- Email: [email protected]
Hypertensive disorders in pregnancy
HYPERTENSIVE DISORDERS IN PREGNANCY
Leon C. Chesley,
PhD
ABSTRACT Hypertensive disorders in pregnancy are the leading cause of maternal death in the United States and in many other parts of the world. A recent prospective study has indicated that the susceptibility to preeclampsia-eclampsia is inherited and probably is determined by a single recessive gene. However, the causes are still unknown. The incidences, prevalences, definitions, cardinal signs, and patients at increased risk for hypertensive disorders in pregnancy are discussed. Successful management of these disorders is early detection. Further discussions are made on the management of preeclampsia, eclampsia, and chronic hypertension in regard to treatment, intrapartum course, and maternal and perinatal outcome.
The hypertensive disorders, chiefly eclampsia, are the leading cause of maternal death in the United States, I England and Wales, 2 and in many other parts of the world. Moreover, they predispose the mother to potentially lethal complications such as abruptio placentae, acute renal failure, circulatory collapse, disseminated intravascular coagulation, and cerebral h e m o r r h a g e . T h e y also greatly increase fetal and neonatal morbidity and mortality. Although there are no reliable data for the overall frequency, the combined incidences and prevalences of the several hypertensive disorders are said to be about 6 to 8%, with wide w~riations in some populations. Black American w o m e n , for instance, have a two to three times higher prevalence of chronic hypertension than do white women, but, contrary to popular belief, the incidence of preeclampsia is similar in the two races. The incidence of preAddress correspondence to: Department of Obstetrics and Gynecology, State University of New York Downstate Medical Center, Brooklyn, NY.
eclampsia varies with the mix of primigravidas and multiparas because preeclampsia is predominantly a disease of the first pregnancy. The incidence of eclampsia and eclamptic deaths depends largely on the availability, quality, and use of prenatal care, b e c a u s e early detection and treatment of preeclampsia, or termination of pregnancy, often can prevent progression of the disease. Almost any hypertensive disease occurring in n o n p r e g n a n t w o m e n may complicate pregnancy; additionally, pregnant women may develop a disease peculiar to pregnancy, such as p r e e c l a m p s i a - e c l a m p s i a . The Committee on Terminology of the American College of Obstetricians and Gynecologists 3 has proposed the following definitions for the hypertensive disorders in pregnancy:
convulsions in a woman with preeclampsia, provided that the convulsions are not attributable to epilepsy, cerebral h e m o r r h a g e or thrombosis, or water intoxication. Chronic hypertensive disease is the presence of sustained hypertension of any cause before, during, and after pregnancy. The discovery of hypertension before the 20th week of gestation is taken as presumptive e v i d e n c e for its having antedated pregnancy.
Preeclampsia is the development of
1. Hypertension is a sustained rise of
hypertension, with proteinuria or facial, digital, or generalized edema after the 20th week of gestation. It may appear earlier in association with trophoblastic dis-
30 m m H g or m o r e a b o v e the usual level of systolic blood pressure, or a sustained increase of 15 m m H g or more in the diastolic pressure, or a sustained absolute level of 140 mmHg or higher in the systolic pressure, or a sus-
eases.
Eclampsia is the development of
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985 Copyright ,6 1985 by the American College of Nurse-Midwives
Superimposed preeclampsia or eclampsia is the d e v e l o p m e n t of preeclampsia or eclampsia in a woman with chronic hypertension or renal disease. The three signs, hypertension, proteinuria, and edema, are defined as follows:
99 0091-2182/85/$03.30
tained diastolic pressure of 90 mmHg or higher. The presence of any one of these four conditions indicates hypertension in pregnancy, provided that the pressures are observed on at least two occasions six hours or more apart. 2. Proteinuria is the urinary excretion of more than 0.3 g/L of protein in a clean 24-hour collection of urine, or more than 1 g/L in a clean random sample. Again, the observations must be made on at least two occasions six hours or more apart. 3. E d e m a is the accumulation of fluid in the tissues, commonly manifested by facial, digital, or generalized swelling. A gain in weight of more than 2.25 kg in a week is indicative of edema. Pedal edema has a mechanical cause, is c o m m o n in normal pregnancy, and as an isolated finding it does not bear upon the diagnosis of preeclampsia. Actually, facial and digital edema are c o m m o n in normal pregnancy and are ignored in some classifications of the hypertensive disorders.
Dr. Leon Chesley is a member of the American Committee on Maternal Welfare. He is internationally known for his life-long research, writing, and contribution in the field of hypertensive disorders in pregnancy. Dr. Chesley has a doctoral degree in zoology from Duke University. He did his major research work at Margaret Hague Maternity Hospital in New Jersey and at Kings County Hospital in Brooklyn, NY. He is Professor Emeritus of the State University of New York at Downstate Medical Center. His many memberships include American College of Obstetricians and Gynecologists, International Society for the Study of Hypertension in Pregnancy, and Diplomate of American Board of Clinical Chemistry. Dr. Chesley is a frequent visiting professor in this country and abroad.
100
In the older classifications, and in some today, preeclampsia can be diagnosed on the sole basis of elevations in blood pressure, but m a n y such diagnoses are erroneous. In an attempt to improve the accuracy of the diagnosis of preeclampsia, the Committee on Terminology3 has set up a new category: transient, late, or gestational hypertension. It is characterized by the appearance of hypertension in pregnancy, labor, or early puerperium, with return of the blood pressure to normal within ten days after delivery. Proteinuria and abnormal edema are absent. Sometimes gestational hypertension is early preeclampsia, but more often it is a manifestation of latent essential hypertension and it predicts a high likelihood of future essential hypertension. It recurs in later pregnancies in about 80% of women having it, and it has been the basis for the erroneous diagnosis of preeclampsia in multiparas. PATIENTS AT INCREASED RISK FOR HYPERTENSIVE DISORDERS IN PREGNANCY
Several factors have been established as predisposing to the development of preeclampsia, and their presence calls for closer observation of the patient. The absence of such factors does not preclude the possibility that preeclampsia will develop. Predisposing Factors Nulliparity. Primigravidas and nulliparas with previous abortions are eight times more susceptible to preeclampsia than are multiparas. Familial history of preeclampsia-eclampsia. A recently completed 49-year prospective study has indicated that the susceptibility to preeclampsia-eclampsia is inherited and probably is determined by a single recessive gene. Using eclamptic women as probands, it was found that 38% of their 147 sisters had the
disorder in first pregnancies; 25% of 248 daughters had preeclampsia or eclampsia in first pregnancies; one in 35 had eclampsia; and 16% of their 74 granddaughters had preeclampsia. In contrast, only 6% of the daughters-in-law (controls) had preeclampsia. Moreover, the numbers of cases per family corresponded closely with predictions based on the hypothesis that a single gene determines the development of the disease. Plural pregnancy. The incidence of preeclampsia is increased five to six times in association with twin pregnancy, and even more with multiple fetuses. Diabetes mellitus. The incidence of preeclampsia is increased several fold in women with diabetes. Also, the prevalence of other hypertensive disorders is increased. Hydatidiform mole. A large, rapidly growing mole increases the incidence of preeclampsia tenfold, in both primigravidas and multiparas. Fetal hydrops. Fetal hydrops, of whatever cause, has the same effect as a large mole. Rh isoimmunization alone appears to have no effect. Chronic hypertension. Although s u p e r i m p o s e d p r e e c l a m p s i a is grossly overdiagnosed, chronic bypertension and probably renal disease do increase the risk of preeclampsia. In such cases, the preeclampsia usually appears earlier than in normotensive women, and it is more severe. Although most w o m e n with chronic hypertension have uneventful pregnancies, there is an increased risk of stillbirth of mature fetuses and of abruptio placentae. The major risk is the superimposition of preeclampsia, which carries a high perinatal mortality with marked increases in abruptio placentae, acute renal failure, and other less common
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985
complications such as cardiac failure, cerebral hemorrhage, and even maternal death. The patient with chronic hypertension should be examined weekly beginning as early as the 28th week of gestation, as preeclampsia tends to appear early. Most pregnant women with chronic hypertension have not had it long e n o u g h or in severe enough form for it to have caused significant renal or vascular disease, but in the few who do have the secondary changes, the fetal prognosis is poor. Therapeutic abortion should be considered if there are grade 3 or 4 changes in the eyegrounds (hemorrhages and exudates, or papilledema), or if renal function is significantly impaired (plasma creatinine level of 1.5 mg/dL, or higher), or if hypertensive cardiac disease has advanced to functional class 2 or worse. There is no good evidence that pregnancy accelerates permanently the course of essential hypertension or renal disease.
Extremes of age. The age-specific incidences of eclampsia are significantly higher before age 16 and after age 35 than in the intermediate age groups. Several other factors have been alleged to predispose to preeclampsia, but probably do not. Contrary to popular belief, short, squat, obese women are not at increased risk for eclampsia or preeclampsia, although they are at increased risk for gestational hypertension and ultimate essential hypertension. Socioeconomic status has little if anything to do with the incidence of preeclampsia, but impow~,rished women tend to have more severe manifestations of the disease because they often do not seek prenatal care. Polyhydramnios probably has no effect, although it frequently is associated with plural pregnancy, diabetes, and fetal hydrops, which do predispose to preeclampsia. There is no good evidence that diet plays any significant role in the d e v e l o p m e n t of pre-
eclampsia. For several centuries, eclampsia was believed to be a disease of upper class women, as diets high in protein were thought to be the cause. In the past half century, however, the nutritionists have changed their views. A simple test that helps to identify women at increased risk is the rollover test, although it is not wholly reliable. It is performed, preferably between the 28th and 32nd weeks of gestation, by having the patient lie on her side until the diastolic pressure stabilizes (about 20 minutes). The patient then rolls over to lie on her back, and the blood pressure is checked at one and five minutes. In a positive test, the diastolic pressure rises more than 20 mmHg, predicting that the patient has about a 65% chance of developing preeclampsia. Lesser rises in diastolic pressure constitute a negative test, and few of these w o m e n are expected to develop preeclampsia. Preeclampsia is rare before the 24th week of gestation, unusual before the 28th week, and develops with increasing frequency as pregnancy approaches term. Evaluation of the patient at shorter and shorter intervals as pregnancy progresses is therefore advised. Obviously, patients identified as being at high risk should be seen more frequently than in the routine schedule for supposedly normal women. Oncoming preeclampsia is sometimes heralded by the appearance of facial or digital edema, but the sign is not specific. It may appear before, at the same time as, or after the blood pressure increases, or not at all. The same is true with sudden inordinate weight gains. Although the majority of normal pregnant women gain more than 0.90 kg per week at some time in the latter half of pregnancy, seeing such a gain in weight should call for another examination within a week. The most common clinical sign of early preeclampsia is an abrupt rise in blood pressure, especially in the diastolic pressure.
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985
Occasionally the pressure increases over time, and obviously, such a trend calls for close observation. If the diastolic pressure reaches 90 mmHg or higher, the patient should be admitted to the hospital; there is no place for the ambulatory management of preeclampsia. MANAGEMENT OF HYPERTENSIVE DISORDERS IN PREGNANCY Preeclampsia
The two keys to the successful management of preeclampsia are to detect it early and never to be complacent. Early detection usually, but not always, enables treatment or termination of pregnancy to prevent progression of the disease. In the dayto-day management of patients, any acute rise in blood pressure must be regarded as preeclampsia, possibly leading to eclampsia, and potentially lethal. Dieckmann 4 shows that 22% of his eclamptic patients had no recorded systolic pressure exceeding 140 mmHg before the onset of convulsions. Their eclampsia was not mild, as about 14% died of it. My own observations have been similar; about one-quarter of all eclamptic w o m e n have had so-called mild or even barely diagnosable preeclampsia when the first convulsion occurred. Proteinuria is almost always a late sign in the course of preeclampsia, so late that perhaps 10% of eclamptic women have the first convulsion before its appearance. Preeclampsia is classified as severe in the presence of any one or more of the following: Systolic pressure of 160 mmHg or higher, or diastolic of 110 mmHg or higher, observed at least twice, six hours or more apart, with the patient resting in bed. Proteinuria of at least 5 g/L (3 or 4 plus in clinical tests). Oliguria (less than 400 mL of urine per 24 hours).
101
Cerebral or visual disturbances. Pulmonary edema or cyanosis. Abnormal hepatic function. Consumptive coagulopathy. Hemoconcentration. Epigastric pain. Possibly hyperreflexia. Patients with severe preeclampsia, as defined, are more likely to have convulsions than are those with socalled mild preeclampsia. However, one-quarter of all eclamptic women have had mild preeclampsia until the onset of convulsions. Obviously, we need more reliable criteria for assessing the inherent severity of preeclampsia. The diagnosis of mild preeclampsia cannot be established until after the patient has been delivered and discharged from the hospital. Severe preeclampsia is recognizable and calls for immediate treatment, often with prompt termination of the pregnancy. If the patient with any degree of preeclampsia is within two weeks of term there is little to be gained by carrying the pregnancy further if labor seems to be inducible. The pregnancy should not be permitted to go much past term, as the perinatal mortality increases. If the patient is far from term and the preeclampsia appears to be mild and not progressing, delivery may be delayed. At the Southwestern Medical School in Dallas, Gilstrap et al~ admitted 576 primigravidas whose diastolic blood pressure rose to 90 mmHg or higher. Thirty-one left the hospital against advice, and most of them returned with severe hypertension, with four stillbirths. The patients with severe preeclampsia on admittance were delivered within 24 hours unless the disease had abated significantly within that period. Those with such improvement, and all others, were kept in the High-Risk Unit for an average of 24 days (range from two to 120 days). The perinatal mottality in that group was only nine per 1000, about one-third that in the whole clinic population. Many of the women probably had gestational hy102
pertension rather than preeclampsia, yet many had preeclampsia, and the perinatal salvage is truly impressive. The patients were not confined to bed, but their physical activity was less than what it would have been if they had been at home. They were given the house diet without restriction of sodium, but did not have access to salty foods and colas (which may not be relevant). The only medication was ferrous sulfate. Blood pressures were recorded four times per day and urines were tested for protein daily. The patients were weighed three times per week and creatinine clearances were measured weekly. If the patient was far from term, the fetal growth was monitored by periodic sonography. Within five days of admittance to the hospital, the blood pressures fell to normal in 81% of the women, but rose again before or during labor in 87% (the preeclampsia was not cured; only delivery does that). Of the 19% in whom blood pressure did not return to normal, the hypertension was mild and intermittent in 13% (of all patients). In 6% of patients, significant hypertension persisted, and in all of these the pregnancies were terminated within a week; one of them developed eclampsia. The indications for delivery were: increasing blood pressure, onset or aggravation of proteinuria, sudden inordinate gain in weight, appearance of symptoms, decreased frequency of fetal movements, cessation of fetal growth, or a confirmed decrease in creatinine clearance. In the absence of such indications, pregnancies were allowed to continue until the onset of labor, term, or until the cervix was favorable for the induction of labor late in pregnancy. Induction of labor was successful in 286 (53%) women. The indicafions were: persistent or recurrent bypertension in 200 women, pregnancy at term in 57 women, and near term with a favorable cervix in 29 women. Cesarean sections were
performed in 156 (29%) women. The indications were failed induction of labor in 76 women and obstetric reasons in the others. The total perinatal mortality included one intrapartum stillbirth and four neonatal deaths. Only four infants were small for gestational age, and nine developed respiratory distress. The results prove that temporization in mild preeclampsia is practicable, but only with close observation of the patient and prompt intervention when the preeclampsia worsens. It has been recognized for three centuries that labor often precipitates convulsions in w o m e n with preeclampsia. For that reason, we frequently give parenteral magnesium sulfate to preeclamptics in labor, following the schedule described in the next section. Beyond doubt, many women so treated do not need it, but in the light of Dieckmann's 4 observation it is highly probable that occasionally we have prevented eclampsia in unidentifiable women.
Severe preeclampsia. The objectives in treating severe preeclampsia are to prevent convulsions and to salvage the fetus with as little trauma as possible. Our most efficacious agent for the prevention of convulsions is magnesium sulfate. Termination of the pregnancy within a few hours is usually desirable. Our practice is to give intravenously 3 g of magnesium sulfate (30 mL of 10% solution). The injection must be given slowly, over a period of three to five minutes. Immediately thereafter, we give 10 g of magnesium sulfate (20 mL of 50% solution) intramuscularly. The solution is mixed in the syringe with 1 or 2 mL of 2% lidocaine, and 10 mL is injected deep into the upper outer quadrant of each buttock, being sure that the needle is not in a blood vessel. The total dose of 13 g is safe, but further doses may not be given unless certain precautions are taken. The second or any later dose should be given only if: T e n d o n reflexes, such as the knee jerk, are present (as
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985
the plasma level of magnesium increases, the tendon reflexes disappear and with still higher levels, respiration is depressed, then arrested. Thus, the disappearance of the knee jerk indicates that the level of magnesium is approaching toxic concentrations); the respiratory rate is not depressed or below 16 breaths per minute (iit is not likely to be if the knee jerk is active, but it must be checked); the urinary output has been at least 100 mL since the last dose, (magnesium is excreted almost solely by the kidney, and severe renal impairment may lead to toxicity if the injections are continued); and the antidote to magnesium toxicity is readily at hand, (10 mL of 10% calcium gluconate for intravenous injections is effective). If all of the requirements are met, 5 g of magnesium sulfate (10 mL of 50% solution) is given intramuscularly every four hours, alternating the buttocks as the sites of injection. The treatment is continued for about 24 houn~ after delivery. It almost always stops convulsions in eclampsia, and ~have seen only one woman with preeclampsia develop convulsions while under treatment with magnesium sulfate. If the diastolic pressure is maintained at 110 mmHg or higher, hydralazine (Apresoline) is used to reduce it to between 90 and 100 mmHg, but not to normal. The placental blood flow, which is the lifeline of the fetus, is markedly reduced in preeclampsia and decreasing the maternal blood pressure may reduce it further. The initial dose of hydralazine is 5 or 10 mg, given intravenously as a bolus. If the diastolic pressure does not go down to the desired level by the end of 20 minutes, another dose of 10 mg is given. AImost always, a total dose of from 5 to 20 mg suffices in preeclamptic and eclamptic hypertension. Injections are repeated whenever the diastolic pressure rises again to 110 mmHg or higher, which may be within an hour, several hours, or not at all. Lactated Ringer's solution con-
taining 5% dextrose is given by infusion at a rate of from 60 to 150 mL per hour, unless there is oliguria (lower rate) or excessive loss of fluids (higher rate). Diuretic agents are contraindicated. Unless there is some contraindication to vaginal delivery, induction of labor with oxytocin should be initiated within a few hours. Procrastination increases the risk of fetal morbidity and mortality, and of abruptio placentae.
Eclampsia The treatment of eclampsia is essentially the same as that outlined for severe preeclampsia. Pritchard 6,7 has reported the best maternal and fetal salvage rates ever attained in eclampsia, and it is probably significant that his treatment, just described, is the simplest of the hundreds that have been tried. Parenteral magnesium sulfate is the only drug used in many cases; if the diastolic pressure is 110 mmHg or higher, he uses hydralazine as described. That is all, apart from the induction of labor or cesarean section as soon as the patient regains consciousness and is oriented. He uses no diuretic drugs, no sedation except for labor, no hypertonic solutions, no plasma expanders, and no heparin. In the unusual case of eclampsia in which convulsions continue, Pritchard administers another 2 g of magnesium sulfate intravenously, and in the rare cases with continuing convulsions, he gives another 2 g if the patient is large, or he gives a slow infusion of up to 250 mg of sodium amobarbital. Pritchard delivered about 26% of 214 fetuses of antepartum and intrapartum eclamptics by cesarean section, 56% of them because of failed induction of satisfactory labor. Nearly 80% of the attempted inductions were successful, even in patients far from term. He reported only one maternal death in 245 consecutive cases of eclampsia, and that one was accidental. An inexperienced attendant
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985
mistakenly gave 20 g of magnesium sulfate intravenously, which caused cardiac arrest. The perinatal mortality among the 214 fetuses and infants of antepartum and intrapartum eclamptic women was 33 (15.4%), but 12 were dead at the time of admittance to the hospital. With the conventional exclusion of those weighing less than 1000 g at birth, the corrected perinatal mortality was only 8.4%. Remarkably, there was only one stillbirth. In earlier years and under older m a n a g e m e n t the rate of stillbirth was 25% and up. If the patient's usual blood pressure had been less than 110/70 mmHg, as often is the case in young primigravidas, we would use hydralazine when the diastolic pressure exceeds 100 mmHg, seeking to reduce it to between 80 and 90. The reason for such treatment is that lowering the blood pressure may decrease the risk of cerebral hemorrhage, which causes about one-half of all eclamptic deaths? O t h e r treatments. Many obstetricians abroad do not use magnesium sulfate. Diazepam (Valium) is an anticonvulsant drug that has been used, but studies in Asia indicate that it fails to stop eclamptic convulsions in about 10% of cases, whereas magnesium sulfate fails in only 2 to 4% of cases. Moreover, diazepam has adverse effects upon the newborn infant, who cannot metabolize it. Cree et al8 found that doses as small as 15 mg cross the placenta rapidly and persist in the blood stream of the infant for up to eight days. The Apgar score is often depressed, the infant is atonic or even flaccid, the infant may have to be fed by tube for several days because the sucking reflex is depressed, and the infant has impaired thermogenesis. The continuous infusion of magnesium sulfate has been adopted in some clinics, as an alternative to the periodic intramuscular injections. A priming dose of 4 g is injected intravenously, followed by the infusion of 1, 1.5, 2 g or more per hour. Sibai 103
et al9 observed that the usual rate of 1 g per hour did not suffice to give therapeutic levels in the blood, and that nine patients developed convulsions while receiving the infusions. Even 2 g per hour was insufficient in some cases, and they increased the rate to 3 g per hour, which equals a total dose of 76 g per day. Although they did not observe magnesium toxicity in mothers or infants, such doses are potentially dangerous and call for close observation of the patient. The cases of magnesium toxicity that have been reported in infants have been associated with continuous infusions given to the mother, and the levels in blood attained by periodic intramuscular injections are more predictable than are those attained by infusion. Another variation has been to give the hydralazine by continuous infusion, but it is more efficacious if given by bolus, as required, whenever necessary.
Chronic Hypertension Several large clinical trials have shown that the reduction of hypertensive blood pressures by antihypertensive drugs decreases the morbidity and mortality in men, by retarding the progression of secondary vascular disease. The findings have set off a furor for treating all hypertension, but closer analysis of the data reveals that the beneficial results probably are limited to men aged 50 or more, patients with significant secondary vascular disease, and those whose diastolic pressure exceeds 105 mmHg. I° Very few p r e g n a n t w o m e n m e e t those criteria, and w o m e n have long b e e n known to withstand hypertension better than men. In passing, the rationale for the use of antihypertensive drugs does not apply to the acute and transient hypertension of preeclampsia. The most dreaded complication of chronic hypertension in pregnancy is the superimposition of preeclampsia, but nine studies have shown that control of the blood pressure does 104
not decrease its incidence. Moreover, control of the blood pressure often masks its onset until it appears suddenly in fulminant form. There are few controlled studies and in these the perinatal mortality was not significantly reduced, although late abortions were somewhat more frequent in control than in treated patients. Our practice is to treat chronic hypertension only if the diastolic pressure is sustained at 110 mmHg or higher, and again, we do not seek to reduce the pressure to normal. Diuretic drugs are not used. Most of the obstetric experience with antihypertensive drugs has been with ~-methyldopa (Aldomet), which we use. The initial dose is 250 mg three times daily. After three or four days, the dose is adjusted, up or down, depending on the response. The total dose should not e x c e e d 2.5 g per day, as larger doses increase side effects without much improvement of antihypertensive effect. Hydralazine, which we usually reserve for preeclamptic hypertension, may be added or substituted for c~-methyldopa if the initial response is not satisfactory. The fetal status is assessed frequently during the third trimester, with the nonstress test as the usual mainstay. DISCUSSION
The causes of preeclampsia and of most other hypertensive disorders are unknown, and for that reason, treatments are empiric, too often symptomatic, and in some respects, are based on imitative magic. Treatment is subject to fads. Twenty years ago, most p r e g n a n t w o m e n were given diuretic drugs to rid them of e d e m a and "to p r e v e n t preeclampsia." Several controlled studies have proved that the drugs do not prevent preeclampsia or have a beneficial effect in its treatment, and diuretic drugs are now believed to be contraindicated in preeclampsia. The current fad is to reduce even mild hy-
pertension to normal levels, but no beneficial effect has b e e n d e m o n strated. In the past, when maternal mortality in eclampsia was from 20 to 70%, treatment probably killed more women that did the disease. Pritchard's 7,8 u n m a t c h e d record of maternal and fetal salvage in eclampsia well may depend largely on the simplicity of his treatment. The method is empiric, but it works.
REFERENCES 1. Quilligan EJ, Little AB, Oh W: Pregnancy, birth and the infant. Washington, D.C., US Department of Health and Human Services, Public Health Service, National Institutes of Health, 1981, pp 2-6. 2. Editorial: Treatment of moderate hypertension in pregnancy. Br Med J 280:1483-1484, 1980. 3. Hughes EC (ed): Obstetric-gynecologic terminology. Philadelphia, Davis, 1972, pp 422-423. 4. Dieckmann WJ: The toxemias of pregnancy, 2nd ed. St. Louis, C. V. Mosby, 1952, p 420. 5. Gilstrap LC, Cunningham FG, Whalley PJ: Management of pregnancyinduced hypertension in the nulliparous patient far from term. Semin Perinatol 2:73-81, 1978. 6. Pritchard JA: Standardized treatment of 154 consecutive cases of eclampsia. Am J Obstet Gynecol 123:543-549, 1975. 7. Pritchard JA, Cunningham FG, Pritchard SA: The Parkland Hospital protocol for treatment of eclampsia: Evaluation of 245 cases. Am J Obstet Gynecol 145:951-963, 1984. 8. Cree JE, Meyer J, Hailey DM: Diazepam in labour: Its metabolism and effect on the clinical condition and thermogenesis of the newborn. Br Med J 4:251-255, 1973. 9. Sibai BM, Lipshitz J~ Anderson GD, et al: Reassessment of intravenous MgSO 4 therapy in preeclampsiaeclampsia. Obstet Gyneco157:199-202, 1981. 10. Alderman MH: The indications for treatment with antihypertensive drugs, in Sleight P, Freis ED, (eds), Cardiology 1, Hypertension. London, Butterworth Scientific, 1982, pp 248-270.
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985
Leon C. Chesley,
PhD
ABSTRACT Hypertensive disorders in pregnancy are the leading cause of maternal death in the United States and in many other parts of the world. A recent prospective study has indicated that the susceptibility to preeclampsia-eclampsia is inherited and probably is determined by a single recessive gene. However, the causes are still unknown. The incidences, prevalences, definitions, cardinal signs, and patients at increased risk for hypertensive disorders in pregnancy are discussed. Successful management of these disorders is early detection. Further discussions are made on the management of preeclampsia, eclampsia, and chronic hypertension in regard to treatment, intrapartum course, and maternal and perinatal outcome.
The hypertensive disorders, chiefly eclampsia, are the leading cause of maternal death in the United States, I England and Wales, 2 and in many other parts of the world. Moreover, they predispose the mother to potentially lethal complications such as abruptio placentae, acute renal failure, circulatory collapse, disseminated intravascular coagulation, and cerebral h e m o r r h a g e . T h e y also greatly increase fetal and neonatal morbidity and mortality. Although there are no reliable data for the overall frequency, the combined incidences and prevalences of the several hypertensive disorders are said to be about 6 to 8%, with wide w~riations in some populations. Black American w o m e n , for instance, have a two to three times higher prevalence of chronic hypertension than do white women, but, contrary to popular belief, the incidence of preeclampsia is similar in the two races. The incidence of preAddress correspondence to: Department of Obstetrics and Gynecology, State University of New York Downstate Medical Center, Brooklyn, NY.
eclampsia varies with the mix of primigravidas and multiparas because preeclampsia is predominantly a disease of the first pregnancy. The incidence of eclampsia and eclamptic deaths depends largely on the availability, quality, and use of prenatal care, b e c a u s e early detection and treatment of preeclampsia, or termination of pregnancy, often can prevent progression of the disease. Almost any hypertensive disease occurring in n o n p r e g n a n t w o m e n may complicate pregnancy; additionally, pregnant women may develop a disease peculiar to pregnancy, such as p r e e c l a m p s i a - e c l a m p s i a . The Committee on Terminology of the American College of Obstetricians and Gynecologists 3 has proposed the following definitions for the hypertensive disorders in pregnancy:
convulsions in a woman with preeclampsia, provided that the convulsions are not attributable to epilepsy, cerebral h e m o r r h a g e or thrombosis, or water intoxication. Chronic hypertensive disease is the presence of sustained hypertension of any cause before, during, and after pregnancy. The discovery of hypertension before the 20th week of gestation is taken as presumptive e v i d e n c e for its having antedated pregnancy.
Preeclampsia is the development of
1. Hypertension is a sustained rise of
hypertension, with proteinuria or facial, digital, or generalized edema after the 20th week of gestation. It may appear earlier in association with trophoblastic dis-
30 m m H g or m o r e a b o v e the usual level of systolic blood pressure, or a sustained increase of 15 m m H g or more in the diastolic pressure, or a sustained absolute level of 140 mmHg or higher in the systolic pressure, or a sus-
eases.
Eclampsia is the development of
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985 Copyright ,6 1985 by the American College of Nurse-Midwives
Superimposed preeclampsia or eclampsia is the d e v e l o p m e n t of preeclampsia or eclampsia in a woman with chronic hypertension or renal disease. The three signs, hypertension, proteinuria, and edema, are defined as follows:
99 0091-2182/85/$03.30
tained diastolic pressure of 90 mmHg or higher. The presence of any one of these four conditions indicates hypertension in pregnancy, provided that the pressures are observed on at least two occasions six hours or more apart. 2. Proteinuria is the urinary excretion of more than 0.3 g/L of protein in a clean 24-hour collection of urine, or more than 1 g/L in a clean random sample. Again, the observations must be made on at least two occasions six hours or more apart. 3. E d e m a is the accumulation of fluid in the tissues, commonly manifested by facial, digital, or generalized swelling. A gain in weight of more than 2.25 kg in a week is indicative of edema. Pedal edema has a mechanical cause, is c o m m o n in normal pregnancy, and as an isolated finding it does not bear upon the diagnosis of preeclampsia. Actually, facial and digital edema are c o m m o n in normal pregnancy and are ignored in some classifications of the hypertensive disorders.
Dr. Leon Chesley is a member of the American Committee on Maternal Welfare. He is internationally known for his life-long research, writing, and contribution in the field of hypertensive disorders in pregnancy. Dr. Chesley has a doctoral degree in zoology from Duke University. He did his major research work at Margaret Hague Maternity Hospital in New Jersey and at Kings County Hospital in Brooklyn, NY. He is Professor Emeritus of the State University of New York at Downstate Medical Center. His many memberships include American College of Obstetricians and Gynecologists, International Society for the Study of Hypertension in Pregnancy, and Diplomate of American Board of Clinical Chemistry. Dr. Chesley is a frequent visiting professor in this country and abroad.
100
In the older classifications, and in some today, preeclampsia can be diagnosed on the sole basis of elevations in blood pressure, but m a n y such diagnoses are erroneous. In an attempt to improve the accuracy of the diagnosis of preeclampsia, the Committee on Terminology3 has set up a new category: transient, late, or gestational hypertension. It is characterized by the appearance of hypertension in pregnancy, labor, or early puerperium, with return of the blood pressure to normal within ten days after delivery. Proteinuria and abnormal edema are absent. Sometimes gestational hypertension is early preeclampsia, but more often it is a manifestation of latent essential hypertension and it predicts a high likelihood of future essential hypertension. It recurs in later pregnancies in about 80% of women having it, and it has been the basis for the erroneous diagnosis of preeclampsia in multiparas. PATIENTS AT INCREASED RISK FOR HYPERTENSIVE DISORDERS IN PREGNANCY
Several factors have been established as predisposing to the development of preeclampsia, and their presence calls for closer observation of the patient. The absence of such factors does not preclude the possibility that preeclampsia will develop. Predisposing Factors Nulliparity. Primigravidas and nulliparas with previous abortions are eight times more susceptible to preeclampsia than are multiparas. Familial history of preeclampsia-eclampsia. A recently completed 49-year prospective study has indicated that the susceptibility to preeclampsia-eclampsia is inherited and probably is determined by a single recessive gene. Using eclamptic women as probands, it was found that 38% of their 147 sisters had the
disorder in first pregnancies; 25% of 248 daughters had preeclampsia or eclampsia in first pregnancies; one in 35 had eclampsia; and 16% of their 74 granddaughters had preeclampsia. In contrast, only 6% of the daughters-in-law (controls) had preeclampsia. Moreover, the numbers of cases per family corresponded closely with predictions based on the hypothesis that a single gene determines the development of the disease. Plural pregnancy. The incidence of preeclampsia is increased five to six times in association with twin pregnancy, and even more with multiple fetuses. Diabetes mellitus. The incidence of preeclampsia is increased several fold in women with diabetes. Also, the prevalence of other hypertensive disorders is increased. Hydatidiform mole. A large, rapidly growing mole increases the incidence of preeclampsia tenfold, in both primigravidas and multiparas. Fetal hydrops. Fetal hydrops, of whatever cause, has the same effect as a large mole. Rh isoimmunization alone appears to have no effect. Chronic hypertension. Although s u p e r i m p o s e d p r e e c l a m p s i a is grossly overdiagnosed, chronic bypertension and probably renal disease do increase the risk of preeclampsia. In such cases, the preeclampsia usually appears earlier than in normotensive women, and it is more severe. Although most w o m e n with chronic hypertension have uneventful pregnancies, there is an increased risk of stillbirth of mature fetuses and of abruptio placentae. The major risk is the superimposition of preeclampsia, which carries a high perinatal mortality with marked increases in abruptio placentae, acute renal failure, and other less common
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985
complications such as cardiac failure, cerebral hemorrhage, and even maternal death. The patient with chronic hypertension should be examined weekly beginning as early as the 28th week of gestation, as preeclampsia tends to appear early. Most pregnant women with chronic hypertension have not had it long e n o u g h or in severe enough form for it to have caused significant renal or vascular disease, but in the few who do have the secondary changes, the fetal prognosis is poor. Therapeutic abortion should be considered if there are grade 3 or 4 changes in the eyegrounds (hemorrhages and exudates, or papilledema), or if renal function is significantly impaired (plasma creatinine level of 1.5 mg/dL, or higher), or if hypertensive cardiac disease has advanced to functional class 2 or worse. There is no good evidence that pregnancy accelerates permanently the course of essential hypertension or renal disease.
Extremes of age. The age-specific incidences of eclampsia are significantly higher before age 16 and after age 35 than in the intermediate age groups. Several other factors have been alleged to predispose to preeclampsia, but probably do not. Contrary to popular belief, short, squat, obese women are not at increased risk for eclampsia or preeclampsia, although they are at increased risk for gestational hypertension and ultimate essential hypertension. Socioeconomic status has little if anything to do with the incidence of preeclampsia, but impow~,rished women tend to have more severe manifestations of the disease because they often do not seek prenatal care. Polyhydramnios probably has no effect, although it frequently is associated with plural pregnancy, diabetes, and fetal hydrops, which do predispose to preeclampsia. There is no good evidence that diet plays any significant role in the d e v e l o p m e n t of pre-
eclampsia. For several centuries, eclampsia was believed to be a disease of upper class women, as diets high in protein were thought to be the cause. In the past half century, however, the nutritionists have changed their views. A simple test that helps to identify women at increased risk is the rollover test, although it is not wholly reliable. It is performed, preferably between the 28th and 32nd weeks of gestation, by having the patient lie on her side until the diastolic pressure stabilizes (about 20 minutes). The patient then rolls over to lie on her back, and the blood pressure is checked at one and five minutes. In a positive test, the diastolic pressure rises more than 20 mmHg, predicting that the patient has about a 65% chance of developing preeclampsia. Lesser rises in diastolic pressure constitute a negative test, and few of these w o m e n are expected to develop preeclampsia. Preeclampsia is rare before the 24th week of gestation, unusual before the 28th week, and develops with increasing frequency as pregnancy approaches term. Evaluation of the patient at shorter and shorter intervals as pregnancy progresses is therefore advised. Obviously, patients identified as being at high risk should be seen more frequently than in the routine schedule for supposedly normal women. Oncoming preeclampsia is sometimes heralded by the appearance of facial or digital edema, but the sign is not specific. It may appear before, at the same time as, or after the blood pressure increases, or not at all. The same is true with sudden inordinate weight gains. Although the majority of normal pregnant women gain more than 0.90 kg per week at some time in the latter half of pregnancy, seeing such a gain in weight should call for another examination within a week. The most common clinical sign of early preeclampsia is an abrupt rise in blood pressure, especially in the diastolic pressure.
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985
Occasionally the pressure increases over time, and obviously, such a trend calls for close observation. If the diastolic pressure reaches 90 mmHg or higher, the patient should be admitted to the hospital; there is no place for the ambulatory management of preeclampsia. MANAGEMENT OF HYPERTENSIVE DISORDERS IN PREGNANCY Preeclampsia
The two keys to the successful management of preeclampsia are to detect it early and never to be complacent. Early detection usually, but not always, enables treatment or termination of pregnancy to prevent progression of the disease. In the dayto-day management of patients, any acute rise in blood pressure must be regarded as preeclampsia, possibly leading to eclampsia, and potentially lethal. Dieckmann 4 shows that 22% of his eclamptic patients had no recorded systolic pressure exceeding 140 mmHg before the onset of convulsions. Their eclampsia was not mild, as about 14% died of it. My own observations have been similar; about one-quarter of all eclamptic w o m e n have had so-called mild or even barely diagnosable preeclampsia when the first convulsion occurred. Proteinuria is almost always a late sign in the course of preeclampsia, so late that perhaps 10% of eclamptic women have the first convulsion before its appearance. Preeclampsia is classified as severe in the presence of any one or more of the following: Systolic pressure of 160 mmHg or higher, or diastolic of 110 mmHg or higher, observed at least twice, six hours or more apart, with the patient resting in bed. Proteinuria of at least 5 g/L (3 or 4 plus in clinical tests). Oliguria (less than 400 mL of urine per 24 hours).
101
Cerebral or visual disturbances. Pulmonary edema or cyanosis. Abnormal hepatic function. Consumptive coagulopathy. Hemoconcentration. Epigastric pain. Possibly hyperreflexia. Patients with severe preeclampsia, as defined, are more likely to have convulsions than are those with socalled mild preeclampsia. However, one-quarter of all eclamptic women have had mild preeclampsia until the onset of convulsions. Obviously, we need more reliable criteria for assessing the inherent severity of preeclampsia. The diagnosis of mild preeclampsia cannot be established until after the patient has been delivered and discharged from the hospital. Severe preeclampsia is recognizable and calls for immediate treatment, often with prompt termination of the pregnancy. If the patient with any degree of preeclampsia is within two weeks of term there is little to be gained by carrying the pregnancy further if labor seems to be inducible. The pregnancy should not be permitted to go much past term, as the perinatal mortality increases. If the patient is far from term and the preeclampsia appears to be mild and not progressing, delivery may be delayed. At the Southwestern Medical School in Dallas, Gilstrap et al~ admitted 576 primigravidas whose diastolic blood pressure rose to 90 mmHg or higher. Thirty-one left the hospital against advice, and most of them returned with severe hypertension, with four stillbirths. The patients with severe preeclampsia on admittance were delivered within 24 hours unless the disease had abated significantly within that period. Those with such improvement, and all others, were kept in the High-Risk Unit for an average of 24 days (range from two to 120 days). The perinatal mottality in that group was only nine per 1000, about one-third that in the whole clinic population. Many of the women probably had gestational hy102
pertension rather than preeclampsia, yet many had preeclampsia, and the perinatal salvage is truly impressive. The patients were not confined to bed, but their physical activity was less than what it would have been if they had been at home. They were given the house diet without restriction of sodium, but did not have access to salty foods and colas (which may not be relevant). The only medication was ferrous sulfate. Blood pressures were recorded four times per day and urines were tested for protein daily. The patients were weighed three times per week and creatinine clearances were measured weekly. If the patient was far from term, the fetal growth was monitored by periodic sonography. Within five days of admittance to the hospital, the blood pressures fell to normal in 81% of the women, but rose again before or during labor in 87% (the preeclampsia was not cured; only delivery does that). Of the 19% in whom blood pressure did not return to normal, the hypertension was mild and intermittent in 13% (of all patients). In 6% of patients, significant hypertension persisted, and in all of these the pregnancies were terminated within a week; one of them developed eclampsia. The indications for delivery were: increasing blood pressure, onset or aggravation of proteinuria, sudden inordinate gain in weight, appearance of symptoms, decreased frequency of fetal movements, cessation of fetal growth, or a confirmed decrease in creatinine clearance. In the absence of such indications, pregnancies were allowed to continue until the onset of labor, term, or until the cervix was favorable for the induction of labor late in pregnancy. Induction of labor was successful in 286 (53%) women. The indicafions were: persistent or recurrent bypertension in 200 women, pregnancy at term in 57 women, and near term with a favorable cervix in 29 women. Cesarean sections were
performed in 156 (29%) women. The indications were failed induction of labor in 76 women and obstetric reasons in the others. The total perinatal mortality included one intrapartum stillbirth and four neonatal deaths. Only four infants were small for gestational age, and nine developed respiratory distress. The results prove that temporization in mild preeclampsia is practicable, but only with close observation of the patient and prompt intervention when the preeclampsia worsens. It has been recognized for three centuries that labor often precipitates convulsions in w o m e n with preeclampsia. For that reason, we frequently give parenteral magnesium sulfate to preeclamptics in labor, following the schedule described in the next section. Beyond doubt, many women so treated do not need it, but in the light of Dieckmann's 4 observation it is highly probable that occasionally we have prevented eclampsia in unidentifiable women.
Severe preeclampsia. The objectives in treating severe preeclampsia are to prevent convulsions and to salvage the fetus with as little trauma as possible. Our most efficacious agent for the prevention of convulsions is magnesium sulfate. Termination of the pregnancy within a few hours is usually desirable. Our practice is to give intravenously 3 g of magnesium sulfate (30 mL of 10% solution). The injection must be given slowly, over a period of three to five minutes. Immediately thereafter, we give 10 g of magnesium sulfate (20 mL of 50% solution) intramuscularly. The solution is mixed in the syringe with 1 or 2 mL of 2% lidocaine, and 10 mL is injected deep into the upper outer quadrant of each buttock, being sure that the needle is not in a blood vessel. The total dose of 13 g is safe, but further doses may not be given unless certain precautions are taken. The second or any later dose should be given only if: T e n d o n reflexes, such as the knee jerk, are present (as
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985
the plasma level of magnesium increases, the tendon reflexes disappear and with still higher levels, respiration is depressed, then arrested. Thus, the disappearance of the knee jerk indicates that the level of magnesium is approaching toxic concentrations); the respiratory rate is not depressed or below 16 breaths per minute (iit is not likely to be if the knee jerk is active, but it must be checked); the urinary output has been at least 100 mL since the last dose, (magnesium is excreted almost solely by the kidney, and severe renal impairment may lead to toxicity if the injections are continued); and the antidote to magnesium toxicity is readily at hand, (10 mL of 10% calcium gluconate for intravenous injections is effective). If all of the requirements are met, 5 g of magnesium sulfate (10 mL of 50% solution) is given intramuscularly every four hours, alternating the buttocks as the sites of injection. The treatment is continued for about 24 houn~ after delivery. It almost always stops convulsions in eclampsia, and ~have seen only one woman with preeclampsia develop convulsions while under treatment with magnesium sulfate. If the diastolic pressure is maintained at 110 mmHg or higher, hydralazine (Apresoline) is used to reduce it to between 90 and 100 mmHg, but not to normal. The placental blood flow, which is the lifeline of the fetus, is markedly reduced in preeclampsia and decreasing the maternal blood pressure may reduce it further. The initial dose of hydralazine is 5 or 10 mg, given intravenously as a bolus. If the diastolic pressure does not go down to the desired level by the end of 20 minutes, another dose of 10 mg is given. AImost always, a total dose of from 5 to 20 mg suffices in preeclamptic and eclamptic hypertension. Injections are repeated whenever the diastolic pressure rises again to 110 mmHg or higher, which may be within an hour, several hours, or not at all. Lactated Ringer's solution con-
taining 5% dextrose is given by infusion at a rate of from 60 to 150 mL per hour, unless there is oliguria (lower rate) or excessive loss of fluids (higher rate). Diuretic agents are contraindicated. Unless there is some contraindication to vaginal delivery, induction of labor with oxytocin should be initiated within a few hours. Procrastination increases the risk of fetal morbidity and mortality, and of abruptio placentae.
Eclampsia The treatment of eclampsia is essentially the same as that outlined for severe preeclampsia. Pritchard 6,7 has reported the best maternal and fetal salvage rates ever attained in eclampsia, and it is probably significant that his treatment, just described, is the simplest of the hundreds that have been tried. Parenteral magnesium sulfate is the only drug used in many cases; if the diastolic pressure is 110 mmHg or higher, he uses hydralazine as described. That is all, apart from the induction of labor or cesarean section as soon as the patient regains consciousness and is oriented. He uses no diuretic drugs, no sedation except for labor, no hypertonic solutions, no plasma expanders, and no heparin. In the unusual case of eclampsia in which convulsions continue, Pritchard administers another 2 g of magnesium sulfate intravenously, and in the rare cases with continuing convulsions, he gives another 2 g if the patient is large, or he gives a slow infusion of up to 250 mg of sodium amobarbital. Pritchard delivered about 26% of 214 fetuses of antepartum and intrapartum eclamptics by cesarean section, 56% of them because of failed induction of satisfactory labor. Nearly 80% of the attempted inductions were successful, even in patients far from term. He reported only one maternal death in 245 consecutive cases of eclampsia, and that one was accidental. An inexperienced attendant
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985
mistakenly gave 20 g of magnesium sulfate intravenously, which caused cardiac arrest. The perinatal mortality among the 214 fetuses and infants of antepartum and intrapartum eclamptic women was 33 (15.4%), but 12 were dead at the time of admittance to the hospital. With the conventional exclusion of those weighing less than 1000 g at birth, the corrected perinatal mortality was only 8.4%. Remarkably, there was only one stillbirth. In earlier years and under older m a n a g e m e n t the rate of stillbirth was 25% and up. If the patient's usual blood pressure had been less than 110/70 mmHg, as often is the case in young primigravidas, we would use hydralazine when the diastolic pressure exceeds 100 mmHg, seeking to reduce it to between 80 and 90. The reason for such treatment is that lowering the blood pressure may decrease the risk of cerebral hemorrhage, which causes about one-half of all eclamptic deaths? O t h e r treatments. Many obstetricians abroad do not use magnesium sulfate. Diazepam (Valium) is an anticonvulsant drug that has been used, but studies in Asia indicate that it fails to stop eclamptic convulsions in about 10% of cases, whereas magnesium sulfate fails in only 2 to 4% of cases. Moreover, diazepam has adverse effects upon the newborn infant, who cannot metabolize it. Cree et al8 found that doses as small as 15 mg cross the placenta rapidly and persist in the blood stream of the infant for up to eight days. The Apgar score is often depressed, the infant is atonic or even flaccid, the infant may have to be fed by tube for several days because the sucking reflex is depressed, and the infant has impaired thermogenesis. The continuous infusion of magnesium sulfate has been adopted in some clinics, as an alternative to the periodic intramuscular injections. A priming dose of 4 g is injected intravenously, followed by the infusion of 1, 1.5, 2 g or more per hour. Sibai 103
et al9 observed that the usual rate of 1 g per hour did not suffice to give therapeutic levels in the blood, and that nine patients developed convulsions while receiving the infusions. Even 2 g per hour was insufficient in some cases, and they increased the rate to 3 g per hour, which equals a total dose of 76 g per day. Although they did not observe magnesium toxicity in mothers or infants, such doses are potentially dangerous and call for close observation of the patient. The cases of magnesium toxicity that have been reported in infants have been associated with continuous infusions given to the mother, and the levels in blood attained by periodic intramuscular injections are more predictable than are those attained by infusion. Another variation has been to give the hydralazine by continuous infusion, but it is more efficacious if given by bolus, as required, whenever necessary.
Chronic Hypertension Several large clinical trials have shown that the reduction of hypertensive blood pressures by antihypertensive drugs decreases the morbidity and mortality in men, by retarding the progression of secondary vascular disease. The findings have set off a furor for treating all hypertension, but closer analysis of the data reveals that the beneficial results probably are limited to men aged 50 or more, patients with significant secondary vascular disease, and those whose diastolic pressure exceeds 105 mmHg. I° Very few p r e g n a n t w o m e n m e e t those criteria, and w o m e n have long b e e n known to withstand hypertension better than men. In passing, the rationale for the use of antihypertensive drugs does not apply to the acute and transient hypertension of preeclampsia. The most dreaded complication of chronic hypertension in pregnancy is the superimposition of preeclampsia, but nine studies have shown that control of the blood pressure does 104
not decrease its incidence. Moreover, control of the blood pressure often masks its onset until it appears suddenly in fulminant form. There are few controlled studies and in these the perinatal mortality was not significantly reduced, although late abortions were somewhat more frequent in control than in treated patients. Our practice is to treat chronic hypertension only if the diastolic pressure is sustained at 110 mmHg or higher, and again, we do not seek to reduce the pressure to normal. Diuretic drugs are not used. Most of the obstetric experience with antihypertensive drugs has been with ~-methyldopa (Aldomet), which we use. The initial dose is 250 mg three times daily. After three or four days, the dose is adjusted, up or down, depending on the response. The total dose should not e x c e e d 2.5 g per day, as larger doses increase side effects without much improvement of antihypertensive effect. Hydralazine, which we usually reserve for preeclamptic hypertension, may be added or substituted for c~-methyldopa if the initial response is not satisfactory. The fetal status is assessed frequently during the third trimester, with the nonstress test as the usual mainstay. DISCUSSION
The causes of preeclampsia and of most other hypertensive disorders are unknown, and for that reason, treatments are empiric, too often symptomatic, and in some respects, are based on imitative magic. Treatment is subject to fads. Twenty years ago, most p r e g n a n t w o m e n were given diuretic drugs to rid them of e d e m a and "to p r e v e n t preeclampsia." Several controlled studies have proved that the drugs do not prevent preeclampsia or have a beneficial effect in its treatment, and diuretic drugs are now believed to be contraindicated in preeclampsia. The current fad is to reduce even mild hy-
pertension to normal levels, but no beneficial effect has b e e n d e m o n strated. In the past, when maternal mortality in eclampsia was from 20 to 70%, treatment probably killed more women that did the disease. Pritchard's 7,8 u n m a t c h e d record of maternal and fetal salvage in eclampsia well may depend largely on the simplicity of his treatment. The method is empiric, but it works.
REFERENCES 1. Quilligan EJ, Little AB, Oh W: Pregnancy, birth and the infant. Washington, D.C., US Department of Health and Human Services, Public Health Service, National Institutes of Health, 1981, pp 2-6. 2. Editorial: Treatment of moderate hypertension in pregnancy. Br Med J 280:1483-1484, 1980. 3. Hughes EC (ed): Obstetric-gynecologic terminology. Philadelphia, Davis, 1972, pp 422-423. 4. Dieckmann WJ: The toxemias of pregnancy, 2nd ed. St. Louis, C. V. Mosby, 1952, p 420. 5. Gilstrap LC, Cunningham FG, Whalley PJ: Management of pregnancyinduced hypertension in the nulliparous patient far from term. Semin Perinatol 2:73-81, 1978. 6. Pritchard JA: Standardized treatment of 154 consecutive cases of eclampsia. Am J Obstet Gynecol 123:543-549, 1975. 7. Pritchard JA, Cunningham FG, Pritchard SA: The Parkland Hospital protocol for treatment of eclampsia: Evaluation of 245 cases. Am J Obstet Gynecol 145:951-963, 1984. 8. Cree JE, Meyer J, Hailey DM: Diazepam in labour: Its metabolism and effect on the clinical condition and thermogenesis of the newborn. Br Med J 4:251-255, 1973. 9. Sibai BM, Lipshitz J~ Anderson GD, et al: Reassessment of intravenous MgSO 4 therapy in preeclampsiaeclampsia. Obstet Gyneco157:199-202, 1981. 10. Alderman MH: The indications for treatment with antihypertensive drugs, in Sleight P, Freis ED, (eds), Cardiology 1, Hypertension. London, Butterworth Scientific, 1982, pp 248-270.
Journal of Nurse-Midwifery • Vol. 30, No. 2, March/April 1985