There is no universally accepted strict deinition of HELLP syndrome, and thus its incidence varies by investigator. In the previously noted study of 183 women with HELLP syndrome, 40 percent had adverse outcomes, and two mothers died (Haddad, 2000). Complications included eclampsia in 6 percent, placental abruption-10 percent, acute kidney injury-5 percent, and pulmonary edema-10 percent. Stroke, hepatic hematoma, coagulopathy, acute respiratory distress syndrome, and sepsis were other serious complications.
Women with preeclampsia and HELLP syndrome typically have worse outcomes than preeclamptic women without the HELLP constellation (Kozic, 2011; Martin, 2012, 2013). In one review of693 women with HELLP syndrome, 10 percent had concurrent eclampsia (Keiser, 2011). Sep and associates (2009) described a significantly higher risk for complications in women with HELLP syndrome compared with those with "isolated preeclampsia." These included eclampsia-15 versus 4 percent; preterm birth-93 versus 78 percent; and perinatal mortality rate-9 versus 4 percent, respectively. Because of these marked clinical diferences, it has been postulated that HELLP syndrome has a distinct pathogenesis (Reimer, 2013; Vaught, 2016).
Headaches and visual symptoms are common with severe preeclampsia, and associated convulsions deine eclampsia. The earliest anatomical descriptions of brain involvement came from autopsy specimens, but CT and MR imaging and Doppler studies have added many important insights.
FIGURE 40-10 This autopsy brain slice shows a fatal hypertensive hemorrhage in a primigravida with eclampsia.
From early anatomical descriptions, brain pathology accounted for only about a third of fatal cases such as the one shown in Figure 40-10. In fact, most deaths were from pulmonary edema, nd brain lesions were coincidental. Thus, lthough gross intracerebral hemorrhage was seen in up to 60 percent of eclamptic women, it was fatal in only half of these (Melrose, 1984; Richards, 1988; Sheehan, 1973). s shown in Figure 40-11, other principal lesions found at autopsy of eclamptic women were cortical and subcortical petechial hemorrhages. The classic microscopic vascular lesions consist of fibrinoid necrosis of the arterial wall and perivascular micro infarcts and hemorrhages. Other frequently described major lesions include subcortical edema, multiple nonhemorrhagic areas of "sotening" throughout the brain, and hemorrhagic areas in the white matter (Hecht, 2017). here also may be hemorrhage in the basal ganglia or pons, sometimes with rupture into the ventricles.
Clinical, pathological, and neuroimaging findings have led to two general theories to explain cerebral abnormalities with eclampsia. Importantly, endothelial cell dysfunction that characterizes the preeclampsia syndrome likely is a key in both. The first theory suggests that in response to acute and severe hypertension, cerebrovascular overregulation leads to vasospasm (Trommer, 1988). In this scheme, diminished cerebral blood low is hypothesized to result in ischemia, cytotoxic edema, and eventually tissue infarction. Little objective evidence supports this mechanism.