is intravascular activation of clotting. Abruption is the most common cause of clinically profound consumptive coagulop athy in obstetrics-and indeed, probably in all of medicine (Cunningham, 2015).
An important consequence of intravascular coagulation is the activation of plasminogen to plasmin, which lyses ibrin microemboli to maintain microcirculatory patency. With placental abruption severe enough to kill the fetus, there are always pathological levels of ibrinogen-ibrin degradation products and D-dimers in maternal serum (Erez, 2015). heir quantiication is not clinically useful. In a third of women with an abruption severe enough to kill the fetus, the plasma ibrinogen level will be < 150 mg/ dL. hese levels are dependent on the maternal preabruption ibrinogen level, and thus higher levels are "protective" (Cunningham, 2015; Wang, 2016). Clinically signiicant low levels may cause troublesome surgical bleeding. Levels of several other coagulation factors are also variably decreased. In addition, thrombocytopenia, sometimes profound, may accompany severe hypoibrinogenemia initially and becomes common after repeated blood transfusions.
Consumptive coagulopathy is more likely with a concealed abruption because intrauterine pressure is higher. his forces more thromboplastin into the large veins draining the implantation site. With a partial abruption and a live fetus, severe coagulation defects are less common. Our experience has been that if serious coagulopathy develops, it is usually evident by the time abruption symptoms appear.
At the time of cesarean delivery, it is not uncommon to ind widespread extravasation of blood into the uterine musculature and beneath the serosa (Fig. 41-18). It is named after Couvelaire, who in the early 1900s termed it uteroplacental apoplexy. hese myometrial hemorrhages seldom cause uterine atony, and alone they are not an indication for hysterectomy. Efusions of blood are also seen beneath the tubal serosa, between the leaves of the broad ligaments, in the substance of the ovaries, and free in the peritoneal cavity.
FIGURE 41-18 Couvelaire uterus from total placental abruption ater cesarean delivery. Blood markedly infiltrates the myometrium to reach the serosa, especially at the cornua. The small serosaloleio myoma seen on the lower anterior uterine surface is an incidental finding. (Used with permission from Dr. Angela Fields Walker.)
Acute kidney injury AI) is a general term describing renal dysfunction from many causes (Chap. 53, p. 1036). Delayed or incomplete treatment of hypovolemia with severe placental abruption can be one. However, even with abruption complicated by severe disseminated intravascular coagulation, prompt and vigorous treatment of hemorrhage with blood and crystalloid solution usually prevents clinically signiicant renal dysfunction. The risk for renal injury with abruption is magnified when preeclampsia coexists (Alexander, 2015; Drakeley, 2002). Most cases of AKI are reversible and not so severe as to require dialysis. Generally, long-term outcomes are good (Arazi, 2015). That said, irreversible acute cortical necrosis encountered in pregnancy can be associated with abruption (Gopalakrishnan, 2015).
Rarely, pituitary failure-Sheehan syndrome-follows severe intrapartum or early postpartum hemorrhage. Described in Chapter 58 (1133), the exact pathogenesis is not well understood, especially because endocrine abnormalities are infrequent even in women who sufer catastrophic hemorrhage (Matsuwaki, 2014; Robalo, 2012).