Asphyxia-related Risk Factors and Spastic Cerebral Palsy

Abstract & Commentary

By John C. Hobbins, MD, Professor and Chief of Obstetrics, University of Colorado Health Sciences Center, Denver, is Associate Editor for OB/GYN Clinical Alert.

Dr. Hobbins reports no financial relationship to this field of study.

Synopsis: There appears to be a strong relationship between placental infarcts and small-for-gestational age (SGA) with spastic cerebral palsy, and a possible link between the finding of a cord around the neck and this condition.

Source: Nielsen LF, et al. Asphyxia-related risk factors and their timing in spastic cerebral palsy. BJOG 2008;115:1518-1528.

This interesting study just surfaced in the British Journal of Obstetrics and Gynecology that addressed the relationship between spastic cerebral palsy (CP) and asphyxia-related causes. The authors searched the antepartum and peripartum records of women whose children were ultimately diagnosed to have spastic CP. They identified 271 children with this condition who were born in Denmark between 1982 and 1990, and then matched each one with 271 not having this condition who were born at the same time in gestation. Since the authors indicated they would be analyzing data separately for a potential infectious etiology for CP, they concentrated in this study on findings or perinatal events that would have the potential to cause fetal or neonatal asphyxia. These dependent variables were too numerous to list, but from my standpoint the authors seemed to cover all bases.

Along with some expected findings there were also some surprises. In the expected category, 9.4% of those with spastic CP had cord pH values below 7.0, compared with none of the controls. Placental abruption and placenta previa had no relationship to CP and, outside of a cord around the neck (CAN), other cord abnormalities were not seemingly associated with CP.

Now, the punch line! The strongest association with spastic quadriplegia in this study was the presence of placental infarction, as noted by visual post-delivery examination, which was 4-fold higher after controlling for prepartum factors and 11-fold higher after factoring out other intrapartum events. Another strongly associated factor was a SGA infant which, when combined with placental infarction, increased the risk of spastic CP by a whopping 16-fold.

The result that needs to be put into proper perspective was the relationship between CAN and spastic CP. Children with CP had an incidence of CAN of 17.4% vs 8.7% in control children. Also, although not statistically significant because of small numbers, there was a 4-fold greater chance of neonatal seizures in the control group when a CAN was found.


What can be learned from this study? First, an infarcted placenta, extensive enough to be seen by gross examination after delivery, could be a sign of spastic CP to surface later, with or without immediate neonatal signs, and this tendency increases substantially if the infant is SGA. This means to me that we should look very carefully for signs of placental compromise through Doppler waveform analysis of the umbilical arteries and the uterine arteries when the estimated fetal weight falls below the 10th percentile, or when there is a predisposition towards infarction, such as in thrombophilia, a history of previous SGA, or preeclampsia.

With CAN the answer obviously is not so clear. First, the incidence of CAN was quite low in the control group, which may have skewed the results. Second, the authors concentrated on a condition (spastic CP) that has a very low prevalence and then looked back for factors that may have been related to it. Although such a study is important scientifically, it does not help appreciably in deciding what to do prospectively when one runs across a finding (CAN) that is so common and, in general, has so little chance of causing trouble.

To put this conundrum into proper perspective, in one study involving 11,200 deliveries, 19.9% of infants were born with one loop of cord around the neck; 5.3% had two loops, and 1.3% had three loops — so the prevalence of this finding is very high.1 In another study looking at perinatal outcome, 118 infants born consecutively with CAN were matched with 233 controls.2 There were no differences in time of birth, need for Cesarean section, abnormal fetal heart rate patterns, Apgar scores, or length of neonatal stay. Another study listed in the references had similarly reassuring outcomes with CAN.3

So, what does one do when one inadvertently finds a CAN during a routine ultrasound examination? If you poll 5 different authors you will get five different answers. What is clear is that we have the potential to scare the heck out of the 1 in 5 patients in whom we find a CAN. For this reason, if we are apprising a patient of this finding, it should be couched generally in very reassuring terms. Variables that would suggest a greater chance of trouble would be a double or triple loop of CAN, one that is tight around the neck (one study suggests increased morbidity with this finding, while the above featured Danish study did not), or decreased perceived fetal movement.

A fetal non-stress test (NST) could detect significant cord impingement through the presence of variable decelerations, or chronic hypoxia through decreased beat-to-beat variability. A biophysical profile would provide even more information regarding the integrity of the CNS. However, perhaps the best indicator of early cord impingement is a notch in the systolic downslope of the umbilical artery waveform, as described by Abuhamad in a publication on velamentous insertions of the cord.4

Until new information surfaces, I would do an NST or biophysical profile only on those patients in whom two or more loops of cord were noted around the neck. Also, at the time the CAN is found with ultrasound, one could simply move quickly to the umbilical artery to look for a notch in the Doppler waveform. If the studies are normal, then these patients can be reassured and advised simply to report any major decrease in fetal movement, which, in turn, would trigger another evaluation of the fetus. Although this approach will not completely preclude a future adverse event, it would appreciably diminish the chances of a later disaster, while lessening patient anxiety levels by many angst units.


  1. Sornes T. Umbilical cord encirclement and fetal growth restriction. Obstet Gynecol 1995;86:725-728.
  2. Gonzalez-Quintero VH, et al. Outcomes of pregnancies with sonographically detected nuchal cords remote from delivery. J Ultrasound Med 2004;23:43-47.
  3. Peregrine E, et al. Ultrasound detection of nuchal cord prior to labor induction and the risk of Cesarean section. Ultrasound Obstet Gynecol 2005;25:160-164.
  4. Abuhamad A, et al. Umbilical artery Doppler waveform notching: Is it a marker for cord and placental abnormalities? J Ultrasound Med 2002;21:857-860.