Causes of onset of labor: Hormonal and Mechanical Theories

Causes of onset of labor

The exactl cause of the onset of labor is still uncertain, but it appears to be multifactorial in origin, being combination of Hormonal and Mechanical factors. There is evidence that something triggers the fetal hypothalamus to produce releasing factors which stimulate the anterior pituitary gland to produce adrenoconticotrophic hormone (ACTH) which stimulate the fetal adrenal glands to secrete cortisol, this causes changes in the relative level of placental hormones, Oestrogen and Progesterone. Oxytocin is also released. This gives reason to some theories as to the causes of onset of labour.”

Hormonal theories:

Oxytoxin: A hormone produced from the posterior pituitarygland which the uterine muscle is very sensitive to. It is released in high dose at the end of pregnancy leading to contraction of the uterine muscle. Maybe as a result in progesterone: Oestrogen ratio, also the reduction in the level of oxytocinase in the blood stream makes the muscles more sensitive to oxytocin. Oestrogen facilitates the release of oxytocin. Oxytocin stimulates the release of protaglandins from the myometrium of the hormone.

Progesterone deprivation theory: During pregnancy,progesterone is secreted in high level which has a sedative

effect on the uterine muscle making it remain relaxed. As pregnancy advances the level of progesterone get reduced so the uterus becomes more active so that a diminished amount leads to onset of labor. Progesterone has opposite effect to that of oestrogen, making the myometrium less sensitive to stimuli.

Oestrogen Stimulation Theory: there is an opinion that therising level of oestrogen during the last few weeks of pregnancy results in the formation of oxytocic receptors in the uterine muscle cells. This makes the muscle respond more easily to stimuli or to oxytocin.

Protaglandins: Is found in high level in the amniotic fluidand blood stream during labour. They initiate uterine contraction. The rising level of oestrogen increases oxytocin receptors in the myometrium. Oxytocin stimulates the release of prostaglandin from the deciduas and membranes. The role played by this hormone is yet to be fully investigated but it is known to have oxytoxic effect on uterine muscles.

Foetal Endocrine Control: there is interaction between thefetal adrenal gland and the uterus. At term the fetal adrenal gland secret corticoid steroid which is believed to trigger the release of prostaglandin in the maternal decidua,a mechanism leading to labour. By stimulate the precosol to prostaglandin synthesized in the decidua at term.

Mechanical Theories:

Overdistension/Uterine stretch theory: During pregnancythe uterus is in pace with its content, but when it stretches to it’s maximum it starts to contract to expel it’s content . This evidence can be seen in multiple pregnancy and Polyhydramnios.

Increase contractibility:As the end of pregnancyapproaches the normal Baxton Hicks contractions becomes exaggerated as the uterus becomes more sensitive to stimuli.

Pressure of the Presenting part: On the cervical nerveendings is thought to stimulation nerve plexus (known as cervical ganglion) which result in secretion of oxytoxin by the Posterior Pituitary Gland (PTG). This gives the reason why labour is very fast with engaged head.

Circulatory Deprivation theory: Towards end of pregnancythe placental functions become inefficient thereby leading to reduction in circulatory nutrition and blood supply to the fetus.

Other conditions:

·              Hyperpyrexia

·              Strong Emotions

·              Cyanosis e.g. Eclampsia