Severe preeclampsia is frequently accompanied by hemolysis, which manifests as elevated serum lactate dehydrogenase levels and reduced haptoglobin levels. Other evidence comes from schizocytosis, spherocytosis, and reticulocytosis in peripheral blood (Cunningham, 1985; Pritchard, 1954, 1976). hese derangements result in part from microangiopathic hemoysis caused by endothelial disruption with platelet adherence and ibrin deposition. Cunningham and coworkers (1995) postulated that erythrocyte morphology was partially caused by serum lipid alterations. Related, substantively decreased longchain fatty acid content is found in erythrocytes of preeclamptic women (Mackay, 2012).
Mter early reports of hemolysis and thrombocytopenia with severe preeclampsia, descriptions were added of abnormally elevated serum liver transaminase levels that indicated hepatocellular necrosis (Chesley, 1978). Weinstein (1982) referred to this combination of events as the HELLP syndrome-and this term now is used worldwide. Also, facets of the HELLP syndrome are included in criteria that diferentiate severe from nonsevere preeclampsia (see Table 40-2). he HELLP syndrome is discussed further in that section (p. 722).
Subtle changes consistent with intravascular coagulation, and less often erythrocyte destruction, commonly are found with preeclampsia and especially eclampsia (Cunningham, 2015; Kenny, 2015). Some of these changes include elevated factor VIII consumption, increased levels of ibrinopeptides A and B and of D-dimers, and reduced levels of regulatory proteinsantithrombin III and proteins C and S. Coagulation aberrations generally are mild and are seldom clinically signiicant (Kenny, 2015; Pritchard, 1984). Unless placental abruption is comorbid, plasma ibrinogen levels do not difer remarkably from levels found in normal pregnancy. Fibrin degradation products such as D-dimers are minimally elevated. As preeclampsia worsens, so do abnormal indings with thromboelastography (Pisani-Conway, 2013). Despite these changes, routine laboratory assessments of coagulation, such as prothrombin time (PT), activated partial thromboplastin time (aPTT), and plasma ibrinogen level, are not required in the management of pregnancy-associated hypertensive disorders.
Plasma levels of renin, angiotensin II, angiotensin 1-, aldosterone, deoxycorticosterone, and atrial natriuretic peptide (ANP) are substantively augmented during normal pregnancy. ANP is released during atrial wall stretching from blood volume expansion, and it responds to cardiac contractility (Chap. 4, p. 63). Levels of serum ANP rise in pregnancy, and its secretion is further enhanced in women with preeclampsia (Luft, 2009). Levels of its precursor-proatrial natriuretic peptide-are also increased in preeclampsia (Sugulle, 2012). Vasopressin levels are similar in nonpregnant, normally pregnant, and preeclamptic women even though the metabolic clearance is elevated in the latter two (Durr, 1999) .