Presentation on theme: "Hypertensive Disorders in Pregnancy"— Presentation transcript:
1Hypertensive Disorders in Pregnancy Azza AlyamaniProf. of Obstetrics & Gynecology
2ClassificationWomen who are pregnant and hypertensivemust be divided into :* chronic hypertension.* pregnancy induced hypertension (PIH)or gestational hypertension.those with PIH further subdivided :* proteinuric PIH (preeclampsia)minority* non-proteinuric PIH majority
3Therefore :women with hypertension in pregnancy are classified as having:1. preeclampsia (proteinuric hypertension).2. non – proteinuric hypertension.3. chronic hypertension:•primary (essential) hypertension. 95%.•secondary hypertension.5%...renal dis...adrenal dis...hyperthyroidism.The aetiology and management of the three conditions are different .
4Worldwide , maternal mortality from hypertensive Incidence:Worldwide , maternal mortality from hypertensivedisease accounts for :deaths per year.preeclampsia occurs in 5% .non – proteinuric PIH 15%.it accounts to 15 – 20% of maternal mortality inthe developed cuonteris.
5Definition: pregnancy induced hypertension (PIH) is : Hypertension that occurs after 20 weeks gestation and unrelated to other pathology.protienuria is the excretion of 300mg or more of protein in 24 hours urine.hypertension and protienuria define preeclampsia.
6Preeclampsia :* is a multisystem disorder involving the placenta , liver , kidneys , blood , neurological andcardiovascular systems.* both maternal and fetal morbidity / mortality are more likely to occur with early – onset disease as;placental abruption ,acute renal failure ,cerebral Hge ,DIC and IUGR ,prematurity as delivery isthe only cure.therefore , ANC is directed towards identifying women with hypertension and protienuria.
7* severity ranges from : a mild disorder (transient hypertension in the later part of the pregnancy) toa life-threatening disorder with seizure HELLP syndrome, fetal hypoxia, and growth retardation.* more severe disease: 0.5 per deliveries
8Chronic Hypertension : is the presence of persistent hypertension of whatever cause , before 20 weeks gestationorpersistent hypertension beyond 6 weekspostpartum.sustained bl. p of 140/90 mmHg or > on two occasions 6 hours apart is consideredhypertensive.
9Aetiology Pregnancy induced hypertension (PIH) Preeclampsia: is unknown , believed to be involved := immune maladaptation.= placental ischemia.= oxidative stress.= genetic predisposition.
10Genetic Predisposition Faulty interplay bet. invading trophoblast and deciduaDecreased bl. supply to feto-placental unitRelease of circulating factorsEndothelial cell alterationIUGRHypertensionProteinuria
11Management Screening for preeclampsia : Risk Factors1. +ve family history in the first –degree relativeincrease the risk of PET 4 – 8 fold.2. primiparety3. medical disorders as :* history of PET.* chronic hypertension.* diabetes.* obesity.* antiphospholipid syndrome.* molar pregnancy.* multiple pregnancy.* hydrops fetalis.
12Screening and assessment for chronic hypertension :Women who is found to be hypertensive before pregnancy can be advised about :1. weight loss.2. restrict salt and alcohol intake.3. change her antihypertensive agents , diuretics ,angiotensin-converting enzyme (ACE) inhibitorsand β blockers to other alternatives.
13Diagnosis Screening tests: to predict PET and superimposed preeclampsiaon chronic hypertension.(1) USit is quick ,non-invasive and inexpensive .Uterine artery Doppler :analysis of its waveform is an early predictor ofpoor placental perfusion and development of PET ,there is resistance circulation with notch.Its predictive value is greater at 24 weeks or more.
15(2) Biochemical tests in preeclampsia : * HB , and Hematocrit concentrations.* CBC with platelets count.* serum uric acid .* endothelial activation markers are increased.* urinary excretion of Ca and microalbuminuria
16in severe chronic hypertension: * urine analysis.* 24h urine for protein , creatinine clearance,catecholamine metabolites and free cortisol.* bl. Urea and electrolytes as Na & k.* Lupus anticoagulant and anticardiolipin in APS.* serum lipids.in addition(3) fundoscopy.(4) ECG & ECHO.(5) X ray chest.
19= blood pressure : > 160 mmHg systolic or > 110 mm Hg diastolic * Criteria of severe preeclampsia= blood pressure : > 160 mmHg systolic or> 110 mm Hg diastolic= Proteinuria: > 3 g in 24 hours= Persistent and severe cerebral or visual disturbances (headache, blurred vision)= Persistent and severe epigastric pain or right upper quadrant pain.= Pulmonary edema or cyanosis.= Oliguria ( < 500 ml urine / 24 hour).= Eclampsia ( grand mal seizures).= HELLP syndrome.
20Maternal and fetal assessment: * the GA at which woman present with hypertensionis an important factor in establishing risk .Late onset hypertension after 37weeks rarely result in serious maternal or fetal complications.* Superimposed pre eclampsia on chronic hypertension is diagnosed by identifying proteinuria, raised uric acid levels or failing platelets count .chronic hypertension is associated with preeclampsiain 20% and abruptio placenta in 2%.
21* Uterine artery Doppler velocity waveforms is used to assess risk . * bl.pressure and urine analysis are checkedevery 2 weeks.sudden and profound rise should alert theclinician to the possibility of PET.* high uric acid and low platelet countmay pre –date proteinuria by someweeks.
22Pre eclamptic Toxaemia ManagementPre eclamptic ToxaemiaA) PET remote from termEarly onset PET is associated with :a. placental insufficiencyresulting in IUGR and fetal death. Therefore ;Fetal Wellbeing must be carefully considered.1. monitoring of fetal movements.2. serial symphesis -fundal height .3. serial US to confirm fetal growth ,AFvolume and Umbilical A. Dopplerwaveform .
23b. involvement of other organ systems resulting in increased maternal morbidityand mortality.1.serial platelets countas platelets are consumed due to endothelialactivation Thrompocytopenia< /ml. delivery should be considered.2.increased HB and haematocrit values indicatehypovolaemia.3.clotting abnormalities indicate DIC..
244.raised uric acida measure of fine renal tubular function is usedto assess severity of the disease.raised urea and creatinineindicate late renal involvement .5.severe proteinuria> 3g /24 hours urine resulting in fall ofcirculating albumin and increasing the risk ofpulmonary edema.
25it is severe variant of PET, Haemolysis , 5.HELLP syndromeit is severe variant of PET, Haemolysis ,Elevated Liver enzymes and Low Platelets .PET can cause subcapsular hematoma, liverrupture and hepatic infarction which result inraised liver transaminases as AST indicatinghepatocellular damage andliver involvementand the need to consider delivery.
26Delivery :should be considered once fetal lung maturity is likely ( at 32 weeks gestation) ,especially if eithermulti-organ involvement or fetal compromise isproved.Corticosteroids are given to enhance fetal lung maturity. Steroid therapy may enhance recovery from HEELP syndrome.Delivery before term is usually by CS .such patients are risk of thromboembolism and should be given prophylactic SC heparin and stockings.
27Indications of termination of pregnancy in PET :1. uncontrollable hypertension.2. deteriorating liver or renal function.3. progressive fall in platelets.4. neurological complications as cerebral Hge.5. deteriorating fetal condition as non-reactiveCTG.
28Lat onset preeclampsia rarely results in B) PET near termLat onset preeclampsia rarely results inserious morbidity to mother or fetus .Drug therapy should be considered:a) antihypertensivethe aim is to lower the bl. pressure andlower the risk of maternal cerebrovacularaccident without uterine bl. flow andcompromising the fetus.
291. Labetolol ą &β blockers . can be given IV and orally. safe during pregnancy.2. Methyldopacentrally acting agent.very safe during pregnancy.only given orally .takes 24 h for its effect.3. Nifedipineis Ca channel blocker .with rapid onset of action.cause severe headache.
30associated fetal death and preterm delivery. NB:Diuretics ,Angiotensin-converting enzyme (ACE)inhibitors and β-blockers are contraindicated .b) Low dose aspirinresults in significant reduction in preeclampsiaassociated fetal death and preterm delivery.c) for prophylaxisCa , fish oil , antioxidants , vit. C , vit. E
31Management of severe fulminating preeclampsia and impending eclampsia : 1. IV antihypertensiveHydralazine / labetololIV infusion titration rapidly against changes inthe blood pressure .2. Anticonvulsant therapyMagnesium Sulfate :* it is the anticonvulsant of choice as ttt. ofeclampsia and also as prophylaxis whichreduce the risk of fits to half.Diazepam and phenytoin can be used butless effective .
32* mode of action = anticonvulsant. = muscle relaxant. =vasodilator. reduce the intracerebral ischaemia.* dose2 g IV as a loading dose then1-2 g / h as maintenance infusion.* toxicity is detected by :absence of the patellar reflexes.respiratory arrest .may be cardiac arrest.* antidote is:10 ml of 10% Ca gluconate.
333. Fluid managementa Folly′s catheter should be inserted and fluidbalance recorded.* oliguria without a rising serum urea orcreatinine is a manifestation of severe PETand not renal failure.however , if creatinine or potassium rises ,haemodialysis is necessary.* diuretics should only be given if there aresigns of pulmonary edema.
34* in severe PET and eclampsia, a severe type of Postpartum Care* in severe PET and eclampsia, a severe type ofof eclamptic fits occur postpartum , intensivemonitoring is required for 48 h. after delivery.* bl. Pressure is frequently at its highest levels3 -4 days after delivery . Therefore ,antihypertensive therapy is need to becontinued after discharge home.
35* a postnatal care visit 6 -8 w. is mandatory for measuring bl.p , urine analysis , RFT, LFT andpredisposing factors as thrompophilia or APSshould be excluded.* in women with severe chronic hypertensionmust be carefully monitored for at least 48hafter delivery as they are at increased risk ofrenal failure , pulmonary edema andhypertensive encephalopathy.