Uterine Tachysystole, Hypertonus and Hyperstimulation: An Urgent Need to get the Definitions Right to Avoid Intrapartum Hypoxic-Ischemic Brain Injury

Abstract

Onset of labour is due to the hormonal changes initiated by the hypo-thalamo-pituitary axis followed by local changes in the chorio-amnion that result in the production of prostaglandins (PGs). Prostaglandins cause softening and effacement of the cervix and uterine contractions that are key elements for the onset and progress of labour. Uterine contractions have four important parameters: the frequency, strength, duration, and the basal “resting” tone, and if any of these parameters are excessive, a reduction in fetal oxygenation may occur. It is important to understand that any increase in uterine activity (frequency, strength, duration or the basal “resting” tone) can affect the utero-placental oxygenation and the patency of the blood vessels within the umbilical cord. Any disturbance in fetal oxygenation secondary to an increase in the frequency, duration and strength or the basal tone of the uterine contractions sufficient to cause fetal hypoxia can cause changes in the fetal heart rate patterns. There is a wide variation in current National and International Guidelines on what constitutes excessive uterine activity, and most guidelines do not consider the duration, strength or increased basal tone in their definition of uterine hyperstimulation. This may lead to the failure of recognition of an ongoing excessive uterine activity leading to poor maternal and perinatal outcomes.