“Third stage indeed is the unforgiving stage of labor, and in it there lurks more unheralded treachery than in both the other stages combined. The normal case can, within a minute, become abnormal and successful delivery can turn swiftly to disaster.”
Despite the above fact third stage of labor is relatively little thought or little teaching seems to be devoted to the third stage of labor compared with that given to the first and second stages.
DEFINITION
The third stage of labor commences with the completed delivery of the fetus and ends with the completed delivery of the placenta and its attached membranes.1 The risk of complications continues for some period after delivery of the placenta. For this reason, many authorities have advocated a so-called fourth stage of labor, which begins with the delivery of the placenta and lasts for an arbitrary period afterward for one to four hours.
SIGNIFICANCE
Significant complications can occur in this period. The most common is postpartum hemorrhage (PPH). Severe PPH, retained placenta, and uterine inversion may require emergency management and cause significant morbidity and mortality.
Duration
The most commonly accepted duration is 1 hour; however, periods as long as 4 hours have been suggested. The length of the third stage itself is usually 5–15 minutes. The absolute time limit for delivery of the placenta, without evidence of significant bleeding, remains unclear. Periods ranging from 30–60 minutes have been suggested. The third stage of labor is diagnosed as prolonged if not completed within 30 minutes of the birth of the baby with active management and 60 minutes with physiological management.1
Physiology of Third Stage of Labor
The physiology of the third stage can only be realistically considered in relation to some of the elements which occur in the preceding months of pregnancy. The first significant consideration is the changes in hemodynamics as the pregnancy progresses. The maternal blood volume increases by a factor of about 50%. There is disproportionate increase in the plasma volume over the RBC volume resulting in physiological fall in both Hb and hematocrit values. The evolutionary physiology behind this change revolves around the fact that the uteroplacental unit has low resistance perfusion demands which are better served by a high circulating blood volume and it also provides a buffer for the inevitable blood loss that occurs at the time of delivery.2 The high progesterone levels also reduce the general vascular tone thereby increase venous pooling (Fig. 1.1).
Along with these hemodynamic changes number of physiological changes occur in coagulation system in pregnancy. There is seen to be a sharp increase in the quantity of most of the clotting factors in the blood and a functional decrease in the fibrinolytic activity. Platelet levels are observed to fall. Relevance of these considerations is clear when we consider that one of the main hazards facing the mother during the third stage of labor is that of hemorrhage,3 and the changes in the hemodynamics are largely germinal to this fact.
Fig. 1.1: Physiology of labor. (A) Placenta and fetus before birth; (B) Uterus and placenta after birth
The other major factor in our considerations is the efficiency of the hemostasis produced by the uterine contraction in the third stage of labor. The prime agent in the immediate control of blood loss after separation of the placenta is uterine contraction which can exert a physical pressure on the arterioles to reduce immediate blood loss. Clot formation and the resultant fibrin deposition, although they occur rapidly, only become functional after the coagulation cascade has triggered off and progressed. Once operative, however, this secondary mechanism becomes dominant in securing hemostasis in the days following delivery (Fig. 1.2).4
During parturition, uterine contractions start from fundus of the uterus and spread downwords. For 10 to 45 minutes after birth of the baby, the uterus continues to contract to a smaller and smaller size, which causes a shearing effect between the walls of the uterus and the placenta, thus, separating the placenta from its implantation site.5 This is thought to be mainly a physical phenomenon as the uterus is capable of contraction, whereas the placenta (being devoid of muscular tissue) is not. The characteristic of the myometrium which is unique in the animal kingdom, and this is the ability of the myometrial fibres to maintain its shortened length after each contraction and then to be able to contract further with subsequent contractions. This characteristic results in a progressive and (normally) fairly rapid reduction in the overall surface area of the placental site.6 By this mechanism, the placenta is undermined, detached, and propelled into the lower uterine segment.
6Placental separation also occurs by virtue of the physical separation engendered by the formation of a subplacental hematoma. This is brought about by the dual mechanisms of venous occlusion and vascular rupture of the arterioles and capillaries in the placental bed and is secondary to the uterine contractions.7 The physiology of the normal control of this phenomenon is both unique and complex. The structure of the uterine side of the placental bed is a lattice work of arterioles that spiral around and inbetween the meshwork of interlacing and interlocking myometrial fibrils. As the myometrial fibers progressively shorten, they effectively actively constrict the arterioles by kinking them. It is referred to as living ligature and physiological sutures of uterus (Fig. 1.3).
Several agents cause uterine contraction. The sensitivity of the myometrium to oxytocin, a nonapeptide produced in the posterior pituitary, increases greatly in late pregnancy and even more so during labor. Locally produced and exogenous prostaglandins, especially those of the F series, also cause myometrial contraction. Synthetic ergot alkaloids cause strong tetanic contraction of the uterus.
Agents that cause uterine relaxation can lead to dangerous bleeding following delivery. Beta-sympathomimetics (e.g. ritodrine, terbutaline, salbutamol) relax the uterus via beta-2 stimulation. Nonsteroidal anti-inflammatory agents have a dual action, with both antiprostaglandin and antiplatelet activity. The former effect makes them useful for treating dysmenorrhea and afterpains, both due to uterine cramping; however, in the postpartum period and especially following PPH, strong uterine contraction is desired. Calcium antagonists, such as nifedipine and, to a lesser extent, magnesium sulfate, may also inhibit uterine contractions. Nitroglycerin and some inhalational anesthetic agents also decrease uterine contractility. All women who deliver are at risk of complications in the third stage of labor.
7These complications include PPH, retained placenta, and uterine inversion. Others include conditions that commonly manifest for the first time during the third stage (e.g. placenta accreta and its variants). Most complications of the third stage occur in low-risk women; therefore, caregivers and institutions must have management strategies in place to deal with these problems promptly when they arise.
Signs of Placental Separation
The fundus rises and becomes smaller, harder, and rounder. There may be a small gush of blood from the vagina and the cord outside the vulva lengthens. When these have occurred, the placenta is expelled by grasping the fundus uteri in the hollow of the hand, and as soon as it is felt to harden, strong and firm pressure is made upon it, downwards and backwards, in the axis of the pelvic brim.8
Management of Third Stage of Labor
The controversy surrounding third-stage management exists between authorities who advocate the expectant or physiological approach and those who advocate the active approach.
Proponents of physiological management argue that the natural processes outlined above promote normal separation and delivery of the placenta and lead to fewer complications. If PPH develops, it may be effectively managed with available techniques and drugs. Proponents express concern that active management increases PPH and uterine inversion rates due to cord traction and increases the risk of retained placenta due to entrapment caused by uterotonic agents. Delivery of the placenta occurs by uterine contractions and maternal expulsive efforts, and cord traction is prohibited. Concern also exists regarding the case of an undiagnosed second twin, if uterotonics are routinely used at the time of delivery.
Advocates of active management argue that administering prophylactic uterotonic agents promotes strong uterine contractions and leads to faster retraction and placental delivery. This decreases the amount of maternal blood loss and the rate of PPH. They also argue that the more effective uterine activity leads to a reduction in the incidence of retained placenta.
Gentle cord traction is only applied when the uterus is well contracted, and the uterus is manually controlled above the level of the symphysis with countertraction (Brandt-Andrews maneuver). This maneuver is referred to as controlled cord traction (CCT). Cord traction must never be applied in the absence of countertraction and is applied in the axis of the birth canal. Advocates point out that an undiagnosed second twin is rare problem and that clinical assessment in labor and following delivery of the first baby can establish the diagnosis before uterotonic administration.7
Several large, randomized, controlled trials have addressed the question of whether physiological management or active management is 8 preferable. These trials have consistently shown that active management leads to several benefits compared to physiological management. These trials use 1 of 3 uterotonic agents: ergonovine, oxytocin, or syntometrine, (a combination of ergometrine and oxytocin).
NICE clinical guidelines for intrapartum care suggest following guidelines for management of labor:
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Active management of the third stage is recommended, which includes the use oxytocin (10 international units [IU] by intramuscular injection), followed by early clamping and cutting of the cord and controlled cord traction
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Women should be informed that active management of the third stage reduces the risk of maternal hemorrhage and shortens the third stage
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Women at low risk of postpartum hemorrhage who request physiological management of the third stage should be supported in their choice
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Changing from physiological management to active management of the third stage is indicated in the case of:
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Hemorrhage
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Failure to deliver the placenta within 1 hour
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The woman's desire to artificially shorten the third stage of labour.
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Pulling the cord or palpating the uterus should only be carried out after administration of oxytocin as part of active management
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In the third stage of labor neither umbilical oxytocin infusion nor prostaglandins should be used routinely.
Complications of Third Stage of Labor
Most dreaded complication is postpartum hemorrhage. The others include retained placenta, placenta accrete, and uterine inversion. These complications and their management have been discussed in this book in the other chapters. Caretakers must know the basic physiology and basic management of third stage of labor to diagnose and manage the complications that may arise in timely and systematic way.
REFERENCES
- NICE clinical guideline 55 - intrapartum care, 2007.
- Dansereau J, Joshi A K, Helewa M E, et al. Double-blind comparison of carbetocin versus oxytocin in prevention of uterine atony after cesarean section. Am J Obstet Gynecol 1999; 180(3 Pt 1): 670–6.
- Soltani H, Dickinson F, Symonds I. Placental cord drainage after spontaneous vaginal delivery as part of the management of the third stage of labour. Cochrane Database Syst Rev 2005; CD004665.
- Guyton and Hall- Textbook of Physiology.
- Sanborn B M, C Yue, W Wang, KL Dodge. G protein signalling pathways in myometrium: affecting the balance between contraction and relaxation Rev. Reprod 1998; 3: 196–205.
- Sharma J B, Pundir P, Malhotra M. Evaluation of placental drainage as a method of placental delivery in vaginal deliveries. Arch Gynecol Obstet 2005; 271 (4): 343–5.
- Wilson T Roddie. Blood loss during third stage of labour. Ulster Med J 1956; 25 (1): 23–6.