MEDLINE Abstracts: Pharmacotherapy for Hypertension During Pregnancy
MEDLINE Abstracts: Pharmacotherapy for Hypertension During Pregnancy
What's the latest in drug treatment of hypertension during pregnancy? Find out in this easy-to-navigate collection of recent MEDLINE abstracts compiled by the editors at Medscape Pharmacotherapy.
Lydakis C, Lip GY, Beevers M, Beevers DG
Am J Hypertens. 1999;12(6):541-7
Atenolol use may be associated with growth retardation when given in pregnancy, although the relationship to trimester of initiation, duration of treatment, and its use as monotherapy is still uncertain. To compare the obstetric and fetal outcome between women receiving atenolol (as monotherapy) and other antihypertensive drug monotherapies, and also to investigate the effect of duration of treatment on fetal growth, we performed a retrospective cohort study of 312 pregnancies in 223 women attending an Antenatal Hypertension Clinic. Atenolol (as monotherapy) was given in 78 pregnancies (25.0%), other types of antihypertensive drugs as monotherapy were given in 53 pregnancies (17.0%), and multiple drug combinations were given in 90 pregnancies (28.8%). In 91 pregnancies (29.2%) no antihypertensive drugs were given. Atenolol was found to be associated with lower birth weight and ponderal index values, with a trend toward a higher prevalence of preterm (<37 weeks) delivery and small-for-gestational-age babies when compared to other antihypertensive drugs as monotherapy, or to no treatment. The adverse effect of atenolol was more pronounced in women receiving the drug earlier in their pregnancy, and continuing the drug for a longer duration. In conclusion, atenolol should be avoided in the early stages of pregnancy and given with caution at the later stages, as it is associated with fetal growth retardation, which is related to duration of treatment.
Hall DR, Odendaal HJ, Steyn DW, Smith M
BJOG. 2000;107(6):759-65
Objective: To determine whether nifedipine or prazosin is the more appropriate second-line antihypertensive agent in pregnancy.
Design: Randomised controlled trial. SETTING: Tygerberg Hospital, a tertiary referral centre. POPULATION: Women with early, severe pre-eclampsia or hypertension in pregnancy, whose blood pressure could not be adequately controlled by methyldopa 2 g/day, but were otherwise stable.
Methods: Nifedipine or prazosin were given and increased as necessary in a stepwise fashion. Once the maximum dose was reached, the other drug was added in a crossover pattern. Failure to control blood pressure, or the onset of maternal/fetal complications were indications for delivery. Patients reaching a minimum gestation of 34 weeks without complications were delivered electively.
Main Outcome Measures: Antenatal days gained; major maternal complications and perinatal survival.
Results: Days gained on the second antihypertensive agent did not differ significantly (P = 0.9), while more days were gained using nifedipine as the crossover 'third agent' (P = 0.01). In the nifedipine group better renal function was recorded, but more cases with isolated low platelet counts occurred. More cases of pulmonary oedema as well as more nonviable mid-trimester and third trimester intrauterine deaths occurred in the prazosin group.
Conclusion: Nifedipine and prazosin as second agents allowed comparable amounts of time to be gained, although this changed when used as crossover third-line agents. The efficacy and safety of nifedipine in this study are consistent with the results of other studies. A greater number of intrauterine deaths occurred in the prazosin group.
Gazzolo D, Visser GH, Russo A, Scopesi F, Santi F, Bruschettini PL
Early Hum Dev. 1998;50(2):149-57
In 21 pregnancies complicated by pregnancy-induced hypertension (PIH) which was treated by antihypertensive drugs (labetalol, nifedipine), fetal behavioural recordings (quiet state, C1F; active state, C2F; no coincidence, NOC) and Doppler measurements of blood flow velocity in the umbilical artery (UA) (resistance index, RI) were made on two occasions (27-32 and 33-36 weeks of gestation). Data were compared to those of a control group of normally grown fetuses (n = 96); in 15 cases we were able to match fetuses from the study group for age (+/- 1 week) and weight (+/- 150 g) at birth with fetales from a control group. It was the aim of this study to investigate if there are disturbances in the development of fetal behavioural states and if possible disturbances are due to poor fetal growth or to antihypertensive therapy. Our results show that in PIH treated by antihypertensive drugs, there are disturbances in the development of fetal behavioural states with higher percentages of NOC and C1F, lower percentages of C2F, and higher UA RI values. These disturbances are mainly due to coexisting placental impairment and poor fetal growth rather than to nifedipine or labetalol therapy, although these drugs may cause some redistribution of states.
Tomlinson AJ, Campbell J, Walker JJ, Morgan C
Ann Pharmacother. 2000;34(2):180-2
Objective: To report a case of a patient treated with an angiotensin-converting enzyme (ACE) inhibitor with a good neonatal outcome.
Case Report: A 39-year-old African-Caribbean patient who had chronic hypertension presented at 18 weeks' gestation with acute hypertension. She was being treated for chronic hypertension with lisinopril, but had self-discontinued treatment. Attempts to control her hypertension with labetolol, nifedipine, and methyldopa were ineffective. She was therefore offered termination of pregnancy so treatment with lisinopril could be restarted. The patient elected to continue with the pregnancy in spite of the fetal risks associated with the use of an ACE inhibitor. She was delivered of a girl at 26 weeks' gestation. The baby initially had renal failure and also developed acute necrotizing enterocolitis. The renal failure improved simultaneously with the latter complication, and it is postulated that there was enteric excretion of lisinopril. The baby was discharged home on day 102 with no further complications.
Discussion: ACE inhibitors are acceptable medications to use in the first trimester of pregnancy; however, fetal malformations and neonatal complications have been associated with their use later in pregnancy, and they have a perinatal mortality rate of 97/1000. Lisinopril is excreted in urine and feces unchanged, and its half-life is prolonged in anuric neonates. Peritoneal dialysis eliminates lisinopril; however, this neonate improved after treatment for necrotizing enterocolitis and simultaneous improvement in bowel function.
Conclusions: ACE inhibitors should not be used in pregnancy beyond the end of the first trimester. In exceptional cases, they may be indicated for the control of severe hypertension when the patient is refractory to other medications. The patient should be fully counseled about the adverse effect profile and neonatal outcome. This case report documents a successful outcome for mother and baby in these circumstances.
von Dadelszen P, Ornstein MP, Bull SB, Logan AG, Koren G, Magee LA
Lancet. 2000;355(9198):87-92
Background: We investigated the relation between fetoplacental growth and the use of oral antihypertensive medication to treat mild-to-moderate pregnancy hypertension.
Methods: The study design was a metaregression analysis of published data from randomised controlled trials. Data from a paper that was regarded as an extreme statistical outliner were excluded from primary analyses. The change in (group) mean arterial pressure (MAP) from enrolment to delivery was compared with indicators of fetoplacental growth.
Findings: Greater mean difference in MAP with antihypertensive therapy was associated with the birth of a higher proportion of small-for-gestational-age (SGA) infants (slope: 0.09 [SD 0.03], r2=0.48, p=0.006, 14 trials) and lower mean birthweight significant after exclusion of data from another paper regarded as an extreme statistical outliner (slope: -14.49 [6.98] r=0.16, p=0.049, 27). No relation with mean placental weight was seen (slope -2.01 [1.62], r2=0.15, p=0.25, 11 trials).
Interpretation: Treatment-induced falls in maternal blood pressure may adversely affect fetal growth. Given the small maternal benefits that are likely to be derived from therapy, new data are urgently needed to elucidate the relative maternal and fetal benefits and risks of oral antihypertensive drug treatment of mild-to-moderate pregnancy hypertension.
Conway DL, Longer O
J Matern Fetal Med. 2000;9(1):66-9
The choice of an antihypertensive agent for the pregnant woman with diabetes involves many factors. We seek to avoid adverse fetal effects while optimizing maternal outcome, both short- and long-term. This article examines the existing literature to define therapeutic goals of antihypertensive therapy during pregnancy as compared to the therapeutic goals of antihypertensive therapy in the setting of diabetes mellitus and to integrate this information for the treatment of pregnant women in whom diabetes mellitus and hypertension coexist.
Vermillion ST, Scardo JA, Newman RB, Chauhan SP
Am J Obstet Gynecol. 1999;181(4):858-61
Objective: We sought to compare the efficacies of oral nifedipine and intravenous labetalol in the acute management of hypertensive emergencies of pregnancy.
Study Design: We performed a randomized double-blind trial of oral nifedipine (10 mg) and intravenous labetalol (20 mg) in 50 peripartum patients with sustained systolic blood pressure of ≥170 mm Hg or diastolic blood pressure of ≥105 mm Hg. Both agents were repeated at sequentially escalating dosages every 20 minutes until a therapeutic goal of systolic blood pressure of <160 mm Hg and diastolic blood pressure of <100 mm Hg was achieved. Crossover occurred if the treatment goal was not achieved after 5 doses. Primary outcome was time to achievement of the therapeutic goal. Secondary outcome variables were agent failure, urinary output, and adverse effects. Data were analyzed by unpaired t test, Mann-Whitney U test, and analysis of variance for repeated measures.
Results: The time to achieve the blood pressure goal was significantly shorter with nifedipine (mean +/- SD, 25 +/- 13.6 minutes) than with labetalol (43.6 +/- 25.4 minutes; P =.002). No patients required crossover therapy. Urine output was significantly increased (P <.001) at 1 hour after nifedipine dosing (99 +/- 99 mL) compared with labetalol (44.8 +/- 19.1 mL) and remained significantly increased at 2, 6, 12, 18, and 24 hours after initial administration. Adverse effects were infrequent. There were no differences in maternal age, gestational age, number of antepartum patients, or enrollment blood pressures between groups.
Conclusions: Both oral nifedipine and intravenous labetalol are effective in the management of acute hypertensive emergencies of pregnancy; however, nifedipine controls hypertension more rapidly and is associated with a significant increase in urinary output.
Gilson GJ, Kramer RL, Barada C, Izquierdo LA, Curet LB
J Matern Fetal Med. 1998;7(3):142-7
We investigated whether use of labetalol, a beta adrenoreceptor blocking antihypertensive agent commonly employed as an alternative to hydralazine, is independently associated with pulmonary edema in women with severe preeclampsia. We retrospectively evaluated women with severe preeclampsia who were given labetalol by intravenous bolus for MAP > 120 mm Hg. Outcome variables included: achieving MAP < 120 mm Hg with < 300 mg of labetalol, incidence of adverse effects of the drug, including pulmonary edema, hypotension, and maternal bradycardia. Total intravenous fluid intake exceeding output (+ delta I/O) and presence or absence of preeclamptic liver involvement were noted. Statistical analysis included unpaired t-tests and Fisher's exact test. Fifty-one women were studied, 7 (13.7%) of whom developed pulmonary edema. Demographic and pregnancy characteristics were not different between patients who did or did not develop pulmonary edema. No patient had detectable underlying heart disease. Patients with or without pulmonary edema did not differ as regards entry MAP (130 +/- 14 vs. 129 +/- 18 mm Hg), total dose of labetalol (209 +/- 83 vs. 193 +/- 39 mg/24 hours), incidence of bradycardia or hypotension (0/7 vs. 8/44), or presence of hepatic involvement (1/7 vs. 9/44). However, there was a significant difference in degree of positive fluid balance. Patients developing pulmonary edema had a net gain of 1,466 +/- 429 mL of fluid in the 24 hours in which they received labetalol than those who did not (659 +/- 1152 mL, P = .003). Initial central hemodynamic monitoring data revealed no impairment of cardiac performance (mean cardiac output 7.7 +/- 1.8 L/min, cardiac index 4.0 +/- 0.8 L/min/m2, left ventricular stroke work index 73 +/- 9 g.m.m-2) despite high pulmonary capillary wedge pressures (22 +/- 4 mm Hg). We conclude that the incidence of pulmonary edema in patients with severe preeclampsia who are treated with labetalol appears to be a result of an increase in third space fluid accumulation as a manifestation of the severity of their disease, not a direct effect of the drug on cardiac performance.
Perloff D
Cardiol Clin. 1998;16(1):79-101
Pregnant women with hypertension can be divided into two groups: normotensive women who develop the uniquely pregnancy-related syndrome of preeclampsia, which is characterized by hypertension, proteinuria, and edema; and women with chronic hypertension who become pregnant and are at increased risk for developing superimposed preeclampsia. Preeclampsia is a syndrome of generalized endothelial dysfunction initiated by abnormal placentation and consequent placental under-perfusion, release of cytokines and other toxins, and vasoconstriction and platelet activation. Preeclampsia is the major cause of both maternal and fetal morbidity and mortality and may be complicated by eclampsia (seizures) and hepatic and renal failure. The process is completely reversible by delivery of the fetus and placenta, but intrauterine growth retardation and premature delivery pose major threats to the fetus and may require care in tertiary care center. Treatment of preexisting or pregnancy-induced hypertension does not prevent or reverse the process, but is justified to prevent maternal cardiovascular complications, especially during labor and delivery.
What's the latest in drug treatment of hypertension during pregnancy? Find out in this easy-to-navigate collection of recent MEDLINE abstracts compiled by the editors at Medscape Pharmacotherapy.
Lydakis C, Lip GY, Beevers M, Beevers DG
Am J Hypertens. 1999;12(6):541-7
Atenolol use may be associated with growth retardation when given in pregnancy, although the relationship to trimester of initiation, duration of treatment, and its use as monotherapy is still uncertain. To compare the obstetric and fetal outcome between women receiving atenolol (as monotherapy) and other antihypertensive drug monotherapies, and also to investigate the effect of duration of treatment on fetal growth, we performed a retrospective cohort study of 312 pregnancies in 223 women attending an Antenatal Hypertension Clinic. Atenolol (as monotherapy) was given in 78 pregnancies (25.0%), other types of antihypertensive drugs as monotherapy were given in 53 pregnancies (17.0%), and multiple drug combinations were given in 90 pregnancies (28.8%). In 91 pregnancies (29.2%) no antihypertensive drugs were given. Atenolol was found to be associated with lower birth weight and ponderal index values, with a trend toward a higher prevalence of preterm (<37 weeks) delivery and small-for-gestational-age babies when compared to other antihypertensive drugs as monotherapy, or to no treatment. The adverse effect of atenolol was more pronounced in women receiving the drug earlier in their pregnancy, and continuing the drug for a longer duration. In conclusion, atenolol should be avoided in the early stages of pregnancy and given with caution at the later stages, as it is associated with fetal growth retardation, which is related to duration of treatment.
Hall DR, Odendaal HJ, Steyn DW, Smith M
BJOG. 2000;107(6):759-65
Objective: To determine whether nifedipine or prazosin is the more appropriate second-line antihypertensive agent in pregnancy.
Design: Randomised controlled trial. SETTING: Tygerberg Hospital, a tertiary referral centre. POPULATION: Women with early, severe pre-eclampsia or hypertension in pregnancy, whose blood pressure could not be adequately controlled by methyldopa 2 g/day, but were otherwise stable.
Methods: Nifedipine or prazosin were given and increased as necessary in a stepwise fashion. Once the maximum dose was reached, the other drug was added in a crossover pattern. Failure to control blood pressure, or the onset of maternal/fetal complications were indications for delivery. Patients reaching a minimum gestation of 34 weeks without complications were delivered electively.
Main Outcome Measures: Antenatal days gained; major maternal complications and perinatal survival.
Results: Days gained on the second antihypertensive agent did not differ significantly (P = 0.9), while more days were gained using nifedipine as the crossover 'third agent' (P = 0.01). In the nifedipine group better renal function was recorded, but more cases with isolated low platelet counts occurred. More cases of pulmonary oedema as well as more nonviable mid-trimester and third trimester intrauterine deaths occurred in the prazosin group.
Conclusion: Nifedipine and prazosin as second agents allowed comparable amounts of time to be gained, although this changed when used as crossover third-line agents. The efficacy and safety of nifedipine in this study are consistent with the results of other studies. A greater number of intrauterine deaths occurred in the prazosin group.
Gazzolo D, Visser GH, Russo A, Scopesi F, Santi F, Bruschettini PL
Early Hum Dev. 1998;50(2):149-57
In 21 pregnancies complicated by pregnancy-induced hypertension (PIH) which was treated by antihypertensive drugs (labetalol, nifedipine), fetal behavioural recordings (quiet state, C1F; active state, C2F; no coincidence, NOC) and Doppler measurements of blood flow velocity in the umbilical artery (UA) (resistance index, RI) were made on two occasions (27-32 and 33-36 weeks of gestation). Data were compared to those of a control group of normally grown fetuses (n = 96); in 15 cases we were able to match fetuses from the study group for age (+/- 1 week) and weight (+/- 150 g) at birth with fetales from a control group. It was the aim of this study to investigate if there are disturbances in the development of fetal behavioural states and if possible disturbances are due to poor fetal growth or to antihypertensive therapy. Our results show that in PIH treated by antihypertensive drugs, there are disturbances in the development of fetal behavioural states with higher percentages of NOC and C1F, lower percentages of C2F, and higher UA RI values. These disturbances are mainly due to coexisting placental impairment and poor fetal growth rather than to nifedipine or labetalol therapy, although these drugs may cause some redistribution of states.
Tomlinson AJ, Campbell J, Walker JJ, Morgan C
Ann Pharmacother. 2000;34(2):180-2
Objective: To report a case of a patient treated with an angiotensin-converting enzyme (ACE) inhibitor with a good neonatal outcome.
Case Report: A 39-year-old African-Caribbean patient who had chronic hypertension presented at 18 weeks' gestation with acute hypertension. She was being treated for chronic hypertension with lisinopril, but had self-discontinued treatment. Attempts to control her hypertension with labetolol, nifedipine, and methyldopa were ineffective. She was therefore offered termination of pregnancy so treatment with lisinopril could be restarted. The patient elected to continue with the pregnancy in spite of the fetal risks associated with the use of an ACE inhibitor. She was delivered of a girl at 26 weeks' gestation. The baby initially had renal failure and also developed acute necrotizing enterocolitis. The renal failure improved simultaneously with the latter complication, and it is postulated that there was enteric excretion of lisinopril. The baby was discharged home on day 102 with no further complications.
Discussion: ACE inhibitors are acceptable medications to use in the first trimester of pregnancy; however, fetal malformations and neonatal complications have been associated with their use later in pregnancy, and they have a perinatal mortality rate of 97/1000. Lisinopril is excreted in urine and feces unchanged, and its half-life is prolonged in anuric neonates. Peritoneal dialysis eliminates lisinopril; however, this neonate improved after treatment for necrotizing enterocolitis and simultaneous improvement in bowel function.
Conclusions: ACE inhibitors should not be used in pregnancy beyond the end of the first trimester. In exceptional cases, they may be indicated for the control of severe hypertension when the patient is refractory to other medications. The patient should be fully counseled about the adverse effect profile and neonatal outcome. This case report documents a successful outcome for mother and baby in these circumstances.
von Dadelszen P, Ornstein MP, Bull SB, Logan AG, Koren G, Magee LA
Lancet. 2000;355(9198):87-92
Background: We investigated the relation between fetoplacental growth and the use of oral antihypertensive medication to treat mild-to-moderate pregnancy hypertension.
Methods: The study design was a metaregression analysis of published data from randomised controlled trials. Data from a paper that was regarded as an extreme statistical outliner were excluded from primary analyses. The change in (group) mean arterial pressure (MAP) from enrolment to delivery was compared with indicators of fetoplacental growth.
Findings: Greater mean difference in MAP with antihypertensive therapy was associated with the birth of a higher proportion of small-for-gestational-age (SGA) infants (slope: 0.09 [SD 0.03], r2=0.48, p=0.006, 14 trials) and lower mean birthweight significant after exclusion of data from another paper regarded as an extreme statistical outliner (slope: -14.49 [6.98] r=0.16, p=0.049, 27). No relation with mean placental weight was seen (slope -2.01 [1.62], r2=0.15, p=0.25, 11 trials).
Interpretation: Treatment-induced falls in maternal blood pressure may adversely affect fetal growth. Given the small maternal benefits that are likely to be derived from therapy, new data are urgently needed to elucidate the relative maternal and fetal benefits and risks of oral antihypertensive drug treatment of mild-to-moderate pregnancy hypertension.
Conway DL, Longer O
J Matern Fetal Med. 2000;9(1):66-9
The choice of an antihypertensive agent for the pregnant woman with diabetes involves many factors. We seek to avoid adverse fetal effects while optimizing maternal outcome, both short- and long-term. This article examines the existing literature to define therapeutic goals of antihypertensive therapy during pregnancy as compared to the therapeutic goals of antihypertensive therapy in the setting of diabetes mellitus and to integrate this information for the treatment of pregnant women in whom diabetes mellitus and hypertension coexist.
Vermillion ST, Scardo JA, Newman RB, Chauhan SP
Am J Obstet Gynecol. 1999;181(4):858-61
Objective: We sought to compare the efficacies of oral nifedipine and intravenous labetalol in the acute management of hypertensive emergencies of pregnancy.
Study Design: We performed a randomized double-blind trial of oral nifedipine (10 mg) and intravenous labetalol (20 mg) in 50 peripartum patients with sustained systolic blood pressure of ≥170 mm Hg or diastolic blood pressure of ≥105 mm Hg. Both agents were repeated at sequentially escalating dosages every 20 minutes until a therapeutic goal of systolic blood pressure of <160 mm Hg and diastolic blood pressure of <100 mm Hg was achieved. Crossover occurred if the treatment goal was not achieved after 5 doses. Primary outcome was time to achievement of the therapeutic goal. Secondary outcome variables were agent failure, urinary output, and adverse effects. Data were analyzed by unpaired t test, Mann-Whitney U test, and analysis of variance for repeated measures.
Results: The time to achieve the blood pressure goal was significantly shorter with nifedipine (mean +/- SD, 25 +/- 13.6 minutes) than with labetalol (43.6 +/- 25.4 minutes; P =.002). No patients required crossover therapy. Urine output was significantly increased (P <.001) at 1 hour after nifedipine dosing (99 +/- 99 mL) compared with labetalol (44.8 +/- 19.1 mL) and remained significantly increased at 2, 6, 12, 18, and 24 hours after initial administration. Adverse effects were infrequent. There were no differences in maternal age, gestational age, number of antepartum patients, or enrollment blood pressures between groups.
Conclusions: Both oral nifedipine and intravenous labetalol are effective in the management of acute hypertensive emergencies of pregnancy; however, nifedipine controls hypertension more rapidly and is associated with a significant increase in urinary output.
Gilson GJ, Kramer RL, Barada C, Izquierdo LA, Curet LB
J Matern Fetal Med. 1998;7(3):142-7
We investigated whether use of labetalol, a beta adrenoreceptor blocking antihypertensive agent commonly employed as an alternative to hydralazine, is independently associated with pulmonary edema in women with severe preeclampsia. We retrospectively evaluated women with severe preeclampsia who were given labetalol by intravenous bolus for MAP > 120 mm Hg. Outcome variables included: achieving MAP < 120 mm Hg with < 300 mg of labetalol, incidence of adverse effects of the drug, including pulmonary edema, hypotension, and maternal bradycardia. Total intravenous fluid intake exceeding output (+ delta I/O) and presence or absence of preeclamptic liver involvement were noted. Statistical analysis included unpaired t-tests and Fisher's exact test. Fifty-one women were studied, 7 (13.7%) of whom developed pulmonary edema. Demographic and pregnancy characteristics were not different between patients who did or did not develop pulmonary edema. No patient had detectable underlying heart disease. Patients with or without pulmonary edema did not differ as regards entry MAP (130 +/- 14 vs. 129 +/- 18 mm Hg), total dose of labetalol (209 +/- 83 vs. 193 +/- 39 mg/24 hours), incidence of bradycardia or hypotension (0/7 vs. 8/44), or presence of hepatic involvement (1/7 vs. 9/44). However, there was a significant difference in degree of positive fluid balance. Patients developing pulmonary edema had a net gain of 1,466 +/- 429 mL of fluid in the 24 hours in which they received labetalol than those who did not (659 +/- 1152 mL, P = .003). Initial central hemodynamic monitoring data revealed no impairment of cardiac performance (mean cardiac output 7.7 +/- 1.8 L/min, cardiac index 4.0 +/- 0.8 L/min/m2, left ventricular stroke work index 73 +/- 9 g.m.m-2) despite high pulmonary capillary wedge pressures (22 +/- 4 mm Hg). We conclude that the incidence of pulmonary edema in patients with severe preeclampsia who are treated with labetalol appears to be a result of an increase in third space fluid accumulation as a manifestation of the severity of their disease, not a direct effect of the drug on cardiac performance.
Perloff D
Cardiol Clin. 1998;16(1):79-101
Pregnant women with hypertension can be divided into two groups: normotensive women who develop the uniquely pregnancy-related syndrome of preeclampsia, which is characterized by hypertension, proteinuria, and edema; and women with chronic hypertension who become pregnant and are at increased risk for developing superimposed preeclampsia. Preeclampsia is a syndrome of generalized endothelial dysfunction initiated by abnormal placentation and consequent placental under-perfusion, release of cytokines and other toxins, and vasoconstriction and platelet activation. Preeclampsia is the major cause of both maternal and fetal morbidity and mortality and may be complicated by eclampsia (seizures) and hepatic and renal failure. The process is completely reversible by delivery of the fetus and placenta, but intrauterine growth retardation and premature delivery pose major threats to the fetus and may require care in tertiary care center. Treatment of preexisting or pregnancy-induced hypertension does not prevent or reverse the process, but is justified to prevent maternal cardiovascular complications, especially during labor and delivery.
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