In women with severe preeclampsia, the volume of extracellular luid, manifest as edema, is usually much greater than that in normal pregnant women. As discussed, the mechanism responsible for pathological luid retention is endothelial injury (Davidge, 2015). In addition to generalized edema and proteinuria, these women have reduced plasma oncotic pressure. his reduction creates a iltration imbalance and further displaces intravascular luid into the surrounding interstitium. Electrolyte concentrations do not difer appreciably in women with preeclampsia compared with those of normal pregnant women.
Following an eclamptic convulsion, the serum pH and bicarbonate concentration are lowered due to lactic acidosis and compensatory respiratory loss of carbon dioxide. he intensity of acidosis relates to the amount of lactic acid producedmetabolic acidosis-and the rate at which carbon dioxide is exhaled-respiratory acidosis.
During normal pregnancy, renal blood flow and glomerular filtration rate rise appreciably (Chap. 4, p. 65). With preeclampsia, several reversible anatomical and pathophysiological changes ensue. Of clinical importance, renal perfusion and glomerular iltration are reduced. Levels that are much less than normal nonpregnant values are infrequent and are the consequence of severe disease. Most of the decrement in glomerular filtration is from higher renal aferent arteriolar resistance that may be elevated up to fivefold (Conrad, 2015; Comelis, 201r1). Morphological changes are characterized by glomerular endotheliosis, which blocks the barrier that allows filtration. Diminished iltration causes serum creatinine levels to rise to values seen in nonpregnant individuals, that is, 1 mg/ mL, and sometimes higher (Lindheimer, 2008a). Abnormal values usually begin to normalize 10 days or later after delivery (Comelis, 2011; Spaan, 2012a).
In most preeclamptic women, the urine sodium concentration is elevated. Urine osmolality rises, urine:plasma creatinine ratio is elevated, and fractional excretion of sodium is low, which all indicated that a prerenal mechanism is involved. Sodium-containing crystalloid infusion raises left ventricular illing pressure, and although oliguria temporarily improves, rapid infusions may cause clinically apparent pulmonary edema. Intensive intravenous fluid therapy is not indicated as "treatment" for preeclamptic women with oliguria unless urine output is diminished from hemorrhage or luid loss from vomiting or fever.
Plasma uric acid concentration is typically elevated in preeclampsia. The elevation exceeds that attributable to the reduction in glomerular filtration rate and likely is also due to enhanced tubular reabsorption (Chesley, 1945). At the same time, preeclampsia is associated with diminished urinary excretion of calcium, perhaps because of greater tubular reabsorption (Taufield, 1987).
As shown in Table 40-1, detection of proteinuria helps to establish the diagnosis of preeclampsia. Abnormal protein excretion is empirically deined by 24-hour urinary excretion exceeding 300 mg; a urine protein:creatinine ratio �0.3; or persistent protein values of 30 mg/ dL (1 + dipstick) in random urine samples. Although worsening or nephrotic-range proteinuria has been considered by most to be a sign of severe disease, this does not appear to be the case (Airoldi, 2007). Certainly, this concept was not accepted by the 20r13 Task Force.