William F. Rayburn, MD

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xperts discuss  potential complications of gestational hypertension, as well as the  role of home blood-pressure (BP) monitoring as an adjunct in managing  these cases.

: Hypertensive disorders-specifically chronic  hypertension, gestational hypertension, and pre-eclampsia/eclampsia-are  the most common medical complications of pregnancy, and remain a major  cause of maternal and perinatal morbidity. Differential diagnosis of  these conditions is critical (Table 1).

 One difficulty encountered in  any discussion of these conditions is the lack of consistent  terminology. So let’s define our terms.

: We’ll start with hypertension. Early pregnancy entails  numerous physiologic changes, including a reduction in vascular  resistance that results in a drop in BP. The decline in diastolic  pressure usually ranges from 9 to 17 mm Hg. BP tends to reach its nadir  at 20 weeks’ gestation. During the third trimester, it usually rises to  prepregnancy levels.4 Hypertension is defined as a systolic BP of 140 mm  Hg or greater and diastolic BP of 90 mm Hg or greater while receiving antihypertensives.

: BP should always be measured in a consistent manner,  with a correctly sized cuff. Patients should be seated with their arm at  heart level. Although most health care personnel think of BP during  pregnancy as a fixed entity, it varies throughout the day. Repeated  findings of elevated BP during routine prenatal office visits may prove  inadequate; increasing evidence supports the usefulness of home BP  monitoring to clarify diagnosis and facilitate treatment.

Although office readings are usually obtained using a mechanical  sphygmomanometer, home readings can be obtained with an electronic BP  monitor (Table 2). Intermachine variation has been small for the best  machines. Also, many of them are manufactured to adhere to one of two  international premarket accuracy standards.

: How does patients’ home BP monitoring complement readings obtained in the office?

: Self-recordings of BP are dynamic, and are combined  with conventional office measurements to provide an extra degree of  accuracy necessary to plan management. Home monitoring allows patients  to actively participate in their treatment, provides instant visual  evidence of BP and response to therapy, enhances compliance, may aid  physicians in making treatment decisions, may result in a reduction of  drug doses with attendant benefits, and may permit longer intervals  between scheduled office visits.

: Do you have data to support your view about the benefits of adjunctive home BP monitoring?

: Yes. Our study demonstrated that home BP  measurements, as compared with office measurements, were lower in 52% of  cases and equivalent in 28% of cases. It is important to get an  indication of “true” BP so that we treat only those cases of  hypertension that are verifiable.

 Home BP monitoring helps  to make that possible. Portable electronic or mechanical aneroid devices  suitable for home use may be purchased at most retail department stores  and pharmacies. We do not recommend use of wrist cuffs or finger cuffs, as they are not as accurate as arm cuffs.

: How does chronic hypertension during pregnancy cloud the clinical picture?

: Chronic hypertension is defined as hypertension  present either before pregnancy or diagnosed before 20 weeks’ gestation.  Reported rates in the United States range from 1% to 5%.

 In addition, chronic hypertension  is the suggested diagnosis if it develops during pregnancy and lasts for  longer than 6 weeks postpartum. The risk for chronic hypertension  increases with age. Hence, as the number of women in their 40s who  become pregnant has been increasing over the years, the incidence of  chronic hypertension in pregnancy has been rising too.

 When evaluating gravidas with  chronic hypertension, clinicians must rule out secondary causes of the  elevated BP, as these may have a separate impact on the viability of the  pregnancy. Such secondary causes include pheochromocytoma, renal  parenchymal disease, coarctation of the aorta, and hyperaldosteronism.  Management of women with chronic hypertension should begin before  pregnancy and should include counseling about potential complications  associated with pregnancy.

: As mentioned previously, BP declines during early  pregnancy. As this decrease reaches its nadir midway during pregnancy,  some women with chronic hypertension may not be diagnosed until after 20  weeks’ gestation, when BP starts to rise again. However, elevated BP  appearing after 20 weeks in gravidas not previously known to be  hypertensive is typically diagnosed as gestational hypertension.

: To make the diagnosis of gestational hypertension, I  would add that elevated BP should be persistent on at least two  separate occasions at least 6 hours apart but not more than 1 week  apart. Gestational hypertension is fairly common among nulliparas,  occurring in 7% to 18% of them. Time of onset is usually 36 weeks’  gestation or later; in 20% to 30% of cases, it progresses to pre-eclampsia.

 A study of pregnancy  outcomes showed that a greater proportion of women with gestational  hypertension than those with normal BPs underwent preterm induction  (19.4% vs 11.2%) or cesarean delivery (29.1% vs 13.3%).

: In many of these cases, it seems that health care  providers deliberately choose to terminate what may be an achievable  full-term pregnancy. I fear that they have a rather rapid “trigger  finger,” but at what added cost to the health care system and at what  added health risk to mothers and their infants?

: Ms Ravin’s concern seems warranted. In my opinion,  management of gestational hypertension should be more conservative  (i.e., relative bed rest, weekly visits for evaluation, and antenatal  measurements of hematocrit, platelet count, and liver enzymes).  Observation for progression to pre-eclampsia should be made. Indications  for more expedient delivery include gestational age beyond 40 weeks,  abnormal fetal test findings, hematologic abnormalities, and/or  development of symptoms of pre-eclampsia.

: How does home BP monitoring contribute to a conservative management strategy for women with gestational hypertension?

: This strategy works well in patients whose BPs are  borderline (140/90 mm Hg) or mildly elevated in the clinic but normal at  home. Those whose BPs are consistently elevated both at the clinic and  at home should receive antihypertensives; home BP readings are still  useful as an adjunct to office readings in monitoring treatment  response. A 2-year investigation conducted at our clinic showed that  among women who had hypertension and learned home BP monitoring, 50%  were able to stop their medications (mostly diuretics).

: How do you teach your patients to take their BP accurately?

: Our nurses teach them. The Korotkoff I sound is  easily taught. Although diastolic BP measured as the Korotkoff IV sound  corresponds better with intra-arterial diastolic pressure, some  controversy exists about whether to use the Korotkoff IV or V sound.

 We handle this by recording  all three: I, IV, and V. As BP is lowest in the morning and highest in  the afternoon, we instruct patients to take daily measurements at those  times. We also give them written instructions about whom to call if they  should note a series of elevated readings. We counsel them that  readings of 135/85 mm Hg are considered normal, and that a diastolic  pressure of 85 to 89 mm Hg during pregnancy requires further evaluation.  Pressures consistently higher at home have generally been infrequent  but certainly require confirmation.

 Our study showed that  home BP monitoring lowered the cost of obstetric prenatal care:  Antepartum hospitalization for hypertension-related concerns was more  than twice as common for women whose BPs were monitored only in the  office than it was for those followed both at home and in the office,  with no difference in pregnancy outcomes.

: To manage chronic hypertension conservatively and  effectively, patients should undergo a physical examination and  hypertensive evaluation at the first prenatal visit. Clinicians should  pay particular attention to the degree and duration of hypertension, the  use of medications, and the presence of lab test abnormalities (e.g.,  proteinuria, elevated serum urate, hemoconcentration, thrombocytopenia,  elevated liver enzyme values).

Based on these findings, patients are classified as having low- or  high-risk chronic hypertension. This sequestration puts them on widely  different paths of scrutiny, with high-risk patients requiring frequent  prenatal visits and likely use of antihypertensive medication, repeat  laboratory testing, ultrasonography starting at 28 weeks and repeated  every 3 weeks, and evaluation for suspected pre-eclampsia. High-risk  patients include those with a systolic BP greater than 160 mm Hg and a  diastolic BP greater that 110 mm Hg, and those with hypertension for  more than 5 years or disease showing target-organ impact. Women with  previous pre-eclampsia are also at high risk. Antihypertensive  drugs/classes such as atenolol, angiotensin-converting enzyme  inhibitors, or angiotensin receptor blockers should be discontinued  within the first trimester. Patients can be treated with methyldopa, if  needed, or nifedipine. Low-risk patients can be seen at regular  intervals of prenatal care; use of antihypertensive drugs is optional.

: Dr Sibai, how do we define pre-eclampsia?

: It’s defined as hypertension plus either proteinuria  or an abnormal platelet count, elevated liver enzyme values, or the  presence of symptoms of pre-eclampsia. It’s more common in primagravidas  (incidence, 6%) and in women whose mother or sisters have had it.  Pre-eclampsia is also more common in women having multiple births, and  in young teen mothers. Medical conditions, including existing  hypertension, type 1 diabetes, and renal dysfunction, can predispose to  it. No single test is diagnostic. Although most women with pre-eclampsia  can deliver healthy babies, 10% to 20% of them progress to severe  pre-eclampsia, putting themselves and their babies at risk.

: Although most cases of pre-eclampsia end in an  uneventful delivery and recovery, some patients experience severe  multisystem decompensation, cardiovascular collapse, and death. No  single satisfactory unifying explanation has been advanced for the  origin of the protein manifestation of this disorder, but it has been  attributed to an excessive placental mass, an immunologic basis,  placental ischemia, and genetic abnormalities.

 Two additional pathophysiologic entities, endothelial cell damage and prostacyclin/thromboxane imbalances, can account for many of the manifestations.

: Accurate diagnosis of pre-eclampsia is paramount.  Although knowledge of high-risk populations helps, we can’t assume that  any specific patient will or will not develop pre-eclampsia. Recently  evaluated clinical data fail to distinguish the independent significance  of known risk factors and physiologic markers [personal communication:  Poole, JH: Physiologic Markers for Preeclampsia. Doctoral dissertation  (unpublished), University of South Carolina (Columbia), 1999].

: I agree; establishing the correct diagnosis is  critical. Mild pre-eclampsia is associated with elevated BP (>140/90  mm Hg, with two measurements at least 6 h apart) and/or proteinuria  (>300 mg/24 h or >1+ on two consecutive urine specimens). Severe  disease may include central nervous system disorders (blurry vision,  scotomata, severe headache, altered sensorium), pulmonary edema,  eclampsia (seizures or postictal state), persistently elevated BP  (>160/110 mm Hg), proteinuria (>5 g/24 h), oliguria (<100 mL/4  h, <400 mL/24 h), liver involvement, the HELLP syndrome (hemolysis,  elevated liver enzymes, and low platelet count), and fetal growth  retardation.

: Before we discuss management of pre-eclampsia, let’s  address nonpharmacologic approaches to preventing it. We all seem to  favor use of prenatal vitamins without much additional  supplementation-iron being an exception in special situations-and we do  not favor supplementation with fish oil. But how about sodium  restriction, added magnesium, or the use of aspirin to ward off pre-eclampsia?

: Strict sodium restriction and alteration of  medium-chain triglycerides have been attempted to prevent pre-eclampsia.  Other approaches include dietary supplementation with zinc, magnesium,  and/or calcium. Sodium restriction can be useful in cases of severe  hypertension, but it can also endanger fetal development. Dietary  magnesium supplementation has enjoyed an intuitive popularity based on  the use of intravenous magnesium sulfate in the treatment of clinical pre-eclampsia.

 Calcium supplementation has also been proposed.

 In general, I would  concur that adequate dietary intake of these nutrients is all that is  needed. We do not have solid evidence that low-dose aspirin (40–100  mg/d) is beneficial in this regard.

: Now let’s turn to management. Previous data  indicated that prolonged hospitalization for patients with mild  pre-eclampsia remote from term might improve outcomes,

 but other data suggest that  outpatient management of hypertension and mild pre-eclampsia using home  BP self-monitoring is not only safe but also substantially reduces the  number of days of hospitalization.

To address this issue of hospitalization versus outpatient  management in cases of mild pre-eclampsia and no evidence of maternal or  fetal distress, clinicians can use a simple algorithm.

: In essence, then, treatment of pre-eclampsia involves  discerning whether and when expedited delivery is needed. The type and  aggressiveness of the intervention depend on symptom severity and  gestational age at diagnosis. Following a complete hypertensive  evaluation (Table 3), patients are followed closely. In stable and  compliant patients with mild disease, management includes bed rest with  close fetal and maternal monitoring. For motivated patients, this  includes dipstick urinalysis and home BP monitoring. Semiweekly fetal  biophysical testing is also suggested, either at home or in the clinic.  Patients are managed until the spontaneous onset of labor or until a  favorable Bishop cervical score is obtained, allowing for safe preterm  induction of labor if medically indicated. In general, any patient with  mild pre-eclampsia and a mature fetus, or any patient with severe  disease regardless of fetal maturity status, is best served by delivery.  One possible exception is fetal gestation of 24 to 27 weeks in which  expedited delivery is frequently associated with high fetal mortality  and morbidity. Cautious extension of such patients may yield a small  percentage of viable neonates, but the overall prognosis remains  guarded.

: Can any maternal guidelines assist us in determining the need for expedited delivery in women with pre-eclampsia?

: Expedited delivery within 72 hours is indicated in  women who present with one or more of these conditions: uncontrolled  hypertension, eclampsia, platelet count below l00,000 per &L,  aspartate transaminase (AST) or alanine transaminase (ALT) greater than 2  times the upper limit of normal with epigastric pain or right upper  quadrant (RUQ) tenderness, pulmonary edema, compromised renal function,  and persistent severe headache or visual changes. Conservative  management is indicated in patients who present with one or more of  these conditions: controlled hypertension, oliguria that resolves with  routine fluid and food intake, and AST or ALT less than 2 times the  upper limit of normal without epigastric pain or RUQ tenderness.

 Proteinuria should not be a factor in delivery decisions.

: What are fetal guidelines for expedited delivery?

: These include one or more of the following: nonreassuring fetal heart rate,  amniotic fluid index of 2 or lower, ultrasound-estimated fetal weight  in the 5th percentile or lower (unless gestational age is <27 wk),  and reverse umbilical artery diastolic flow. Guidelines for conservative  management include one or more of the following: biophysical profile of  6 or higher, amniotic fluid index score greater than 2, and  ultrasound-estimated fetal weight greater than the 5th percentile.

: Let’s consider intrapartum management of  pre-eclampsia that has progressed to the point at which eclamptic  convulsions can be expected without medical intervention. What do we do  next?

: Once pre-eclampsia has progressed to a point at which  delivery is required, the priority is to prevent progression of the  disease to eclamptic convulsions. Although therapy remains  controversial, the mainstay is magnesium sulfate, at least in the United States.

 It is common practice to  use magnesium sulfate during the intrapartum period for prevention and  to continue this treatment for at least 24 hours after delivery. Because  eclampsia is potentially life-threatening and because most seizures  will occur either intrapartum or within the first 24 hours postpartum,  most clinicians concentrate prophylactic efforts within that time frame.  Although magnesium sulfate has a wide margin of safety, serious  complications have been associated with its use. It is increasingly  common to monitor serum magnesium levels, which should be between 4 and 8  mEq per L. Cardiopulmonary arrest can occur at levels above 12 mEq per  L, and respiratory depression at levels between 8 and 10 mEq per L. 

Outside the United States, other agents, including phenytoin and diazepam, are used to manage severe pre-eclampsia.

 Both agents have  fairly long histories in neurology, but their potential in managing  pre-eclampsia is not clear. Diazepam has been shown to have adverse  effects on the fetus, including reduced tone, hypothermia, and  respiratory depression. Phenytoin does not have these effects, and may  ultimately prove to have a role in treatment. However, two recent  studies have shown that magnesium sulfate was superior to both of these  agents in preventing recurrent seizures, and superior to phenytoin in  preventing initial seizures, making magnesium sulfate the drug of choice.

Once patients with severe pre-eclampsia or eclampsia have delivered,  postpartum management should consist of close monitoring of BP,  intravascular volume, and urinary output. Treatment should continue for  24 hours or longer. Transient thrombocytopenia is usually managed expectantly.

: I hope that the information provided in this forum  will be useful to our readers in their daily clinical practices, and  that it will help to improve maternal and fetal outcomes. Many experts  have been pleading for more conservative management of women with  gestational hypertension, chronic hypertension during pregnancy, or mild  pre-eclampsia. This conservative management may include the use of home  BP monitoring. I thank the panelists for taking time from their busy  schedules to participate in this discussion.

1.        The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1997;157: 2413â2446.

2.        Sibai BM. Diagnosis and management of chronic hypertension in pregnancy. Obstet Gynecol. 1991;78:451â461.

3.        Sibai BM. Treatment of hypertension in pregnant women. N Engl J Med. 1996;335: 257â265.

Articles

Experts discuss potential complications of gestational hypertension, as well as the role of home blood-pressure (BP) monitoring as an adjunct in managing these cases.

Author | William F. Rayburn, MD

Articles

Gestational Hypertension: Implications for Pre-eclampsia and Eclampsia