Hypertensive Disorders of Pregnancy Blok 25 Revisi 2013

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HYPERTENSIVE DISORDERS OF PREGNANCY Adrian Setiawan, M.D. Department of Obstetrics and Gynecology,Faculty of Medicine KRIDA WACANA CHRISTIAN UNIVERSITY

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Transcript of Hypertensive Disorders of Pregnancy Blok 25 Revisi 2013

HYPERTENSIVE DISORDERS OF PREGNANCY

HYPERTENSIVE DISORDERS OF PREGNANCYAdrian Setiawan, M.D.Department of Obstetrics and Gynecology,Faculty of MedicineKRIDA WACANA CHRISTIAN UNIVERSITYGeneral ClassificationPreeclampsia or Eclampsia (hypertension and proteinuria unique to pregnancy)Chronic hypertensionChronic hypertension with superimposed preeclampsiaGestational or transient hypertension(National Institutes of Health Working Group Report on High Blood Pressure in Pregnancy,2000. Adopted by ACOG ,2002)Diagnosis of HypertensionBlood pressure readings vary depending on maternal position and the gestational age of the pregnancy.Tends to be lower in the LLD position, higher in the sitting position.In the supine position some elevated pressure, some have supine hypotension due to compression of the vena cava by the uterus.Arterial blood pressure normally declines during 1st and 2nd trimesterThe diagnosis of hypertension should be reserved for patients with a systolic greater than or equal to 140 mmHg or a diastolic greater than or equal to 90 mmHg.BP should be taken in the sittting or lateral decubitus position after woman has rested at least 10 minutes.PREECLAMPSIAA syndrome unique to pregnancy, characterized by the new onset of hypertension and proteinuria in the latter half of gestation divided into mild and severe preeclampsia.Classically affecting the first pregnancy, but also occurs in multiparas or change in husbandTwo criteria for diagnosis of preeclampsia : the BP 140/90 mmHg and development of new onset proteinuria after 20th wks AOG.Proteiunuria defined as 0.3 gram protein in a 24 hour urine collection , usually correlates 30 mg/dl (+1 on dipstick)Criteria for Severe PreeclampsiaBP 160/110 mmHg at rest on two occasions at least 6 hr apartProteinuria 5 gram in a 24 h urine collection or qualitative +3 Oliguria (< 500 ml in 24 hr)Cerebral or visual disturbancesPulmonary edema or cyanosisEpigastric or right upper quadrant painImpaired liver function (elevated liver enzyme)ThrombocytopeniaFetal growth restriction

(ACOG, Practice Bulletin No.33, Washington,DC,2002)EclampsiaIs the presence of tonic clonic seizures in a woman with preeclampsia that cannot be attributed to other causes.Chronic HypertensionThe diagnosis of chronic hypertension requires at least one of the following : known hypertension before pregnancy, development of hypertension before 20 weeks gestation, or, in cases in which hypertension is first noted during pregnancy, persistence of elevated blood pressures greater than 12 weeks postpartum.Chronic Hypertension with Superimposed PreeclampsiaThe diagnosis of superimposed preeclampsia should be reserved for those women with chronic hypertension who develop new onset proteinuria (0.3 g in a 24 hour collection) after 20th week of gestation. In pregnant women with preexisting hypertension and proteinuria, the diagnosis of superimposed preeclampsia should considered if they experience sudden significant increases in blood pressure or proteinuria or any of the other signs and symptoms consistent with severe preeclampsia.Gestational HypertensionThe diagnosis of gestational hypertension is made if hypertension without proteinuria first appears after 20 weeks gestation or within 48 to 72 hours after delivery and resolves by 12 weeks postpartum.The diagnosis of gestational hypertension can only be made in retrospect, if the pregnancy has been completed without the development of proteinuria and if the blood pressure has returned to normal before the 12 week postpartum.Etiology Preeclampsia / EclampsiaPreeclampsia is called a disease of theories, because genetic,immunologic,vascular, hormonal, nutritional, and behavioral factors have all been proposed as causes. No single definitive cause has been identified and the origins of the disease are considered to be multifactorial.Placental ischemia, or hypoxia appears to be central to the development of the disease and has been attributed to failure of the cytotrophoblasts to adequately invade the uterine spiral arteries and establish the low resistance uteroplacental circulation characteristic of normal pregnantIt is postulated that uteroplacental ischemia results in oxidative stress leading to production and release of toxins that enter the circulation and cause widespread inflammation, endothelial dysfunction and activation of the coagulation system.Endothelial dysfunction leads to imbalance between different classes of locally produced vasoconstrictors and vasodilators.Endothelial changes also appear to involve a relative deficiency in the production of nitric oxide, a vasodilator and inhibitor of platelet aggregation along with increased production of endothelin-1. Endothelin 1 is an extremely potent vasoconstrictor and activator platelets.The net effect of these processes would be spread vasoconstriction leading to hypoxic and ischemic damage in different vascular beds,systemic hypertension, the HELLP syndrome or DIC and worsening placental ischemia.PathophysiologyGeneralized vasospasmGFR and renal blood flow are significantly lowerDamage of glomerular membranes , increasing their permeability to proteins and leading to proteinuria.Cerebral vascular resistance is high in patients with PE and EclampsiaPathologyLack of decidualization of the myometrial segments of the spiral arteriesGlomerular capillary endotheliosisIschemia, hemorrhage and necrosis in many organs, presumably secondary to arteriolar constriction.Clinical and laboratory manifestationsWeight gain and edemaElevation of blood pressureProteinuriaIncrease serum uric acid concentrationThrombocytopeniaLiver function : elevated serum enzyme levels (alanine aminotransferase and aspartate aminotransferase)Retroplacental hemorrhage or abruptioVisual disturbanceLaboratory : CBC, platelet count,LDH, Ureum, creatinin and uric acid, urinalysis 24 hour urine for protein and creatinine, liver function tests.PREVENTION1.BMI and diet.Several authors have shown that women with BMI> 30 had an increase risk of gestational hypertension, preeclampsia, gestational diabetes and fetal macrosomia. The influence maybe due to inflammation.2. Low dose AspirinIn PIH patients circulating levels of Thromboxane A2(TXL-A2 vasoconstrictor) increased and Prostacyclin (PGI, vasodilator) decreased. Low dose Aspirin effectively inhibit TXA2 .

Many Authors concluded that low dose aspirin have moderate benefits when used for prevention of preeclampsia.3. High dose CalciumOral intake of high dose calcium (2 Gm/day) has been proposed to prevent pre-eclampsia. High dose calcium exerts a negative feedback effect on parathyroid hormone > lowering intracellular calcium ion levels > smooth muscle relaxation and diminished responsiveness to pres-sor stimuli.Management of Mild Preeclampsia and Gestational HypertensionInitial hospitalization to obtain baseline data and monitor feto-maternal status. The mother is also instructed to perform fetal movement counts daily and low salt, high calcium diet.OPD follow up basically consist of review of fetal movement, BP reading and NST (Non Stress Test)We prefer to give oral methyldopa, low dose aspirin and high dose calciumWe tend to push the mild preeclampsia patient to near term as possible provided feto-maternal status is not impaired.Evaluation and managementDelivery is the only definitive cure for preeclampsia and eclampsia after a period of stabilization, regardless of the gestational age of the fetus.Seizure prophylaxis : magnesium sulfateAntihypertensive therapy : hydralazine, labetalol, nifedipine, methyldopaManagement of Severe Preeclampsia and EclampsiaControl of convulsionsThe anti convulsant of choice is Magnesium Sulfate although some prefer diazepam. The RCT has shown the superiority of MgSO4 over diazepam and phenytoin.Give a loading dose of 4 Gm slow IV bolus over 5 minutes followed by a maintenance dose of 1-2 Gms per hour IV drip.The safety of MgSO4 is monitored at the bedside using the following points :- the presence of deep tendon reflexes- respiratory rate of > 12 per minute- urine output of at least 100 cc/4 hours- Serum magnesium for greater accuracy- Antidote calcium gluconas 10 % is prepared2. Control of Hypertension- Hydralazine initial dose 5 mg IV bolus followed by 5 mg incremental increases half hourly if diastolic BP does not improve up to total dose of 20 mg- Nifedipine - Labetalol - Methyldopa3. Optimum time and Mode of DeliveryImmediate delivery may be done for the following :- all cases of eclampsia regardless of age of gestation- severe preeclampsia who are at least 34 weeks AOG in the presence of a mature fetal lung and adequate nursery facilities.

- evidence of uncontrollable hypertension of 160/110 mmHg, oliguria < 40 cc hours, trombocytopenia < 100.000, pulmonary edema and impending eclampsia- evidence of fetal compromise based on abnormal fetal movement counting, CTG, BPS monitoringIn the presence of clinical disease at < 34 weeks AOG , conservative management should focus on the evaluation of maternal and fetal status plus therapy with anticonvulsant, antihypertensive, corticosteroid for lung maturity.Mode of delivery : vaginal is more preferable than CS.THANK YOU.....