Third_Stage_of_Labour

Introduction The third stage of labour refers to the period from delivery of the baby to the delivery of the placenta. The placenta separates as a result of shearing force between the placental surface and the uterine wall in the presence of uterine muscular contraction. The major complication is post-partum haemorrhage. PPH is the most common cause of maternal death. The degree of blood loss associated with placental separation and delivery depends on the efficiency of uterine muscle contraction and the time taken to expel the placenta from the uterus. The length of the third stage of labour is usually 5-15 minutes. Physiology of the third stage of labour Placenta is an organ attached to the uterine wall throughout the pregnancy. It connects the developing foetus with uterine wall and supplies nutrients and oxygen to the foetus from the maternal blood. The placenta is expelled shortly after the delivery of the baby. Placental separation occurs due to the shearing placental surface with uterine contractions after the delivery of the baby. Gus of blood, lengthening of the umbilical cord and anterior cephalad movement of the uterus are considered the signs of placental separation. The fundus becomes firmer and globular. Placental explusion occurs due to a combination of events including spontaneous uterine contractions, downward pressure from the developing retro-placental haematoma and increase in intra-abdominal pressure. These changes in the uteroplacental region are divided into four phases: latent, contraction, detachment and expulsion phase.1 Latent phase determines the duration of the third stage of labour. It is characterised by beginning of periodic myometrial contractions. These contractions at the placental site continue throughout the contraction phase.1 Thickening of the placenta-site wall occurs towards the end of the latent phase which causes cessation of the basal blood flow between the placenta and myometrium, thus preventing excessive blood loss during placental separation. Thickening and reduction in the surface area of the placental-site wall during the detachment phase results in the shearing of the placental edge. The shearing begins at the lower segment of the placental margin and progresses along adjacent sites of the placental attachment like a 'wave of separation' travelling upwards. Therefore, the uppermost part of the placenta detaches last.2 The placenta is then expelled from the uterus. Oxytocin is a peptide hormone synthesized in the hypothalamus and released from the posterior pituitary. It is secreted naturally during labour. It plays a key role in third stage of labour. During pregnancy, the concentration of oxytocin receptors increases in myomterium by 100-200 folds. This leads to increased myomterial senstivity to circulating oxytocin levels during the later stages of pregnancy. After the delivery of the baby, there is natural surge of oxytocin. It leads to strong uterine contractions causing separation of the placenta from the uterine wall.3 Maternal blood volume increases by 50%, clotting factors increase and fibrinolytic activity decrease over the course of the pregnancy and since, there is constant blood flow to the placenta site even after the placenta is detached, another surge of oxytocin occurs contracting the uterus to clamp down on the detachment area followed by rapid clot formation and fibrin deposition, thereby preventing haemorrhage.4 The myometrium of the uterine wall is composed of smooth muscle cells arranged in longitudinal, transverse, oblique as well in criss cross manner with intervening blood vessels. This arrangement is referred to as ‘living ligatures’ and is the main mechanism in control of postpartum haemorrhage. Uterine contractions are a result of activation of the myometrium. It is characterised by increased expression of a series of contraction associated proteins (CAPs) and myometrial receptors for prostaglandins and oxytocin, activation of specific ion channels and increase in connexin-43, a key component of gap junctions. An increase in formation of gap junctions between adjacent myocytes leads to electrical synchromy within the myometrium and allows for effective co-ordinated contractions.5 These contractions are mediated by ATP-dependent binding of the myosin to actin. Prostaglandin and oxytocin binds to cell-specific surface receptors and promotes the opening of the ligand regulated calcium channels and release of calcium ions from the sarcoplasmic reticulum. As the calcium begin to enter the cell, drop in intracellular electronegativity occurs promoting opening of large number of voltage-regulated calcium channels producing a rapid movement of calcium ions into the cell. Calcium then binds to calmodulin to from calmodulin-calcium complex. This complex activates myosin light chain kinase and leads to phosphorylation of myosin light chains causing ATPase activity leading to sliding of myosin over the actin filaments causing myometrial contractions.6