Approach To Hypertensive Disorders In Pregnancy - JSciMed Central
Central Bringing Excellence in Open AccessAnnals of Clinical and Experimental HypertensionMini Review*Corresponding authorNatrajSetty HS, Assistant Professor of Cardiology, SriJayadeva Institute of Cardiovascular Sciences andResearch, Bangalore, Karnataka, India, Tel: 26580051,Fax No: 080-22977261, #493, 4th Cross, 7th Main, J.P.Nagar 3rd Phase, Bangalore 69, Email:Approach to HypertensiveDisorders in PregnancySubmitted: 20 October 2016HS Natraj Setty*, Vijay kumar, BC Srinivas, Nagesh, BabuReddy, and CN ManjunathAccepted: 28 October 2016Sri Jayadeva Institute of Cardiovascular Sciences and Research, IndiaISSN: 2373-9258Published: 05 November 2016CopyrightAbstract 2016 Natraj Setty et al.Hypertensive disorders of pregnancy, including preeclampsia, complicate up to10% of pregnancies worldwide, constituting one of the greatest causes of maternaland perinatal morbidity and mortality worldwide. Preeclampsia is a leading causeof maternal and perinatal morbidity mortality, with an estimated 50,000-60,000Preeclampsia – related deaths per year worldwide. Hypertensive disorders ofpregnancy are major contributors to prematurity. Preeclampsia is a risk factor forfuture cardiovascular disease and metabolic disease in women. Within the past 10years substantial advances in the understanding of preeclampsia pathophysiology aswell as increased efforts of obtain evidence to guide therapy have emerged. However,this information has not translated into improved clinical practice. New best practicerecommendations are greatly needed to guide clinicians in the care of women withall forms of preeclampsia and hypertension that occur during pregnancy, particularlywomen with severe hypertension and superimposed preeclampsia. Also needed is asystem for continually updating these guidelines integrating them into daily obstetricpractice.OPEN ACCESSINTRODUCTIONHypertension occurs in approximately 10% of firstpregnancies and 8% of all pregnancies. Preeclampsia (PE),defined as new onset of hypertension with proteinuria after 20weeks’ gestation, is a leading cause of maternal and neonatalmortality worldwide [1]. Though maternal mortality fromPreeclampsia has fallen in developed countries, it remains acommon cause of preterm delivery of low birth weight babiesfrom intrauterine growth retardation [2]. Moreover, the rate ofpreeclampsia is increasing, likely from increasing maternal ageand more multiple births [3]. Special attention will be directedat maternal obesity, which increases the risk for hypertensionduring pregnancy with resultant increases in large babies andcaesarean delivery [4]. At present, 0.2–4% of all pregnancies arecomplicated by cardiovascular diseases (CVD), [5] and the numberof the patients who develop cardiac problems during pregnancyis increasing. However, knowledge of the risks associated withCVD during pregnancy and their management are of pivotalimportance for advising patients before pregnancy. Therefore,guidelines on disease management in pregnancy are of greatrelevance. Such guidelines have to give special considerationto the fact that all measures concern not only the mother, butthe fetus as well. Therefore, the optimum treatment of bothmust be targeted. A therapy favourable for the mother can beassociated with an impairment of the child, and in extreme casestreatment measures which protect the survival of the mothercan cause the death of the fetus. Counselling and managementKeywords Hypertensive Disorders Proteinuria Maternal ageof women of childbearing age with suspected cardiac diseaseshould start before pregnancy occurs; they should be managedby interdisciplinary teams; high risk patients should be treated inspecialized centres; and diagnostic procedures and interventionsshould be performed by specialists with great expertise in theindividual techniques and experience in treating pregnantpatients. Registries and prospective studies are urgently neededto improve the state of knowledge. Hypertension is the mostcommon medical problem encountered in pregnancy and is aleading cause of perinatal and maternal morbidity and mortality[6]. A rise in blood pressure (BP) during the peripartum periodrequires evaluation and review [7].CLASSIFICATION [8,9]Gestational HypertensionGestational hypertension, formerly known as pregnancyinduced hypertension or PIH, is the new onset of hypertensionafter 20 weeks of gestation.Also known as transient hypertension.The diagnosis requires that the patient have:Elevated blood pressure (systolic 140 or diastolic 90mm Hg, the latter measured using the fifth Korotkoff sound),Previously normal blood pressures, No protein in the urine, Nomanifestations of preeclampsia, increased incidence of up to30% in multiple gestation, 15-25% of women initially diagnosedwith gestation HTN develop preeclampsia and earlier onset ofgestation HTN are more likely to progress to preeclampsia [10].Cite this article: Natraj Setty HS, Vijay Kumar, Srinivas BC, Reddy ND, Manjunath CN (2016) Approach to Hypertensive Disorders in Pregnancy. Ann Clin ExpHypertension 4(2): 1039.
Natraj Setty et al. (2016)Email: Central Bringing Excellence in Open AccessChronic Hypertension in pregnancyChronic hypertension is high blood pressure that eitherprecedes pregnancy, is diagnosed within the first 20 weeks ofpregnancy, or does not resolve by the 12-week postpartum checkup. Two categories of severity are recognized: mild (up to 179mm Hg systolic and 109 mm Hg) and severe ( 180 systolicor 110 diastolic). Chronic hypertension complicates about 5%of all pregnancies, and prevalence rates are increasing due todelayed childbearing. Medications should be reviewed whenpregnancy is first diagnosed. Chronic hypertension accounts for adisproportionate amount of maternal and perinatal morbidity andmortality, mostly because of an increased risk of superimposedpreeclampsia. There is an increased risk of prematurity, birthof infants who are small for their gestational age, intrauterinedeath, placental abruption, and caesarean delivery.Complication rates are directly related to the severity andduration of elevated blood pressures. Patients with severehypertension in the first trimester have a greater than 50% riskof developing superimposed preeclampsia About 20-25% ofwomen with chronic hypertension develop preeclampsia duringpregnancy. All hypertensive patients should undergo increasedsurveillance, serial laboratory tests throughout pregnancy, serialultrasound scans to follow growth, and antenatal testing. Thebaby should be delivered vaginally if possible.When a patient’s blood pressure is persistently greaterthan 150 to 180/100 to 110 mm Hg, pharmacologic treatmentis needed to prevent maternal end-organ damage. Methyldopa ,labetalol, and nifedipine are oral agents commonly used to treatchronic hypertension in pregnancy. Angiotensin-convertingenzyme inhibitors and angiotensin-II receptor antagonistsare not used because of teratogenicity, intrauterine growthrestriction (IUGR), and neonatal renal failure [11].PreeclampsiaPreeclampsia is a multiorgan disease process of unknownetiology characterized by the development of hypertensionand protein uria after 20 weeks of gestation. There are varioustheories of pathogenesis of preeclampsia. The most populartheory is immunologic. During a normal pregnancy, fetal syncytialtrophoblasts penetrate and remodel maternal spiral arteries,causing them to dilate into large, flaccid vessels. This remodelingaccommodates the vast, increased maternal circulation neededfor adequate placental perfusion. This remodeling is somehowprevented in preeclamptic pregnancies: the placenta is unableto properly burrow into the maternal blood vessels, leading tointrauterine growth restriction and other fetal manifestationsof the disorder. Investigators speculate that this incompleteplacentation is due to maternal immunologic intolerance offoreign fetal genes. Evidence in support of this theory is that therisk of preeclampsia is highest in a first pregnancy and decreaseswith the length of time a woman has lived with the fatherbefore becoming pregnant. Others theories of pathogenesis ofpreeclampsia are angiogenic factors (increased sFlt-1, decreasedplacental growth factor levels) cardiovascular maladaptationand vasoconstriction, genetic predisposition (maternal, paternal,thrombophilias) immunologic intolerance between fetoplacentaland maternal tissue, platelet activation, vascular endothelialAnn Clin Exp Hypertension 4(2): 1039 (2016)damage or dysfunction. Development of HTN proteinuria inducedby pregnancy generally in the second half of gestation. Morefrequent at the extremes of reproductive years. Preeclampsiamay present in two forms [12].Mild: BP- Systolic greater than 140mmHg and/or diastolicgreater than 90 mmHg. Proteinuria-Greater than 300 mg on 24hours collection of 1 on single sample.Severe: BP-Systolic greater than 160-180 mmHg and/ordiastolic greater than 110 mmHg. Proteinuria- Greater than5g on 24 hours collection or 2 on single sample, multi systemalteration.EPIDEMIOLOGYThe etiology of preeclampsia must explain the followingfeatures, as delineated by Chesley (1985): It occurs almostexclusively during the first pregnancy; nulliparas are six to eighttimes more susceptible than are multiparas. Older primigravidasare more susceptible than are younger. Cardiovascular riskfactors associated with increased probability of preeclampsia,as are maternal age older than 40 years, diabetes, obesity andpre-existing hypertension. The increased prevalence of chronichypertension and other comorbid medical illnesses in womenolder than 35 years may explain the increased frequencyof preeclampsia among older women [13]. It occurs morefrequently in those with multiple fetuses, hydatidiform mole,or diabetes. The incidence increases as term approaches; it isunusual before the end of the second trimester. The features ofthe syndrome are hypertension, edema, proteinuria, and, whenadvanced, convulsions and coma. There is characteristic hepaticand renal pathology. The syndrome has a hereditary tendency;in the families of women who had preeclampsia, the syndromedeveloped in 25% of their daughters and granddaughters but inonly 6% of their daughters-in law. It rapidly disappears when thepregnancy is terminated [14].PATHOPHYSIOLOGYThe pathogenesis of preeclampsia is thought to be triggeredby excessive maternal immune response to the developingtrophoblast leading to placental oxidative stress, hypoperfusion,and hypoxia, and the subsequent release of placental factorscausing widespread endothelial dysfunction in the maternalcirculation. In turn, the resulting placental hypoperfusion isprobably further aggravated by reduced activity of growthfactors, including vascular endothelial growth factor (VEGF),placental growth factor, and transforming growth factor β 1.Antiangiogenic factors, such as soluble fms-like tyrosine kinase-1a soluble form of the VEGF-1 receptor, and soluble endoglin, apart of the transforming growth factor β receptor, are releasedfrom apoptotic trophoblast cells and interact with and reduce thesystemic and local levels of VEGF, placental growth factor, andtransforming growth factor β 1 [15].Uterine vascular changesTrophoblastic-mediated vascular changes - decreasedmusculature in spiral arterioles- development of low resistance.Low pressure, high-flow system, Inadequate maternal vascularresponse, Endothelial damage is also noted within the vessels.2/5
Natraj Setty et al. (2016)Email: Central Bringing Excellence in Open AccessHemostatic changesIncreased platelet (PLT) activation with increased increasedendothelial fibronection and decreased ant thrombin III and α-2antiplasminfurther endothelial damage is thought to promotefurther vasospasm.Changes in prostanoidsDuring pregnancy, both prostaglandin (PGI 2) (vasodilatationand decreased PLTaggregation) and thromboxane A2(TXA 2)(vasoconstriction and PLT aggregation) are increased withbalance favored to PGI 2, In preeclampsia TXA 2 is favoredChanges in endothelium-derived factorsDecreased in nitric oxide promoting vasoconstriction [16].DIAGNOSISHypertension developing after the 20th week of gestation withproteinuria in a young nullipara is preeclampsia, particularlyif she has a positive family history for the syndrome. Becausepatients usually have no symptoms, prenatal care is crucialto detect the signs early and thereby prevent the dangeroussequelae of the fully developed syndrome. In keeping with the listof known risk factors, women with the following features shouldbe more closely evaluated and monitored [17]. First pregnancy Previous preeclampsia 10 years since last baby Multiple pregnancy Underlying medical causes Preexisting hypertension Preexisting renal disease Preexisting diabetes Presence of antihypertensive phospholipid antibodiesTREATMENTNonpharmacologic ManagementSmoking Cessation: Through 2007, 26% of mothers smokedduring pregnancy and their children had more hypertension, butthis was mainly ascribed to their obesity [18].Bed Rest: In women who were hospitalized for variouspreterm indications, strict bed rest was said to reduce theincidence of preeclampsia and IUGR [19].Exercise: Most studies find a protection against preeclampsiaby moderate exercise [20].Sodium: Maintenance of usual sodium intake has beenrecommended to avoid further reducing placental perfusion [21].Calcium Supplements: Although once claimed to be effectivefor prevention of preeclampsia in high-risk populations, they arenot useful for therapy. However, in an in vitro study, calciumprotected endothelial activation by trophoblastic debris [22].Pharmacologic Therapy Body mass index 35 Family history of preeclampsia (mother or sister) Patient had low birth weight Diastolic BP 80 mm Hg Proteinuria ( on more than one occasion and 300 mgper 24 hours)The indications for drug therapy for hypertension duringpregnancy remain uncertain since there is no evidence that suchtherapy improves neonatal outcomes. As stated by the 2013ESH/ESC guidelines (Table 2)Risks to Mother and FetusWomen with chronic hypertension have a 30% increased riskTable 1: Definition and Hypertension Disorders during PregnancyElevation of blood pressure (BP) is 140 mmHg systolic and/or 90 mmHg diastolic and on two occasions at least 6 hours apart.TypesPregnancy-induced HTN(PIH)Chronic HTN preceding pregnancyChronic HTN with superimposed PIHEclampsiaAnn Clin Exp Hypertension 4(2): 1039 (2016)DescriptionGestational HTN:-Mild-to-moderate HTN after 20 weeks of pregnancy sustained systolic BP at or above 140 mmHg, or adiastolic BP 90 mmHg or greater.Preeclampsia:Development of HTN proteinuria induced by pregnancy generally in the second half of gestation.Mild:BP- Systolic greater than 140mmHg and/or diastolic greater than 90 mmHg.Proteinuria-Greater than 300 mg on 24 hours collection of 1 on single sample.Severe:BP-Systolic greater than 160-180 mmHg and/or diastolic greater than 110 mmHg.Proteinuria- Greater than 5g on 24 hours collection or 2 on single sample, multi system alteration.Eclampsia:Addition of convulsions in a woman with preeclampsia.Systolic pressure is greater than or equal to 140 mmHg, diastolic pressure greater than 90 mmHg orboth present before 20th week of pregnancy or persist longer than 12- week postpartum. Superimposed preeclampsia Superimposed eclampsiaPreeclampsia with seizures that cannot be attributed to other causes. Seizures may appear 2 or moredays after delivery.3/5
Natraj Setty et al. (2016)Email: Central Bringing Excellence in Open Accessfor superimposed preeclampsia and placental abruption, and atleast their male babies have a threefold greater risk for perinatalmortality. Hormonal changes occur during pregnancy which leadsto histological changes in the aorta, increasing the susceptibilityto dissection. Dissection occurs most often in the last trimesterof pregnancy (50%) or the early postpartum period (33%). Inall women with known aortic disease and/or an enlarged aorticroot diameter, the risks of pregnancy should be discussed beforeconception [25]. Even without superimposed preeclampsia,women with chronic hypertension have more complicatedpregnancies with more intrauterine growth retardation andperinatal mortality. For those with serum creatinine exceeding2.0 mg/dL, a one in three chance of entering end-stage renalfailure after pregnancy has been reported, so that these womenshould be strongly advised against pregnancy. Nonetheless,successful pregnancies have been reported in most women whoconceive during chronic dialysis [26].CONCLUSIONHypertensive disorders of pregnancy are one of the mostserious complications in pregnancy because they cause seriousmaternal and perinatal morbidity and mortality. Althoughnumerous hypertensive patients have relatively good outcome,difficulty in differentiating among various hypertensiveconditions, inability to predict which patients are at highest risk,Table 2: Oral Drugs for Treatment Of Chronic Hypertension in betalolCalcium antagonists(nifedipine)DiureticsACEIs, A-II receptorblockers, direct rennininhibitorsPreferred on the basis of long –term followup studies supporting safetyReports on intrauterine growthretardation(atenlol)Increasing preferred to methyldopa becauseof reduces side effects.Limited dataNo increase in major teratogenicity withexposureNot first-line agentsProbably safe to reduce fluid retention otheragentsContraindicated: Reported fetal toxicity anddeathTable 3: Treatment of Acute Severe Hypertension in Preeclampsia prusside(rarely whenothers fail)Comments5mg IV bolus, then 10 mg every 20-30 minutes toa maximum of 25 mg, repeat in several hours asnecessary20 mg IV bolus, then 40 mg 10 minutes lates, 80mg every 10 minutes for two additional doses to amaximum of 220 mg10 mg PO, repeat every 20 minutes to a maximumof 30 mg. Caution when using nifedipine withmagnesium sulphate, can see precipitous BP drop.0.25 µg/kg/min to a maximum of 5 µg/kg/min. Fetalcyanide poisoning may occur if used for 4 hAnn Clin Exp Hypertension 4(2): 1039 (2016)and variability in the progression of preeclampsia make thesedisorders the greatest challenge of clinical medicine in obstetricsREFERENCES1. Abalos E, Cuesta C, Grosso AL, Chou D, Say L. Global and regionalestimates of preeclampsia and eclampsia: A systematic review . Eur JObstet Gynecol Reprod Biol. 2013; 170: 1-7.2. Sibai BM, Lindheimer M, Hauth J, Steve Caritis, Peter VanDorsten, MarkKlebanoff, et al. Risk factors for preeclampsia, abruptio placentae, andadverse neonatal outcomes among women with chronic hypertension.N Engl J Med. 1998; 339: 667-671.3. Wallis AB, Saftlas AF, Hsia J, Atrash HK, et al. Secular trends in the ratesof preeclampsia, eclampsia, and gestational hypertension, UnitedStates, 1987-2004. Am J Hypertens. 2008; 21: 521-526.4. 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Natraj Setty et al. (2016)Email: Central Bringing Excellence in Open Accessbedrest on the prevention of hypertensive diseases of pregnancy andgrowth restriction. Hypertens Pregnancy. 2008; 27: 197-205.et al. 2013 ESH/ESC guidelines for the management of arterialhypertension. J Hypertens. 2013; 31: 1281-1357.20. Genest DS, Falcao S, Gutkowska J, Lavoie JL. Impact of exercise trainingon preeclampsia: Potential preventive mechanisms. Hypertension.2012; 60: 1104-1009.24. Norwitz ER, Funai EF. Expectant management of severe preeclampsiaremote from term: Hope for the best, but expect the worst. Am J ObstetGynecol. 2008; 199: 209-212.22. Chen Q, Tong M, Wu M, Stone PR, Snowise S, Chamley LW, et al. Calciumsupplementation prevents endothelial cell activation: possiblerelevance to preeclampsia. J Hypertens. 2013; 31: 1828-1836.26. Chappell LC, Enye S, Seed P, Briley AL, Poston L, Shennan AH, et al.Adverse perinatal outcomes and risk factors for preeclampsia inwomen with chronic hypertension: A prospective study. Hypertension.2008; 51: 1002-1009.21. Knuist M, Bonsel GJ, Zondervan HA, et al. Low sodium diet andpregnancy-induced hypertension: A multi-centre randomisedcontrolled trial. Br J Obstet Gynecol. 1998; 105: 430-434.23. Mancia G, Fagard R, Narliewicz K, Redón J, Zanchetti A, Böhm M,25. Manalo-Estrella P, Barker AE. Histopathologic findings in humanaortic media associated with pregnancy. Arch Pathol. 1967; 83: 336341.Cite this articleNatraj Setty HS, Vijay Kumar, Srinivas BC, Reddy ND, Manjunath CN (2016) Approach to Hypertensive Disorders in Pregnancy. Ann Clin Exp Hypertension 4(2):1039.Ann Clin Exp Hypertension 4(2): 1039 (2016)5/5
Gestational hypertension, formerly known as pregnancy-induced hypertension or PIH, is the new onset of hypertension after 20 weeks of gestation.Also known as transient hypertension. The diagnosis requires that the patient have: Elevated blood pressure (systolic 140 or diastolic 90 . mm Hg, the latter measured using the fifth Korotkoff .
principles of hypertensive crisis and in most recent guide-lines termed “compelling conditions” (Whelton 2017). For the general treatment of hypertensive crisis, patients should be classified as having hypertensive emergency or hypertensive urgency. Hypertensive urgency often requires initiating, reini-
3.4 Management of HELLP Syndrome 3.5 Anaesthesia and Hypertensive Disorders in Pregnancy 3.6 Fetal Surveillance in Hypertensive Disorders in Pregnancy 3.7 Discharge and Follow-up Strategies . SECTION 4 : REFERRAL PROCEDURES AND MANAGEMENT IN TRANSIT SECTION 5 : DIFFERENTIAL DIAGNOSIS .
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I10 Essential (primary) hypertension I16.0 Hypertensive urgency I16.1 Hypertensive emergency I16.9 Hypertensive crisis, unspecified I25.10 Atherosclerotic heart disease of native coronary artery without angina pectoris I25.110 Atherosclerotic heart disease of
Norway who had a stillbirth had pregnancy-induced hypertension [3, 6]. Cardiovascular disease (CVD) is a leading cause of morbidity and mortality for women globally. Women . Incidence of hypertensive disorders of pregnancy (HDP) and CVD The crude incidence of GH decreased over the study period, before increasing again to 3.7% by 2014, while
