Richard Torpin, M.D.
(Student of the Human Placenta)
Medical College of Georgia
1931 - 1974

It has been estimated that 30% of births have some type of umbilical cord finding. This statistic implies a potential for fetal harm that may not be appreciated by scientific and public health authorities. Not knowing how many fetuses are harmed by their umbilical cords prevents research into the issue. If neurological harm can occur as the result of umbilical cord problems, then this mechanism of harm to the fetus needs to be investigated.

Every fetus should have the opportunity to begin life with all its God-given talents and abilities. Realistically, this may not be possible, but some physically normal newborns could benefit from a reduction in the risks of a cord mishap. It is estimated that learning disabilities may represent 15% of children today. What if one-third of these learning disabilities are due to some type of cord complication? The issue of cerebral palsy is important, but currently no solution and few insights exist as to its origin. Preventing the stillbirth of a normal infant would be an important step in identifying cord-related harm. What is the size of the problem, and what best describes each part of the problem of umbilical cord mishaps?

Disruption of the umbilical cord's supply line is a major source of harm to the developing fetus. It is estimated that every third to fourth delivery has an identifiable umbilical cord abnormality or anomaly. What is unknown is how these findings affect the fetus in degrees. The obvious effect is that stillbirth can result from the closing of the supply line.

The expectant mother can play a role in solving the tragedy of umbilical cord accidents. While it is unknown how much time is needed for a fetus to die, it is believed that some fetuses die slowly. Fetal behavior is consistent and can have a repetitive (circadian) rhythm. As discussed later, awareness of fetal movements, sleep-wake cycles and tendencies may provide an initial warning of a compromised fetus. Verbalizing these changes to the obstetrician may alert everyone of the need for a closer look at the fetus with ultrasound and fetal monitoring.

To understand umbilical cord related complications, an understanding of fetal developmental physiology is imperative. The umbilical cord begins to form between four and six weeks, as the embryonic disc takes a cylindrical shape. Located at the lower third of the embryo, the proximal portion of the umbilical cord begins to form and develops a sac (herniation). The proximal portion houses the guts (intestines) until the tenth week of gestation. At this time the umbilical cord is short, usually shorter than the head-to-tail (crown-rump) length of the embryo and of proportionately large diameter. It is not able to tolerate rotation about itself or the formed embryo. In fact, as the umbilical cord elongates, the proximal cord encompassing the intestinal pouch cannot be disturbed. This initial stalk develops in the center of the implantation site, which is the reason the cord presents at the center of the afterbirth (placenta).

By ten weeks, the intestines leave the proximal cord and return to the stomach, the elongation of the cord begins, and the location of the umbilicus (bellie button) positions in the middle third of the embryo. The elongation of the umbilical vein and arteries coincides with the development of Wharton's jelly, an umbilical cord connective tissue.

The responsibilities of the cord are numerous. For example, the cord manages its own growth, elongation, and expansion, accommodates increasing blood flow, and possibly assists the fetal heart. It also must regulate blood flow and its fluidity (thickness/thinness). In addition, the umbilical arteries and vein contain muscular coats that allow constriction of the vessels at birth or dilation of the vessels during growth. The umbilical cord also must produce its own chemistry to prepare for its role in birth and separation from the newborn umbilicus (a process which takes 7 to 10 days).

Located within the cord are the umbilical vein and arteries. The relationship of the umbilical vein to the umbilical arteries changes with development. These changes can result in cord abnormalities which will be discussed in the next chapter. Initially, two arteries send blood with waste products from the embryo to the afterbirth (placenta), and the one umbilical vein sends oxygen and nutrient-enriched blood to the embryo from the placenta. This circulation pattern must respond over time to the constantly changing fetal requirements and demands.

Rare developmental changes which can occur to the embryonic umbilical cord are persistence of the right "vitelline" vein, creating a four-vessel cord with two arteries and two veins. The reverse of this is obliteration of an artery and vein and the development of a two-vessel cord with one artery and one vein. There also exists a description of a "double cord" with separate vessel duplication.

Genetic problems are seen with two-vessel cords where fetuses with multiple malformations have defective organs which are not compatible with life. Maldevelopment of the genitourinary system such as bladder and kidney has been noticed. Although these relationships are known, obstetrics currently does not place any added concern on pregnancies with two-vessel cords. No remedy for these anomalies presently exists.

Umbilical cord vessels may multiply and branch under stressful conditions. For example, heavy smoking is associated with "multiple channels" in the umbilical cord. Hypoxia (the decrease of available oxygen) has been determined as the stimulus for opening of early "vestigal" vessels of the cord, once closed at 10 weeks. These findings of "re-channeled" embryonic vessels are also associated with fetal compromise and stillbirths. A trend was also noted in which first time pregnancies had more vascular branching than multiple birth mothers. Research indicates a 2% probability of this cord finding.

How the umbilical cord elongates and grows is unknown. As it grows, it changes the relationship between the vein and arteries. These changes may or may not predispose the growing fetus to blood flow disturbances or mechanical disturbances between the fetus and umbilical cord.

The umbilical cord is traditionally thought to "stretch" or "elongate" depending on the activity of the fetus. Active fetuses are believed to have longer cords on the whole than less active fetuses. Twins and triplets, because of restricted movement, have been shown to have cords on the average shorter than their single counterparts. Boys have longer cords than girls. Non-identical twins have varying cord lengths when compared to each other. Non-identical twin A can have a cord twice the length of twin B. Also twins A and B can have different cord architectures where one is straight and one is helical.

Rare instances exist in which no cord develops at all, the fetus being attached directly to the placenta at the umbilicus. Other reports in Chinese and French literature cite cords as long as 300 cm in length.

The umbilical cord appears to have organ-like properties. These properties are prone to disturbance under certain conditions which can affect the fetus. Just as a heart can fail pumping, or the liver and kidney can fail filtering the body's chemistry and waste products, the umbilical cord can fail in its role of being a "supply line."

Umbilical cords without much Wharton's jelly are more prone to compression, and complete absence is usually associated with fetal death. If an umbilical cord is twisted or knotted, it is more likely to tighten where there is less resistance, such as an area low in Wharton's jelly.

It is believed that males have more Wharton's jelly content than do females and that good nutrition increases the amount. Wharton's jelly tends to reduce with gestational age and can disappear when pregnancies go beyond 40 weeks. Because these cases tend to have fetal heart rate changes, the level of Wharton's jelly is a consideration when obstetricians plan the deliveries of pregnancies low on amniotic fluid.

Cord length can be associated with neurologic abnormalities and fetal positioning. To understand this correlation, it is important to understand the physiology of the human umbilical cord. Cord length has been frequently measured. One of the largest studies was completed by Pathologist Dr. Richard Naeye. In his book Disorders of the Placenta, Fetus, and Neonate, Dr. Naeye averages the lengths of different umbilical cords at progressively older gestational ages. The cord is believed to elongate until as late as 36 weeks although rapid change occurs until 28 weeks, then slows. The final length of the umbilical cord averages about 61 cm, or 24 inches, according to Percy Malpas, M.D., a British obstetrician who studied cord length in the 1960s. The first pregnancy tends to generate a shorter cord than subsequent pregnancies. Although no published report of a genetic relationship exists, there may be one.

So why 61 cm? Umbilical cords of whales, porpoises, goats and other mammals are relatively shorter than the human cord. Walker and Rye of Cambridge surmised in the British Medical Journal in 1960 that prehistoric humans evolved length for protection. Nature's purpose was to allow the mother to pick up the newborn without disturbing the placenta. The event of breast feeding would then separate the placenta - an event which could attract predators. Having the fetus in tow would allow escape for mother and child.

Today, cord length correlates to several "outcomes." Cords too short and cords too long predispose the fetus to intrauterine dangers. A short cord has a length of less than 32 cm. This length was determined in 1910 by a famed Chicago obstetrician, Dr. Joseph B. DeLee. Dr. DeLee believes 32 cm to be the minimal length necessary for a term fetus to deliver. The concept changes, however, when cord insertion site and cord entanglement are considered. This idea is called a relatively short cord. Very short cords less than 20 cm are associated with genetic malformations. When cord lengths were evaluated for IQ, short cords showed a higher incidence of neurologic abnormalities.

Cord length may also influence fetal position. Torgrim Sornes, M.D., a Norwegian researcher, observed this. His work suggests that Breech-positioned fetuses have shorter cords due to less activity. This insight suggests that if the fetus persists at remaining Breech, a cord etiology should be considered, and the obstetrician should watch for fetal difficulties during labor.

Umbilical cord circumference and diameter are also important measurements. On average, normal umbilical cords are 3.7 cm in circumference with a range of 3 - 5 cm. The diameter range of 1.0 cm to 3.0 cm can suggest an abnormal cord with edema, tumor, or hernia. Dimensions greater than 6 cm circumference should prompt an examination of the cord and fetus. Are shorter cords thicker than longer cords? Although rarely published, it appears that this may be the case. Before cutting any thick cord, it should be checked to ensure that the fetal intestine is not present within the cord.

Growth and development of the umbilical cord are dependent upon many factors. Disturbance of these events can lead to fetal compromise or result in fetal compromise. These effects will be described in the next chapter.

How the umbilical cord is built has long been of interest to anatomists. A look at all mammals shows a variety of design adaptations. In humans, it has been determined that there are several designs. What these differences mean to the fetus is unknown. Attempts by several noted scientists to understand how the umbilical cord works have taught us that the cord is more like an organ rather than a rigid conduit (pipeline).

Not all cords are alike. Just as there are different kinds of hair (curly/straight, thick/thin), there are different kinds of cords. Most cords (99%) have three vessels, although some (1%) have only two, and even less have four.

The relationship between the normal vein and two arteries is usually parallel (Figure 7). This parallel configuration can vary, however, and may imply effects which can alter blood supply to the fetus. Variances include arteries that are together, or separated with each artery lateral to the vein (Figure 8). Another variance is arteries that wind around the vein while the vein remains central in the cord. This is sometimes referred to as spiralled arteries, but helical is the preferred term (Figure 9). The vein can also parallel the arteries in a helical configuration, and the vein can wind around the arteries.

The location of umbilical cord attachment to the fetus and placenta is also important. Placental attachments can be in the center, off center, on the edge, or in the membranes. Membranous insertions of the umbilical cord are called Velamentous Insertions. These placental-cord designs have flaws which can lead to cord tears. Currently, little research has been done to develop prenatal diagnostic criteria.

Umbilical attachment of the cord can vary and predispose the infant to hernias at the umbilicus and "constriction" of the cord. Although these are uncommon findings, future research will allow a more accurate evaluation of the umbilicus. Amniotic bands can interfere with both ends of the umbilical cord. For example, the amniotic membrane can leave remnants in the form of fibrous bands which can stiffen and occlude the blood circulation through the cord. These events are reproductive mishaps that have no current remedy. In order to begin the process of creating solutions to umbilical cord related complications, understanding cord function and design must be thorough.

Throughout human history, stillbirths have been associated with umbilical cord findings. These findings vary, and some are more common than others.

Scientifically, umbilical cord changes and effects are described several ways. To start, the umbilical cord can develop design flaws which can lead to fetal harm. These flaws are called Umbilical Cord Abnormalities:

Short Umbilical Cords (less than 35 cm) are predisposed to rupture and prevention of fetal descent during labor. Very short cords, less than 25 cm, are associated with genetic malformations. Short umbilical cords need to be considered relative to their attachments to the placenta. The further the attachment is from the cervix, the less likely the fetus can be born vaginally, requiring a C-section.

In addition, fetal heart rate changes will be more likely to occur during monitoring, creating concern for all involved in the labor process. Very short umbilical cords, less than 25 cm, have been associated with neurologic disorders, IQs less than 80, and cerebral palsy. There is an increase in stillbirth risk with short and relatively short cords. This risk may be as much as six times more likely, especially when other factors like toxemia are involved. Short cords and cigarette smoking tend to result in small babies, called IUGR (Intrauterine Growth Retarded). It is difficult to unravel the relationships mentioned above since some fetuses may incur neurologic damage which predisposes them to decreased activity and leads to decreased cord length.

Long Umbilical Cords (longer than 70 cm) are associated with a number of circumstances which can impact fetal life. Leonardo da Vinci studied cord length and believed it was a proportional/natural relationship of 1 to 1 (cord length = fetal age in weeks). Although this is not precisely correct, da Vinci was correct in that it is proportional. Biological and physical principles which dictate the shape of a star fish, tree leaf, or nautilus shell determine the positive or negative relationship between the fetus and its umbilical cord (and probably placenta).

Fetal activity is believed to determine umbilical cord growth. This mechanical stimulus may be a direct or indirect factor. How does the umbilical cord grow and elongate? Biochemical and cellular mechanisms must be at work. All of these molecular-genetic pieces are potentially at risk for failure by inside or outside disturbances. Growth factors have been identified in the umbilical cord. In addition, studies in twins suggest a genetic control or modulation of length. Length can also be influenced by amniotic fluid volume and anything that constricts fetal movement. Umbilical cords are also innervated to a degree near the umbilicus. The role this plays or whether there is an influence on cord development is currently unknown. Of all those multiple variables influencing cord length, the most important variable needs to be determined. It is unknown whether individual cell enlargement or cell division and multiplication cause cord growth. Many different cells such as muscle cells, endothelial cells, fibroblasts, connective cells and amniotic cells all must do the same thing. Insight into this aspect of fetal development may help understand anomalies of the cord.

Microscopic comparison of long and short cords may reveal differences of structure. Thickness or thinness of vessel walls, composition of Wharton's jelly, and artery-vein interrelationships may be important findings which explain long cord susceptibility to various events.

Two Vessel Cords occur in about 1% of births. The connection to fetal harm or well-being is unclear. These umbilical cords have one artery and one vein. The dominant artery origination (left or right inside the fetus) determines whether or not congenital malformations may be present. It is accepted that these cords may predispose the fetus to stillbirth compared to a normal three vessel cord. The risk of stillbirth can be six times greater than normal especially when other factors such as toxemia exist. Whether or not other variables are involved remains to be determined. Development of a single umbilical artery cord may be associated with maternal smoking, drug exposure, placental abnormalities and maternal diabetes. Whether or not all infants with a two vessel cord are predisposed to some difficulty remains to be seen. The mechanism of how one artery is obliterated versus undeveloped may be important to understanding this issue.

Four vessel umbilical cords are rare and are mentioned to emphasize the vulnerability of cord vessels to malformation. Not all umbilical cords are alike, and non-identical twins can have non-identical cords. Proper development of the embryo and its supply line are important steps toward a healthy fetus and newborn. Maldevelopment of the supply line from the start can predispose the fetus to harm.

Another important step in umbilical cord development is the connection of the fetus and placenta to each other. The fetal connection is specialized and has a specific architecture. This design needs to function as a secure tether for the fetus, as a disrupter for umbilical separation (in mammals the cord tears free or is chewed fee), perhaps as a sensor for blood flow into the fetus, and must merge with the skin.

Researchers have identified nerve endings near the umbilical insertion of the cord in the Wharton's jelly. These "end nests" may play a role in communicating with fetal "valves" called shunts relative to blood volume wave properties entering the fetal circulation through the umbilical vein at the level of the liver and heart. When the umbilical end is malformed, constriction or coarctation occurs, stopping blood flow. How this happens is unknown. At the other end of the supply line, the fetal arteries enter the placenta with a membranous support tether and distribute in a branching manner. When the placenta develops it sometimes "migrates" and "dissolves" from its original site. This sometimes can result in what appears to be a relocation of the placenta. The placenta tissue dissolves, leaving a membrane (the amnion) remaining which can then be the connection (insertion) site of the umbilical cord. This results in the umbilical cord placental end looking like it is connected to the edge of the placenta (called a marginal or Battledore insertion) and a membranous insertion called a (Velamentous) insertion. (Figure 10)

Another variation is called a furcate cord insertion in which the cord does not connect to the placenta but its branching elements do; however, no membranous insertion exists. These malformations account for another 0.5% to 1% of all births and are observed increased in premature labor, premature birth, fetal stillbirth, and neurologic harm.

The risk of cord vessel rupture is increased with an abnormal cord insertion. The difficulty of managing an incident such as cord rupture is great. What makes the mystery even more complicated is the location of the cord insertion in the uterus. If the membranous insertion is over the cervical opening, the risk of tearing and fetal blood loss is great. If a marginal insertion is against the sacrum (lower backbone), the risk of compression and fetal circulation disruption is great as the fetus descends into the pelvis. This relationship of vessel location to fetal location has caused sudden fetal distress and the need to activate a surgical team for an emergency C-section. It is unknown how often this happens during day-to-day obstetrical care as the attention is on the fetus, not the placenta, its location, or its cord insertion architecture.

Umbilical cords may have eight different types of design. The extremes are very helical cords (95%) and completely straight cords (5%). The association between umbilical vein and arteries can vary where veins wind around arteries, veins and arteries are parallel, and arteries wind around veins. The veins can be parallel with the arteries as well (10%). Very helical designs (spiraled, coiled, and curled) may predispose the fetus to certain blood flow changes, and very straight designs may be susceptible to compression. It is unknown what the fetal effects are but some evidence points to supply line vulnerability when the design is faulty. Add to this other variables such as placental location and umbilical cord insertion site, and the combination becomes a significant factor in determining the well-being of the fetus. Knowing these details may provide important insights into the development of fetal harm.

Wharton's jelly, although apparently inert looking, may be an important chemical factory for the fetus. Additionally, its components and cellular make-up can predispose the fetus to the formation of tumors, cysts, and edema. Edema is not an infrequent finding at delivery of a newborn (10%). It is usually limited to small sections of the umbilical cord and associated with trauma due to fetal behavior. Extensive involvement of the cord is associated with complications of pregnancy such as toxemia and infections. When cause is due to fetal circulatory disturbances, fetal heart failure may predispose the cord to edema which is associated with an increased risk of stillbirth. Tumors can develop in Wharton's jelly. Although rare, "teratomas" have been reported. Teratomas grow to large sizes and can disrupt vessels and blood flow.

Embryonic features of the umbilical cord can produce six types of remnants, some of which look like "hemangiomas," blood vessels which together look like small varicose veins in a bundle. Other structures such as "Viteline duct remnants" and "Urachal duct remnants" can be seen. Those changes are very infrequent but should be considered if an enlargement or localized "mass" is seen in the cord. Hematomas (bleeds into the substance of the cord) can occur and mimic these rare tumors. The possible association with fetal defects must always be considered. As the fetus ages, it is believed that Wharton's jelly recedes. This becomes an important issue when deciding to deliver a "post date infant" where the due date has been passed without delivery. Loss of Wharton's jelly may put the fetus at risk of cord compression and therefore fetal harm.

Growths and Swellings of Umbilical Cord Vessels
Back to Chapter 1 Topic Menu

Human umbilical arteries consist of two layers of muscle fibers, the outer layer being 3/4 of the wall thickness and an inner layer. The design of the muscle cells is parallel where the inner layer runs with the vessel lengthwise, and the outer layer surrounds the vessel like a spiral staircase. A thin layer of cells line the vessel opening, and an outer layer is formed by connective tissue and Wharton's jelly. This architecture allows constriction and shortening of the vessel. Defects in this structure can occur which may predispose the umbilical arteries to failure.

A type of architectural defect is called "umbilical cord vessel segmental thinning." In this malformation (1%), umbilical vessel walls are missing a layer of muscle, therefore weakening the vessel. Related observations include fetal anomalies and perinatal problems. These fetuses are predisposed to stillbirth, meconium, and fetal heart rate decelerations.

All in all, when a combination of defects results, the risk of umbilical cord failure begins to become important. It is unknown how many placentas and umbilical cords contain a variety of architectural anomalies or abnormalities that lead to miscarriage. It is unknown how much fetal harm may be the result of faulty placentation and cord alterations such as straight cord segments resulting from the molding of Wharton's jelly due to long-term compression of an entangled cord. Future research into these issues will be both exciting and fruitful. The integration of the anatomy (structure), biochemistry (substance), and physiology (function) of the umbilical cord will allow the emergence of a new awareness of three structures to manage in pregnancy: the placenta, umbilical cord, and fetal unit.

What is remarkable about the umbilical cord is that it is a blood vessel without branches. This is unique compared to the large blood vessels of the adult body, the aorta and vena cava. Its properties, therefore, are different in some respects and alike in others. The umbilical cord has two-way traffic: the arteries carry blood pumped by the heart away from the fetus, and this circulation surrounds the vein normally; the umbilical vein returns blood to the fetus from the placenta rejuvenated with oxygen and nutrients and devoid of waste products.

How this happens is still surrounded by mystery. The fetal heart cannot expand or work harder because it is surrounded by a fluid-filled lung, like pushing against a water bed. Therefore, as the fetus steadily grows exponentially and three-dimensionally, how does it accommodate the increased blood volume it needs over time? As the fetus grows, the cord elongates and grows in diameter. The fetus has to work against a larger column of fluid and tissue resistance at the placental end. It has been estimated that by 31 weeks, the umbilical cord must carry 70 quarts of blood per day, moving at 4 miles an hour.

This remarkable organ also must participate in fetal growth milestones; additionally, it may act as an assist pump to the fetal heart. This assist pump may be designed to help the fetus over difficult growth proportions which may exist at 20 weeks, 24 weeks, 28 weeks, and 32 weeks - times that are known for premature labor to appear. The extra stress on the fetus may require that the cord be designed correctly so that it can have properties of an assist mechanism or pump. This theory, proposed in the 1950s, requires that the arteries surround the vein in the proper architecture. If this is so, then future research into this issue may explain fetal effects secondary to cord design. To date, no assist pump property has been detected in the umbilical cord.

How blood flow is regulated in addition to being carried by the umbilical cord is unclear. Cord length does not significantly affect blood flow dynamics; however, blood flow must meet some resistance for the circulation to work. As a result, the umbilical arteries are surrounded with four layers of smooth muscle to maintain a certain amount of muscular tone. The umbilical vein is not as musculated. The system operates fully dilated, but stimuli from chemistry or hormones can affect the system and cause constriction. This must happen at birth to reduce blood loss. In larger mammals, the cord must constrict from the placenta to the fetus for the fetus to avoid anemia. In the human, similar mechanisms may be available chemically. Regulation of blood flow, vessel constriction at birth, and blood loss prevention may be the roles of these vessel-active substances. Some of these substances originate in the placenta.

Researchers using ultrasonography recently have been able to measure umbilical blood flow with color Doppler imaging. This technique allows visualization of the blood vessels based on the movement of the blood itself. These studies also suggest that the umbilical vein, arteries, and placenta act as an assist pump of sorts to the fetal heart. Measurement of blood flow allows the obstetrician to determine whether enough blood volume is circulating in the placenta to provide nutrition and oxygen to the fetus. Under certain conditions this blood flow can be reduced and circulation in the placenta altered to create a growth-affected fetus, Intrauterine Growth Retardation (IUGR). In essence, it is a way of determining the fetus' blood pressure.

These findings become important because, in addition to the potential for fetal harm or stillbirth, important lifetime tendencies are emerging. The fetus seems to have the ability to set its vital signs for its adult life. If stressed, the IUGR fetus sets blood pressure and heart function, which can predispose the fetus to adult heart attack. These mechanisms are just beginning to be understood, and the umbilical cord may be an important part of the mystery.