Abstract

SUMMARY: In a controlled experiment, term lambs born of caesarean sacrifice, normal or artificially prolonged birth were examined at autopsy to determine the role of vaginal birth in the pathogenesis of presumed birth injury to the fetal CNS characterised by subdural and extradural haemorrhage, subarachnoid haemorrhage and congestion, and blood‐stained cerebrospinal fluid in and around the cranial and spinal meninges of lambs dying during or within 7 days of birth. Additional material, comprising near‐term fetuses, was examined at an abattoir to determine the prevalence of meningeal lesions in unborn fetuses.Mean durations of parturition in the caesarean‐born controls, natural and artifically‐delayed vaginal deliveries were 0 min., 56 min., and 185 min. respectively. The experimental treatments influenced the frequency of cranial lesions only. Single lambs were more prone to injury than twin lambs. The incidence of affected lambs in delayed births was 8.9 times higher than that in caesarean births and 1.7 times higher than that in normal births. Within the delayed group the incidence of affected single lambs in the subgroups was similar despite wide differences in the nature of parturition. It was concluded that the induced lesions resembled those associated with the perinatal mortality of livestock and infants and that pathogenetic variables included interactions between the duration and the vigour of the birth process. Repeated stretching and relaxation of the rostral fetal cranio‐vertebral skeleton during Stage 2 labour may be involved in pathogenesis. At that stage of delivery, the fetus is relatively fixed because the chest and shoulders have firmly engaged the pelvic inlet, while the head and neck are exposed to the lower pressure of the vagina and atmosphere. Intrafetal pressure is hydrostatically continuous with intrauterine pressure which is higher than atmospheric pressure. Rises in intrauterine pressure due to labour are probably transmitted hydraululically to the fetal cranio‐vertebral canal leading to stretching of the head and neck. Because the fetal CNS is firmly anchored to the cranio‐vertebral skeleton such movement may set up the shearing action necessary to rupture small vessels in the cranial and cervical meninges.

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