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Pregnancy Induced Hypertension

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PIH : Etiology, Clinical features & Management

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Pregnancy Induced Hypertension

  1. 1. Pregnancy Induced Hypertension Dr. Ayshwarya Revadkar OBGY UNIT 3,YCMH
  2. 2. INTRODUCTION Multisystem disorder with varied and still unknown etiology with unpredictable outcome, with increase in maternal & fetal morbidity and mortality.
  3. 3. Intro conti… Also known as “Toxaemia of pregnancy” Major cause of maternal mortality in India. Asso with poor outcome of pregnancy if uncared for. It affects 7 – 15 % of all pregnancies.
  4. 4. Hypertension In Pregnancy Definition (ACOG) : Diastolic BP of 90mm Hg or higher or systolic BP of 140mm Hg or higher after 20wks of gestation in a woman with previously normal BP. It should be documented on atleast 2 occasions measured 4hrs apart. Proteinuria : It is defined as the urinary excretion of 300mg/L or more of protein in a 24hr urine collection. (correlates with reagent strip >1+ i.e. >30mg/dl)
  5. 5. CLASSIFICATION OF HYPERTENSION IN PREGNANCY1) Chronic HTN : HTN present before the 20th week of pregnancy or that present before pregnancy.2) Chronic HTN with superimposed Preeclampsia : defined as proteinuria developing for first time during pregnancy in a woman with known chronic HTN.3) Gestational HTN : HTN without proteinuria developing after 20wks of gestation during labor or the peurperium in previously normotensive non proteinuric woman.
  6. 6. 4) Preeclampsia : Gestational HTN asso with proteinuria .5) Eclampsia : Convulsions occuring in a pt with preeclampsia.* HELLP Syndrome : Severe form of preeclampsia char by hemolysis (abnormal PBS, bil > 1.2mg/dl), thrombocytopenia (platelets<1lakh/mm3) and elavated liver enzymes (AST>70, U/L, LDH>600 U/L)
  7. 7. Physiological changes in pregnancy : Normal pregnancy is char by :1. Increase in plasma volume(preload), starts to increase by 6th wk, & plateaus at 30wks. (+50%) so fall in haematocrit.2. Increase in CO, starts to increase in 5th week, peak at 30-34 weeks then remains static till term, increases further in labor & immediately following delivery.3. Decrease in PVR4. So results in a physiological decrease in mean BP during 2nd trimester but it rises to normal value as pregnancy advances.
  8. 8. Conti.. Hypercoagulable state : Increase (50%) in fibrinogen to 300-600 Fall in platelets (15%) Raised ESR 4 times of normal. (so no diagnostic value) Decreased fibrinolytic activity Increase in clotting factors 1 7 9 10 but others decreased so difference in CT. All these help to effectively control blood loss & achieve hemostasis after placental separation.
  9. 9. Chronic HTN & Pregnancy :  Etiology : 1. Most common : Essential HTN 2. Secondary HTN : 1. Renal : parenchymal or renovascular 2. Endocrine : pheochromocytoma, prim aldosteronism, cushings syndrome. 3. Neurogenic : increased ICT 4. Vascular : Aortic coarctation 3. Systolic HTN : Thyrotoxicosis, hyperkinetic circulation.
  10. 10. 2 categories : First one responding to medications & without complications, good outcome of pregnancy Second one : HTN difficult to control, require multiple drugs, fetal hazards or end organ damage, demanding delivery, Risk factors : severe HTN (HTN crisis, risk of stroke and abruption), superimposed PIH, IUGR, abruptio placenta.
  11. 11. Important points to note : Difficult to differentiate from PIH as Pts came for ANC mainly after 20th week & very few pts diagnosed in pre-pregnant state. Pre-conceptional counseling : for determination of cause, organ functions, exercise & weight loss, salt restriction Change of medications : eg omit ACE inhibitors & ARBs Daily self monitoring of BP twice at home Don’t lower BP rapidly: harm to fetus
  12. 12. Antihypertensives used in Pregnancy :1. Diuretics : Furosemide, chlorthiazide2.Vasodilators : Labetalol, Nifedipine, Prazosin, Hydralazine.3. Drugs that decrease CO : Beta blockers, Propanalol4. Centrally acting : Methyldopa
  13. 13.  30% pts have chance to develop super- imposed preeclampsia. If this happens, PIH is very severe, occurs early in pregnancy, responds poorly to bed rest. How to differentiate aggrevated HTN from superimposed PIH ? Proteinuria, Urinary Ca excretion,
  14. 14. High risk factors indicating poor outcome Diastolic BP 85 or greater, MAP 95 or greater, in repeated observations 6hrs apart after 14weeks of GA. H/O severe HTN in previous pregnancies. h/o abruption h/o stillbirth or unexplained neonatal death. h/o IUGR AGE > 35yrs or chronic HTN of >15yrs duration Marked obesity Secondary HTN
  15. 15. Management Many pts will have mild disease & progress to term. ANC visits every 2 weekly until 32 wks & then every weekly. Variables to monitor : BP, uterine growth, preterm labor, DFMC, maternal weight Pts with other high risk factor develop complication resulting in preterm delivery.
  16. 16. Gestational HTN Prevalence 6-15% in nulliparas & 2-4% in multiparas. Early : before 30wks, frequently severe, advances to preeclampsia and has a guarded perinatal prognosis. Late : after 30wks, frequently in obese women and multiple pregnancies, due to poor maternal adaptation to physiological changes in pregnancy.
  17. 17. Conti.. Criteria to identify high risk women with gestational HTN :1. BP > 150/100 mm Hg.2. GA < 30wks3. Evidence of end organ damage4. Oligohydramnios5. Fetal growth restriction6. Abnormal CD.7. Nullipara, Age > 35yrs, BMI > 35 kg/m2
  18. 18. PREECLAMPSIAIncidence : 5-15%In primigravida: 10%In Multigravida 5%
  19. 19. Risk factors for Preeclampsia : Primi : younger or elderly Family history of PIH, HTN, DM H/O PIH in previous pregnancy Hyperplacentosis as in molar pregnancy, twins, DM Obesity, Chronic HTN, pre-existing vascular or Renal disease, DM New paternity Thrombophilias : APLA, deficiency of protein C/S, factor 5 leiden,
  20. 20. ETIOLOGY & PATHOGENESIS Basic etiology is abnormal placentation : failure of trophoblast invasion Failure of second wave of endovascular trophoblast migration resulting in reduction of blood supply to fetoplacental unit. 2 main things we should remember : Endothelial Dysfunction due to oxidative stress and inflammatory mediators, Vasospasm due to imbalance b/w vasodilators(PGI2, NO) & vasoconstrictors (TxA2, angiotensin 2, endothelin).
  21. 21. Conti.. All of above result in : Increased vasoconstriction Decreased organ perfusion : utero-placental – IUGR, Kidneys- glomerular endotheliosis,oliguria, liver ischaemia, HELLP, CNS seizures. Increased endothelial dysfunction – capillary leak, oedema, Pulmonary oedema, proteinuria. Activation of coagulation: DIC, low platelets Haemoconcentration
  22. 22. Diagnosis BP > 140/90 mmHg (NICE gudelines mild 140/90 to 149/99, Moderate150/100 to 159/109 & severe 160/110) Proteinuria : 24hr urinary protein >300mg, (>5gm severe PIH) dipstick method > 1+ (30mg/dl) Urinary Protein/creatinine ratio > 30mg/mmol
  23. 23. Other : Pathological oedema Excessive weight gain : is > 0.5kg in one week or >2kg in one month in later months of pregnancy. Clinical e/o vasoconstriction by fundoscopy
  24. 24. s/o Impending Eclampsia : Headache Epigastric or rt upper quadrant pain : particularly in HELLP S due to liver dysfunction. Visual symptoms : scotomas progressing to blurred vision, even blindness. (abnormality lies in occipital cortex, not in retina.) recovers faster post natally. Brisk DTRs : CNS irritabilty.
  25. 25.  “Neverneglect these alarming signs….and u will save a life or two…”
  26. 26. Laboratory findings : Haemoconcentration leads to false Hb. Thrombocytopenia RFTs: Serum Uric Acid >4.5mg/dl, BUL, serum creatinine- derrange only in severe cases. LFTs : raised liver enzymes in severe cases Incresed fibrinogen, it is decreased in abruption.
  27. 27. Abnormal fetal growth IUGR of 2-4 wks in PIH commonly seen. Demands uterine, umbilical & MCA doppler. UA utero-placental circulation Umb A : Placento-umbilical circulation. Doppler weekly in moderate to severe PIH. NST & MBBP twice weekly to assess fetal wel-being.
  28. 28. Management of mild PIH GA > 37 weeks : Deliver. GA b/w 32 & 36 wks : periodic evaluation by NST, Lab, USG & CD. In-hospital management to avoid complications. GA < 32wks : IPD, continuous assessment: daily BP, Weight, daily urine dipstick, LFT & Platelets twice wkly, DFMC, NST twice wkly, doppler wkly,
  29. 29. Conti.. If only pt. is stable : continue pregnancy. If unstable : may require early delivery. Indication for delivery in k/c/o mild PIH: BP>160/110, proteinuria > 5gm in 24hrs urine. Trying to conserve pregnancy in severe PIH by giving antihypertensive : invitation for disaster.
  30. 30. Anti hypertensive Drug of choice: Labetalol orally in dose of 100-400 mg every 8-12hrly. Others : Methyl dopa 250mg-500mg 6-8 hrly. Nifedipine 10-20mg bd - tds. Hydralazine : 10-25mg 12hrly. Iv or oral furosemide, oral thiazide: only after delivery. If s/o severity devlop : MgSO4.
  31. 31. Management Of Severe PIH Criteria for diagnosis of severe preeclampsia : Systolic BP > 160 / Diastolic > 110 on 2 occasions 6hrs apart while pt is in bed rest. Proteinuria of 5 g or higher in 24hr urine or 3+ or greater in 2 samples 4hrs apart. Oliguria of less than 5oo ml urine in 24 hrs. IUGR Cerebral or visual disturbances
  32. 32. Conti.. Pulmonary oedema or cyanosis Epigastric or right uppaer quadrant pain Impaired liver function Thrombocytopenia Very imp : s/o impending eccampsia
  33. 33. Management of severe PIH GA > 34 wks : MgSO4 to prevent seizures Antihypertensive to control BP Delivery : if Cx ripe Induction or Caesarean section. Don’t try to lower BP suddenly, it will impair organ perfusion and result in maternal & fetal morbidity
  34. 34. Hypertnsive crisis BP> 160/110 Labetalol 10-20mg iv every 10min, max upto 300mg iv, maintenance dose 40mg/hr Hydralazine : 5mg iv every 30min, max 30mg iv, maint dose 10mg/hr Nifedipine : 10-20mg oral, max up to 240mg in 24hrs, for maint 4-6 hrly Nitroglycerine : 5microgm/min iv or Sod nitroprusside 0.25-5 microgm/kg/min iv short term therapy only when other drugs failed.
  35. 35. Regimes of MgSO41. Intra-muscular (PRITCHARD)2. Intra-venous (zuspan or Sibai) 6 gm(25%) iv over 20min f/b maint dose of 2 gm(50%) /hr or 100ml/hr iv infusion.• Therapeutic level 4-7 meq/L.• 4 Actions. Toxicity. Antidote.
  36. 36. Severe PIH : GA 28-33 wks : Postpone delivery for 24-48hrs for action of steroids. GA 24-28 wks : Indivisualised for pt acc to severity.
  37. 37.  Guidelines for expectant management :Bed restDaily weightDaily input & outputAntihypertensive t/tSteroidsLab on alternate daysDaily NSTDFMCCD twice a weekAFI twice a weekUSG to see for fetal growth every 2 weeks
  38. 38. GA < 24 weeks: Severe maternal morbidity if pregnancy conserved Perinatal mortality, IUDs. Only t/t is Delivery.
  39. 39. Ecampsia It is the extremely severe form of PIH char by sudden onset of generalized tonic clonic convulsions. Higher frequency in developing countries. Occurs antepartum in 35-45%, intrapartum in 15- 20%, postpartum in 35-45%. Preceded by impending signs & aura. In 15 % of patients, HTN & protenuria are absent. Preventable in 70% cases. No any long term neurological deficit.
  40. 40. Pathophysiology : In mild HTN or normotension : abnormal autoregulatory response consisting of severe arterial vasospasm with rupture of endothelium & pericapillary haemorhages with development of abnormal electric foci causing convulsion. In severe HTN, limit of autoregulation exceeded, vasodialatation occurs with hyperperfusion causing endothelial capillary damage and interstitial vasogenic edema.
  41. 41. Management of Eclampsia Place pt in lateral decubitus. Mouth gag Suction oral secretions O2 by mask Elevate bedside rails to avoid injury Switch off lights, keep quite environment surrounding pt. Pulse oxymeter, foley’s catheter, iv access MgSO4 Start IV fluids at low rate 100ml/hr. Antihypertensive : 1st drug of choice in severe HTN is iv Labetalol. Deliver the pt.
  42. 42. Conti.. Continue MgSO4 till 24hrs postpartum to avoid convusion. Nimodepine 60 mg oral 4hrly: drug of choice in mild elevated BP with impending signs/ eclampsia. Phenytoin : loading dose 10-15 mg/kg slow iv f/b maint dose 100mg iv every 6-8hrly. For prophylaxis 100mg iv/im 4hrly. Oral phenytoin should be continued in postpartum period. Postpartum i.v. Furosemide should be given aggresively for early recovery.
  43. 43. Fetal Response To Maternal Seizures In majority of cases: transient fetal distress during seizure, normalizes as seizure is over. Occasionaly the tetanic uterine contraction is severe enough to cause abruption & IUD. Thus if fetal distress continues for more than 5 min after end of seizure & despite giving O2, abruption should be suspected & LSCS should be done. In these case both maternal & fetal prognosis is poor.
  44. 44. Increase in LSCS for eclampsia inmodern OBs : Due to Unripe Cx, poor progress in labor IUGR, preterm baby Inadequate control of BP Mainly to avoid adverse maternal & fetal effects of pregnancy continuation.
  45. 45. Postparum care : MgSO4 for atleast 24hrs after delivery Aggressive diuresis & maintained several days Antihypertensive until BP normalizes. Approximately 35% pts will have PIH in subsequent pregnancy.
  46. 46. HELLP SYNDROME Criteria for diagnosis :1) Haemolysis (microangiopathic H.A.) Burr cells, schistocytes on PBS bilirubin > 1.2mg/dl absent plasma haptoglobin2) Elevated liver enzymes AST > 72 IU/L LDH > 600 IU/L3)Low platelets < 1 lakh/mm3
  47. 47. Conti..Maternal morbidity :  Abruption  DIC  Pulmonary oedema  ARF  ARDS  Hepatic rupture leading to DIC & death  Death in 1%
  48. 48. Management Immediate delivery is indicated once diagnosis of HELLP established. Vaginal or LSCS Platelets if count < 50000 or if s/o altered hemostasis. Plasmapheresis is lifesaving if deterioration in course of disease. Better to err by delivering preterm fetus than to conserve for further harm.
  49. 49. Other severe complications of PIH Pulmonary oedema (d/t fluid overload, oligouria & LVF) ARF Abruption Intra-cranial bleeding Visual disorders. Recurrence in next pregn 30% High risk of chronic HTN.
  50. 50. Post natal care Daily BP monitoring till pt is indoor. Once discharged, BP on alt days till normal value settles in. Continue antihypertensive till normalization of BP postpartum. Repeat lab after 48hrs. If abnormal monitor weekly. Do reagent strip for proteinuria at 6wks follow up. If abn, repeat at 3months. Counselling of pt about recurrence of PIH and risk of chronic HTN.
  51. 51. Prevention Research going on without effective solution Low dose aspirin Ca supplementation: cheap & effective ? Anti-oxidants, ? Fish oil supplementation No role of salt restricted diet in PIH Predictive tests.
  52. 52.  “Let us understand PIH better for managing patients more efficiently.” “THANK YOU…”

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