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HYPERTENSIVE DISORDERS IN PREGNANCY

HYPERTENSIVE DISORDERS IN PREGNANCY. DR. SALWA NEYAZI CONSULTANT OBSTETRICIAN GYNECOLOGIST PEDIATRIC & ADOLESCENT GYNECOLOGIST. TYPES OF HYPERTENSIVE DISEASE IN PREGNANCY. 1-Gestational hypertension 2-PET 3-Eclampsia 4-Chronic hypertension 5-PET superimposed on chronic hypertension.

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HYPERTENSIVE DISORDERS IN PREGNANCY

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  1. HYPERTENSIVE DISORDERS IN PREGNANCY DR. SALWA NEYAZI CONSULTANT OBSTETRICIAN GYNECOLOGIST PEDIATRIC & ADOLESCENT GYNECOLOGIST

  2. TYPES OF HYPERTENSIVE DISEASE 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 of PET • 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. 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 INCIDENCE & RISK FACTORS

  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 current hypothesis: • Immunological disturbance  abnormal placental implantation ↓ placental perfusion  production of substances that activate or injure endothelial cells of the blood vessels  multiple organ system involvement

  10. PATHOPHYSIOLOGY MULTIPLE ORGAN SYSTEM INVOLVMENT

  11. 1- CNS • Similar to hypertensive 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 • May occur 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 is reduced, 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 vascular resistance & hyperdynamic ventricular function avoid aggressive fluid adminstration • Loss of the normal refractoriness to angiotensin II

  16. 4-BLOOD • Hemoconcentration • Thrombocytopenia < 150 000  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 with fibrin deposition • Periportal hemorrhagic necrosis ↑↑ serum liver enzymes • Bleeding from these lesions  Subcapsular hematoma  hepatic rupture • Hepatic infarction • HEELP SYNDROME

  19. 8-Endocrine & metabolic changes • ↓↓ 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 oil ineffective • 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 IUGR Oligohydramnios Placental infarcts Placental abruption Prematurity Uteroplacental insufficiency Perinatal death Maternal CNS seizures & stroke DIC ↑↑ CS Renal failure Hepatic failure or rupture Death Fetal & maternal risks

  24. CLASSIFICATION OF PET SEVERE PET • 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

  25. MANEGEMENT OF PET & EC

  26. Manegement OBJECTIVES • Terminaton of pregnancy with 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 • Observe for 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: • Severity of 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 • Term pregnancy 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 • There is 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 for severe 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 agents not 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 OF CONVULSIONS • 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 delivery25% 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 rare due 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%

  35. CHRONIC HYPERTENSION in pregnancy

  36. CHRONIC HYPERTENSION • Incidence of ch 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% • IUGR 10-15% • Stillbirth & fetal distress due to abruptio placentae or ch intrauterine asphyxia

  39. TREATMENT • No benefit of treating 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/S for fetal growth. BPP, NST34wk • 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

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