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The human umbilical cord - Page 3 - Discussion

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Early published studies would suggest that no significant harm results from umbilical cord complications. (25-32) More recently, McLennan et al. noted, in a study of 1115 vaginal deliveries, that no clinical indicators warned of stillbirth risk from umbilical cord complications. (33) Our impression suggests that fetal hiccups may be a clinical indicator of umbilical cord compression. (34) Also noticed was a consistent report by the umbilical cord complication group of decreased fetal movement and fetal heart rate umbilical cord compression patters.(35) A retrospective review of 706 consecutive deliveries in a community hospital reported no poor outcomes in the group with umbilical cord complications.(36)

Larson et al. retrospectively reviewed singleton, vertex term cases with multiple nuchal loops and noticed increased meconium and abnormal fetal heart rate patterns.(37) Our experience was negative for meconium and may relate to delivery by LMP due date.

Torsion was not recognised in these studies.(38,39) The concept of torsion is an integral part of how nuchal cords and true knots are formed. Another discrepancy in previous studies is our observation of type A and type B nuchal cords.(40) These two groups much be studied separately, just as nuchal loops must be distinguished from nuchal cords. Crawford first recognised the need for a definition in 1962; he described a nuchal cord as 'the condition in which the umbilical cord is wound at least once around the neck of the fetus'.(41) This initial description was applied to a study which led to the following conclusion: '[the] nuchal cord is well recognised as being commonly associated with fetal distress and neonatal depression. It is all the more remarkable, therefore, that little work has been published to demonstrate the incidence of the condition, and to analyse its effects during labour and delivery'.

There are several consequences that can occur in fetuses with umbilical cord complications antenatally which resolve and in fetuses experiencing labour with umbilical cord complications. Other than stillbirth, recent studies have noted effects from umbilical cord complications which may include admission to a neonatal intensive care unit (but no longer hospital stays) when compared to controls.(42,43)

Neurological damage is thte worst morbidity outcome. Manning et al. reviewed 84 947 live births. (18) In a low-risk untested group, 4.74/1000 cases of cerebral palsy were noted compared to the tested high-risk group rate of 2/1000. Antenatal asphysia was considered a potentially avoidable cause of cerebral paulsy, specially when biophysical profile testing is considered. The PUCP observed no case of cerebral palsy in either the group with umbilical cord complications or the group without such complications. However, two cases of autism were suspicious for antenatal cord compression as noted by ultrasound and antenatal nonstress tests. Nelson and Grether retrospectively reviewed cases for cerebral palsy and noted an association with tight nuchal cords,(44) although antenatal ultrasound confirmation of tightness was not available. The cerebral palsy rate was 1/1500. Inaddition, 39% of children with unexplained cerebral palsy, 47% of children with quadriplegic cerebral palsy and 19% of control cases had umbilical cord encirclement.

Clapp et al. reviewed nuchal cord cases and their neurodevelopmental performance over a period of one year. They suggested a significant association with subclinical neurological deficits.(45) The Physicians' Insurance Association of America reviewed neurological damage claims and found a significant association with nuchal cords.(46) O'Callaghan et al. suggested that obstetric complications may play a role in nonfamilial schizophrenia.(47) Another study suggested that, in nonfamilial schizophrenia, umbilical cord knots and encirclement was related to development in 23.7% of cases.(48)

Aas the problem of umbilical cord complication is studied it may become possible to identify the fetus as risk and to manage the fetus successfully to avoid injury or stillbirth. Various authors have described the ability to identify umbilical cord complications with ultrasound as an initial step in its management.(49-54) Sherer and manning, in a recent editorial suggested that ultrasound should be considered at 36 weeks to scan for umbilical cord complications.(55)

Once born, the fetus, umbilical cord and placenta should be carefully examined for signs of sbtle compromise. Chorioangiosis (a placental change noted by hypervascularity) is one placental finding which may imply cord compressionleading to ischaemia.(56) Table 26.4 shows a review of cases of true knots at the Pregnancy Insitute which suggests that this may be a helpful indicator.

Table 26.5 lists the stillbirths associated with umbilical cord complications (>26 weeks) in 100 consecutive interviews from parents with stillbirth loss from umbilical cord complications. This unique list, which exceeds any known published data on stillbirth attributed to umbilical cord complications, suggests that the events may be occurring during maternal sleep.(57,58) These data are, of course, not part of a controlled study but the importance of presenting the information is the possibility that these patient insights may lead to clues to the aetiology of how these normal fetuses die. What is needed is a careful interview process with the family when an umbilical cord complication is encountered. It may be worthwhile exploring the possible link with stillbirth during maternal sleep. Good controlled research studies are required to determin whether umbilical cord complications are indeed an important contributor to perinatal morbidity and mortality.

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Table 26.4. Singleton term livebirths with trueknots and associated placental findings
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GP
Weight (g)
Gestational
age (weeks)
Apgar scores
Umbilical
length (cm)
Umbilical weight (g)
Placental
weight (g)
Placental
dimensions (cm)
Histology
UCC

32002
2948
37
8/8
38.1
24
493
16.1x2.7
Normal
K
10000
3260
39
4/6
64.0
54
600
22.0x1.6
Chorioangiosis
K
32002
3969
42
8/8
87.0
80
744
22.0x1.3
Immature
K/NC
54004
4167
43
8/9
62.3
51
638
22.0x2.7
Immature
K
21001
3402
41
8/9
65.5
94
648
20.0x3.6
Normal
K/BL
43003
3884
37
8/8
84.1
98
607
20.7x4.2
Normal
K/NC
54004
3317
40
8/9
81.7
80
645
21.4x3.4
Immature
K
21001
2742
40
8/9
70.5
42
602
20.0x2.4
Chorioangiosis
K/PR
21001
????
40
8/9
66.5
70
470
19.5x1.4
Immature
K
41111
2807
38
8/9
54.5
45
401
17.0x2.0
Normal
K
10000
3147
38
8/8
47.9
34
492
20.0x2.6
Normal
K2/NC2
53103
3856
38
8/9
47.3
59
532
21.7x3.7
Immature
K/NC
20010
3147
39
8/9
48.7
56
390
19.7x2.4
Normal
K2

BL=body loop, GP=gravity parity;Immature=immature placenta with enlarged hypervascular villi, K=true knot, NC=nuchal cord, P=prolapse cord, UCC=umbilical cord complication

Table 26.5
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