ARTICLE
The Umbilical Cord: Normal Parameters GERALD ENTE, M.D., F.R.S.H.
Attending, Department of Pediatrics Nassau County Medical Centre Director Neonatology, Central General Hospital, Plainview, NY 11803, PAUL H. PENZER, M.D. Attending, Department of Pediatrics Nassau
County Medical Centre,
INTRODUCTION
HE UMBILICAL cord is the lifeline of the t foetus. Prenatal survival is dependent on adefunction of the cord. After birth, this item with the placenta is discarded as medical waste, along which may account for the relative lack of knowledge and interest in the umbilical cord. Medical literature contains much information about pathological aspects of the cord such as infections, granulomas, and hernias. But the same body of literature has little quantification of many normal aspects of the cord such as length, circumference, twist, and time of separation. ’All other men, being born of woman, have a navel, by reason of the umbilical vessels inserted into it, which from the placenta carry nourishment to children in the womb of their mothers; but it could not be with our first parents. It cannot be believed that God gave them navels which would have been altogether useless.’ Bishop Richard Cumberland (1632-1718)
1 quate
, I
_ --
’
(Strauss,
196 )8
LENGTH >
performed studies on the umbilical cord. He concluded that the length of the umbilical cord was equal to the height of the newborn infant (Moessinger et al, 1982). During the next five centuries, this measurement has been refined somewhat. At delivery, the average length of the umbilical cbrd LEONARDO DA VINCI
is 50-60cm with 40cm as the lower limit of normal (Naeye, 1985). Short cords may cause traction during vaginal delivery, explaining why these are occasionally associated with delayed completion of the second stages of labour, or may cause placental abruptions, uterine inversions, cord herniations or even cord rupture (Naeye, 1985). Abnormally long cords increase the frequency of cord prolapse, true knots and coiling of the cord around foetal parts, all of which can produce foetal distress through cord compression. A cord must be long enough to reach from the placental site to the vulva, and if the placenta is located in the uterine fundus, a minimal length of 32cm is necessary. Although the mechanical consequences of short and long cords have become well known to physicians, recently researchers have begun to realize that the activity of the foetus and the tension on the cord itself is the basis of umbilical cord elongation (Miller et at, 1982). The tensile strength of the cord is from 8-15 pounds (3.6-6.8kg) (DeLee, 1943). Maldevelopment of the central nervous system is one of the factors that
U.S.A.
East Meadow, NY 11554, U. S.A.
limit foetal movements and subsequently cord length. Abnormal cord length, therefore, is an early marker for developmental abnormalities. The lengths of 35,779 neonatal cords were analyzed as part of the data from the Collaborative Study of the National Institute of Neurological Communicative Disorders and Stroke (Miller et al, 1982). The actual measurements showed a mean length of 57.4cm at 38 to 39 weeks gestation, and a mean length of 59.6cm at 40 to 41 weeks gestation with a standard deviation of ± 12.6cm (Mills et al, 1983). Cord lengths were positively correlated with maternal pregravid weight, height, socioeconomic status, pregnancy weight gain and foetal gender (Moessinger et al, 1981). There was no correlation with neonatal hemoglobin level, maternal hypertension, race, maternal mental retardation, maternal alcoholism, maternal narcotic addiction or maternal cigarette smoking. The cord grows mainly during the first two trimesters of pregnancy and reaches a mean of 32cm at 20 weeks gestation. At 34 weeks, the male cord averages in length, the female cord 51.75cm. At term the lengths are 60.25 and 57cm respectively. The cord grows very slowly after the 35th week and there is practically no growth after the 40th week (Moessinger
Perinatall and
53.75cm
et al, 1982) (Miller et al, 1982).
only 6% of term cords are below 40cm, length has been defined as a short cord (Naeye, 1985). Short cords were found to be associated with low Apgar scores, hypotonia, positive pressure rescuscitation at birth, and jitteriness in the neonatal period. Short cords increased the prognostic value of these neonatal markers for subsequent neurological abnormalities and low IQ scores by a factor of 2 or 3. This correlation proved to be independent of birth, weights and head circumference measurements (Miller et al, 1982; Naeye, 1985). Cords as short as 6.7cm and as long as 198cm have been cited (DeLee, 1943), but these lengths are rare. Because Down syndrome is associated with hypotonicity and reduced foetal activity, and, as has been stated before, foetal motor activity and tension do influence cord growth, newborns with Down syndrome have significantly shorter umbilical cords. A study of 21 Down neonates compared to matched controls showed significantly shorter cords (mean of 45cm compared to controls of 57.3cm (Moessinger, 1986). The Down syndrome cords were 12.5cm (1 standard deviation) shorter than the normals. Clearly, the presence of such Because below this
a
short cord in itself is not
138
Downloaded from rsh.sagepub.com at Purdue University on January 16, 2015
diagnostic
of Down
syndrome nor is the presence of a long cord exclusive of the diagnosis. However, this is another soft physical sign which may be considered in the clinical diagnosis of Down syndrome. Ulrich & Bohm described ’the missing cord syndrome’, or ’dysplasia umbilical-foetalis’ (Ullrich, 1977). This condition is a major malformation complex consisting of maldevelopment of cord, defect of the abdominal wall and other severe lethal congenital anomalies. This defect develops at the end of the third embryonic week during the 7mm stage. The foetus is attached to the placenta through an umbilical hernia. Measurement of cord length at birth, at one time a
standard obstetrical ritual, represents an index of foetal activity, providing that the foetus was allowed adequate space for movement. The physical examination of any newborn includes measurements of body weight, body length and head circumference. Significant deviations from normal cord length suggest selective pathological processes. The quantification of observable measurements of the cord is simple, consumes little time and is value in assessing the newborn. This measuref greatshould be reinstated as one of the routine ewborn measurements which are presently recorded.
ent
CIRCUMFERENCE WE PUBLISHED a paper in 1970 (Ente et al, 1970) entitled ’Giant umbilical cord associated with patent urachus’. We realized that the diameter was unusually large (5cm), but had no data for comparison. Quantification of normal umbilical cords based on a study of 191 full term newborn infants was subsequently reported (Patel et al, 1989). The mean umbilical cord circumference measured at day 1 at its attachment to the umbilicus was 3.77±0.73cm. This mean cord circumference increased with increased birth weight, chest circumference and abdominal circumference. The authors pointed out that an unusually large cord should raise suspicion of a hernia and that the baby should be closely examined by a physician before the cord is
clamped. Although the factors regulating the circumferential growth of the umbilical cord are unknown, Patel and olleagues postulated that ’factors that regulate the z
of the foetus in the growth the umbilical cord’. In the
influence the size of of cord gigantism associated with patent urachus (Ente et al, 1970), it was postulated that retrograde flow of hyperosmolar urine increased the mass of the mucoid connective tissue (Whartons jelly) surrounding the vessels traversing the cord. At term, the average diameter of the cord is 1-2cm (Elhassani, 1984). uterus
case
TWIST
umbilical vein is longer than the umbilical arteries and the arteries are longer than the cord itself, twisting of the vessels occurs. The vein is twisted around the arteries which themselves are twisted within the cord. This spiral action of the cord vessels is well known. The twist, as well as the length at birth depends on foetal activity. Jones and Benirschke collected data on 2334 cords and recorded the direction of the twist. Only five percent had no twist at all. Left twist outnumbered right twist by 7:1, which is the same ratio as the predominance of right handedness over left handedness in the general population (Jones, 1987). BECAUSE THE
(1987)
There was, however, no correlation between the direction of the twist and handedness of the mother or the child. They did show that 37% of infants with a single umbilical artery had an associated major structural abnormality, a multiple malformation syndrome, or foetal death. They also found that an increased incidence of absent twist is independent of hemodymanic forces in the cord itself. The increased incidence of absent twist among intrauterine foetal deaths and twins suggests that decreased foetal movements can impede the forces that lead to normal twisting. Absence of the twist may be associated with a poor
prognosis (Jones, 1987). TIME OF SEPARATION of separation of the umbilical remnant from the baby is partially dependent on microbial factors operating at the site. The precise timing of cord separation is probably the result of a complex interaction of many factors, which include drying, necrosis, collagenase activity and granulocyte activity. Leucocyte dysfunction and recurrent infections may be associated with delayed cord separation. Leucocyte dysfunction may be secondary to defects in chemotaxis, hypomobility, diminished oxidative response, failure of adherence, a deficiency of a high molecular glycoprotein or a primary defect of a contractible protein. Premature birth is yet another factor associated with dysfunctional leucocytes. The method of delivery also affects leucocyte function (Oudesluys-Murphy et al, 1987). Cord separation beyond 21 days is considered ’delayed’. This should serve to warn the physician of the possibility of leucocyte dysfunction, which is often THE TIME
accompanied by recurrent life-threatening infections (Oudesluys-Murphy et al, 1987; Wilson et al, 1985). A common question asked by new mothers is, ’when will the cord fall off?’. A medically insignificant delay in the separation of the umbilical stump may be a genuine cause of maternal concern. Such concern can be prevented if a proper explanation is given along with proper anticipatory guidance. In a study of 911 infants, Oudesluys-Murphy and colleagues (1987) found a mean time of separation 7.4±3.3 days (range 1-29 days). The authors discussed several perinatal factors that affected the time of separation. Separation was delayed in the following conditions: when antibiotics were administered to the neonate; when the infant was born when delivery was by Caesarian section or when the infant had a low birth weight. The cord separated slightly earlier in female than in male infants. For this study, cord care was limited only to dry sterile gauze dressing. The administration of parenteral antibiotics delayed separation by three days. Caesarian section delivery delayed the separation by two days. The cords of males separated on an average of one half day later than those of females. Novack et al, (1988) further found that hyperbilirubinemia was statistically associated with later separation.
prematurely;
The use of topical antibacterial agents may help to explain the two fold increase in the time of cord separation in most nurseries in the developed countries of the world. Several good clinical studies look to this point. Six different methods of umbilical cord care were compared by Gladstone and colleagues (1988). The six methods included: (1) TD/TD triple dye once TD/AL daily until cord separation);
(2)
applied (triple dye
139
Downloaded from rsh.sagepub.com at Purdue University on January 16, 2015
applied once then alcohol applied daily until cord separation); (3) TD (triple dye applied once, with no further antimicrobial treatment); (4) POV ( rovidoneiodine supplied daily until cord (5) SIL (silver sulfadiazine applied daily until cord separation); and (6) BAC (bacitracin ointment applied daily until cord separation). The results are listed in Table I and
weeks of age at present in the era of triple a
large vanability due to multiple factors.
dye care with
separation ;
equally effective for infection control in all groups, but with differing times of cord separation. are
CONCLUSION DESPITE THE
insignificance of the umbilicus in adults, the plays a major role in survival and
umbilical cord
of the foetus in utero. The cord is a viable development index of foetal Much information can be
activity. by examining this structure, simply by visual inspection and measurement. We are urging the observation and recording of these measurements as learned
Newman (1989) in a letter warned that the use of 2% iodine solutions interfered with congenital hypothyroidism screening by suppression of thyroid function. Several other studies have confirmed that with any of the varied modern cord care regimens, the mean time of cord separation is approximately two weeks ± 1 week, with a range of 3-67 days (Novack et al, 1988; Wilson et al, 1985; Arad et al, 1981). In summary, dry cord care has a mean time of separation of 7 days. Dry cord care is, however, not considered safe today. The use of antibacterial agents prolongs the time before separation by another 1-2 weeks. The use of any of the standard cord care regimens are effective for infection control.
SUMMARY See Table II
length of the umbilical cord is 50-60cm in the normal full term newborn infant. The length of the cord is an index of foetal activity and is dependent on the tension caused by the freely movmg foetus, during the second trimester. The short cord is primarily associated with foetal akinesis or maldevelopment of the central nervous system and is a significant early marker of developmental abnormalities including Down syndrome. Abnormal girth of the cord should make one of a patent urachus or an umbilical hernia suspicious and caution should be used before clamping. The importance of the twist is that, if not present, one should suspect congenital anomalies. The twist should be to the left or counter clockwise. The cord stump separates from the baby at about two
THE AVERAGE
part of newborn infant assessment.
-
REFERENCES ARAD I., EYAL F., FAINMESSER P. Umbilical care and cord separation. Arch Dis Child, 1981; 56: 887-88. DELEE J.B., GREENHILL J.P. The principles and practice of obstetrics. 1943; 579-89. Philadelphia: W.B. Sanders. ELHASSANI S.B. The umbilical cord: care, anomalies, and diseases. South Med J., 1984; 77: 730-36. ENTE G., PENZER P.H., KENIGSBERG K. Giant umbilical cord associated with patent urachus. Am J Dis Child, 1970; 120: 82-83. GLADSTONE I.M., CLAPPER L., THORPJ.W., WRIGHT D.I. Randomized study of six umbilical cord care regimens. Clin Peds, 1988; 27: 127-30. JONES B.L., BENIRSCHKE K. The umbilical cord twist; origin, direction, and relevance. Am J Obstet Gynecol, 1987; 157: 833-38. MILLER M.E., JONES M.C., SMITH D.W. Tension: the basis of umbilical cord growth. J Peds, 1982; 844. 101: MILLS J.L., HARLEY E.E., MOESSINGER A.C. Standards for measuring umbilical cord length. Placenta , 1983; 4: 423-26. MOESSINGER A.C., BLANC W.A., MARONE P.A., POLSEN D.C. Umbilical cord length as an index of foetal activity. Ped Res, 1982; 16: 109-112. MOESSINGER A.C., MILLS J.L., HARLEY E.E., RAMAKRISHNAN R., BERENDES M.D., BLANC W.A. Umbilical cord length in Down Syndrome. Am J Dis Child, 1986; 140: 1276-7. NAEYE R.L. Umbilical cord length: Clinical significance. J Peds, 1985; 107: 276-81. NEWMAN N.M. Use of providone-iodine in umbilical cord care. Clin Peds,
37. 28: 1989;
NOVACK A.H., MUELLER B., OCHS H. Umbilical cord separation in normal newborn. Am J Dis Child, 1988; 142: 220-23. OUDESLUYS-MURPHY A.M., EILER G.A.M., DEGROOT C.J. The time of the umbilical cord. 146: 387-89. separation Europ J Peds, 1987; PATEL D., DAWSON M., KALYANAM P., . Umbilical cord circumferet al ence at birth. Am J Dis Child, 1989; 143: 638-9. STRAUSS M.B., ED. Familiar Medical Quotations. 1968; pg318. Boston: Little, Brown
theof
& Co. ULLRICH K. BOHM N.
Early embryonal maldevelopment of the umbilical cord. Beitr Pathol, 1977; 160: 286-97. WILSON C.B., OCHS H.D., ALMQUIST J., DASSELL S., MAUSETH R., OCHS U.H. When is umbilical cord separation delayed? J Peds, 1985; 107: 292-94.
140
Downloaded from rsh.sagepub.com at Purdue University on January 16, 2015
The Umbilical Cord: Normal Parameters GERALD ENTE, M.D., F.R.S.H.
Attending, Department of Pediatrics Nassau County Medical Centre Director Neonatology, Central General Hospital, Plainview, NY 11803, PAUL H. PENZER, M.D. Attending, Department of Pediatrics Nassau
County Medical Centre,
INTRODUCTION
HE UMBILICAL cord is the lifeline of the t foetus. Prenatal survival is dependent on adefunction of the cord. After birth, this item with the placenta is discarded as medical waste, along which may account for the relative lack of knowledge and interest in the umbilical cord. Medical literature contains much information about pathological aspects of the cord such as infections, granulomas, and hernias. But the same body of literature has little quantification of many normal aspects of the cord such as length, circumference, twist, and time of separation. ’All other men, being born of woman, have a navel, by reason of the umbilical vessels inserted into it, which from the placenta carry nourishment to children in the womb of their mothers; but it could not be with our first parents. It cannot be believed that God gave them navels which would have been altogether useless.’ Bishop Richard Cumberland (1632-1718)
1 quate
, I
_ --
’
(Strauss,
196 )8
LENGTH >
performed studies on the umbilical cord. He concluded that the length of the umbilical cord was equal to the height of the newborn infant (Moessinger et al, 1982). During the next five centuries, this measurement has been refined somewhat. At delivery, the average length of the umbilical cbrd LEONARDO DA VINCI
is 50-60cm with 40cm as the lower limit of normal (Naeye, 1985). Short cords may cause traction during vaginal delivery, explaining why these are occasionally associated with delayed completion of the second stages of labour, or may cause placental abruptions, uterine inversions, cord herniations or even cord rupture (Naeye, 1985). Abnormally long cords increase the frequency of cord prolapse, true knots and coiling of the cord around foetal parts, all of which can produce foetal distress through cord compression. A cord must be long enough to reach from the placental site to the vulva, and if the placenta is located in the uterine fundus, a minimal length of 32cm is necessary. Although the mechanical consequences of short and long cords have become well known to physicians, recently researchers have begun to realize that the activity of the foetus and the tension on the cord itself is the basis of umbilical cord elongation (Miller et at, 1982). The tensile strength of the cord is from 8-15 pounds (3.6-6.8kg) (DeLee, 1943). Maldevelopment of the central nervous system is one of the factors that
U.S.A.
East Meadow, NY 11554, U. S.A.
limit foetal movements and subsequently cord length. Abnormal cord length, therefore, is an early marker for developmental abnormalities. The lengths of 35,779 neonatal cords were analyzed as part of the data from the Collaborative Study of the National Institute of Neurological Communicative Disorders and Stroke (Miller et al, 1982). The actual measurements showed a mean length of 57.4cm at 38 to 39 weeks gestation, and a mean length of 59.6cm at 40 to 41 weeks gestation with a standard deviation of ± 12.6cm (Mills et al, 1983). Cord lengths were positively correlated with maternal pregravid weight, height, socioeconomic status, pregnancy weight gain and foetal gender (Moessinger et al, 1981). There was no correlation with neonatal hemoglobin level, maternal hypertension, race, maternal mental retardation, maternal alcoholism, maternal narcotic addiction or maternal cigarette smoking. The cord grows mainly during the first two trimesters of pregnancy and reaches a mean of 32cm at 20 weeks gestation. At 34 weeks, the male cord averages in length, the female cord 51.75cm. At term the lengths are 60.25 and 57cm respectively. The cord grows very slowly after the 35th week and there is practically no growth after the 40th week (Moessinger
Perinatall and
53.75cm
et al, 1982) (Miller et al, 1982).
only 6% of term cords are below 40cm, length has been defined as a short cord (Naeye, 1985). Short cords were found to be associated with low Apgar scores, hypotonia, positive pressure rescuscitation at birth, and jitteriness in the neonatal period. Short cords increased the prognostic value of these neonatal markers for subsequent neurological abnormalities and low IQ scores by a factor of 2 or 3. This correlation proved to be independent of birth, weights and head circumference measurements (Miller et al, 1982; Naeye, 1985). Cords as short as 6.7cm and as long as 198cm have been cited (DeLee, 1943), but these lengths are rare. Because Down syndrome is associated with hypotonicity and reduced foetal activity, and, as has been stated before, foetal motor activity and tension do influence cord growth, newborns with Down syndrome have significantly shorter umbilical cords. A study of 21 Down neonates compared to matched controls showed significantly shorter cords (mean of 45cm compared to controls of 57.3cm (Moessinger, 1986). The Down syndrome cords were 12.5cm (1 standard deviation) shorter than the normals. Clearly, the presence of such Because below this
a
short cord in itself is not
138
Downloaded from rsh.sagepub.com at Purdue University on January 16, 2015
diagnostic
of Down
syndrome nor is the presence of a long cord exclusive of the diagnosis. However, this is another soft physical sign which may be considered in the clinical diagnosis of Down syndrome. Ulrich & Bohm described ’the missing cord syndrome’, or ’dysplasia umbilical-foetalis’ (Ullrich, 1977). This condition is a major malformation complex consisting of maldevelopment of cord, defect of the abdominal wall and other severe lethal congenital anomalies. This defect develops at the end of the third embryonic week during the 7mm stage. The foetus is attached to the placenta through an umbilical hernia. Measurement of cord length at birth, at one time a
standard obstetrical ritual, represents an index of foetal activity, providing that the foetus was allowed adequate space for movement. The physical examination of any newborn includes measurements of body weight, body length and head circumference. Significant deviations from normal cord length suggest selective pathological processes. The quantification of observable measurements of the cord is simple, consumes little time and is value in assessing the newborn. This measuref greatshould be reinstated as one of the routine ewborn measurements which are presently recorded.
ent
CIRCUMFERENCE WE PUBLISHED a paper in 1970 (Ente et al, 1970) entitled ’Giant umbilical cord associated with patent urachus’. We realized that the diameter was unusually large (5cm), but had no data for comparison. Quantification of normal umbilical cords based on a study of 191 full term newborn infants was subsequently reported (Patel et al, 1989). The mean umbilical cord circumference measured at day 1 at its attachment to the umbilicus was 3.77±0.73cm. This mean cord circumference increased with increased birth weight, chest circumference and abdominal circumference. The authors pointed out that an unusually large cord should raise suspicion of a hernia and that the baby should be closely examined by a physician before the cord is
clamped. Although the factors regulating the circumferential growth of the umbilical cord are unknown, Patel and olleagues postulated that ’factors that regulate the z
of the foetus in the growth the umbilical cord’. In the
influence the size of of cord gigantism associated with patent urachus (Ente et al, 1970), it was postulated that retrograde flow of hyperosmolar urine increased the mass of the mucoid connective tissue (Whartons jelly) surrounding the vessels traversing the cord. At term, the average diameter of the cord is 1-2cm (Elhassani, 1984). uterus
case
TWIST
umbilical vein is longer than the umbilical arteries and the arteries are longer than the cord itself, twisting of the vessels occurs. The vein is twisted around the arteries which themselves are twisted within the cord. This spiral action of the cord vessels is well known. The twist, as well as the length at birth depends on foetal activity. Jones and Benirschke collected data on 2334 cords and recorded the direction of the twist. Only five percent had no twist at all. Left twist outnumbered right twist by 7:1, which is the same ratio as the predominance of right handedness over left handedness in the general population (Jones, 1987). BECAUSE THE
(1987)
There was, however, no correlation between the direction of the twist and handedness of the mother or the child. They did show that 37% of infants with a single umbilical artery had an associated major structural abnormality, a multiple malformation syndrome, or foetal death. They also found that an increased incidence of absent twist is independent of hemodymanic forces in the cord itself. The increased incidence of absent twist among intrauterine foetal deaths and twins suggests that decreased foetal movements can impede the forces that lead to normal twisting. Absence of the twist may be associated with a poor
prognosis (Jones, 1987). TIME OF SEPARATION of separation of the umbilical remnant from the baby is partially dependent on microbial factors operating at the site. The precise timing of cord separation is probably the result of a complex interaction of many factors, which include drying, necrosis, collagenase activity and granulocyte activity. Leucocyte dysfunction and recurrent infections may be associated with delayed cord separation. Leucocyte dysfunction may be secondary to defects in chemotaxis, hypomobility, diminished oxidative response, failure of adherence, a deficiency of a high molecular glycoprotein or a primary defect of a contractible protein. Premature birth is yet another factor associated with dysfunctional leucocytes. The method of delivery also affects leucocyte function (Oudesluys-Murphy et al, 1987). Cord separation beyond 21 days is considered ’delayed’. This should serve to warn the physician of the possibility of leucocyte dysfunction, which is often THE TIME
accompanied by recurrent life-threatening infections (Oudesluys-Murphy et al, 1987; Wilson et al, 1985). A common question asked by new mothers is, ’when will the cord fall off?’. A medically insignificant delay in the separation of the umbilical stump may be a genuine cause of maternal concern. Such concern can be prevented if a proper explanation is given along with proper anticipatory guidance. In a study of 911 infants, Oudesluys-Murphy and colleagues (1987) found a mean time of separation 7.4±3.3 days (range 1-29 days). The authors discussed several perinatal factors that affected the time of separation. Separation was delayed in the following conditions: when antibiotics were administered to the neonate; when the infant was born when delivery was by Caesarian section or when the infant had a low birth weight. The cord separated slightly earlier in female than in male infants. For this study, cord care was limited only to dry sterile gauze dressing. The administration of parenteral antibiotics delayed separation by three days. Caesarian section delivery delayed the separation by two days. The cords of males separated on an average of one half day later than those of females. Novack et al, (1988) further found that hyperbilirubinemia was statistically associated with later separation.
prematurely;
The use of topical antibacterial agents may help to explain the two fold increase in the time of cord separation in most nurseries in the developed countries of the world. Several good clinical studies look to this point. Six different methods of umbilical cord care were compared by Gladstone and colleagues (1988). The six methods included: (1) TD/TD triple dye once TD/AL daily until cord separation);
(2)
applied (triple dye
139
Downloaded from rsh.sagepub.com at Purdue University on January 16, 2015
applied once then alcohol applied daily until cord separation); (3) TD (triple dye applied once, with no further antimicrobial treatment); (4) POV ( rovidoneiodine supplied daily until cord (5) SIL (silver sulfadiazine applied daily until cord separation); and (6) BAC (bacitracin ointment applied daily until cord separation). The results are listed in Table I and
weeks of age at present in the era of triple a
large vanability due to multiple factors.
dye care with
separation ;
equally effective for infection control in all groups, but with differing times of cord separation. are
CONCLUSION DESPITE THE
insignificance of the umbilicus in adults, the plays a major role in survival and
umbilical cord
of the foetus in utero. The cord is a viable development index of foetal Much information can be
activity. by examining this structure, simply by visual inspection and measurement. We are urging the observation and recording of these measurements as learned
Newman (1989) in a letter warned that the use of 2% iodine solutions interfered with congenital hypothyroidism screening by suppression of thyroid function. Several other studies have confirmed that with any of the varied modern cord care regimens, the mean time of cord separation is approximately two weeks ± 1 week, with a range of 3-67 days (Novack et al, 1988; Wilson et al, 1985; Arad et al, 1981). In summary, dry cord care has a mean time of separation of 7 days. Dry cord care is, however, not considered safe today. The use of antibacterial agents prolongs the time before separation by another 1-2 weeks. The use of any of the standard cord care regimens are effective for infection control.
SUMMARY See Table II
length of the umbilical cord is 50-60cm in the normal full term newborn infant. The length of the cord is an index of foetal activity and is dependent on the tension caused by the freely movmg foetus, during the second trimester. The short cord is primarily associated with foetal akinesis or maldevelopment of the central nervous system and is a significant early marker of developmental abnormalities including Down syndrome. Abnormal girth of the cord should make one of a patent urachus or an umbilical hernia suspicious and caution should be used before clamping. The importance of the twist is that, if not present, one should suspect congenital anomalies. The twist should be to the left or counter clockwise. The cord stump separates from the baby at about two
THE AVERAGE
part of newborn infant assessment.
-
REFERENCES ARAD I., EYAL F., FAINMESSER P. Umbilical care and cord separation. Arch Dis Child, 1981; 56: 887-88. DELEE J.B., GREENHILL J.P. The principles and practice of obstetrics. 1943; 579-89. Philadelphia: W.B. Sanders. ELHASSANI S.B. The umbilical cord: care, anomalies, and diseases. South Med J., 1984; 77: 730-36. ENTE G., PENZER P.H., KENIGSBERG K. Giant umbilical cord associated with patent urachus. Am J Dis Child, 1970; 120: 82-83. GLADSTONE I.M., CLAPPER L., THORPJ.W., WRIGHT D.I. Randomized study of six umbilical cord care regimens. Clin Peds, 1988; 27: 127-30. JONES B.L., BENIRSCHKE K. The umbilical cord twist; origin, direction, and relevance. Am J Obstet Gynecol, 1987; 157: 833-38. MILLER M.E., JONES M.C., SMITH D.W. Tension: the basis of umbilical cord growth. J Peds, 1982; 844. 101: MILLS J.L., HARLEY E.E., MOESSINGER A.C. Standards for measuring umbilical cord length. Placenta , 1983; 4: 423-26. MOESSINGER A.C., BLANC W.A., MARONE P.A., POLSEN D.C. Umbilical cord length as an index of foetal activity. Ped Res, 1982; 16: 109-112. MOESSINGER A.C., MILLS J.L., HARLEY E.E., RAMAKRISHNAN R., BERENDES M.D., BLANC W.A. Umbilical cord length in Down Syndrome. Am J Dis Child, 1986; 140: 1276-7. NAEYE R.L. Umbilical cord length: Clinical significance. J Peds, 1985; 107: 276-81. NEWMAN N.M. Use of providone-iodine in umbilical cord care. Clin Peds,
37. 28: 1989;
NOVACK A.H., MUELLER B., OCHS H. Umbilical cord separation in normal newborn. Am J Dis Child, 1988; 142: 220-23. OUDESLUYS-MURPHY A.M., EILER G.A.M., DEGROOT C.J. The time of the umbilical cord. 146: 387-89. separation Europ J Peds, 1987; PATEL D., DAWSON M., KALYANAM P., . Umbilical cord circumferet al ence at birth. Am J Dis Child, 1989; 143: 638-9. STRAUSS M.B., ED. Familiar Medical Quotations. 1968; pg318. Boston: Little, Brown
theof
& Co. ULLRICH K. BOHM N.
Early embryonal maldevelopment of the umbilical cord. Beitr Pathol, 1977; 160: 286-97. WILSON C.B., OCHS H.D., ALMQUIST J., DASSELL S., MAUSETH R., OCHS U.H. When is umbilical cord separation delayed? J Peds, 1985; 107: 292-94.
140
Downloaded from rsh.sagepub.com at Purdue University on January 16, 2015
