This is called postpartum preeclampsia. Preeclampsia also includes signs of damage to some of your organs, such as your liver or kidney.

The signs may include protein in the urine and very high blood pressure. Preeclampsia can be serious or even life-threatening for both you and your baby.

What causes preeclampsia? The cause of preeclampsia is unknown. Who is at risk for preeclampsia? You are at higher risk of preeclampsia if you: Had chronic high blood pressure or chronic kidney disease before pregnancy Had high blood pressure or preeclampsia in a previous pregnancy Have obesity Are over age 40 Are pregnant with more than one baby Are African American Have a family history of preeclampsia Have certain health conditions, such as diabetes , lupus , or thrombophilia a disorder which raises your risk of blood clots Used in vitro fertilization, egg donation, or donor insemination What problems can preeclampsia cause?

Preeclampsia can cause: Placental abruption, where the placenta separates from the uterus Poor fetal growth, caused by a lack of nutrients and oxygen Preterm birth A low birth weight baby Stillbirth Damage to your kidneys, liver, brain, and other organ and blood systems A higher risk of heart disease for you Eclampsia, which happens when preeclampsia is severe enough to affect brain function, causing seizures or coma HELLP syndrome, which happens when a woman with preeclampsia or eclampsia has damage to the liver and blood cells.

It is rare, but very serious. What are the symptoms of preeclampsia? Possible symptoms of preeclampsia include: High blood pressure Too much protein in your urine called proteinuria Swelling in your face and hands. Your feet may also swell, but many women have swollen feet during pregnancy.

So swollen feet by themselves may not be a sign of a problem. How is preeclampsia diagnosed? What are the treatments for preeclampsia? They include how severe it is, how many weeks pregnant you are, and what the potential risks to you and your baby are: If you are more than 37 weeks pregnant, your provider will likely want to deliver the baby.

If you are less than 37 weeks pregnant, your health care provider will closely monitor you and your baby. This includes blood and urine tests for you.

Monitoring for the baby often involves ultrasound, heart rate monitoring, and checking on the baby's growth. You may need to take medicines, to control your blood pressure and to prevent seizures. Some women also get steroid injections, to help the baby's lungs mature faster.

If the preeclampsia is severe, you provider may want you to deliver the baby early. Start Here. About Preeclampsia and Eclampsia Eunice Kennedy Shriver National Institute of Child Health and Human Development Also in Spanish High Blood Pressure and Pregnancy Mayo Foundation for Medical Education and Research Also in Spanish High Blood Pressure during Pregnancy American Academy of Family Physicians Also in Spanish High Blood Pressure during Pregnancy March of Dimes Foundation.

What Are the Symptoms of Preeclampsia, Eclampsia, and HELLP Syndrome? Eunice Kennedy Shriver National Institute of Child Health and Human Development Also in Spanish.

Diagnosis and Tests. How Do Health Care Providers Diagnose Preeclampsia, Eclampsia, and HELLP Syndrome? Eunice Kennedy Shriver National Institute of Child Health and Human Development Also in Spanish Magnesium Blood Test National Library of Medicine Also in Spanish.

Treatments and Therapies. What Are the Treatments for Preeclampsia, Eclampsia, and HELLP Syndrome? Related Issues. HELLP Syndrome American Academy of Family Physicians Also in Spanish What Are the Risks of Preeclampsia and Eclampsia to the Fetus?

Eunice Kennedy Shriver National Institute of Child Health and Human Development Also in Spanish What Are the Risks of Preeclampsia and Eclampsia to the Mother?

Postpartum Preeclampsia American Academy of Family Physicians Also in Spanish. Preeclampsia: MedlinePlus Genetics National Library of Medicine. Videos and Tutorials. Preeclampsia Medical Encyclopedia Also in Spanish.

Statistics and Research. High Blood Pressure during Pregnancy Centers for Disease Control and Prevention Who Is at Risk of Preeclampsia? Clinical Trials. gov: Hypertension, Pregnancy-Induced National Institutes of Health ClinicalTrials.

gov: Pre-Eclampsia National Institutes of Health. Article: The Risk of Hypertension and Diabetes Mellitus According to Offspring's Birthweight Article: Association of antenatal corticosteroids with mortality and morbidities in very preterm Many patients have a history of malaise or nonspecific symptoms suggesting an acute viral syndrome.

Laboratory tests are used to diagnose HELLP syndrome Table 3 33 — 35 ; a decreasing platelet count and an increasing l-lactate dehydrogenase level indicative of both hemolysis and liver dysfunction reflect disease severity.

A common regimen for expectant management of mild preeclampsia is outlined in Table 4. Delivery is generally not indicated for women with mild preeclampsia until 37 to 38 weeks of gestation and should occur by 40 weeks 1 , 7 Figure 1 7. Patients with severe preeclampsia are admitted to the hospital, placed on bed rest, and carefully monitored Figure 2 7 and Table 5 1 , 7 , The goals of treatment are to prevent seizures, lower blood pressure to avoid maternal end-organ damage, and expedite delivery.

Magnesium Sulfate. The use of magnesium sulfate helps prevent seizures in women with preeclampsia. Assuming one half of seizures are preventable with magnesium sulfate, 38 women with mild preeclampsia would need to be treated to prevent one seizure.

Magnesium sulfate slows neuromuscular conduction and depresses central nervous system irritability without significant effects on blood pressure. One fourth of women will experience adverse effects, especially flushing.

The antidote is calcium gluconate, 1 g infused intravenously over two minutes. Vital signs blood pressure, pulse, respiration ; deep tendon reflexes; and mental status every 15 to 60 minutes until stable, then every 60 minutes while on magnesium sulfate.

Administer lactated Ringer's solution at 75 mL per hour IV to maintain urine output of 30 to 40 mL per hour; total intake IV and oral should not exceed mL per hour or 3, mL per day. Fetal evaluation: nonstress test on admission; obstetric ultrasonography for estimated fetal weight, amniotic fluid volume, and umbilical artery Doppler measurements.

Loading dose of 4 to 6 g diluted in mL of normal saline, given IV over 15 to 20 minutes, followed by a continuous infusion of 2 g per hour Hydralazine, 5 to 10 mg IV every 15 to 30 minutes maximal dose: 30 mg 7.

Labetalol, 20 mg IV initially; if the initial dose is not effective, double the dose to 40 mg and then 80 mg at minute intervals until target blood pressure is reached or a total of mg has been administered 1 , 7 ; the maximal dose of IV labetalol is mg in a hour period 7 , Calcium gluconate, 1 g IV; keep at bedside in case of respiratory depression from magnesium sulfate use.

Antihypertensive Medications. The optimal level of blood pressure control in pregnancies complicated by hypertension is unknown. Intravenous labetalol and hydralazine are commonly used for the acute management of preeclampsia.

Fluid Management. Excessive fluid administration can result in pulmonary edema, ascites, and cardiopulmonary overload, whereas too little fluid exacerbates an already constricted intravascular volume and leads to further end-organ ischemia.

Urine output should be greater than 30 mL per hour 44 and intravenous fluids limited to mL per hour. Delivery Decisions in Severe Preeclampsia.

Delivery is the only cure for preeclampsia. Decisions regarding the timing and mode of delivery are based on a combination of maternal and fetal factors. Fetal factors include gestational age, evidence of lung maturity, and signs of fetal compromise on antenatal assessment.

Patients with treatment-resistant severe hypertension or other signs of maternal or fetal deterioration should be delivered within 24 hours, irrespective of gestational age or fetal lung maturity. Fetuses older than 34 weeks, or those with documented lung maturity, are also delivered without delay.

Expectant management, with close monitoring of the mother and fetus, delays delivery when possible and reduces neonatal complications and length of stay in the newborn intensive care nursery.

In women with HELLP syndrome, the fetus is delivered at an earlier gestation; specifically, fetuses older than 28 weeks are routinely delivered 24 to 48 hours after the first maternal dose of corticosteroids is administered. Vaginal delivery is recommended for women with severe preeclampsia if there is no evidence of maternal or fetal compromise or other obstetric contraindication.

Postpartum Management. Most patients with preeclampsia respond promptly to delivery with decreased blood pressure, diuresis, and clinical improvement. Eclampsia may occur postpartum; the greatest risk of postpartum eclampsia is within the first 48 hours.

There are no reliable data on postpartum hypertensive management 50 ; however, oral nifedipine is commonly used.

An eclamptic seizure may be preceded by increasingly severe preeclampsia, or it may appear unexpectedly in a patient with minimally elevated blood pressure and no proteinuria.

Blood pressure is only mildly elevated in 30 to 60 percent of women who develop eclampsia. A postictal phase may follow with confusion, agitation, and combativeness. The timing of an eclamptic seizure can be antepartum 53 percent , intrapartum 19 percent , or postpartum 28 percent. Initial management of an eclamptic seizure includes protecting the airway and minimizing the risk of aspiration by placing the woman on her left side, suctioning her mouth, and administering oxygen.

A medical professional skilled in performing intubations should be immediately available. After the convulsion has ended and the patient is stabilized, plans should be made for prompt delivery. In rural or remote areas, physicians need to consider the risk of transfer versus the benefits of tertiary maternal and neonatal care.

It is important to avoid unnecessary interventions and iatrogenic complications. Otherwise, a 6-g loading dose is given intravenously over 15 to 20 minutes, followed by maintenance infusion of 2 g per hour. A total of 8 g of magnesium sulfate should not be exceeded over a short period of time.

Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol. Abalos E, Duley L, Steyn DW, Henderson-Smart DJ. Antihypertensive drug therapy for mild to moderate hypertension during pregnancy. Cochrane Database Syst Rev.

Magee LA, Duley L. Oral beta-blockers for mild to moderate hypertension during pregnancy. ACOG Committee on Practice Bulletins. ACOG Practice Bulletin. Chronic hypertension in pregnancy.

Obstet Gynecol. von Dadelszen P, Ornstein MP, Bull SB, Logan AG, Koren G, Magee LA. Fall in mean arterial pressure and fetal growth restriction in pregnancy hypertension: a meta-analysis.

von Dadelszen P, Magee LA. Antihypertensive medications in management of gestational hypertension-preeclampsia. Clin Obstet Gynecol. Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Barton JR, O'brien JM, Bergauer NK, Jacques DL, Sibai BM.

Mild gestational hypertension remote from term: progression and outcome. Gofton EN, Capewell V, Natale R, Gratton RJ. Obstetrical intervention rates and maternal and neonatal outcomes of women with gestational hypertension.

Buchbinder A, Sibai BM, Caritis S, et al. Adverse perinatal outcomes are significantly higher in severe gestational hypertension than in mild preeclampsia.

Davison JM, Homuth V, Jeyabalan A, et al. New aspects in the pathophysiology of preeclampsia. J Am Soc Nephrol. American College of Obstetricians and Gynecologists..

ACOG Committee on Practice Bulletins—Obstetrics. ACOG Practice Bulletin No. Diagnosis and management of preeclampsia and eclampsia. McMaster MT, Zhou Y, Fisher SJ. Abnormal placentation and the syndrome of preeclampsia.

Semin Nephrol. Merviel P, Carbillon L, Challier JC, Rabreau M, Beaufils M, Uzan S. Pathophysiology of preeclampsia: links with implantation disorders. Eur J Obstet Gynecol Reprod Biol. Levine RJ, Thadhani R, Qian C, et al.

Urinary placental growth factor and risk of preeclampsia. Levine RJ, Maynard SE, Qian C, et al. Circulating angiogenic factors and the risk of preeclampsia.

N Engl J Med. Esplin MS, Fausett MB, Fraser A, et al. Paternal and maternal components of the predisposition to preeclampsia. Morgan T, Ward K. New insights into the genetics of preeclampsia. Semin Perinatol. Lin J, August P. Genetic thrombophilias and preeclampsia: a meta-analysis.

Mignini LE, Latthe PM, Villar J, Kilby MD, Carroli G, Khan KS. Mapping the theories of preeclampsia: the role of homocysteine.

Milne F, Redman C, Walker J, et al. The preeclampsia community guideline PRECOG : how to screen for and detect onset of preeclampsia in the community. Levine RJ, Hauth JC, Curet LB, et al. Trial of calcium to prevent preeclampsia. Sibai BM, Villar MA, Bray E. Magnesium supplementation during pregnancy: a double-blind randomized controlled clinical trial.

Salvig JD, Olsen SF, Secher NJ. Effects of fish oil supplementation in late pregnancy on blood pressure: a randomised controlled trial. Br J Obstet Gynaecol. Poston L, Briley AL, Seed PT, Kelly FJ, Shennan AH for the Vitamins in Preeclampsia VIP Trial Consortium.

Vitamin C and vitamin E in pregnant women at risk for preeclampsia VIP trial : randomised placebo-controlled trial. Hofmeyr GJ, Atallah AN, Duley L. Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems. Duley L, Henderson-Smart DJ, Meher S, King JF.

Antiplatelet agents for preventing preeclampsia and its complications. Canadian Task Force on Preventive Health Care. Prevention of preeclampsia.

Thank you for subscribing! Sorry something went wrong with your subscription Please, try again in a couple of minutes Retry. Show references Pregnancy and high blood pressure. National Heart, Lung, and Blood Institute. Accessed May 16, Preeclampsia and high blood pressure during pregnancy.

American College of Obstetricians and Gynecologists. Ferri FF. In: Ferri's Clinical Advisor Elsevier; Accessed May 18, Melvin LM, et al. Gestational hypertension. Accessed My 16, Battarbee AN, et al. Chronic hypertension in pregnancy.

American Journal of Obstetrics and Gynecology. Hypertension in pregnancy. Merck Manual Professional Version. Gestational hypertension and preeclampsia: ACOG practice bulletin summary, number Obstetrics and Gynecology.

Landon MB, et al. Preeclampsia and hypertensive disorders. In: Gabbe's Obstetrics: Normal and Problem Pregnancies. ACOG practice bulletin No. Reddy S, et al. Hypertension and pregnancy: Management and future risks. Advanced Chronic Kidney Disease. Products and Services Assortment of Compression Products at Mayo Clinic Store A Book: Obstetricks A Book: Mayo Clinic Guide to a Healthy Pregnancy.

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Follow Mayo Clinic. Get the Mayo Clinic app. Oral beta-blockers for mild to moderate hypertension during pregnancy. ACOG Committee on Practice Bulletins.

ACOG Practice Bulletin. Chronic hypertension in pregnancy. Obstet Gynecol. von Dadelszen P, Ornstein MP, Bull SB, Logan AG, Koren G, Magee LA. Fall in mean arterial pressure and fetal growth restriction in pregnancy hypertension: a meta-analysis. von Dadelszen P, Magee LA.

Antihypertensive medications in management of gestational hypertension-preeclampsia. Clin Obstet Gynecol. Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia.

Barton JR, O'brien JM, Bergauer NK, Jacques DL, Sibai BM. Mild gestational hypertension remote from term: progression and outcome. Gofton EN, Capewell V, Natale R, Gratton RJ. Obstetrical intervention rates and maternal and neonatal outcomes of women with gestational hypertension.

Buchbinder A, Sibai BM, Caritis S, et al. Adverse perinatal outcomes are significantly higher in severe gestational hypertension than in mild preeclampsia. Davison JM, Homuth V, Jeyabalan A, et al.

New aspects in the pathophysiology of preeclampsia. J Am Soc Nephrol. American College of Obstetricians and Gynecologists.. ACOG Committee on Practice Bulletins—Obstetrics. ACOG Practice Bulletin No. Diagnosis and management of preeclampsia and eclampsia.

McMaster MT, Zhou Y, Fisher SJ. Abnormal placentation and the syndrome of preeclampsia. Semin Nephrol. Merviel P, Carbillon L, Challier JC, Rabreau M, Beaufils M, Uzan S.

Pathophysiology of preeclampsia: links with implantation disorders. Eur J Obstet Gynecol Reprod Biol. Levine RJ, Thadhani R, Qian C, et al. Urinary placental growth factor and risk of preeclampsia.

Levine RJ, Maynard SE, Qian C, et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med. Esplin MS, Fausett MB, Fraser A, et al. Paternal and maternal components of the predisposition to preeclampsia.

Morgan T, Ward K. New insights into the genetics of preeclampsia. Semin Perinatol. Lin J, August P. Genetic thrombophilias and preeclampsia: a meta-analysis. Mignini LE, Latthe PM, Villar J, Kilby MD, Carroli G, Khan KS. Mapping the theories of preeclampsia: the role of homocysteine.

Milne F, Redman C, Walker J, et al. The preeclampsia community guideline PRECOG : how to screen for and detect onset of preeclampsia in the community. Levine RJ, Hauth JC, Curet LB, et al. Trial of calcium to prevent preeclampsia.

Sibai BM, Villar MA, Bray E. Magnesium supplementation during pregnancy: a double-blind randomized controlled clinical trial. Salvig JD, Olsen SF, Secher NJ. Effects of fish oil supplementation in late pregnancy on blood pressure: a randomised controlled trial.

Br J Obstet Gynaecol. Poston L, Briley AL, Seed PT, Kelly FJ, Shennan AH for the Vitamins in Preeclampsia VIP Trial Consortium. Vitamin C and vitamin E in pregnant women at risk for preeclampsia VIP trial : randomised placebo-controlled trial.

Hofmeyr GJ, Atallah AN, Duley L. Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems. Duley L, Henderson-Smart DJ, Meher S, King JF.

Antiplatelet agents for preventing preeclampsia and its complications. Canadian Task Force on Preventive Health Care. Prevention of preeclampsia. Accessed October 12, Preventive Services Task Force.

Guide to Clinical Preventive Services: Report of the U. Baltimore, Md. Wheeler TL, Blackhurst DW, Dellinger EH, Ramsey PS. Usage of spot urine protein to creatinine ratios in the evaluation of preeclampsia. Weinstein L. Syndrome of hemolysis, elevated liver enzymes, and low platelet count: a severe consequence of hypertension in pregnancy.

Sibai BM, Ramadan MK, Usta I, Salama M, Mercer BM, Friedman SA. Maternal morbidity and mortality in pregnancies with hemolysis, elevated liver enzymes, and low platelets HELLP syndrome.

Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count. Barton JR, Sibai BM. Diagnosis and management of hemolysis, elevated liver enzymes, and low platelets syndrome.

Clin Perinatol. Magann EF, Martin JN. Twelve steps to optimal management of HELLP syndrome. Neilson JP, Alfirevic Z. Doppler ultrasound for fetal assessment in high risk pregnancies. Williams KP, Farquharson DF, Bebbington M, et al.

Screening for fetal well-being in a high-risk pregnant population comparing the nonstress test with umbilical artery Doppler velocimetry: a randomized controlled clinical trial. Altman D, Carroli G, Duley L, et al. Do women with preeclampsia, and their babies, benefit from magnesium sulphate?

The Magpie Trial: a randomised placebo-controlled trial. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. Belfort MA, Anthony J, Saade GR, Allen JC for the Nimodipine Study Group.

A comparison of magnesium sulfate and nimodipine for the prevention of eclampsia. Magnesium sulfate prophylaxis in preeclampsia: evidence from randomized trials.

Duley L, Gülmezoglu AM, Henderson-Smart DJ. Magnesium sulphate and other anticonvulsants for women with preeclampsia. Diagnosis, prevention, and management of eclampsia. Dildy GA. Complications of preeclampsia.

In: Critical Care Obstetrics. Malden, Mass. Martin JN, Thigpen BD, Moore RC, Rose CH, Cushman J, May W. Stroke and severe preeclampsia and eclampsia: a paradigm shift focusing on systolic blood pressure.

Duley L, Henderson-Smart DJ, Meher S. Drugs for treatment of very high blood pressure during pregnancy. Churchill D, Duley L. Interventionist versus expectant care for severe preeclampsia before term. Odendaal HJ, Pattinson RC, Bam R, Grove D, Kotze TJ.

Aggressive or expectant management for patients with severe preeclampsia between 28—34 weeks' gestation: a randomized controlled trial. 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.

Magee L, Sadeghi S. Prevention and treatment of postpartum hypertension. Mattar F, Sibai BM. Risk factors for maternal morbidity. Chames MC, Livingston JC, Ivester TS, Barton JR, Sibai BM. Late postpartum eclampsia: a preventable disease?. Aagaard-Tillery KM, Belfort MA. Eclampsia: morbidity, mortality, and management.

Which anticonvulsant for women with eclampsia? Evidence from the Collaborative Eclampsia Trial [published correction appears in Lancet.

By contrast, testing for proteinuria should be performed at each visit in patients with hypertension as proteinuria changes the diagnosis to preeclampsia. Once a diagnosis of preeclampsia is established, testing for proteinuria is no longer diagnostically or prognostically useful.

See "Proteinuria in pregnancy: Diagnosis, differential diagnosis, and management of nephrotic syndrome" and "Proteinuria in pregnancy: Diagnosis, differential diagnosis, and management of nephrotic syndrome", section on 'Semiquantitative screening ' and "Proteinuria in pregnancy: Diagnosis, differential diagnosis, and management of nephrotic syndrome", section on 'Quantitative diagnostic '.

A calculator that combines maternal characteristics with mean arterial blood pressure, mean uterine artery resistance, and serum PlGF and PAPP-A levels was developed by the Fetal Medicine Foundation for screening patients in early pregnancy to stratify risk of developing preeclampsia later in pregnancy [ 54 ].

It is not used in the United States. See "Early pregnancy prediction of preeclampsia", section on 'Risk prediction models'.

In approximately 5 percent of cases, the signs and symptoms are first recognized postpartum ie, postpartum preeclampsia , usually within 48 hours of birth [ ]. Upper abdominal, retrosternal, or epigastric pain may be the presenting symptom of preeclampsia and reflux is common in pregnant individuals, especially at night; therefore, a high index of suspicion is important to make a timely diagnosis of preeclampsia with severe features rather than reflexively ascribing these symptoms to gastroesophageal reflux.

Rare and atypical presentations. Other disorders with similar signs and symptoms include lupus nephritis, thrombotic thrombocytopenic purpura which may be hereditary , and hemolytic-uremic syndrome.

Differential diagnosis can be challenging table 4. See "Hypertensive disorders in pregnancy: Approach to differential diagnosis".

Hydrops-related Mirror syndrome is most common between 22 and 28 weeks, but rare cases have presented before 20 weeks [ 61,62 ]. See "Nonimmune hydrops fetalis", section on 'Mirror syndrome'. Headache is the most common reason for presentation to a health care provider in patients subsequently diagnosed with late postpartum preeclampsia, and was present in nearly 70 percent of such patients in two large studies [ 59,63 ].

Shortness of breath was also relatively common, affecting 20 to 30 percent of patients. Signs and symptoms can be atypical; for example, the patient may have thunderclap headaches alternating with mild headaches or intermittent rather than persistent hypertension.

Other etiologies for the signs and symptoms should be considered, such as reversible cerebral vasoconstriction syndrome or impending stroke [ ]. See "Overview of thunderclap headache" and "Reversible cerebral vasoconstriction syndrome".

Risk factors for delayed postpartum preeclampsia appear to be similar to those for the typical cases of preeclampsia table 3 , and some patients have no risk factors [ 59,68,69 ].

In a retrospective cohort study including patients with delayed postpartum preeclampsia, Of these patients, Severe features of preeclampsia without hypertension — It is uncommon for patients to exhibit the severe features of preeclampsia without hypertension, but this may be observed in 15 percent of patients with HELLP syndrome which some consider a variant of preeclampsia and others consider a separate disorder and in some patients with eclampsia a possible sequelae of preeclampsia.

It is possible that in such patients, blood pressure is increased above baseline but does not meet diagnostic criteria for hypertension, similar to what has been described in the syndrome of posterior reversible encephalopathy [ 70 ]. See "Eclampsia", section on 'Can eclampsia be predicted and prevented?

Isolated hypertension — Patients with new onset of mild hypertension but no other criteria for preeclampsia or an underlying disease associated with hypertension are given the diagnosis of gestational hypertension.

These patients should be followed closely since up to 50 percent will subsequently develop the full diagnostic criteria for preeclampsia. See "Gestational hypertension", section on 'Risk of progression to preeclampsia'.

Isolated proteinuria — Isolated gestational proteinuria may occur before the diagnostic criteria for preeclampsia have manifested [ 71 ]. We are unaware of prospective studies describing this finding, but in a retrospective study of 95 pregnant patients with new-onset isolated proteinuria who were followed to term, preeclampsia developed in 22 percent: antepartum or intrapartum in 13 patients and postpartum in 8 patients [ 72 ].

Candidates — All pregnant patients with new-onset hypertension or worsening hypertension after 20 weeks of gestation or other potential clinical manifestations of preeclampsia should be promptly evaluated for the disease.

It is estimated that about 30 percent of all pregnancies will undergo evaluation for preeclampsia at some point. Patients with nonsevere hypertension who are asymptomatic may be followed closely as outpatients provided they are seen frequently and the maternal and fetal status is stable.

The decision to monitor patients in the hospital versus in an outpatient setting should be made on a case-by-case basis, taking into consideration both medical and social issues.

See "Preeclampsia: Antepartum management and timing of delivery". Accurate assessment of blood pressure — A standardized validated technique for blood pressure measurement in pregnancy is critically important both in the office and at home.

These techniques are reviewed separately. See "Treatment of hypertension in pregnant and postpartum patients", section on 'Technique for accurate measurement of blood pressure'. Repeated measurements should be performed to confirm hypertension, ideally over several hours or days unless blood pressure is severely elevated thus requiring prompt treatment.

Laboratory tests. Routine — For all patients with suspected preeclampsia, routine laboratory testing includes:. See "Diagnosis of immune TTP". Role of measurement of angiogenic markers — Preeclampsia is associated with abnormal angiogenic imbalance.

Measurement of urinary or plasma antiangiogenic markers, such as soluble fms-like tyrosine kinase-1 sFlt-1 , and angiogenic markers, such as placental growth factor PlGF , or their ratios may be useful for:.

The clinical utility of these tests remains somewhat unclear, due to heterogeneity among studies in measurement of markers, study populations, and outcomes of interest. Despite these limitations, prospective studies and trials suggest that angiogenic markers accurately diagnose preeclampsia and have a high negative predictive value, thus they may be useful in ruling out preeclampsia thereby avoiding unnecessary hospitalization and testing [ ].

See "Preeclampsia: Pathogenesis", section on 'sFlt-1, VEGF, PlGF'. One angiogenic marker test sFltPlGF ratio is commercially available in the United States.

Lastly, they suggest that the test may be of greater benefit in patients at greater risk of adverse maternal outcomes. Evidence — In a meta-analysis of observational studies examining the performance of sFlt-1, PlGF, or the sFltPlGF ratio in predicting adverse outcomes in patients with suspected or confirmed preeclampsia, both PlGF and the sFltPlGF ratio demonstrated pooled area under the summary receiver operating characteristic curve values from 0.

The best available evidence is from the following clinical trials and one large prospective observational study testing the potential benefits of PlGF-based testing:. It was performed in 11 maternity units in the United Kingdom and used the Triage PlGF test [ 76 ].

Maternity units were randomly allocated to a management strategy using PlGF testing that was revealed to the care team or to management without knowledge of PlGF levels concealed. In addition, maternal and neonatal morbidity trended higher in the PlGF testing group. It was based in a single UK tertiary referral hospital and used the Elecsys immunoassay sFltPLGF ratio.

Patients were allocated to management based on knowledge of sFltPlGF levels reveal or to a nonreveal group. Nearly patients were recruited. The test in this study, as in others, had a high sensitivity and negative predictive value for diagnosis of preeclampsia, but this information did not translate into an improvement in pregnancy outcome.

Based on this study, the FDA approved use of sFltPlGF in patients hospitalized with hypertension to predict progression to preeclampsia with severe features within two weeks. Clinical use for managing such patients is discussed separately. See "Preeclampsia: Antepartum management and timing of delivery", section on 'Role of sFltPlGF'.

The findings from this study are not generalizable for clinical use in ambulatory patients with hypertension and limited by the observational design.

Assessment of fetal status — Fetal status is assessed concurrently with the maternal evaluation or post-diagnosis, depending on the degree of concern when the mother is evaluated. At a minimum, a nonstress test or biophysical profile is performed, if appropriate for gestational age. Ultrasound is indicated to evaluate amniotic fluid volume and estimate fetal weight given the increased risk for oligohydramnios and fetal growth restriction FGR.

See "Overview of antepartum fetal assessment". The symptom of sudden onset of severe headache "worst headache of my life" is sufficiently characteristic of subarachnoid hemorrhage that it should prompt neurology consultation and consideration of imaging.

The headache in subarachnoid hemorrhage is lateralized in 30 percent of patients and may be associated with a brief period of altered consciousness, collapse, nausea or vomiting, preretinal subhyaloid hemorrhages, or meningismus.

See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis". Consultation with other services is useful if there is uncertainty about differential diagnosis or management of severe hematologic, renal, hepatic, or cardiopulmonary disease. SPECTRUM OF DISEASE — The clinical findings of preeclampsia result from the underlying pathophysiology of the disease: placental insufficiency, vasoconstriction, increased capillary permeability, and endothelial dysfunction.

Potential clinical findings. Hypertension — All patients with preeclampsia have hypertension, but a small proportion of those with HELLP and rare patients with eclampsia do not meet diagnostic criteria for hypertension in pregnancy.

Hypertension is generally the earliest clinical finding and the most common clinical clue to the presence of the disease. However, in some patients, hypertension develops rapidly, before 34 weeks of gestation, or postpartum. Pheochromocytoma is a rare cause of hypertension during pregnancy and may be difficult to distinguish from preeclampsia.

See "Hypertensive disorders in pregnancy: Approach to differential diagnosis", section on 'Pheochromocytoma'. Hemodynamic profile — Patients with early onset of preeclampsia tend to have a hemodynamic profile of increased total peripheral resistance and decreased cardiac output, while those with onset at term tend to have decreased total peripheral resistance and increased cardiac output [ 85 ].

Some investigators have hypothesized that antihypertensive treatment that aims to normalize the specific underlying hemodynamic abnormalities results in better blood pressure control and may mitigate maternal and fetal risks eg, decrease fetal growth restriction associated with early-onset disease [ 86 ].

Epigastric, upper abdominal, or retrosternal pain — Epigastric, upper abdominal, or retrosternal pain, when present, is a cardinal symptom of the severe end of the disease spectrum. Severe constant pain often begins at night and is usually maximal in the low retrosternal area or epigastrium, but may radiate to the right hypochondrium or back [ 87 ].

Nausea or vomiting sometimes occurs, but when persistent and associated with loss of appetite, fatty liver of pregnancy should be ruled out.

See "Acute fatty liver of pregnancy". On examination, the liver may be tender to palpation due to stretching of Glisson's capsule from hepatic swelling or bleeding. Liver rupture or hemorrhage is rare but should be suspected when there is sudden onset of right upper quadrant pain associated with a decrease in blood pressure.

See "HELLP syndrome hemolysis, elevated liver enzymes, and low platelets ", section on 'Management of hepatic bleeding'. Acute pancreatitis is a rare complication of preeclampsia [ 88 ] and can mimic the epigastric pain of preeclampsia [ 89 ].

Rarely, patients develop chest pain caused by cardiac disease eg, ischemia, acute spontaneous coronary artery dissection. It may be temporal, frontal, occipital, or diffuse [ 90,91 ]. The pain usually has a throbbing or pounding quality but may be piercing. Although not pathognomonic, a feature that suggests preeclampsia-related headache rather than another type of headache is that it persists despite administration of over-the-counter analgesics, and it may become severe ie, incapacitating, "the worst headache of my life".

However, resolution of the headache with analgesics does not exclude the possibility of preeclampsia. The American College of Obstetricians and Gynecologists' criteria for preeclampsia-related headache are "new-onset headache unresponsive to medication and not accounted for by alternative diagnoses" [ 2 ].

The mechanism for headache, as well as other cerebrovascular symptoms of preeclampsia, is poorly understood. These findings may result from generalized endothelial cell dysfunction, leading to vasospasm of the cerebral vasculature in response to severe hypertension, or they may result from loss of cerebrovascular autoregulation, leading to areas of both vasoconstriction and forced vasodilation.

Thus, they could represent a form of posterior reversible leukoencephalopathy syndrome PRES [ 70,94,95 ]. PRES is typically associated with severe hypertension but can also occur with rapid increases in blood pressure in patients with endothelial damage and in patients with only mildly elevated blood pressure [ 96 ].

See "Reversible posterior leukoencephalopathy syndrome" and "Eclampsia", section on 'Clinical findings'. Acetaminophen is commonly used to treat headache.

They are caused, at least in part, by retinal arteriolar spasm, impaired cerebrovascular autoregulation, and cerebral edema [ 70,97 ]. Symptoms may include blurred vision, photopsia flashing lights or sparks , scotomata dark areas or gaps in the visual field [ ], diplopia, or amaurosis fugax blindness in one or both eyes.

Visual disturbances in preeclampsia may be manifestations of PRES [ 95 ]. Cortical blindness is rare and typically transient [ ].

Blindness related to retinal pathology, such as retinal artery or vein occlusion, retinal detachment, optic nerve damage, retinal artery spasm, and retinal ischemia, may be permanent [ ].

Most strokes in this setting are hemorrhagic and preceded by severe headache and severe hypertension especially severe systolic hypertension , but ischemic strokes also occur [ , ]. Eclamptic seizures occur in some, but not all, cases. Lowering blood pressure reduces the risk of stroke.

See "Cerebrovascular disorders complicating pregnancy", section on 'Preeclampsia, eclampsia, and HELLP' and "Treatment of hypertension in pregnant and postpartum patients", section on 'Acute therapy of severe hypertension'.

Sustained ankle clonus may be present. Seizure in a preeclamptic patient upstages the diagnosis to eclampsia. Eclamptic seizures develop in 1 in patients with preeclampsia without severe features and in 1 in 50 patients with preeclampsia with severe features.

Histopathologic correlates include brain hemorrhage, petechiae, edema, vasculopathy, ischemic damage, microinfarcts, and fibrinoid necrosis [ , ].

Neuroimaging consistent with PRES may be seen [ ]. See "Eclampsia", section on 'Clinical findings'. Pulmonary edema — Pulmonary edema is a feature of the severe end of the disease spectrum and was observed in approximately 10 percent of 63 cases of preeclampsia with severe features in a prospective study [ ].

The etiology of pulmonary edema in preeclampsia is multifactorial [ ]. Excessive elevation in pulmonary vascular hydrostatic pressure combined with decreased plasma oncotic pressure may produce pulmonary edema in some patients, particularly in the postpartum period.

However, not all preeclamptic patients with pulmonary edema demonstrate this phenomenon. Other causes of pulmonary edema are capillary leak from endothelial activation, left heart failure, acute severe hypertension, and iatrogenic volume overload.

There may be some overlap between preeclampsia and peripartum cardiomyopathy as the two disorders may coexist [ , ]. See "Peripartum cardiomyopathy: Etiology, clinical manifestations, and diagnosis". Oliguria — Patients with preeclampsia commonly have transient oliguria less than mL over 4 hours in labor or the first 24 hours postpartum.

Oliguria in preeclampsia is due to contraction of the intravascular space secondary to vasospasm, leading to increased renal sodium and water retention, as well as intrarenal vasospasm [ ].

The glomerular filtration rate GFR may fall by over 25 percent. Rarely, patients with preeclamptic liver disease develop polyuria due to transient diabetes insipidus of pregnancy.

The mechanism in these cases is decreased degradation of vasopressinase due to hepatic dysfunction. See "Polyuria and diabetes insipidus of pregnancy".

Generalized edema — Many pregnant individuals have peripheral edema whether or not they have preeclampsia. It occurs in less than 1 percent of pregnancies with preeclampsia without severe features but 3 percent of those with severe features [ ].

It has been attributed to ischemia-reperfusion injury in maternal uteroplacental vessels. See "Acute placental abruption: Pathophysiology, clinical features, diagnosis, and consequences" and "Acute placental abruption: Management and long-term prognosis".

Potential laboratory findings. See "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults", section on 'hour versus spot urine collection'.

This value can be used to estimate the hour protein excretion calculator 1 [ ]. Measurement of proteinuria is discussed in detail separately. See "Proteinuria in pregnancy: Diagnosis, differential diagnosis, and management of nephrotic syndrome", section on 'Measurement'.

Proteinuria generally increases as preeclampsia progresses, but increased urinary protein excretion may be a late finding [ , ]. Preeclampsia is the most common cause of severe proteinuria in pregnancy. Proteinuria is due, in part, to impaired integrity of the glomerular filtration barrier and altered tubular handling of filtered proteins leading to increased nonselective protein excretion [ ].

Both size and charge selectivity of the glomerular barrier are affected [ , ]. Using special studies, podocyturia urinary excretion of podocytes has been observed in patients with preeclampsia [ , ].

Urinary shedding of podocytes may indicate podocyte loss from the glomerulus, which may lead to a disruption of the glomerular filtration barrier and consequent proteinuria. Deficient vascular endothelial growth factor VEGF signaling appears to account, at least in part, for these findings.

See "Preeclampsia: Pathogenesis", section on 'Role of systemic endothelial dysfunction in clinical findings'. Kidney histology is reviewed below. See 'Potential histologic findings' below. The serum creatinine concentration in patients with preeclampsia generally remains in this range or only slightly elevated.

Some guidelines also include doubling of the patient's baseline creatinine in the absence of other kidney disease as indicative of the severe end of the disease spectrum. The rise in serum creatinine is due primarily to a fall in GFR; renal plasma flow also decreases but to a lesser degree.

Thrombocytopenia is the most common coagulation abnormality in preeclampsia. Microangiopathic endothelial injury and activation result in formation of platelet and fibrin thrombi in the microvasculature.

Accelerated platelet consumption leads to thrombocytopenia; immune mechanisms may also play a role [ ]. See "Thrombocytopenia in pregnancy", section on 'List of causes'. Elevation in the serum indirect bilirubin level also suggests hemolysis.

Elevations in lactate dehydrogenase LDH are usually related to liver dysfunction but can be due to hemolysis or both. Hematocrit typically increases range 36 to 43 percent in one study [ ].

When both hemolysis and hemoconcentration occur concurrently, the effects on hematocrit may negate each other, resulting in a normal value. Abnormalities in liver chemistries are due to reduced hepatic blood flow from periportal and sinusoidal fibrin deposition and microvesicular fat deposition, potentially resulting in ischemia, necrosis, and periportal hemorrhage [ , ].

Infrequently, subcapsular hematoma, hepatic failure, or rupture occurs. The cause is most likely related to a reduction in GFR. However, the increase in serum uric acid is often greater than expected for mild reductions in GFR, leading to the hypothesis that decreased tubular secretion or increased reabsorption in the proximal renal tubules plays a role [ ].

Although meta-analyses have concluded that uric acid levels are not an accurate predictor of complications associated with preeclampsia [ ], this issue remains controversial because of inconsistency among studies. For example, data from a prospective international study of patients admitted to the hospital with preeclampsia showed that serum uric acid corrected for gestational age is clinically useful in predicting adverse perinatal, but not maternal, outcomes [ ].

Lower levels of parathyroid hormone, compared with normal pregnancy, have also been reported [ ]. A very small subgroup of patients with severe preeclampsia may develop myocardial damage or global diastolic dysfunction [ ].

Therefore, troponin I levels should be obtained when clinically indicated, such as when the patient complains of chest pain suggestive of myocardial ischemia or new electrocardiogram changes are observed [ , ].

Potential sonographic findings. Fetal growth restriction FGR may be accompanied by oligohydramnios due to redistribution of the fetal circulation away from the kidneys and toward more vital organs, particularly the brain.

By contrast, preeclampsia that develops clinically at term tends to be associated with appropriate growth for gestational age and normal amniotic fluid volume; in some cases, the fetus may be large for gestational age [ ].

Fetal hydrops is rarely observed and is the cause rather than the result of preeclampsia. Hydrops of any etiology can be associated with preeclampsia-like symptoms and is called Mirror syndrome.

However, this finding is neither sensitive nor specific for preeclampsia. See "Early pregnancy prediction of preeclampsia", section on 'Uterine artery Doppler velocimetry'.

Increased resistance in placental blood vessels is reflected by rising Doppler indices of the umbilical artery. Absent and reversed end diastolic flow are the most severe abnormalities and are associated with a poor perinatal outcome.

See "Doppler ultrasound of the umbilical artery for fetal surveillance in singleton pregnancies". Changes in cardiac function and morphology may be seen on echocardiography at an asymptomatic early stage and progress with increasing disease severity [ ].

Preeclampsia does not affect the myocardium directly, but the heart responds to physiologic changes induced by the disease. Left ventricular ejection fraction usually remains within normal limits [ ], but reductions in longitudinal, circumferential, and radial systolic strain have been observed [ ].

The decrement in left ventricular performance has been attributed to a physiologic response to increased afterload [ ,, ], but other factors may play a role since systolic strain was depressed in preeclamptic patients compared with pregnant patients with nonproteinuric hypertension and similar resting blood pressure [ ].

The high afterload in preeclampsia is associated with elevated cardiac filling pressures, reflected by fourfold higher concentrations of natriuretic peptides in patients with preeclampsia compared with pregnant patients who are normotensive or who have chronic hypertension [ ].

Intravascular volume may be reduced in preeclampsia especially with severe features compared with a normal pregnancy [ ]. There is no evidence of underfilling of the arterial circulation; rather, the reduced volume appears to be a consequence of vasoconstriction from enhanced responses to vasoactive substances.

Activation of the renin angiotensin aldosterone system RAAS increases vascular tone and renal reabsorption of sodium and water. In normal pregnancy, despite lower blood pressure compared with the nonpregnant state, the RAAS is upregulated, an appropriate physiologic response to vasodilation.

Sensitivity to angiotensin II is reduced [ ]. In contrast, in multiple studies of patients with preeclampsia, levels of renin and angiotensin I and II were reduced compared with normal pregnancy and sensitivity to angiotensin II was increased, consistent with vasoconstriction, reduced sodium excretion, and possibly some overfilling of the circulation, similar to what is observed in acute glomerulonephritis [ , ].

Potential histologic findings. In blinded studies, the pooled prevalence of villous lesions in preeclamptic and normal pregnancies was 42 and 19 percent, respectively, and the pooled prevalence of vascular lesions was 39 and 10 percent, respectively [ ].

The parenchymal finding most characteristically associated with preeclampsia on routine hematoxylin and eosin staining is acute atherosis ie, fibrinoid necrosis of the vessel wall with an accumulation of lipid-laden "foamy" macrophages and a mononuclear perivascular infiltrate.

Cytotrophoblast invasion of the interstitial uterine compartment is frequently shallow, with incomplete invasion and remodeling of spiral arteries in many places [ ]. This maldevelopment of the uteroplacental circulation can result in reduced placental perfusion, leading to placental infarcts, villous hypoplasia, and, in some cases, the clinical sequelae of FGR.

Research studies using more advanced techniques eg, special stains have described additional findings eg, reduced uterine natural killer cells in the decidua. Placental histology is described in detail separately. See "The placental pathology report", section on 'Preeclampsia'.

Podocyte foot process effacement is not a prominent feature, despite marked proteinuria. Glomerular endotheliosis shares some histologic features with nonpreeclamptic thrombotic microangiopathies [ ], except thrombi are rare in preeclampsia although fibrin deposition may be observed by immunofluorescence microscopy.

Patients treated with anti-VEGF chemotherapy have also been found to have glomerular endotheliosis, along with hypertension and proteinuria [ ]. Rarely, it may be present without proteinuria and in nonpregnant females [ , ]. However, several other disorders can manifest some or many of the signs and symptoms of preeclampsia.

Differential diagnosis is reviewed separately. Overview — Preeclampsia can be a progressive disease. It is important to note that severe sequelae significant end-organ dysfunction, death can occur in patients without severe hypertension. Chest pain, dyspnea, and low platelet count appear to be particularly predictive of fatal or life-threatening complications [ ].

In most patients, resolution of the maternal signs and symptoms of the disease occurs variably in the postpartum period, with some symptoms disappearing in a matter of hours eg, headache , while others may take weeks or months eg, proteinuria. Typically, mobilization of third-space fluid and diuresis begin within 48 hours postpartum.

Hypertension may worsen during the first, and occasionally the second, postpartum week but normalizes in most patients within four weeks after giving birth [ ]. Rarely, hypertension persists beyond three months. Proteinuria usually begins to improve within a few days; however, in patients with several grams of protein excretion, complete resolution may take weeks to months [ ].

In some patients, signs and symptoms of preeclampsia are first recognized postpartum ie, postpartum preeclampsia , usually within 48 hours of birth.

Even though it is not clear why signs and symptoms of preeclampsia may be first recognized or worsen after birth, postpartum preeclampsia is not caused by large fragments of retained placenta. Curettage may slightly accelerate the fall of the soluble fms-like tyrosine kinase-1 sFlt-1 concentration by removing residual cytotrophoblast in the decidua basalis.

Randomized trials have reported conflicting data about the value of curettage for hastening recovery from preeclampsia and eclampsia [ ] and progression of prepartum preeclampsia to postpartum eclampsia has been reported after cesarean hysterectomy, suggesting fragments of retained placenta are not a causal factor [ ].

Therefore, we recommend not performing postpartum curettage as an adjunctive treatment of the disorder. Risk of maternal death — Patients with preeclampsia are at an increased risk for life-threatening obstetric or medical complications cerebrovascular hemorrhage, pulmonary edema, acute kidney injury, liver rupture, abruption, eclampsia.

Among maternal deaths in the US that occurred during delivery hospitalization to , approximately one-quarter had documented pregnancy-associated hypertension gestational hypertension, preeclampsia, eclampsia, chronic hypertension with superimposed preeclampsia and one-third had documented hypertension chronic, pregnancy-associated, or unspecified [ ].

In low- and middle-income countries, the maternal mortality rate from preeclampsia is higher, approximately 40 per , live births in one study [ ]. Maternal mortality is particularly high in patients with both preeclampsia and heart disease. In a worldwide prospective registry of nearly pregnancies in patients with heart disease, developed preeclampsia and six of these patients died 3.

Maternal mortality was much less 0. Fetal complications — For the fetus, preeclampsia can lead to growth restriction and oligohydramnios as well as medically or obstetrically indicated preterm birth.

Fetal growth restriction results from inadequate placentation, usually associated with early-onset preeclampsia.

As a result, perinatal morbidity and mortality are increased, with the highest risk in pregnancies with onset of preeclampsia before 34 weeks of gestation [ ].

Late-onset preeclampsia may not affect fetal growth. See 'Potential sonographic findings' above. Long-term outcomes — Long-term maternal prognosis recurrence risk, increased risk for related obstetric complications in future pregnancies, increased risk for cardiovascular and renal disease in later life and long-term prognosis for offspring are reviewed separately.

See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Prognosis'. SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately.

See "Society guideline links: Hypertensive disorders of pregnancy". These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 th to 12 th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword s of interest. The approach to diagnosis of these disorders is shown in the algorithm algorithm 1.

Preeclamptic patients with severe hypertension or signs of significant end-organ dysfunction meet criteria for the severe end of the disease spectrum table 2. High-risk factors include a past history of preeclampsia, multiple gestation, type 1 or type 2 diabetes, chronic hypertension, chronic kidney disease, or autoimmune disease with potential vascular complications APS, SLE.

Moderate risk factors include nulliparity, obesity, and family history of preeclampsia in a mother or sister. See 'Risk factors' above.

The value of any laboratory or imaging test as a screening tool, including routine assessment of proteinuria at each visit, has not been established. See 'Screening and risk reduction' above. These findings typically become apparent after 34 weeks of gestation and progress until birth, but some patients develop symptoms earlier in gestation, intrapartum, or postpartum.

Patients with preeclampsia are at increased risk for life-threatening events, including placental abruption, acute kidney injury, cerebral hemorrhage, hepatic failure or rupture, pulmonary edema, stroke, cardiac failure, and progression to eclampsia.

See 'Spectrum of disease' above and 'Overview' above and 'Risk of maternal death' above. The fetus is at increased risk for growth restriction and medically or obstetrically indicated preterm birth.

See 'Fetal complications' above. Placental delivery always results in complete resolution of the maternal signs and symptoms of the disease over a variable period of time.

Some patients initially present with gestational hypertension or proteinuria alone. Others present with significant end-organ dysfunction and minimal or even absent hypertension or proteinuria; these patients are classified as HELLP syndrome hemolysis, elevated liver enzymes, low platelets.

See 'Rare and atypical presentations' above. See 'Laboratory tests' above and 'Potential laboratory findings' above. At a minimum, a nonstress test or biophysical profile is performed if appropriate for gestational age.

Ultrasound is used to evaluate amniotic fluid volume and estimate fetal weight, given the increased risk for oligohydramnios and growth restriction. See 'Assessment of fetal status' above and 'Potential sonographic findings' above. See 'When to obtain consultation' above.

Why UpToDate? Product Editorial Subscription Options Subscribe Sign in. Learn how UpToDate can help you. Select the option that best describes you. View Topic. Font Size Small Normal Large. Preeclampsia: Clinical features and diagnosis. Formulary drug information for this topic.

No drug references linked in this topic. Find in topic Formulary Print Share. View in. Language Chinese English. Authors: Phyllis August, MD, MPH Baha M Sibai, MD Section Editor: Charles J Lockwood, MD, MHCM Deputy Editor: Vanessa A Barss, MD, FACOG Contributor Disclosures. All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jan This topic last updated: Jan 25, Potential clinical findings Hypertension — All patients with preeclampsia have hypertension, but a small proportion of those with HELLP and rare patients with eclampsia do not meet diagnostic criteria for hypertension in pregnancy.

An elevated serum indirect bilirubin level suggests hemolysis. Report of the Canadian Hypertension Society Consensus Conference: 1. Definitions, evaluation and classification of hypertensive disorders in pregnancy.

CMAJ ; Gestational Hypertension and Preeclampsia: ACOG Practice Bulletin, Number Obstet Gynecol ; e Reaffirmed Sisti G, Colombi I. Eur J Obstet Gynecol Reprod Biol ; Slade LJ, Wilson M, Mistry HD, et al. The American College of Cardiology and American Heart Association blood pressure categories in the second half of pregnancy-a systematic review of their association with adverse pregnancy outcomes.

Am J Obstet Gynecol ; Payne B, Magee LA, von Dadelszen P. Assessment, surveillance and prognosis in pre-eclampsia. Best Pract Res Clin Obstet Gynaecol ; Visintin C, Mugglestone MA, Almerie MQ, et al. Management of hypertensive disorders during pregnancy: summary of NICE guidance.

BMJ ; c Magee LA, Pels A, Helewa M, et al. Diagnosis, evaluation, and management of the hypertensive disorders of pregnancy: executive summary. J Obstet Gynaecol Can ; Roberts JM, Rich-Edwards JW, McElrath TF, et al.

Subtypes of Preeclampsia: Recognition and Determining Clinical Usefulness. Hypertension ; Lisonkova S, Joseph KS. Incidence of preeclampsia: risk factors and outcomes associated with early- versus late-onset disease.

Harmon QE, Huang L, Umbach DM, et al. Risk of fetal death with preeclampsia. Obstet Gynecol ; Mifsud W, Sebire NJ. Placental pathology in early-onset and late-onset fetal growth restriction.

Fetal Diagn Ther ; Valensise H, Vasapollo B, Gagliardi G, Novelli GP. Early and late preeclampsia: two different maternal hemodynamic states in the latent phase of the disease.

Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count. Magee LA, Brown MA, Hall DR, et al. Pregnancy Hypertens ; Abalos E, Cuesta C, Grosso AL, et al. Global and regional estimates of preeclampsia and eclampsia: a systematic review.

Fingar KR, Mabry-Hernandez I, Ngo-Metzger Q, et al. Healthcare Cost and Utilization Project HCUP Statistical Briefs, Agency for Healthcare Research and Quality US , Rockville MD Hutcheon JA, Lisonkova S, Joseph KS. Epidemiology of pre-eclampsia and the other hypertensive disorders of pregnancy.

Wallis AB, Saftlas AF, Hsia J, Atrash HK. Secular trends in the rates of preeclampsia, eclampsia, and gestational hypertension, United States, Am J Hypertens ; Lisonkova S, Sabr Y, Mayer C, et al.

Maternal morbidity associated with early-onset and late-onset preeclampsia. Elawad T, Scott G, Bone JN, et al. Risk factors for pre-eclampsia in clinical practice guidelines: Comparison with the evidence.

BJOG ; Duckitt K, Harrington D. Risk factors for pre-eclampsia at antenatal booking: systematic review of controlled studies. BMJ ; Bartsch E, Medcalf KE, Park AL, et al. Clinical risk factors for pre-eclampsia determined in early pregnancy: systematic review and meta-analysis of large cohort studies.

BMJ ; i Sibai BM, el-Nazer A, Gonzalez-Ruiz A. Severe preeclampsia-eclampsia in young primigravid women: subsequent pregnancy outcome and remote prognosis. van Rijn BB, Hoeks LB, Bots ML, et al. Outcomes of subsequent pregnancy after first pregnancy with early-onset preeclampsia.

Sibai BM, Mercer B, Sarinoglu C. Severe preeclampsia in the second trimester: recurrence risk and long-term prognosis. Gaugler-Senden IP, Berends AL, de Groot CJ, Steegers EA. Severe, very early onset preeclampsia: subsequent pregnancies and future parental cardiovascular health.

Campbell DM, MacGillivray I, Carr-Hill R. Pre-eclampsia in second pregnancy. Br J Obstet Gynaecol ; Xiong X, Fraser WD, Demianczuk NN. History of abortion, preterm, term birth, and risk of preeclampsia: a population-based study.

Dekker GA, Sibai BM. Etiology and pathogenesis of preeclampsia: current concepts. Roberts JM, Redman CWG, Global Pregnancy Collaboration. Global Pregnancy Collaboration symposium: Prepregnancy and very early pregnancy antecedents of adverse pregnancy outcomes: Overview and recommendations.

Placenta ; Sutton EF, Hauspurg A, Caritis SN, et al. Maternal Outcomes Associated With Lower Range Stage 1 Hypertension. Wu DD, Gao L, Huang O, et al. Increased Adverse Pregnancy Outcomes Associated With Stage 1 Hypertension in a Low-Risk Cohort: Evidence From 47 Cases.

Reddy M, Rolnik DL, Harris K, et al. Challenging the definition of hypertension in pregnancy: a retrospective cohort study. Sutton EF, Rogan SC, Lopa S, et al. Early Pregnancy Blood Pressure Elevations and Risk for Maternal and Neonatal Morbidity. O'Brien TE, Ray JG, Chan WS. Maternal body mass index and the risk of preeclampsia: a systematic overview.

Epidemiology ; Nevis IF, Reitsma A, Dominic A, et al. Pregnancy outcomes in women with chronic kidney disease: a systematic review. Clin J Am Soc Nephrol ; Bramham K, Briley AL, Seed PT, et al. Pregnancy outcome in women with chronic kidney disease: a prospective cohort study.

Reprod Sci ; Multiple gestation pregnancy. The ESHRE Capri Workshop Group. Hum Reprod ; Sibai BM, Hauth J, Caritis S, et al. Hypertensive disorders in twin versus singleton gestations.

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J Am Soc Nephrol ; Nilsson E, Salonen Ros H, Cnattingius S, Lichtenstein P. The importance of genetic and environmental effects for pre-eclampsia and gestational hypertension: a family study. Tsujimoto Y, Kataoka Y, Banno M, et al. Association of low birthweight and premature birth with hypertensive disorders in pregnancy: a systematic review and meta-analysis.

J Hypertens ; Macedo TCC, Montagna E, Trevisan CM, et al. Prevalence of preeclampsia and eclampsia in adolescent pregnancy: A systematic review and meta-analysis of , adolescents worldwide since Grønvik T, Fossgard Sandøy I.

Complications associated with adolescent childbearing in Sub-Saharan Africa: A systematic literature review and meta-analysis. PLoS One ; e Watanabe N, Fujiwara T, Suzuki T, et al. Is in vitro fertilization associated with preeclampsia? A propensity score matched study.

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Risk for preeclampsia. The Fetal Medicine Foundation. Cunningham FG, Lindheimer MD. Hypertension in pregnancy. Pitfalls in diagnosis and management of preeclampsia.

Yancey LM, Withers E, Bakes K, Abbott J. Postpartum preeclampsia: emergency department presentation and management. J Emerg Med ; Matthys LA, Coppage KH, Lambers DS, et al. Blood pressure is the force of your blood pushing against the walls of your arteries as your heart pumps blood.

High blood pressure , or hypertension, is when this force against your artery walls is too high. There are different types of high blood pressure in pregnancy:. If you go on to develop HELLP syndrome, you may also have bleeding or bruising easily, extreme fatigue, and liver failure.

Your health care provider will check your blood pressure and urine at each prenatal visit. They may include blood tests other lab tests to look for extra protein in the urine as well as other symptoms.

Delivering the baby can often cure preeclampsia. When making a decision about treatment, your provider take into account several factors. They include how severe it is, how many weeks pregnant you are, and what the potential risks to you and your baby are:.

The symptoms usually go away within 6 weeks of delivery. In rare cases, symptoms may not go away, or they may not start until after delivery postpartum preeclampsia. This can be very serious, and it needs to be treated right away. The information on this site should not be used as a substitute for professional medical care or advice.

Contact a health care provider if you have questions about your health. High Blood Pressure in Pregnancy. On this page Basics Summary Start Here Symptoms Diagnosis and Tests Treatments and Therapies.

Learn More Related Issues Specifics Genetics. See, Play and Learn Videos and Tutorials. Research Statistics and Research Clinical Trials Journal Articles.

Resources Find an Expert. For You Patient Handouts. What is high blood pressure in pregnancy? There are different types of high blood pressure in pregnancy: Gestational hypertension is high blood pressure that you develop while you are pregnant.

It starts after you are 20 weeks pregnant. You usually don't have any other symptoms. In many cases, it does not harm you or your baby, and it goes away within 12 weeks after childbirth. But it does raise your risk of high blood pressure in the future.

It sometimes can be severe, which may lead to low birth weight or preterm birth. Some women with gestational hypertension do go on to develop preeclampsia. Chronic hypertension is high blood pressure that started before the 20th week of pregnancy or before you became pregnant.

Some women may have had it long before becoming pregnant but didn't know it until they got their blood pressure checked at their prenatal visit. Sometimes chronic hypertension can also lead to preeclampsia.

Preeclampsia is a sudden increase in blood pressure after the 20th week of pregnancy. It usually happens in the last trimester. In rare cases, symptoms may not start until after delivery.

This is called postpartum preeclampsia. Preeclampsia also includes signs of damage to some of your organs, such as your liver or kidney.

The signs may include protein in the urine and very high blood pressure. Preeclampsia can be serious or even life-threatening for both you and your baby.

What causes preeclampsia? The cause of preeclampsia is unknown. Who is at risk for preeclampsia? You are at higher risk of preeclampsia if you: Had chronic high blood pressure or chronic kidney disease before pregnancy Had high blood pressure or preeclampsia in a previous pregnancy Have obesity Are over age 40 Are pregnant with more than one baby Are African American Have a family history of preeclampsia Have certain health conditions, such as diabetes , lupus , or thrombophilia a disorder which raises your risk of blood clots Used in vitro fertilization, egg donation, or donor insemination What problems can preeclampsia cause?

Preeclampsia can cause: Placental abruption, where the placenta separates from the uterus Poor fetal growth, caused by a lack of nutrients and oxygen Preterm birth A low birth weight baby Stillbirth Damage to your kidneys, liver, brain, and other organ and blood systems A higher risk of heart disease for you Eclampsia, which happens when preeclampsia is severe enough to affect brain function, causing seizures or coma HELLP syndrome, which happens when a woman with preeclampsia or eclampsia has damage to the liver and blood cells.

It is rare, but very serious. What are the symptoms of preeclampsia?

The recommendations in this guideline represent the view of NICE, arrived at after careful consideration of the evidence available. When exercising their judgement, professionals and practitioners are expected to take this guideline fully into account, alongside the individual needs, preferences and values of their patients or the people using their service.

It is not mandatory to apply the recommendations, and the guideline does not override the responsibility to make decisions appropriate to the circumstances of the individual, in consultation with them and their families and carers or guardian.

All problems adverse events related to a medicine or medical device used for treatment or in a procedure should be reported to the Medicines and Healthcare products Regulatory Agency using the Yellow Card Scheme. Local commissioners and providers of healthcare have a responsibility to enable the guideline to be applied when individual professionals and people using services wish to use it.

They should do so in the context of local and national priorities for funding and developing services, and in light of their duties to have due regard to the need to eliminate unlawful discrimination, to advance equality of opportunity and to reduce health inequalities.

Nothing in this guideline should be interpreted in a way that would be inconsistent with complying with those duties. Epidemiology of pre-eclampsia and the other hypertensive disorders of pregnancy. Best Pract Res Clin Obstet Gynaecol. Bateman BT, Shaw KM, Kuklina EV, Callaghan WM, Seely EW, Hernandez-Diaz S.

Hypertension in women of reproductive age in the United States: NHANES PLoS ONE. Callaghan WM, Creanga AA, Kuklina EV. Severe maternal morbidity among delivery and postpartum hospitalizations in the United States. Creanga AA, Berg CJ, Ko JY, Farr SL, Tong VT, Bruce FC, et al.

Maternal mortality and morbidity in the United States: where are we now? J Womens Health Larchmt. Macdonald-Wallis C, Tilling K, Fraser A, Nelson SM, Lawlor DA.

Associations of blood pressure change in pregnancy with fetal growth and gestational age at delivery: findings from a prospective cohort. Centers for Disease Control and Prevention. Treating for two: medicine and pregnancy.

Accessed May 22, Liu Y, Croft JB, Wheaton AG, Kanny D, Cunningham TJ, Lu H, et al. Clustering of five health-related behaviors for chronic disease prevention among adults, United States, Prev Chronic Dis.

Mayo Clinic. Postpartum preeclampsia. Matthys LA, Coppage KH, Lambers DS, Barton JR, Sibai BM. Delayed postpartum preeclampsia: an experience of cases. Am J Obstet Gynecol. Data on selected pregnancy complications in the United States. American College of Obstetricans and Gynecologists.

Preeclampsia and high blood pressure during pregnancy. Preventive Services Task Force. If you have high blood pressure due to another condition chronic hypertension , you will need to see your doctor to make sure your blood pressure returns to safe levels. However, your risk is increased, especially if you have a medical condition such as hypertension, kidney disease, diabetes or lupus.

Call Pregnancy, Birth and Baby to speak to a maternal child health nurse on or video call. Available 7am to midnight AET , 7 days a week. Learn more here about the development and quality assurance of healthdirect content. During pregnancy, very high blood pressure severe hypertension can cause complications for both you and your baby.

Read more on RANZCOG - Royal Australian and New Zealand College of Obstetricians and Gynaecologists website. Pre-eclampsia, also known as pre-eclamptic toxaemia, or just toxaemia, occurs in pregnancy, causing problems for the baby and mother.

Read more on myDr website. There is no evidence that preeclampsia is caused by emotional stress, working too hard or not getting enough rest. Read more on Better Health Channel website. Too much sodium salt can cause high blood pressure and many other health conditions.

Pre-eclampsia is a condition that affects some pregnant women usually during the second half of pregnancy or immediately after delivery. Some women will experience complications such as bleeding, itching high blood pressure or severe vomiting during pregnancy that will require treatment.

If a pregnant woman is rhesus Rh negative and her fetus is Rh positive, the fetus and any subsequent fetus may be at risk of health problems. Read more on Heart Foundation website. Swollen ankles and feet are very common during pregnancy.

Learn how to help relieve some of the discomfort and know whether any symptoms are serious. Atrial septal defect is a birth defect that occurs when there is a hole in the septum that divides the upper chambers of the heart. Learn more about it. Read more on HeartKids website.

Pregnancy, Birth and Baby is not responsible for the content and advertising on the external website you are now entering. Video call. Healthdirect Australia acknowledges the Traditional Owners of Country throughout Australia and their continuing connection to land, sea and community.

We pay our respects to the Traditional Owners and to Elders both past and present. This information is for your general information and use only and is not intended to be used as medical advice and should not be used to diagnose, treat, cure or prevent any medical condition, nor should it be used for therapeutic purposes.

The information is not a substitute for independent professional advice and should not be used as an alternative to professional health care.

There are medicines your doctor can prescribe for pre-eclampsia. Both you and your baby will also need to be closely monitored. Remember that pre-eclampsia can become worse very quickly.

If this happens, you may need to go to hospital or give birth to your baby early. If you have high blood pressure, both you and your baby will be closely monitored during the pregnancy. You may have an intravenous drip to give you fluid and medicines. If your condition seems to be worsening during labour, you may need an emergency caesarean.

If you have pre-eclampsia, your doctor may recommend that you have your baby in a large maternity hospital so you and your baby can get expert care if you need it. It may mean the baby is born early or is smaller than expected. High blood pressure in pregnancy usually disappears once the baby is born.

However, there may still be some complications during the first few days after the birth. You will need to be monitored carefully for several weeks. If you have high blood pressure due to another condition chronic hypertension , you will need to see your doctor to make sure your blood pressure returns to safe levels.

However, your risk is increased, especially if you have a medical condition such as hypertension, kidney disease, diabetes or lupus. Call Pregnancy, Birth and Baby to speak to a maternal child health nurse on or video call. Available 7am to midnight AET , 7 days a week.

Learn more here about the development and quality assurance of healthdirect content. During pregnancy, very high blood pressure severe hypertension can cause complications for both you and your baby.

Read more on RANZCOG - Royal Australian and New Zealand College of Obstetricians and Gynaecologists website. Pre-eclampsia, also known as pre-eclamptic toxaemia, or just toxaemia, occurs in pregnancy, causing problems for the baby and mother.

Read more on myDr website. There is no evidence that preeclampsia is caused by emotional stress, working too hard or not getting enough rest.

Read more on Better Health Channel website. Too much sodium salt can cause high blood pressure and many other health conditions. Pre-eclampsia is a condition that affects some pregnant women usually during the second half of pregnancy or immediately after delivery.

Some women will experience complications such as bleeding, itching high blood pressure or severe vomiting during pregnancy that will require treatment.

If a pregnant woman is rhesus Rh negative and her fetus is Rh positive, the fetus and any subsequent fetus may be at risk of health problems.

Read more on Heart Foundation website. Swollen ankles and feet are very common during pregnancy. Learn how to help relieve some of the discomfort and know whether any symptoms are serious.

Atrial septal defect is a birth defect that occurs when there is a hole in the septum that divides the upper chambers of the heart.

Learn more about it. Read more on HeartKids website. Pregnancy, Birth and Baby is not responsible for the content and advertising on the external website you are now entering.

Video call. Healthdirect Australia acknowledges the Traditional Owners of Country throughout Australia and their continuing connection to land, sea and community. We pay our respects to the Traditional Owners and to Elders both past and present.

This information is for your general information and use only and is not intended to be used as medical advice and should not be used to diagnose, treat, cure or prevent any medical condition, nor should it be used for therapeutic purposes.

The information is not a substitute for independent professional advice and should not be used as an alternative to professional health care. If you have a particular medical problem, please consult a healthcare professional. American College of Obstetricians and Gynecologists..

ACOG Committee on Practice Bulletins—Obstetrics. ACOG Practice Bulletin No. Diagnosis and management of preeclampsia and eclampsia. McMaster MT, Zhou Y, Fisher SJ. Abnormal placentation and the syndrome of preeclampsia. Semin Nephrol.

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Urinary placental growth factor and risk of preeclampsia. Levine RJ, Maynard SE, Qian C, et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med. Esplin MS, Fausett MB, Fraser A, et al. Paternal and maternal components of the predisposition to preeclampsia.

Morgan T, Ward K. New insights into the genetics of preeclampsia. Semin Perinatol. Lin J, August P. Genetic thrombophilias and preeclampsia: a meta-analysis.

Mignini LE, Latthe PM, Villar J, Kilby MD, Carroli G, Khan KS. Mapping the theories of preeclampsia: the role of homocysteine.

Milne F, Redman C, Walker J, et al. The preeclampsia community guideline PRECOG : how to screen for and detect onset of preeclampsia in the community. Levine RJ, Hauth JC, Curet LB, et al. Trial of calcium to prevent preeclampsia.

Sibai BM, Villar MA, Bray E. Magnesium supplementation during pregnancy: a double-blind randomized controlled clinical trial. Salvig JD, Olsen SF, Secher NJ.

Effects of fish oil supplementation in late pregnancy on blood pressure: a randomised controlled trial. Br J Obstet Gynaecol. Poston L, Briley AL, Seed PT, Kelly FJ, Shennan AH for the Vitamins in Preeclampsia VIP Trial Consortium.

Vitamin C and vitamin E in pregnant women at risk for preeclampsia VIP trial : randomised placebo-controlled trial. Hofmeyr GJ, Atallah AN, Duley L. Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems.

Duley L, Henderson-Smart DJ, Meher S, King JF. Antiplatelet agents for preventing preeclampsia and its complications. Canadian Task Force on Preventive Health Care. Prevention of preeclampsia.

Accessed October 12, Preventive Services Task Force. Guide to Clinical Preventive Services: Report of the U. Baltimore, Md. Wheeler TL, Blackhurst DW, Dellinger EH, Ramsey PS.

Usage of spot urine protein to creatinine ratios in the evaluation of preeclampsia. Weinstein L. Syndrome of hemolysis, elevated liver enzymes, and low platelet count: a severe consequence of hypertension in pregnancy. Sibai BM, Ramadan MK, Usta I, Salama M, Mercer BM, Friedman SA.

Maternal morbidity and mortality in pregnancies with hemolysis, elevated liver enzymes, and low platelets HELLP syndrome. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count.

Barton JR, Sibai BM. Diagnosis and management of hemolysis, elevated liver enzymes, and low platelets syndrome. Clin Perinatol. Magann EF, Martin JN. Twelve steps to optimal management of HELLP syndrome.

Neilson JP, Alfirevic Z. Doppler ultrasound for fetal assessment in high risk pregnancies. Williams KP, Farquharson DF, Bebbington M, et al.

Screening for fetal well-being in a high-risk pregnant population comparing the nonstress test with umbilical artery Doppler velocimetry: a randomized controlled clinical trial.

Altman D, Carroli G, Duley L, et al. Do women with preeclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lucas MJ, Leveno KJ, Cunningham FG.

A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. Belfort MA, Anthony J, Saade GR, Allen JC for the Nimodipine Study Group. A comparison of magnesium sulfate and nimodipine for the prevention of eclampsia.

Magnesium sulfate prophylaxis in preeclampsia: evidence from randomized trials. Duley L, Gülmezoglu AM, Henderson-Smart DJ. Magnesium sulphate and other anticonvulsants for women with preeclampsia.

Diagnosis, prevention, and management of eclampsia. Dildy GA. Complications of preeclampsia. In: Critical Care Obstetrics. Malden, Mass. Martin JN, Thigpen BD, Moore RC, Rose CH, Cushman J, May W. Stroke and severe preeclampsia and eclampsia: a paradigm shift focusing on systolic blood pressure.

Duley L, Henderson-Smart DJ, Meher S. Drugs for treatment of very high blood pressure during pregnancy. Churchill D, Duley L. Interventionist versus expectant care for severe preeclampsia before term.

Odendaal HJ, Pattinson RC, Bam R, Grove D, Kotze TJ. Aggressive or expectant management for patients with severe preeclampsia between 28—34 weeks' gestation: a randomized controlled trial. 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.

Magee L, Sadeghi S. Prevention and treatment of postpartum hypertension. Mattar F, Sibai BM. Risk factors for maternal morbidity. Chames MC, Livingston JC, Ivester TS, Barton JR, Sibai BM. Late postpartum eclampsia: a preventable disease?. Aagaard-Tillery KM, Belfort MA.

Eclampsia: morbidity, mortality, and management. Which anticonvulsant for women with eclampsia? Evidence from the Collaborative Eclampsia Trial [published correction appears in Lancet. Duley L, Henderson-Smart D. Magnesium sulphate versus phenytoin for eclampsia.

Magnesium sulphate versus diazepam for eclampsia. This content is owned by the AAFP. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP.

search close. PREV Jul 1, NEXT. B 27 For women with mild preeclampsia, delivery is generally not indicated until 37 to 38 weeks of gestation and should occur by 40 weeks.

A 42 Intravenous labetalol or hydralazine may be used to treat severe hypertension in pregnancy because neither agent has demonstrated superior effectiveness.

Expectant management, with close monitoring of the mother and fetus, reduces neonatal complications and stay in the newborn intensive care nursery. Chronic Hypertension. Gestational Hypertension. LAWRENCE LEEMAN, MD, MPH, is an associate professor of family and community medicine and obstetrics and gynecology at the University of New Mexico School of Medicine, Albuquerque.

He is also director of family practice maternity and infant care and co-medical director of the mother-baby unit at the University of New Mexico Hospital, Albuquerque. Lee-man received his medical degree from the University of California, San Francisco, School of Medicine, and completed a family medicine residency at the University of New Mexico School of Medicine and a fellowship in obstetrics at the University of Rochester NY School of Medicine and Dentistry.

He is an associate editor of the ALSO syllabus. She received her medical degree from the University of Michigan Medical School, Ann Arbor, and completed a family medicine residency at the University of Minnesota North Memorial Health Care Residency Program, Robbinsdale.

She is managing editor of the ALSO syllabus. of Family and Community Medicine, MSC09 , Tucker N. Continue Reading.