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.
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.
Sibai: 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).1–3 One difficulty encountered in any discussion of these conditions is the lack of consistent terminology. So let’s define our terms.
|Clinical Finding||Chronic Hypertension||Gestational Hypertension||Pre-eclampsia|
|Onset of hypertension||<20 weeks’ gestation||Usually in third trimester||≥20 weeks’ gestation|
|Degree of hypertension||Mild or severe||Mild||Mild or severe|
|Sodium urate >5.5 mg/dL||Rare||Absent||Present in almost all cases|
|Hepatic dysfunction||Absent||Absent||Severe disease|
Repke: 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.
Rayburn: 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.5
|ALARIS Medical Systems||Instromedix||QD|
|Becton Dickenson & Co||Assure||A30|
|Becton Dickenson & Co||Assure||W20|
|Omron Healthcare Inc||Omron||HEM-403c|
|Omron Healthcare Inc||Omron||HEM-705CP|
|Omron Healthcare Inc||Omron||HEM-706|
|Omron Healthcare Inc||Omron||HEM-711|
|Omron Healthcare Inc||Omron||HEM-713c|
|Omron Healthcare Inc||Omron||HEM-722c|
|Terumo Medical Corporation||Terumo||ES-H51|
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.6
Ravin: How does patients’ home BP monitoring complement readings obtained in the office?
Rayburn: 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.7
Sibai: Do you have data to support your view about the benefits of adjunctive home BP monitoring?
Rayburn: 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.5 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.8,9
Repke: How does chronic hypertension during pregnancy cloud the clinical picture?
Sibai: 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%.4 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.10,11 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.
Repke: 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.
Sibai: 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.12 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%).13
Ravin: 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?
Sibai: 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.
Ravin: How does home BP monitoring contribute to a conservative management strategy for women with gestational hypertension?
Rayburn: 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).14
Repke: How do you teach your patients to take their BP accurately?
Rayburn: 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.15 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.16 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.14
Sibai: 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.
Repke: Dr Sibai, how do we define pre-eclampsia?
Sibai: 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.17,18
Repke: 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.19–21 Two additional pathophysiologic entities, endothelial cell damage and prostacyclin/thromboxane imbalances, can account for many of the manifestations.21–24
Ravin: 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].
Repke: 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.
Sibai: 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?
Repke: 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.25,26 Calcium supplementation has also been proposed.19,27 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.22,23
Sibai: Now let’s turn to management. Previous data indicated that prolonged hospitalization for patients with mild pre-eclampsia remote from term might improve outcomes,28 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.29–33
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.
Repke: 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.
|Lungs||Rule out congestive heart failure|
|Deep tendon reflexes||Look for clonus|
|Epigastric/RUQ palpation||Liver congestion|
|Uterus||Rule out evolving abruption|
|Cervical examination||Aids delivery planning|
Ravin: Can any maternal guidelines assist us in determining the need for expedited delivery in women with pre-eclampsia?
Repke: 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.34,35 Proteinuria should not be a factor in delivery decisions.
Sibai: What are fetal guidelines for expedited delivery?
Repke: 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.34,35
Sibai: 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?
Repke: 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.36,37 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.37,38 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.39,40
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.41
Sibai: 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.
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9. Schwartz WJ 3rd, Rayburn WF, Turnbull GL, Christensen HD. Blood pressure monitoring during pregnancy: accuracy of portable devices designed for obese patients. J Reprod Med. 1996;41:581â585.
10. Burt VL, Whelton P, Rocella EJ, et al. Prevalence of hypertension in the US adult population: results from the Third National Health and Nutrition Examination Sur-vey, 1988â1991. Hypertension. 1995;25: 305â313.
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13. Hauth JC, Ewell MG, Levine RJ, et al. Pregnancy outcomes in healthy nulliparas who developed hypertension: Calcium for Preeclampsia Prevention Study Group. Obstet Gynecol. 2000;95:24â28.
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15. Rubin P. Measurement of diastolic blood pressure in pregnancy. BMJ. 1996; 313:4â5.
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17. Sibai BM, Caritis SN, Thom E, et al. Prevention of preeclampsia with low-dose aspirin in healthy nulliparous pregnant women. N Engl J Med. 1993;329: 1213â1218.
18. Caritis S, Sibai BM, Hauth J, et al. Low-dose aspirin therapy for the prevention of preeclampsia in high-risk women. N Engl J Med. 1998;338:701â705.
19. Repke JT. Prevention of preeclampsia. Clin Perinatol. 1991;18:779â792.
20. Roberts JM, Taylor RN, Musci TJ, Rodgers GM. Serum from preeclamptic women contains a factor which damages human endothelial cells. Clin Exp Hypertens. 1989;8:119.
21. Friedman SA, Taylor RN, Roberts JM. Pathophysiology of pre-eclampsia. Clin Perinatol. 1991;18:661â682.
22. Schiff E, Peleg E, Goldenberg M, et al. The use of aspirin to prevent pregnancy-induced hypertension and lower the ratio of thromboxane A2 to prostacyclin in relatively high-risk pregnancies. N Engl J Med. 1989;321:351â356.
23. Benigni A, Gregorini G, Frusca T, et al. Effective low dose aspirin on fetal and maternal generation of thromboxane by platelets in women at risk for pregnancy-induced hypertension. N Engl J Med. 1989;321:357â362.
24. Caritis S, Sibai B, Hauth J, et al. Low dose aspirin to prevent preeclampsia in women at high risk. N Engl J Med. 1998; 338:701â705.
25. Conradt A, Weidinger H, Algayer H. On the role of magnesium in fetal hypotrophy, pregnancy-induced hypertension, and preeclampsia. Magnesium Bull. 1984;6:68.
26. Spatling L, Spatling G. Magnesium supplementation in pregnancy: a double blind study. Br J Obstet Gynaecol. 1988; 95:120â125.
27. Repke JT. Prevention and treatment of pregnancy-induced hypertension. Compr Ther. 1991;17(5):25â31.
28. Gilstrap LC, Cunningham FG, Whalley PE. Management of pregnancy-induced hypertension in the nulliparous patient remote from term. Semin Perinatol. 1978; 2:73â81.
29. Sibai BM, Gonzalez AR, Mabie WC, Moretti ML. A comparison of labetalol plus hospitalization versus hospitalization alone in the management of preeclampsia remote from term. Obstet Gynecol. 1987; 70:232â237.
30. Sibai BM, Barton JR, Akl S, et al. A randomized prospective comparison of nifedipine and bed rest versus bed rest alone in the management of preeclampsia remote from term. Am J Obstet Gynecol. 1992;167:879â884.
31. Tuffnell DJ, Liliford RJ, Buchan PC, et al. Randomized controlled trial of day care for hypertension in pregnancy. Lancet. 1992;339:224â227.
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34. Sibai BM, Mercer BM, Schiff E, Friedman SA. Aggressive versus expectant management of severe preeclampsia at 28 to 32 weeks’ gestation: a randomized controlled trial. Am J Obstet Gynecol. 1994;171: 818â822.
35. Schiff E, Friedman SA, Sibai BM. Conservative management of severe preeclampsia remote from term. Obstet Gynecol. 1994;84:626â630.
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37. Pritchard JA, Cunningham FG, Pritchard SA. The Parkland Memorial Hospital protocol for treatment of eclampsia: evaluation of 245 cases. Am J Obstet Gynecol. 1984;148:951â963.
38. Domisse J. Phenytoin, sodium and magnesium sulfate in the management of eclampsia. Br J Obstet Gynaecol. 1990; 7:104.
39. The Eclampsia Trial Collaborative Group. Which anti-convulsant for women with eclampsia? Evidence from the Collaborative Eclampsia Trial. Lancet. 1995;345: 1455â1463.
40. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. N Engl J Med. 1995;333: 201â205.
41. Martin JN, Blake PG, Lowry SL, et al. Pregnancy complicated by preeclampsia/ eclampsia with the syndrome of hemolysis, elevated liver enzymes, and low platelet count: how rapid is postpartum recovery? Obstet Gynecol. 1990;76:737â741.
Baha M. Sibai, MD, Moderator, is a Professor and Chief, Division of MaternalâFetal Medicine, Department of Obstetrics and Gynecology, University of Tennessee, Memphis. John T. Repke, MD, is Chris J. and Marie A. Olsen Professor and Chair, Department of Obstetrics and Gynecology, University of Nebraska Medical Center, Omaha. William F. Rayburn, MD, is a Professor and Chair, Department of Obstetrics and Gynecology, University of New Mexico School of Medicine, Albuquerque. Claudia Reid Ravin, MSN, CNM, is Manager, Professional Development Programs, Association of Women’s Health, Obstetric and Neonatal Nurses, Washington, DC.
*Members of the Gestational Hypertension Roundtable convened in Chicago on June 12, 1999. The roundtable was hosted by the Association of Women’s Health, Obstetric and Neonatal Nurses, through an educational grant from A&D Medical.
Originally published in The Female Patient -- November, 2000
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