Obstetrical hemorrhage continues along with hypertension and infections as one of the infamous “triad” of causes of maternal deaths in both developed and underdeveloped countries. It is a leading reason for admission of pregnant women to intensive care units (ICUs) (Crozier, 2011; Small, 2012; Zeeman, 2003; Zwart, 2008). Hemorrhage was a direct cause of nearly 13 percent of 4693 pregnancy-related maternal deaths in the United States documented by the Pregnancy Mortality Surveillance System of the Centers for Disease Control and Prevention (Berg, 2010). Similarly, Clark and coworkers (2008) reported that 12 percent of maternal deaths recorded in the Hospital Corporation of America database were caused by hemorrhage. In developing countries, its contribution is even more striking. Indeed, hemorrhage is the single most important cause of maternal death worldwide and is responsible for half of all postpartum deaths in developing countries (Lalonde, 2006; McCormick, 2002).
The decreasing maternal mortality rate from hemorrhage in this country has been a major achievement. Decreased deaths from hemorrhage have been a major contributor to the decrease in the maternal mortality rate during the 20th century—from approximately 1000 to only 10 per 100,000 births (Hoyert, 2007). But, as discussed in Chapter 1 (Maternal Mortality), probably half of maternal deaths are not reported, and at least a third are considered preventable. It thus seems unlikely that deaths from hemorrhage have reached an irreducible minimum.
Mechanisms of Normal Hemostasis
A major concept in understanding the pathophysiology and management of obstetrical hemorrhage is the mechanism by which hemostasis is achieved after normal delivery. Recall that near term an incredible amount of blood—at least 600 mL/min—flows through the intervillous space (Pates, 2010). As described in Chapter 5 (Maternal Circulation), this prodigious flow circulates through the spiral arteries, which average 120 in number. Also recall that these vessels have no muscular layer because of their endotrophoblastic remodeling, which creates a low-pressure system. With placental separation, these vessels at the implantation site are avulsed, and hemostasis is achieved first by myometrial contraction, which compresses this formidable number of relatively large vessels (Chap. 2, Cervix). Contractions are followed by clotting and obliteration of vessel lumens.
If after delivery, the myometrium within and adjacent to the denuded implantation site contracts vigorously, fatal hemorrhage from the placental implantation site is unlikely. Importantly, an intact coagulation system is not necessary for postpartum hemostasis unless there are lacerations in the uterus, birth canal, or perineum. At the same time, however, fatal postpartum hemorrhage can result from uterine atony despite normal coagulation. Adhered placental pieces or large blood clots that prevent effective myometrial contraction will serve to impair hemostasis at the implantation site.