HELLP syndrome. Hemolysis (H), elevated liver proteins (EL), and low platelets (LP)—or a combination of these (HELLP)—are well-recognized complications of preeclampsia-eclampsia. Several of the signs, symptoms, and laboratory abnormalities that constitute HELLP syndrome may be confused with similar findings that are usually present in a number of distinct medical and surgical disorders (TABLE 9). This is particularly true when they manifest remote from term. Diagnosis often is delayed, and management frequently is complicated by inappropriate medical and surgical treatments that may be dangerous to both mother and fetus. Not surprisingly, complications related to this syndrome are a major cause of litigation claiming failure to diagnose preeclampsia or failure to diagnose syndromes that can mimic preeclampsia.
The typical HELLP patient is white and complains of epigastric or RUQ pain at less than 36 weeks’ gestation. Some women experience nausea and vomiting (40% to 50%) or diarrhea (5% to 10%), and others have nonspecific viral syndrome-like symptoms. Most patients report a history of malaise for the few hours or days leading up to presentation. Some of these women may complain of flank or shoulder pain, hematuria, bleeding from the gums, or jaundice. Hypertension or proteinuria may be slight or absent. Physical examination will show RUQ tenderness, significant weight gain (ascites, generalized edema), petechiae, or purpura.
Patients with preeclampsia are at increased risk for convulsions during labor and for the first 12 to 24 hours postpartum.
Some patients may have a variety of signs and symptoms, none of which are diagnostic of classic preeclampsia. For this reason, all gravidas beyond 20 weeks’ gestation having any of these symptoms should undergo a platelet count and liver enzyme determinations, regardless of maternal BP. Since 30% of HELLP syndrome cases develop postpartum, similar evaluation should be performed in all women having these complaints within 2 weeks of delivery.
TABLE 4
Clinical factors to be considered in management
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TABLE 5
Indications for delivery in mild preeclampsia
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| FHR=fetal heart rate; IUGR=intrauterine growth restriction; RUQ=right upper quadrant |
| * Nonreactive nonstress test confirmed by biophysical profile or contraction test. |
TABLE 6
Characteristics of patients eligible for outpatient management of mild preeclampsia
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TABLE 7
Antepartum management of mild preeclampsia
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TABLE 8
Indications for delivery during expectant management of severe preeclampsia
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TABLE 9
Imitators of HELLP syndrome
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| HELLP=hemolysis, elevated liver proteins, and low platelets |
Intrapartum management
Some of the medicolegal claims involving intrapartum management of hypertensive disorders concern the failure to give magnesium sulfate to prevent convulsions, the failure to distinguish bleeding of a “bloody show” from abruptio placentae, the failure to use antihypertensive drugs to treat a certain BP level, the mode of delivery, and the association of abnormal fetal-heart-rate (FHR) tracings with neonatal outcome.
In some women, hypertension first develops in labor. These patients should undergo urine protein and blood tests to confirm the presence or absence of preeclampsia and should then be managed accordingly.
Preventing convulsions. Patients with preeclampsia are at increased risk for convulsions during labor and for the first 12 to 24 hours postpartum. The risks are slight in those with mild disease (1%), but may reach 3% to 10% in women with severe disease at less than 32 weeks’ gestation and in patients with HELLP syndrome.9 Therefore, all patients with diagnosed preeclampsia should receive parenteral magnesium sulfate during labor and for at least 12 hours postpartum; in patients with severe preeclampsia or HELLP syndrome, magnesium sulfate should be continued for at least 24 hours postpartum. A typical regimen is a loading dose of 6 g given over 20 minutes, followed by a maintenance dose of 2 g per hour as a continuous intravenous (IV) solution (5% dextrose in lactated Ringer’s solution).