Evaluation of the cervix by ultrasound for the prediction of preterm birth

In 2001 the United States incidence of preterm birth was 11.9%, the highest level observed in over 2 decades [1]. The incidence of preterm birth has not changed appreciably in over 20 years and its short- and long-term neonatal morbidities account for annual medical expenditures in excess of 5 billion dollars [2]. Thus, preterm-birth prevention is the, most important problem in obstetrics. Most preterm births are spontaneous and not indicated for maternal or fetal complications'[3]. Spontaneous preterm birth may best be characterized as a syndrome. The multiple underlying pathophysiologic events are poorly understood and may vary, not only among individual. patients, but also among successive pregnancies in the same woman. The three principal components of the preterm-birth syndrome are: decidual activation and loss of chorioamnionic integrity (premature rupture of membranes); myometrial activity (preterm labor); and premature cervical ripening (diminished cervical competence) [4]. Recognized inciting factors include intrauterine infection, inflammation, local or systemic hormonal effects, vascular disruption, fetal signals, and mechanical stressors. Genetic predisposition and lack of adequate host defenses may change the threshold for the clinical expression of these stimulants, while congenital defects in the uterus and cervix may also contribute to the process. These causative factors interact with the principal anatomic components of the syndrome through unpredictable pathways, which ultimately result in the pathophysiologic expression of spontaneous preterm birth. Investigations into the etiology and prevention of preterm birth have largely been focused on uterine activity and premature rupture of membranes. Recently research has been expanded to include the cervix and its underlying role in pathways to prematurity [5,6].