Cardiovascular disturbances are common with preeclampsia syndrome. hese are related to: (1) greater cardiac afterload caused by hypertension; (2) cardiac preload, which is reduced by a pathologically diminished volume expansion during pregnancy and which is increased by intravenous crystalloid or oncotic solutions; and (3) endothelial activation leading to interendothelial extravasation of intravascular fluid into the extracellular space and, importantly, into the lungs.
The cardiovascular aberrations of pregnancy-related hypertensive disorders vary depending on several modifiers. These factors include preeclampsia severity, hypertension severity, presence of underlying chronic disease, and the part of the clinical spectrum in which these are studied. In some women, these cardiovascular changes may precede hypertension (De Paco, 2008; Easterling, 1990; Khalil, 2012; Melchiorre, 2013). Nevertheless, with the clinical onset of preeclampsia, cardiac outpur declines, due at least in part to greater peripheral resistance. When assessing cardiac function in preeclampsia, consideration is given to echo cardiographic measures ofmyocardial function and to clinically relevant ventricular function.
blood loss incurred at delivery. Anemia may also partially result from greater erythrocyte destruction as subsequently described.
The platelet count is routinely measured in women with any form of gestational hypertension. Decreased platelet concentra tions with eclampsia were described more than 100 years ago.
The frequency and intensity of thrombocytopenia vary and are dependent on the severity and duration of the preeclampsia syn drome (Heilmann, 2007; Hupuczi, 2007). Overt thrombocy topenia-deined by a platelet count < 100,000/�L-indicates severe disease (see Table 40-2). In general, the lower the platelet count, the higher the rates of maternal and fetal morbidity and mortality (Leduc, 1992). In most cases, delivery is advisable because worsening thrombocytopenia usually ensues. Mter delivery, the platelet count may continue to decline for the irst day or so. It then usually rises progressively to reach a normal level within 3 to 5 days. As discussed later (p. 722), in some instances with HELLP syndrome, the platelet count continues to fall after delivery. If these do not reach a nadir until 48 to 72 hours, then preeclampsia syndrome may be incorrectly attrib uted to one of the thrombotic microangiopathies discussed in
Chapter 56 (p. 1088).
Myriad other platelet alterations are attributed to the preeclampsia syndrome. hese were reviewed by Kenny and coworkers (2015) and include platelet activation with increased .-degranulation producing �-thromboglobulin, factor 4, and enhanced clearance. Paradoxically, in most studies, in vitro platelet aggregation is reduced compared with the normal increase that is characteristic of pregnancy. This likely is due to platelet "exhaustion" following in vivo activation. Although the cause is unknown, immunological processes or simply platelet deposition at sites of endothelial damage may be implicated. Levels of platelet-bound and circulating platelet-bindable immunoglobulins are elevated, which suggests platelet surface alterations.
Abnormally low platelets do not develop in the fetuses or neonates born to preeclamptic women despite severe maternal thrombocytopenia (Kenny, 2015; Pritchard, 1987). Thus, maternal thrombocytopenia in a hypertensive woman is not a etal indication or cesarean delivery.