In 1986 I had embarked upon a career in obstetrics and gynaecology. Luckily for me, I was working with an academic who could think laterally and stimulate a young obstetrician to think beyond the conventional schools of thought. At the time, ‘active management’ was de rigueur in most maternity units. It was during this period that I reviewed the paper by Cardozo et al. (Br J Obstet Gynaecol 1982;89:33–8) for a Journal Club. The concept was simple; observe the rate of cervical dilatation and try to make a diagnosis of the type of labour dysfunction on the basis of cervimetric progress. The success in the correction of the labour pattern using oxytocin was then observed and labour and neonatal outcomes were reported. This was one of the first attempts to classify the labour aberrations into groups and monitor the effects of treatment.
The cases that most intrigued me were those that that did not respond to oxytocin, particularly those cases of primary dysfunctional labour. The 10% that failed to respond had a particularly poor outcome. It had occurred to us that the resistance arising from the cervix could not only affect labour progress but also result in the generation of higher intrauterine pressures (from Laplace's Law) and cause fetal distress. This led to a series of investigations, starting with a study to measure the intrauterine pressure and real-time cervical dilatation during labour. This study (Oláh et al. Br J Obstet Gynaecol 1993;100:635–40; Oláh et al. Br J Obstet Gynaecol 1994;101:341–3) showed that the cervix not only responds differently to uterine activity in the latent phase compared with the active phase of labour, but also that the uterine pressure generated is a direct reflection of uterine wall tension, which is greater where the cervix is either contracting (the latent phase of labour) or of firm consistency. These high pressures then lead to decreased placental perfusion, fetal distress and, because of its association with an unfavourable cervix, failure to progress.
The other studies that led on from that work, such as a magnetic resonance imaging assessment of the cervix, electromyogram studies and eventually assessment of the inflammatory cytokine response around the cervix and lower segment of the uterus, have led to the theory of ‘synchronous maturation’, in which the collagen of the cervix and membranes of the lower uterine pole are degraded in spontaneous labour (Oláh and Neilson Br J Obstet Gynaecol 1994;101:1–3), and combined with the onset of contractions will result in low-risk labour. The membranes are not ‘forced’ to rupture, they are ‘biochemically punctured’. The combined body of work entitled An Analysis of the Pathophysiology of Abnormal Patterns of Cervical Dilatation in Labour was awarded the RCOG Harold Malkin Prize, 1992/3.
Although I continue to have an academic interest in obstetrics, I will never forget the clinical studies that initiated my path of research. The principles of pressure generation within the uterus and the effect that the cervix plays in this and in labour progress aids the understanding of the management of preterm labour, preterm prelabour rupture of membranes and abnormal labour patterns. The cervix truly is an enigmatic and amazing structure.