Although mild degrees of acute kidney injury are encountered, clinically apparent acute tubular necrosis is almost invariably induced by comorbid hemorrhage with hypovolemia and hypotension (Chap. 41, p. 755). his is usually caused by severe obstetrical bleeding-especially placental abruption-coupled with inadequate blood replacement. Drakeley and coworkers (2002) described 72 women with preeclampsia and renal failure. Half had HELLP syndrome, and a third had placental abruption. In one review of 183 women with HELLP syndrome, 5 percent had kidney injury (Haddad, 2000). Of those with renal injury, half had placental abruption, and most had postpartum hemorrhage. Last, irreversible renal cortical necrosis develops rarely (Chap. 53, p. 1037).
Ofwomen with preeclampsia, serial echocardiographic studies document diastolic dysfunction in 40 to 45 percent (Guirguis, 2015; Melchiorre, 2012). With this dysfunction, ventricles do not properly relax and cannot ill properly. In some of these women, functional diferences persist up to 4 years after delivery (Evans, 2011; Orabona, 2017). Diastolic dysfunction stens from ventricular remodeling, which is judged to be an adaptive response to maintain normal contractility despite the increased afterload ofpreeclampsia. High levels ofantiangiogenic proteins may be contributory (Shahul, 2016). In the otherwise healthy pregnant woman, these changes are usually clinically inconsequential. But when combined with underlying ventricular dysfunction-for example, concentric ventricular hypertrophy from chronic hypertension-further diastolic dysfunction may cause cardiogenic pulmonary edema (Wardhana, 2017). his is discussed further in Chapters 47 (p. 918) and 49 (p. 964).
Despite the relatively high frequency of diastolic dysfunction with preeclampsia, clinical cardiac function in most afected women is appropriate (Hibbard, 2015). In some preeclamptic women, cardiac troponin levels are slightly elevated, and amino-terminal pro-brain natriuretic peptide (Nt pro-BNP) levels are elevated with severe preeclampsia (Pergialiotis, 2016; Zachary, 2017). Importantly, both normally pregnant women and those with preeclampsia syndrome can have normal or slightly hyperdynamic ventricular function (Fig. 40-5). hus, both have a cardiac output that is appropriate for leftsided illing pressures. Filling pressures are dependent on the volume of intravenous fluids. Thus, aggressive hydration results in overtly hyperdynamic ventricular function. his is .J,
FIGURE 40-5 Ventricular function in normally pregnant women (striped area) and in women with eclampsia (boxed area) is plotted on a Braunwald ventricular function cur e. Normal values are from Clark (1989), and those for eclampsia are from Hankins (1984). PCWP = pulmonary capillary wedge pressure; LVSWI = left ventricular stroke work index.
accompanied by elevated pulmonary capillary wedge pressures, and pulmonary edema may develop despite normal ventricular function. This is because of an alveolar endothelial-epithelialrleak, and it is compounded by decreased oncotic pressure from a low serum albumin concentration. In sum, aggressive fluid administration to otherwise normal women with severe preeclampsia substantially elevates normal leftsided filling pressures and raises a physiologically normal cardiac output to hyperdynamic levels.