As in Williams' time, obstetrical hemorrhage continues along with hypertension and infection to be one part of the infamous "triad" of maternal death causes. It also is a leading reason for admission of pregnant women to intensive care units (Chantry, 2015; Crozier, 2011; De Greve, 2016; Guntupalli, 2015). Hemorrhage was a direct cause of 11r.4 percent of 5367 pregnancy-related maternal deaths from 2006 to 2013 in the United States (Creanga, 2015, 2017). Similarly, 16 percent of1102 maternal deaths recorded in the Nationwide Inpatient Sample were caused by hemorrhage (Kuriya, 2016). In developing countries, hemorrhage's contribution is even more striking, and it is the single most important cause of maternal death worldwide (Gofman, 2016; Oladapo, 2016; Thomas, 2016). Despite these numbers, a declining maternal mortality rate from hemorrhage in the United States has been a seminal achievement. But, as discussed in Chapter 1 (p. 5), it 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 mLi min-flows through the intervillous space (Pates, 2010). his prodigious flow circulates through the spiral arteries, which average 120 in number. Also, recall that these vessels have no muscular layer because of their remodeling by trophoblasts, 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 large vessels. Compression is followed by clotting and obliteration of vessel lumens.
If, after delivery, the myometrium contracts vigorously, fatal hemorrhage from the placental implantation site is unlikely.
Importanty, an intact coagulation system is not necessary or postpartum hemostasis unless there are lacerations in the uterus, birth cana, or perineum. At the same time, however, fatal postpartum hemorrhage can result from uterine atony despite normal coagulation.
70 he blood volume of a pregnant D < 500 mL woman with normal pregnancy-induced hypervolemia usually rises by half, but individual increases range from 30 to 60
D 1000-1e500 mL percent, that is, 1500 ) • > 2500 mL average-sized woman (Pritchard, 1965).
) 40 The equation to calculate blood volume is shown in Table It is axiomatic ) ates, without any decrease in postpartum ..e hematocrit, blood loss at delivery that approaches the volume of blood that she added during pregnancy. Thus, if blood loss is less than the pregnancy-added vol ume, the hematocrit remains the same acutely and during the irst several days delivery delivery with hysterectomy postpartum. It then rises as nonpregnant
FIGURE 41-1 Blood loss associated with vaginal delivery, repeat cesarean delivery, and plasma volume normalizes during the repeat cesarean delivery plus hysterectomy. (Data from Pritchard, 1962.)