associated with HELLP syndrome. First, Fonseca and associates (2005) randomly assigned 132 women with HELLP syndrome to either dexamethasone or placebo administration. Outcomes assessed included hospitalization length, recovery time of abnormal laboratory test results, resolution of clinical parameters, and complications that included acute renal fail ute, pulmonary edema, eclampsia, and death. None of these was signiicantly diferent between the two groups. In another study, 105 postpartum women with HELLP syndrome were assigned to dexamethasone or placebo treatment (Katz, 2008). Outcomes were analyzed similarly to the Fonseca study, and no advantage to dexamethasone was found (Fig. 40-15). In the third study, preeclamptic women were given either placebo or methylprednisolone if their platelet count was between 50,000 and 150,000/�L (Pourrat, 2016). No benefits were gained from corticosteroid therapy. Because of these indings, the 2013 Task Force does not recommend corticosteroid treatment for thrombocytopenia with HELLP syndrome.
In several preliminary studies, therapies have attempted to lower serum levels or mitigate the action of antiangiogenic factors. Some of these include therapeutic apheresis, done to lower sFlt-1 levels (Thadhani, 2016). Pravastatin has been given for preeclampsia prevention (Cleary, 2014). Sildenail citrate, a phosphodiesterase inhibitor, has been provided to promote vasodilation (Trapani, 2016; Vigil-De Gracia, 2016). In a recent randomized trial of 120 women with early-onset preeclampsia, an recombinant antithrombin infusion compared and occasionally anuria develops. There may be hemoglobinuria, but hemoglobinemia is rare. Often, facial and peripheral edema is pronounced, but it may be absent (Fig. 40-17).
FIGURE 40-1 7 Severe edema in a young nullipara with antepartum preeclampsia. (Used with permission from Dr. Nidhi Shah.)
As with severe preeclampsia, urinary output rises after delivery and is usually an early sign of improvement. With renal dysfunction, serum creatinine levels are serially monitored. Proteinuria and edema ordinarily disappear within a week postpartum. In most cases, blood pressure returns to normal within a few days to 2 weeks after delivery (Berks, 2009). As subsequently discussed, persisting and severe hypertension likely predicts underlying chronic vascular disease (Podymow, 2010).
In antepartum eclmpsia, labor may begin spontaneously shortly ater convulsions ensue and may progress rapidly. If the convulsions occur during labor, contractions may increase in frequency and intensity, and the duration oflabor may be shortened. Because of maternal hypoxemia and lactic acidemia caused by convulsions, fetal bradycardia oten follows a seixure (Fig. 40-18). he fetal heart rate usually recovers within 2 to 10 minutes (Ambia, 2018). If it persists more than about 10 minutes, another cause of bradycardia, such as placental abruption or imminent delivery, should be considered.