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0 HYPERTENSIVE DISORDERS IN PREGNANCY.ppt
- 1. HYPERTENSIVE DISORDERS IN PREGNANCY DR.SALWA NEYAZI CONSULTANT OBSTETRICIAN GYNECOLOGIST PEDIATRIC & ADOLESCENT GYNECOLOGIST
- 2. TYPES OF HYPERTENSIVEDISEASE IN PREGNANCY 1-Gestational hypertension 2-PET 3-Eclampsia 4-Chronic hypertension 5-PET superimposed on chronic hypertension
- 3. 1-Gestational hypertension BP ≥140/90 mm Hg for the first time during pregnancy No proteinuria BP returns to N < 12 Wk postpartum Final Dx made only postpartum May have other signs of PET eg. Headache, epigastric discomfort or thrombocytopenia
- 4. PET Minimum criteria BP ≥140/90 mm Hg after 20 Wk gestation Proteinuria ≥ 300 mg/24 hrs or ≥ 1+ dipstick Increased certainty of PET BP ≥ 160/110 mm Hg Proteinuria ≥ 2 gm/24 hrs or ≥ 2+ dipstick Serum creatinine > 1.2 mg/dl unless known to be previously elevated Platelets < 100 000/mm³
- 5. Increased certainty ofPET Microangiopathic hemolysis (increased LDH) Elevated ALT or AST Persistant headache or other cerebral/ visual disturbance Persistant epigastric pain ECLAMPSIA Seizures that can not be attributed to other causes in a woman with PET. 1% of Pt with PET develop EC
- 6. CHRONIC HYPERTENSION BP ≥140/90 mm Hg before pregnancy or Dx before 20 Wk gestation HPT first Dx after 20 Wk gestation & persistant after 12 Wk postpartum PET SUPERIMPOSED ON CHRONIC HYPERTENSION New onset proteinuria ≥ 300 mg/24 hrs in hypertensive women but no proteinuria before 20 Wk gestation A sudden increase in proteinuria or BP or Plt count < 100 000/ mm³in women with HPT & proteinuria before 20 Wk gestation
- 7. INCIDENCE & RISKFACTORS PET occurs in 6-8% of all live birth RISK FACTORS Extremes of reproductive age 15 < & >35 Y Nulliparity Black race Hx of PET in a 1st degree female relative Hx of PET in prior pregnancy DM Chronic renal disease Ch HPT Multiple pregnancy twins 13 vs 6% Hydatidiform mole Nonimmune hydrops fetalis Obesity 4.3% BMI < 19.8 kg/m² 13.3% BMI ≥ 35 kg/m² Smoking ↓ risk of HPT
- 8. PATHOGENESIS Endothelial cell injury↓ ↓ prostacyclin & ↑ thromboxaneA2 Rejection phenomenon (inadequate matenal Ab response) Compromised placental perfusion Altered vascular reactivity ↑sensitivity to vaspressin EPN, NEPN & angiotensin ↓ GFR with retention of salt & water ↓ intravascular volume ↑ CNS irritability DIC Uterine muscle stretch & ischemia Dietary factors Genetic factors
- 9. PATHOGENESIS Summary of currenthypothesis: Immunological disturbance abnormal placental implantation ↓ placental perfusion production of substances that activate or injure endothelial cells of the blood vessels multiple organ system involvement
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- 11. 1- CNS Similar tohypertensive encephalopathy Petechial Hg Gross hemorrhages due to ruptured arteries Thrombosis of the arterioles Microinfarcts Fibrinoid necrosis in the walls of blood vessels Cerebral edema confusion, blurred vision / coma Brain stem herniation is a serious complication of cerebral edema death MECHANISM cerebral hyperperfusion ,vasospasm &forced dilation
- 12. 1- CNS CT Scan ½ of the pt focal hypodensities in the white matter / post half of the cerebral hemisphere & occasionally in the grey matter may represent petechial Hg Severe cases IV Hg or subarachnoid Hg MRI Abnormalities in the cortical & subcortical white matter of the occipital & parietal areas EEG nonspecific changes
- 13. 2-PULMONARY SYSTEM Pulmonary edema Mayoccur with sever PET OR EC Usually postpartum May be due to excessive fluid administration with crystalloids + ↓ plasma colloid pressure due to proteinuria ↑ in Pt with ch HPT & hypertensive cardiac disease Aspiration of gastric content with EC
- 14. 3-CVS Plasma volume isreduced, the cause is unknown theories: 1-Generalized vasoconstriction with ↑ vascular permeability Advocate the use of vasodilators 2-1ry hypovolemia hypoperfusion of the uterus release of pressor substances HPT Advocate the use of volume expanders & avoidance of diuretics
- 15. 3-CVS High systemic vascularresistance & hyperdynamic ventricular function avoid aggressive fluid adminstration Loss of the normal refractoriness to angiotensin II
- 16. 4-BLOOD Hemoconcentration Thrombocytopenia < 150000 15-20% of PT Fibrinogen ↑ Thrombin time ↑ in 1/3 of the Ptwith EC FDP ↑ 20% of the Pt DIC 5% Microangiopathic hemolytic anemia 5% HEELP hemolytic anemia, ↑↑ liver enzymes, low Plt -LDH > 600 U/L -T bilirubin >1.2 mg/dl -AST > 70U/L -Plt < 100 000/mm³ Found in 10% of the Pt with severe PET
- 17. 5-KIDNEY Characteristic lesion glomeruloendotheliosis swelling of the gromelular capillary endothelium ↓↓GFR ↓↓ creatinine clearance/ ↑↑plasma creatinine ↑↑ uric acid Proteinuria Renal tubular necrosis &renal failure 6-Eyes Visual disturbances due to retinal artery vasospasm Retinal detachment Cortical blindness occipital lobe ischemia infarction or edema lasting hrs –up to 8 days
- 18. 7-Liver Minimal involvement withfibrin deposition Periportal hemorrhagic necrosis ↑↑ serum liver enzymes Bleeding from these lesions Subcapsular hematoma hepatic rupture Hepatic infarction HEELP SYNDROME
- 19. 8-Endocrine & metabolicchanges ↓↓ plasma renin, angiotensin II & aldosterone to the normal prepregnancy values Vasopressin levels are N Atrial natriuretic peptide ↑↑ Volume expansion in PET ↑ ANP ↑ COP &↓ periephal vascular resistance Expansion of the extracellular fluid volume (edema) Proteinuria ↓↓ plasma oncotic pressure displacement of intravascular fluid to interstitium
- 20. 9-Uteroplacental perfusion Vasospasm compromised placental perfusion ↑↑ perinatal morbidity & mortality Doppler velocimetry (systolic /diastolic velocity ratio of umbilical& uterine arteries )20% N 15% N Umbilical / Abnormal uterine 40% Both Abnormal Histological changes in placental bed Defective trophoblastic invasion of spiral arteries / decidual vessels but not myometrial vessels are invaded by trophoblast Charecteristic lipid rich lesions in the uteroplacental arteries
- 21. PREVENTION Calcium supplementation?? Fish oilineffective Low dose aspirin selective supression of throboxane synthesis by the plt & sparing endothelial prostacyclin production Not effective in preventing PET Antioxidants Vit C & E supplementation significant reduction in PET
- 22. SYMPTOMS & SIGNS ↑BP Proteinuria Edema of the face & hands ( but it has been dropped of the definition due to poor predictive value) Headache Visual disturbance Epigastric pain Exaggerated reflexes
- 23. Fetal & maternalrisks Fetal IUGR Oligohydramnios Placental infarcts Placental abruption Prematurity Uteroplacental insufficiency Perinatal death Maternal CNS seizures & stroke DIC ↑↑ CS Renal failure Hepatic failure or rupture Death
- 24. CLASSIFICATION OF PET SEVEREPET Systolic BP >160 mmHg or diastolic >110 mmHg on two occasions at least 6 hrs apart Proteinuria ≥ 5 g/24 hrs Oliguria < 500 cc /24 hrs Cerebral or visual symptoms Epigastric or Rt upper quadrant pain Pulmonary edema or cyanosis Low PLt ↑↑ liver enzymes IUGR MILD PET any PET that is not considered severe
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- 26. Manegement OBJECTIVES Terminaton of pregnancywith the least possible trauma to the mother & fetus Birth of an infant who subsequently thrives Complete restoration of health to the mother 1- Hospitalization Women with new onset BP ≥ 140/90 Worsening BP Development of proteinuria in addition to existing BP
- 27. INITIAL HOSPITAL MANAGEMENT Observefor headache , visual disturbance, epigastric pain & rapid wt gain Wt daily Analysis for proteinuria every 2 days / daily BP in sitting position every 4 hrs except during sleep Blood investigations Hct, Plt, S creatinine, liver enzymes Frequent evaluation of fetal size & AF Reduced physical activity but not absolute bed rest N diet & fluid intake
- 28. FURTHER MANAGEMENT Depends on: Severityof PET Duration of gestation Condition of the Cx Complete resolution of the signs & symptoms does not occur till after delivery Lines of management Termination of pregnancy Antihypertensive therapy Anticonvulsant therapy Home health care if BP improved within few days Pt can be managed as outpatient Home BP & urine protein monitoring . Instruction to come to hospital if she has waning symptoms . Rest at home
- 29. Termination of pregnancy Indications Termpregnancy with mild or severe PET Severe PET regardless of the gestational age Warning signs headache , visual disturbance, epigastric pain, oliguria Eclampsia Pt must be stabilized & delivered immediately Preterm with mild PET Assess fetal wellbeing by NST, BPP, Doppler Methods of termination IOL with prostaglandines to ripen the Cx followed by IV oxytocin Elective CS Severe PET with unfavorable Cx
- 30. Antihypertensive therapy Mild PET Thereis no benefit of antihypertensive therapy Reduction in the maternal BP with labetalol or nifedipine IUGR ACI contraindicated IUGR, boney malformations, limb contracture, PDA, pulmonary hypoplasia, RDS, hypotension &death Severe PET Antihypertensive therapy is used to control BP untill the Pt delivers or in preterm for 48 hrs to allow time for glucocorticoid administration for fetal lung maturity then delivery
- 31. Antihypertensive therapy forsevere PET & EC Hydralazine IV infusion or IV 5-10 mg bolus at 15-20 min interval when diastolic BP ≥100-110 mm Hg or systolic BP ≥ 160 mmHg Nifedipine 10 mg po repeated in 30 min Labetalol 10 mg IV / 20 mg after 10 min/ 40mg after 10min/80 mg (not to exceed 220 mg) Nitroprusside used only in PT not responding to other drugs Diuretics not recommended because intravascular volume depletion already exists in PET
- 32. Fluid therapy Hyperosmotic agentsnot recommended because intravascular influx of fluid subsequent escape of fluid to vital organs pulmonary edema & cerebral edema LR 60-120 ml/hr Excessive fluid administration pulmonary edema & cerebral edema
- 33. PREVENTION /CONTROL OFCONVULSIONS Magnesium sulfate IV infusion 4 gm loading dose in 100 ml of IV fluid over 20 min 2 gm /hr maintenance Measure serum MG level at 4-6hrs maintain at 4-7 mEq /L D/C 24 hrs after delivery25% of seiz occur post partum Avoid toxicity by : -monitoring patellar reflexes -respiratory rate -urine output Antidote calcium gluconate 1gm IV MgS ↓ myometrial contractility Compared to phenytoin or diazepam 50% ↓ in maternal mortality ,67% ↓ in convulsions Infants were less likely to be admitted to NICU/ intubation
- 34. Prognosis Maternal death raredue to cerebral Hg, aspiration pneumonia, hypoxic encephalopathy, thromboembolism, hepatic rupture, renal failure, ansthesia Recurrence 25-33% primipara 70% multipara PG, PET before 30 wk 40% HEELP 5%
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- 36. CHRONIC HYPERTENSION Incidence ofch HPT 0.5-4% 80% essential HPT 20% due to renal disease Symptoms & signs ↑risk in Age > 30, obese, multipara, DM, renal disease, black race, family Hx Difficult to deffirentiate HPT with superimposed PET from HPT with renal disease both have proteinuria
- 37. INVESTIGATIONS Chest x ray cardiomegaly ECG Lt vent hypertrophy ↑ serum creatinine, ↓ creatinine clearance & proteinuria 5-10% MATERNAL COMPLICATIONS Superimposed PET in 1/3 of Pt ↑ risk of abruptio placentae 0.4-10% DIC, acute tubular & cortical necrosis If renal function is well creatinine < 1.5 mg/dl pregnancy does not change the coarse of renal disease If renal function is affected prior to pregnancy deterioration of renal function occur more rapid in pregnancy
- 38. FETAL COMPLICATIONS Prematurity 25-30% IUGR10-15% Stillbirth & fetal distress due to abruptio placentae or ch intrauterine asphyxia
- 39. TREATMENT No benefit oftreating mild CH HPT ( 140-179/90-109) in pregnancy should be monitered for worsening HPT or superimposed PET Pt with severe CH HPT should have their BP controlled before pregnancy & continue Rx in pregnancy α Methyle Dopa Calcium channel blockers B blockers can be used but IUGR Labetalol
- 40. Obstetric management Serial U/Sfor fetal growth. BPP, NST34wk Follow up every 2 wks till 30 then weekly Warn the mother about symptoms of superimposed PET Investigations Renal function test,uric a , calcium ,LFT, 24hrs urine for creatinine clearance & protein, CBC, Urinalysis, ECG.GTT Early U/S for dating of preg Not allowed to continue past 40wks IOL at40 wks Regular diet no salt restriction IOL for superimposed PET,IUGR, fetal distress, worsening renal function