Medical Hypotheses (1989) 29.5-6 0 Longman Group UK Ltd 1989

Hasty Clamping of the Umbilical Cord May Initiate Neonatal lntraventricular Hemorrhage

G. J. HOFMEYR, P. J. M. BEX, R. SKAPINKER and T. DELAHUNT

Department of Obstetrics and Gynaecology, University of the Witwatersrand Medical School, Jubilee Road, Parktown 2193, South Africa.

Abstract - lntraventricular hemorrhage may result from surges in systemic vascular pressure, particularly when cerebral blood flow autoregulation is impaired by asphyxia, and the germinal matrix vasculature is immature. We postulate that early interruption of umbilical arterial blood flow may cause a rise in blood pressure sufficient to contribute to the development of intraventricular hemorrhage in susceptible neonates.

tntrur~nltric,ular Hemorrhage (NH) Perinatal IVH is an important marker for subse- quent mortality and neurological morbidity in preterm infants (1). The following factors are thought to bc important in the genesis of IVH: immaturity of the germinal matrix vasculature (2); fluctuation of systemic blood pressure, related to respiratory distress syndrome, pncu- mothorax and transfusions (3); and impairment of cerebral blood flow autoregulation, related to asphyxia (4) and resulting in fluctuation in cerebral blood flow (5). Most hemorrhages are evident hy 24 hours of age (1, 6). Hemorrhage of early onset is most closely related to obstetric events (6) and has the greatest chance of progression and the highest mortality (7).

Studies of prophylactic neonatal pharmacolo- gical interventions such as administration of tranexamic acid. ethamsylate, vitamin E, indo- methacin, pancuronium and phenobarbital have for the most part been inconclusive or contra-

dictory (1). Antenatal administration to the mother of phenobarbital (8. 9) and vitamin ICI (10) have been reported to be protective.

Most studies of mechanical obstetric intcrven- tions such as cesarcan section, episiotomy and forceps delivery have been retrospective and shown little effect or contradictory results (6. 11. 12).

The timing of umbilical cord clamping has a profound influence on neonatal hemodynamics. Delayed clamping results in the transfusion to the term nconatc held at the level of the uterus of, on avcragc, 80 ml placental blood within 60 seconds and I60 ml within 3-5 minutes (13). Systolic aortic pressure during the first 5 minutes of life is increased from 60 to 80 mmHg ( Id). Placental transfusion is somewhat slower in preterm infants (15). Early clamping of the umbilical cord, which accommodates some 4.5

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6 MEDICAL HYPOTHESES

percent of the combined ventricular output during fetal life (16), may cause an abrupt surge in arterial pressure, particularly if the compen- satory baroreceptor-mediated bradycardic response is impaired by asphyxia.

A theoretical case can thus be made to impli- cate either early or delayed cord clamping in the pathogenesis of IVH. The possible harmful effect of placental transfusion when cord clamping is delayed might be reduced by keeping the neonate above the level of the uterus, on the mother’s abdomen or held in her arms. There is at present no consensus as to the optimal time to clamp the umbilical cord (14).

Hypothesis

We postulate that in the presence of asphyxia- relatad impairment of systemic blood pressure control and cerebral blood flow autoregulation, early clamping of the umbilical cord may result in transmission to the cerebral vasculature of blood pressure surges sufficient to initiate the process of intraventricular hemorrhage.

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