Hemoconcentration is a hallmark ofeclampsia. This concept was precisely quantiied by Zeeman and colleagues (2009), who expanded the prior observations of Pritchard and associates (1984). hey showed in eclamptic women that the normally expected pregnancy blood volume expansion is severely curtailed (Fig. 40-6). Women ofaverage size have a blood volume of 3000 mL, and during the last several weeks of a normal pregnancy, this averages 4500 mL. With eclampsia, however, much or all of the anticipated 1500 mL excess is lost. Such hemoconcentration results from generalized vasospasm that follows endothelial activation and leakage of plasma into the interstitial space. In women with preeclampsia, and depending on its severity, hemoconcentration is usually not as marked.
hese changes have substantial clinical consequences. Importantly, women with severe hemoconcentration are unduly sensitive to blood loss at delivery that otherwise may be considered normal. Vasospasm and endothelial leakage of plasma persist for a variable time ater delivery as the endothelium is restored to normalcy. u this takes place, vasoconstriction reverses, and s the blood volume reexpands, the hematocrit usully falls. Importanty} a substantive cause ofthisall in hematocrit} however} is usualy the :J0
FIGURE 40-6 Total blood volumes in normotensive women compared with those with eclampsia. The vertical extensions are one standard deviation from the mean. In eclamptic women, blood volume is minimally increased compared with a subsequent normotensive pregnancy. (Data from Zeeman, 2009.)
Liver involvement with preeclampsia may clinically display at least three manifestations. Narrow First, pain is considered a sign of interspace severe disease. It typically manifests by moderate-to-severe right upper quadrant or midepigasEndothelial tric pain and tenderness. Such swelling women usually have elevated serum aspartate transaminase (AST) or alanine transaminase (AL T) levels. In some cases, however, the amount of hepatic tissue involved with infarction may be surprisingly extensive yet still clinically insignificant (N elson, 2017). In our experiences, infarction may be worsened by FIGURE 40-7 Schematic showing glomerular capillary endotheliosis. The capillary of the normal hypotension from obstetrical glomerulus shown on the left has wide endothelial fenestrations, and the pedicels emanating hemorrhage, and it occasion from the podocytes are widely spaced (arrow). The illustration on the right is of a glomerulus with changes induced by the preeclampsia syndrome. The endothelial cells are swollen and their fenes called shock liver (Alexander, trae narrowed, as are the pedicels that now abut each other.
2009; Yoshihara, 2016).
Second, elevations of serum • Liver AST and ALT levels are markers for severe preeclampsia. Values seldom exceed 500 U/L, but levels reaching more than 2000
The characteristic hepatic lesions with eclampsia are regions of U/L have been reported (Chap. 55, p. 1058). In general, serumperiportal hemorrhage in the liver periphery (Hecht, 2017).
concentrations inversely follow platelet levels, and they bothHowever, lesions as extensive as those shown in Figure 40-8 are usually normalize within 3 days following delivery.