 59:25-30. 8. Weiner CP, Heilskov J, Pelzer G, et al. Normal values for umbilical venous and amniotic fluid pressures and their alteration by fetal disease. AMJ OBSTET GVNECOL 1989;161: 714-7. 9. Weiner CPo Umbilical pressure measurement in the evaluation of nonimmune hydrops fetalis. AM J OBSTET GVNECOL 1993;168:817-23. 10. Edmonds HW. The spiral twist of the normal umbilical cord in twins and singletons. AM J OBSTET GVNECOL 1954; 67:102-20.
Discussion R. LuPO, Minneapolis, Minnesota. The observations described today by Strong et al. point out a tremendously intriguing association between straight umbilical cords and very poor perinatal outcome. They DR. VIRGINIA
1732 Strong, Finberg; and Mattox
raise the issue of "sidedness," which pops up in obstetrics every so often, each time with a little more concern that there may be simple yet profound reasons why bad things happen to good people in pregnancy. Several years ago the observation was made that when the placenta is predominantly located on one side of the uterus, as opposed to being centrally located, preeclampsia and intrauterine growth retardation are almost three times more common. I Subsequent workers have confirmed discordant uterine artery flow velocity ratios in pregnancies well before clinical evidence of preeclampsia exists. 2 We now find it patently obvious that a unilateral placenta may have less blood flow than one centrally located and that decreased placental perfusion may be related to preeclampsia, but it took a good observer like Strong to find that a noncoiled cord at 20 weeks' gestation is associated with a 16% incidence of fetal anomalies or death. A fact that needs to yet be determined is how reproducible the finding of a noncoiled cord is. Of women noted at a mean gestational age of 20 weeks to have a noncoiled cord, 30% of women with follow-up scans were found to have coiled cords. The mean gestational age of the women with initially coiled cords should be determined, to be certain that the lower incidence of coiling was not just an age-related phenomenon. The interval in which the cords coiled, and the overall incidence of coiling and uncoiling in a given fetus, have not been determined. A cohort of patients must be evaluated prospectively and repeatedly, to be certain that this is not an intermittent finding in normal pregnancy. In addition, the incidence of this finding in a general population must be assessed. The Phoenix Perinatal Associates care for large numbers of problem pregnancies, and their population may be intrinsically skewed by women with underlying diseases that have already been identified by 20 weeks' gestation as at risk enough to merit a referral to this group; perhaps those medical or obstetric risks alone are enough to account for the very concerning outcomes reported today. A previous prevalence study by Strong found that in 894 newborns 4.3% had noncoiled cords, and the incidence of fetal death, preterm delivery, abnormal karyotypes, and assorted distress in labor was significantly higher than in fetuses with coiled cords." It is interesting that the 4.3% rate of noncoiled cords at delivery was greater than the 3.7% identified in the current study and much greater than the 3.7% rate if it had indeed been reduced by 30% further along in pregnancy. We may indeed be seeing different things on ultrasonography than at the time the placenta and cord are sitting on our back table after delivery. As Fleming appreciated the mold that killed his antibiotic cultures and discovered the power of penicillin, fortune favors the prepared mind, and further exploration of the relationship of noncoiled umbilical vessels on perinatal outcome is definitely needed, and the groundwork is well laid in this study. REFERENCES 1. Kofinas A, Penry M, Swain M, Hatjis C. Effect of placental laterality on uterine artery resistance and development of
June 1994 Am J Obstet Gynecol
preeclampsia and intrauterine growth retardation. AM ] OSSTET GYNECOL 1989;161:1536-9. 2. Bower S, Bewley S, Campbell S. Improved prediction of preeclampsia by two-stage screening of uterine arteries using the early diastolic notch and color Doppler imaging. Obstet Gynecol 1993;82:78-83. 3. Strong T, Elliott], Radin T. Non-coiled umbilical blood vessels: a new marker for the fetus at risk. AM ] OSSTET GYNECOL 1993;81:409-11. DR. WIU.IAM D. JONES, Columbus, Indiana. The authors have made a straightforward and uncluttered presentation of potentially helpful information. As a general clinician in private practice, I read this study with a bias toward application in such a setting. To that end I would pose the following questions: (1) The authors state that because the control group was made up of high-risk patients the fetal death and fetal anoml'ly rates were likely higher than would have been expected had all 662 subjects been included. Does this follow? What effect might the closer surveillance have had on outcome? Also, were all 25 patients in the uncoiled group followed up in the same fashion as the control group? (2) Because about 30% of noncoiled cords eventually showed coiling, at what stage of gestation would scanning be most beneficial? Did any coiled cords show uncoiling? (3) What is the typical amount of time necessary to perform complete cord scanning? (4) The study defined a straight cord as one with three vessels following a straight, parallel course along the entire length. Does this exclude two vessel cords (straight or coiled) as well as partially coiled cords? (5) This study was based on data collected from routine ultrasonographic examinations. Because the distribution of the health care dollar is falling under increasingly greater scrutiny, do the authors judge that this study adds greater credibility to the use of routine ultrasonography, especially from a cost effectiveness point of view? (6) Do the authors consider identification of uncoiled cords standard of care at this time? DR. BROOKS RANNEY, Yankton, South Dakota. I will point out what would be called in this day of statistical analysis a confounding factor. On the basis of 7000 deliveries I have no statistics but a general impression that fetal cords that are coiled are also those that have a good amount of Wharton's jelly in them and are thicker and safer and cords that are noncoiled are always thinner and have relatively less protective Wharton's jelly in them. Was any measurement made of the diameter of these cords? DR. GEORGE WILBANKS, Chicago, Illinois. My question is from the view of a morphologist. I wonder if indeed the muscular coats of the arteries in the cords were different. Were any special stains performed on those cords? How about the pathologic characteristics of the placenta? Was the placenta itself any different between the two groups (i.e., insertions of the cord, etc.)? DR. STRONG (Closing). Regarding Dr. Lupo's comments and questions about the reproducibility of the study, both the study and control groups were taken from our high-risk pregnancy population with the hope that we would eliminate the potential confounding factor of high-risk pregnancy being found in the straight cords but not the normally coiled cords.
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There was a bit of a difference in the rate of noncoiled cords in this study compared with that of my previous report; because they were from two separate study populations, I can't compare them statistically. However, both rates do fall within the previously reported rates of 2% to 6% of noncoiling of the umbilical vessels. 10 Regarding Dr. Jones' comments and questions, indeed, we do now more closely monitor our patients with noncoiled cords. Specifically, we place them on a regimen of twice-weekly nonstress testing. We have not seen coiled cords become uncoiled. Among those that were identified to be noncoiled early in pregnancy that subsequently became coiledroughly 30%-none had untoward outcomes. All of the suboptimal outcomes occurred in those fetuses who had noncoiling for the duration of gestation. Moreover, those fetuses who continued to have noncoiled cords on ultrasonography proved to have noncoiled cords when their cords were examined grossly at the time of delivery. Typically, in our population where we are used to doing it, it takes 1 to 2 minutes to ultrasonographically
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survey the umbilical cord. However, a pitfall is that segments that are noncoiled can be identified with segments that are very nicely coiled. We have just completed a study of a low-risk population of patients in which we examined the umbilical coiling patterns. Although we haven't completed our analysis, there appears to be a slight difference among those fetuses with evenly spaced cords versus those with intermittent, or "bunched," coiling. We also found in that same study, which we are just now completing, that some nicely coiled cords were fairly richly jellied, and sometimes we would find equally nicely coiled cords that were not. The diameters of the cord were not specifically addressed in that paper, but we are currently working on that study at our institution. In none of our study patients from the current study did we consistently examine placental pathologic characteristics. However, it's important to note that the two deaths in our study group were unexplained fetal deaths. There were no fetal anomalies at autopsy nor were there placental problems separate and apart from straight umbilical cords.
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