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Umbilical cord length



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Short umbilical cord:


            The mean of term umbilical cord length is 50 to 60 cm. A short cord at term is less than 35 cm. Logically the unentangled cord length must reach from the placental insertion to the vaginal outlet if the infant is to be delivered without complications. In fetal akinesia/ hypokinesia sequence, i.e. the consequences of fetal intrauterine paralysis, there is a very short umbilical cord accompanied by joint contractures, and pulmonary hypoplasia. The accepted theory is that fetal movement creates tension on the umbilical cord that promotes longitudinal growth. A corollary is that the less movement there is in utero, the less cord growth. Therefore short cords could be markers of intrauterine neurologic or muscle disease causing decreased movement not severe enough to produce the other features of the akinesia sequence. There is some evidence supporting this corollary with trisomy 21 and with oligohydramnios.


Long umbilical cords:


            Long umbilical cords, over 70 cm of length at term, are often associated with wrapping of the cord around the fetus. In theory, fetal movement produces a tension on the cord that creates ample free length for delivery plus the length of the wrapped cord. An entangled cord may be at risk for intermittent or partial occlusion of umbilical blood flow. There is some evidence of an increased risk of neurologic handicap in infants with long umbilical cords. Cord length may be increased with polyhydramnios, but this is not well documented.




            The length of the umbilical cord received in the pathology lab can not be used to document a suspected short umbilical cord. The obstetrician needs to document the amount left attached to the infant, and any length not attached to the placenta, e.g. sent for blood gases. These lengths can then be added to the length attached to the placenta.  A short umbilical cord may explain complications of delivery or demonstrate a fetal origin of any future neuro-motor problems in the child. The same considerations apply to a long umbilical cord, except that a cord more than 70 cm long attached to the placenta is a long cord. Documenting any wrapping of the cord in specific detail may help implicate specific forms of cord wrapping as more predictive than just cord length for intrapartum or future neurologic complications.






Literature review


Umbilical cord length


Perhaps the largest series of carefully measured cords in which the intent was to add the cord lengths attached to the placenta, the baby and any removed for other purposes was the Collaborative Perinatal Study of 35,779 singleton pregnancies1. The study used stepwise multiple regression analysis to show a positive correlation of longer length with maternal pregravid body weight, maternal pregnancy weight gain, maternal height, socio-economic index value, and male sex of the fetus. The first four suggest some correlation with maternal size, but the β values do not demonstrate how large an effect. The study defines short cord as less than 40 cm because only 6% of cords were ≤ 40 cm long at 40-41 weeks of gestation. To make matters even more confusing, umbilical cord length was divided by birth weight groups, 1-10th percentile, 11th to 30th percentile, and above 30th percentile. These subgroups were analyzed either for IQ < 80 at 4 years of age, or neurologic abnormalities at 7 years of age. Correlations for neurologic abnormalities at the P<0.05 significance were found for low IQ in the first and third birth weight categories, and for neurologic abnormalities in the first two birth weight categories. The analysis does not ask what effect birth weight alone had. Cases with malformation were excluded which would have excluded the cases with akinesia. It would have been more interesting to see a relationship of the actual length of the cord to the outcome, since the 40 cm cut off seemed quite arbitrary. Still, the article suggests that a short umbilical cord could be a marker of intrauterine neurologic abnormality. The normative data used in this study has also been published as a smooth set of percentile graphs which since males had significantly longer cords, were divided into white singleton male and female graphs2.

            Another paper examined 536 singleton, term, not repeat C-section, non-malformed infants for umbilical cord lengths and complications3. They only measured the length remaining on the infant if the cord was short. They used ≤ 35 cm as the cut off for a short cord (less than 6% of total), and ≥80 cm as a long cord. They found increased cord complications (nuchal cord, knots, or prolapse) with long cords, but 17 of 20 abnormalities were nuchal cords. Both long and short cords had an increased incidence of FHR evidence of cord compression (moderate or severe variable decelerations) at the P<.05 signficance. The authors comment that asphyxia and failure to progress were not increased with short cords because of a paucity of very short cords estimated to be 35 cm if implanted at the fundus, but 20 cm if the placenta was low lying. Of the 5 cases with umbilical cord less than 25 cm, 3 required  Cesaean section. The lead author on this paper  14 years later found no significant difference in umbilical cord blood gases with short or long cords using the same definitions4.

            A earlier paper by Rosen is confusing since it never defines short cord, and although compared to matched controls, there were no statistical tests5. He states that 0.78% were absolutely short (<30 cm) and 17.6% were relatively short from a base of 1,525 deliveries. There were no cases of torn cord or detached placenta. Relatively short apparently included cases of cord wrapping. This is not a useful paper.

            A study of umbilical cord length measured in labor and delivery  in 179 term infants in Indonesia found a mean length in males of 54.4 compared to females 50.7 cm, p=0.026. This study was small but found a linear correlation with length and complications (asphyxia, meconium stained fluid, and cord entanglement).

            An early British study of 177 infants measured a mean cord length of 61 cm with a range of 30 to 129 cm7. The length did not correlate with infant or placental weight.

            A Nigerian study of 1000 umbilical cords measured with both fetal and placental portions found a mean length of 51.5 cm8. There was a significant correlation with both infant and placental weight as well as continued increase in the mean until 42 weeks of gestation. The term twin cord length was significantly shorter, but cords with entanglement were not significantly longer. An earlier Nigerian study of 602 cord lengths measured in labor and delivery had found a mean length of 57.5 cm, and had also found a correlation of length with infant and placental weight9.


Fetal movement and short umbilical cord


An early paper explicitly hypothesizing fetal movement was the cause of fetal cord lengthening compared the cord length of a large number of fetal conditions as reported in the literature10. The data came from other papers and was heavily weighted by acardiac twins and by bands attaching the fetus to the placenta. The paper cites two experimental models in rats of oligohydramnios, and personal information about a rat model with curare. The authors restated their hypothesis a year later.11

            The most definitive experimental work was a set of rat experiments comparing cord length from amnion puncture produced oligohydramnios at 15 to 17 of days gestation, of curare induced paralysis at 18 days of gestation, and of extrauterine pregnancy produced by surgery at 18 days of gestation12. At term, 21 days, the rat cords were measured. Oligohydramnios reduced cord length to 65%, 71% and 75% of control length at 15, 16, and 17 day punctures respectively. Fetal paralysis, with or without oligohydramnios, reduced cord length to approximately 85% of controls. The extrauterine rats free to move in the abdomen had cords 147% of control length, while extrauterine rats that were tethered to the uterine horn had 90% of control length. Depending on the experiment there were 10-16 rat fetuses per group, with approximately a 5 mm standard error in cord length with a mean control length of 30 mm. All groups showed highly significant differences. The authors did not analyze the apparent decreased effect the latter in gestation the experimental manipulation, but this is logical if the cord does not shrink once a stimulus is removed. The authors believe that their data supports the hypothesis that fetal torsion is responsible for normal lengthening of the cord.

            A study of rabbits injected with approximately human therapeutic doses of the β adrenergic blocker, atenolol, from day 7 through 24 of gestation demonstrated a statistically significant reduction in cord length (mean 2.76 versus 3.08 cm) excluding one outlier, with an N of 26 cases, 28 controls13. Another rabbit study compared three groups of rabbits (N=9-12/group) by feeding type, regular chow, liquid diet, and liquid diet with 35% of calories as ethanol14. While both liquid diet groups had somewhat smaller litters, there was a significantly shorter umbilical cord in the ethanol group. The cords were measured at 20 days. Interestingly, the cord length with ethanol at 20 days appeared to be the same as at 19 days of gestation with control chow.  Because some features of fetal alcohol syndrome resemble fetal akinesia, other author’s had postulated that alcohol caused decreased fetal movement. This study suggests that the short cord is due to decreased movement, but the study had no independent measure of fetal movement. The same lead author compared maternal rats given 60mg/kg of cocaine daily from day 14 to 21 of gestation with controls and found that those with cocaine had decreased maternal body weight and significantly shorter umbilical cords, approximately 30 versus 34 mm at 21 days of gestation15. Again this was proffered as evidence of decreased movement, but had no other measure of fetal movement.

            A study of cord length in 9601 deliveries of 28 weeks of gestation or more found significant reduction of length of approximately 4 cm in breech deliveries compared to vertx, of approximately 1.5 cm in females versus males16. There are two potential errors in the study. First the author stated cords were routinely cut leaving 2 cm on the infant, but this did not appear to have been confirmed in each case. Second, premature infants were included because there is no cord growth after 28 weeks. This may not be true. If more premature infants were born breech, this would confound the data. In the discussion, the author’s recognize that there is neither proof that all (or even many) breech presentations are caused by decreased movement, nor that there is an intrauterine sex difference in movement. The same authors using the above sample as control data found that the umbilical cords of twins were a mean of 7.9 cm shorter than singletons (N=59, total 118 cords)17. Only twins less than 1000g were excluded which, as noted above, could create a bias with more twins delivering prematurely.

            Two studies in one paper attempt to throw in doubt a relationship between fetal stretch on the cord and cord growth18. The umbilical cord measured in rats at different gestation demonstrated a linear growth pattern through gestation. They argue that this pattern does not reflect changes in relative amounts of amniotic fluid effecting fetal movement. They then survey 103 human fetuses between 7 and 30 weeks of gestation and also demonstrate a linear growth curve, again not reflecting relative changes in amniotic fluid and space for fetal mobility. In addition, they looked at fetuses that were more than 2 standard deviations long or short from the mean cord length. Of 15 with short cords, 6 had early amnion rupture sequence in which the fetus is tethered to the placenta. Six had central nervous system abnormalities that could have caused immobility, but only 2 had listed clubbed feet as an anomaly. There was one case of oligohydramnios with renal agenesis and clubbed feet. The other 2 had no lesion to suspect immobility. Of those with long cords, eight were recorded as having oligo hydramnios, and one other had sirenomelia. The only one without likely oligohydramnios was a case of trisomy 18. The underlying causes of cases listed as oligohydramios included a sirenomelic and another renal and uterine agenesis. Only one had a diagnosis of amnion nodosum. Interestingly of those with oligohydramnios and long cords, all were less than 25 weeks of gestation, while the case with a short cord appeared to be almost 30 weeks of gestation. There is very little anatomic detail, including the degree of intrauterine postmortem softening. I have no proof, but infants with prolonged post mortem retention seem to have long thin cords, perhaps a postmortem artifact. In any case it would be interesting to know the length of cord and mobility during life of these infants. I don’t think finding a linear growth curve for the umbilical cord disapproves a need for fetal motility for normal growth. This study does require explanation. The authors contend that experimental production of oligohydramnios was more akin to early amnion rupture syndrome.

            The relationship of oligohydramnios was studied in another population of fetuses with somewhat different results. 31 of 41 autopsied fetuses had shorter than average cord length19. The fetuses were classified as either renal agenesis, cystic kidney or bladder outlet obstruction without giving more anatomic detail. Twenty two cases had documented oligohydramnios by ultrasound at some gestation but this feature did not better predict short cord. The authors argue that the longer cords occurred because some of the cases had normal fluid early in gestation. There is some support for this in that some bladder outlet obstructions such as posterior urethral valves can obstruct later than cloacal atresia for example. The same is true for cystic kidneys. Autosomal recessive polycystic kidney disease has variable oliguria, while some non-obstructive multicystic kidneys may be non-functional. Only 2 fetuses with absent kidneys had normal cord lengths, and these were both less than 20 weeks of gestation. More detail including the degree of pulmonary hypoplasia, actual anatomic diagnosis, and extent of limb deformation and amnion nodosum could have clarified some of the questions about onset and severity.

            Using the data from the Collaborative Perinatal Project NINDB, 21 infants with Down syndrome were identified. Using a Z-score (as did the oligohydramnios study, that is the length minus the mean over the standard deviation from the mean), Down syndrome infants had significantly shorter cords than controls20. Two infants had long cords. This finding suggests that wrapping or some other factor can lengthen the cords, even if the average is shorter. The hypothesis was that Down syndrome infants were born hypotonic and therefore were less mobile in utero. However, there was no direct measure of intrauterine activity.

            A retrospective review of umbilical cord length in 15 perinatal lethal cases of osteogenesis imperfecta, 8 cases of thanatophoric dysplasia, and one of camptomelic dysplasia demonstrated that all had shorter cords than the mean for gestation, and that some had very short cords21.


Long cord correlations


            The largest most detailed study of long cords studied 926 umbilical cords over 70 cm long and with available hospital chart from 1268 such cords found in a database of over 30,000 placentas22. Of 800 controls, the charts were reviewed on 285. The cord lengths were based on that measured in pathology, but the hospital protocol was to put all segments in the specimen container. The mean control value was shorter than other published studies, 37 cm, but included all gestational ages, although the mean gestational age was 39 weeks. Cords over 70 cm were more frequent in males and were associated with higher birthweight mean. Of gross lesions there were more markedly twisted cords, as well as more right handed twists. Microscopically, there were increases in nucleated RBCs, chorangiosus, fetal vascular thrombi, meconium macrophages, and single umbilical artery. The most significant clinical correlations were with fetal anomalies (3 Beckwith Weideman), cord entanglement, and non-reassuring fetal status. The authors also attempted to follow up the long term outcome in infants with cords longer than 90 cm. Since 1 control had a neurologic abnormality at 5% that implies 20 controls, but 11 (44%) of cases had neurologic abnormality, hence 25 cases. Statistical analysis found that the long cord was the only statistically significant predictor of outcome. As in all retrospective studies there are unanswered questions. Unless there is a prospective effort, how many cords were entangled may not be accurately accessed. I would be more interested to know the relationship between degree entanglement, length and outcome. There are also questions of definition, such as chorangiosus versus congestion, and of the cord twist or coiling index. The authors consider many theories to explain their results including hyperactivity of the infant, which is hard to prove without a measure of the significant hyperactivity, and as the author’s point our knowing when in gestation it may act. They also discuss that length can directly increase resistance to blood flow. They consider nucleated red cells to be markers of hypoxia rather than episodes of asphyxia.

            A study of 3,019 cord lengths in gestation greater than 34 weeks, in which the infant piece was measured only if short, separated groups into long cords (80-121 cm, N=112), short cords (14-35 cm, N= 61) and normal cords for comparison with umbilical cord blood gases. Long cords had a significant increase p<.01 for a pH <7.2 (N=5)4. The authors note the small numbers, and comment that all cases with pH <7.2 had deep variable decelerations, and in the long cords either cord prolapse or entanglement. They describe one case which developed bradycardia, meconium passage, pH 7.11, and base deficit 19.9 in which a 131 cm cord encircled the fetal neck 4 times.

            Comparative studies in horses also suggest that long umbilical cords can produce fetal injury and death. In a review of a previous study of 145 thoroughbred horses, the mean cord length was 55 cm, and length did correlate with the allantochorion and allantoamnion weight as well as the length of the non-pregnant uterine horn23. Long cords were defined as greater than 83 cm, and 4 cases demonstrated cord entanglement with deep grooves in the foals body, and calcification in allantochorionic vessels. Long cords were also associated with obstructed urachus which normally connects the fetal bladder with the allantoic cavity. In two such cases with long cords the foals survived but the bladder apex failed to close at birth causing a patent urachus after birth. In two other cases the dilation resulted in urachal necrosis with rupture of urine into the amnion. One of these without limb contractions survived, again with patent urachus, and the other foal had limb contractions and was stillborn. In these cases the author believed that the long cords resulted in torsion that caused the urachal obstructions. Other long cords associated with fetal death also had urachal as well as evidence of vascular occlusion that again pointed to torsion as the mechanism. Another study of equine abortion and stillbirth of 1,211 foals or placentas found that 55 (4.5%) were due to a long umbilical cord associated with signs of cord torsion24. As in the previous study, it is unclear why long cords would predispose to lethal torsion. Perhaps the increased length is marker for polyhydramnios or cord entanglement.




The examination of the umbilical cord starts with measuring the length, ideally in the delivery suite. Studies of umbilical cord length have been hampered by failure to measure all pieces, i.e. those attached to the infant or placenta, and any removed fragments. Some studies have measured the infant piece only if the remainder is short. Certainly, the portion of umbilical cord received in the pathology laboratory, even if all pieces are routinely to be sent, can not be deemed a reliable length unless there is clinical documentation. Situations in which less cord remains in the placenta such as cutting a tight nuchal cord before delivery, or during Cesarean delivery of a severely depressed newborn, have the potential to bias studies looking at outcome. Studies have also been compromised by either assuming no significant growth of the third trimester umbilical cord or by failing to assess the reliability of the given gestational age. The studies overall support some third trimester growth, and possibly longer cords in males than females, and shorter cords in twins. The differences in means in these groups are often less than the differences in mean cord length between studies, and are not diagnostically important.

Most interest has been in abnormally long or short cords compared to a mean length of 50-60 cm. Authors have varied definitions of long and short cords. Receiver operator curves or standard deviations based on the institutional norms would perhaps be best, but very roughly, cords less than 35 cm in length are considered short, and over 70 cm are considered long. There is a separate logical group of very short cords that would be shorter than the distance from the uterine fundus to the introitus, and hence more likely to prevent normal vaginal delivery.

Aside from theoretical interest in the mechanism of cord growth, the main investigative interest has been the possible correlation of short or long cords with abnormal neurologic outcome. The best established relationship clinically and experimentally is with fetal akinesia whether from muscle paralysis or intrinsic central nervous system disease. The failure of the fetus to move results in a very short umbilical cord, joint contractions and pulmonary hypoplasia. Lesser degrees of this same syndrome can occur with hypokinesia. This naturally leads to the speculation that more subtle degrees of hypokinesia or decreased muscle tone could result in a shorter than mean umbilical cord without clinical joint or pulmonary abnormalities. A study of Down syndrome infants was suggestive of such a relationship. The Perinatal Collaborative Study found a correlation of short cords with childhood developmental abnormality. Cords are also very short when the fetus is tethered to the placenta by bands as in early amnion rupture sequence. Lesser degrees of intrauterine constraint may also produce shorter umbilical cords. The cord may be shorter in some cases of oligohydramnios. The onset of the oligohydramnios varies with etiology and there is no study looking critically at the timing of restricted movement and cord length. The crowding that occurs with twinning may result in a shorter mean cord length. No study has used a prospective intrauterine measure of fetal movement to predict umbilical cord length in non-paralyzed infants. There is no definitive predictive value of umbilical cord length for poor neurologic outcome.

Some authors have found that a long umbilical cord is associated with neurologic injury. There is no experimental model for a mechanism of neurologic injury. Some authors have proposed that fetal hyperkinesias causes the long cord, inversely analogous to akinesia causing short cords. In this model, the intrinsic neurologic abnormality causes the long cord. Some studies have found an increased incidence of umbilical cord entanglement or wrapping with long cords. Anecdotally, complex wrapping may be associated with fetal heart rate patterns of umbilical cord occlusion. The association of long cord with poor neurologic outcome would then be due to hypoxic-ischemic injury secondary to umbilical cord entanglement. It remains to be proven whether the long umbilical cord occurs first with subsequent entanglement or whether wrapping of a normal length umbilical cord around a fetal part causes secondary elongation of the cord, perhaps by fetal tension on the cord. At least one author has speculated a longer umbilical cord length increases vascular resistance. Since only a very small increase in diameter of the vessel would offset this increase, it may be more likely that a kink or pressure on the cord from the wrapping is the mechanism of umbilical blood flow obstruction. A problem with current studies is that the wrapping is usually described at the time of delivery. This may not represent the fetal state, as cord loops may slip or tighten as the fetus is delivered. Prospective longitudinal studies of fetuses discovered to have intrauterine cord wrapping or entanglement might demonstrate a tighter relationship (pun intended) with neurologic injury. Understanding the mechanism leading to the association of long umbilical cords in horses with lethal torsion of the umbilical cord might also contribute to new insights in humans.

Any relationship of cord length to fetal activity would benefit by a better understanding of the biological mechanisms controlling cord length. The so called stretch or tension hypothesis makes superficial sense in that paralyzed or immobilized fetuses can not stretch the cord. Therefore, fetal tugging on the cord is the signal for elongation. There are some logical questions about this mechanism. Since the cord is longer than the uterine cavity, how often does the fetus actually put tension on the cord? Since short cords are at the mean cord length of 23 weeks of gestation, does cord growth stop in the second trimester, or was it slowed continuously during fetal development. Teleologically, some relationship of cord length to fetal movement would be desirable in wrapped cords. The effective cord length for delivery is from the placenta to the beginning of the wrapped portion. If this effective length is less than the distance needed to deliver the infant, this could result in maternal and fetal death prior to modern medical care. Evolution of a mechanism to lengthen the effective cord in this situation would not be surprising. If movement of the fetus provided tension on the cord until a certain length is reached then this might assure that all cords had a sufficient effective length to deliver the infant. However, wishing does not make it true. There does not appear to be research on the molecular mechanisms of cord length growth. Many growth factors have been documented as bound to the matrix of Whartons jelly, but not active in this highly charged environment. Could physical force on glycoaminoglycan matrix free up these growth factors to stimulate mesenchymal cells in Wharton’s jelly. Cells are bound to the matrix which has a characteristic firmness to which they respond25. Could a change in the physical matrix by tension on the cord stimulate cell division.  This would appear to be an interesting area to study, but I did not see any such studies.





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