Lactated Ringer solution is administered routinely at a rate between 60 and 125 mL per hour, unless luid loss is unusual from vomiting, diarrhea, or diaphoresis, or, more likely, excessive blood loss with delivery. Oliguria is common with severe preeclampsia. hus, coupled with the knowledge that maternal blood volume is likely constricted compared with that of normal pregnancy, it is tempting to administer intravenous fluids more vigorously. But controlled, conservative luid administration is preferred for the typical woman with severe preeclampsia who already has excessive extracellular luid that is inappropriately distributed between intravascular and extravascular spaces. Infusion of large luid volumes enhances the maldistribution and thereby appreciably elevates the risk of pulmonary and cerebral edema (Dennis, 2012a; Sciscione, 2003; Zinaman, 1985). hus, for preeclamptic women with anuria, small incremental boluses can be given to maintain urine output above 30 mL per hour. Diminished intravascular volume from hemorrhage or luid loss from vomiting or fever can similarly be replaced by gradual incremental boluses. For labor analgesia with neuraxial analgesia, crystalloid solutions are infused slowly in graded amounts (Chap. 25, p. 496).
Women with severe preeclampsia who develop pulmonary edema most often do so postpartum (Cunningham, 1986, 2012; Zinaman, 1985). With suspected pulmonary edema in the eclamptic woman, aspiration of gastric contents, which may be the result of convulsions, anesthesia, or oversedation, should be excluded. here are three common causes of pulmonary edema in women with severe preeclampsia syndromepulmonary capillary permeability edema, cardiogenic edema, or a combination of the two.
Some women with severe preeclampsia-especially if given vigorous fluid replacement-will have mild pulmonary congestion secondary to permeability edema. his is caused by normal pregnancy changes magnified by the preeclamp�ia syndrome. Importantly, plasma oncotic pressure drops appreciably in normal term pregnancy because of decreased serum albumin concentration, and oncotic pressure falls even more with preeclampsia (Zinaman, 1985). Moreover, both increased extravascular luid oncotic pressure and increased capillary permeability are found in women with preeclampsia (Brown, 1989; 0ian, 1986).
Knowledge concerning cardiovascular and hemodynamic pathophysiological alterations associated with severe preeclampsia-eclampsia has accrued from studies done using invasive monitoring and a low-directed pulmonary artery catheter (see Fig. 40-5). Two conditions frequently cited as indications are preeclampsia associated with oliguria and that associated with pulmonary edema (Clark, 2010). Somewhat ironically, it is usually vigorous treatment of the former that results in most cases of the latter. The Task Force (2013) recommends against routine invasive monitoring. Such monitoring is best reserved for severely preeclamptic women with accompanying cardiac disease, renal disease, or both or with refractory hypertension, oliguria, and pulmonary edema.
Because the preeclampsia syndrome is associated with hemoconcentration, some have inused various fluids, starch polymers, albumin concentrates, or combinations thereof to expand blood volume (Ganzevoort, 2004). Older observational studies describe serious complications-especially pulmonary edema-with volume expansion (Benedetti, 1985; LOpez-Llera, 1982; Sibai, 1987b).