Hypertensive Disorder Of Pregnancy detailed PPT

Detailed Study on Hypertensive Disorder of Pregnancy

1. Hypertensive Disorder In Pregnancy DR SHRUTHI B J DR SIDDHIKA NAZEEM

2. HYPERTENSION When Bp is ≥ 140/90 mmHg measured Two Times With At least 4 Hour interval but not More than 7 days apart PREGNANCY INDUCED HYPERTENSION The term, 'pregnancy-induced hypertension (PIH)is defined as the hypertension that develops as a direct result of the gravid state. It includes- (i) Gestationalhypertension, (ii) pre-eclampsia and ( iii) eclampsia (iv) Chronic Hypertension

3. Classification of Hypertension In Pregnancy

4. Gestational Hypertension A sustained rise of blood pressure to 140/90 mm Hg or more on at least two occasions 4 or more hours apart beyond the 20th week of pregnancy or within the first 48 hours of delivery in a previously normotensive woman is called gestational hypertension

5. Criteria For Gestational Hypertension (1) Absence of any evidences for the underlying cause of hypertension (2) Generally unassociated with other evidences of preeclampsia (edema or proteinuria). (3) Majority of cases are more than or equal to 37 weeks pregnancy. (4) Generally not associated with hemoconcentration or thrombocytopenia, raised serum uric acid level or hepatic dysfunction. (5) The blood pressure should come down to normal within 12 weeks following delivery.

6. PRE-ECLAMPSIA DEFINITION: It is a multisystem disorder of unknown etiology characterized by development of hypertension to the extent of 140/90 mm Hg or more with proteinuria after the 20th week in a previously nor-motensive and nonproteinuric woman T he pre-eclamptic features may appear even before the 20th week as in cases of hydatidiform mole and acute polyhydramnios.

7. Incidence According to the new guidelines giverby American Congress Of Obstetricians and Gynaecologist (ACOG) in 2013. ln INDIA, the incidence of preeclampsiais reported to be 8-10%. lt occurs more frequently in youngprimigravidae and in mothers over 35yrs of age. Incidence In Primigravida is About 10% & Multigravida 5%

8. Causes Of Pre-Eclampsia Risk factors for pre eclampsia Primigravida Family history : Hypertension , pre eclampsia Placental abnormalities: Hyperplacenatosis ; excessive exposure to chorionic villi - ( molar pregnancy, twins, diabetes) Placental ischemia Obesity : BMI more than 35 kg/m ,insulin resistance New paternity, pregnancy following ART Thrombophilia ( anti phospholipid syndrome ,protein c , & Protein s deficiency

9. Etiopathological factors for pre eclampsia Failure of trophoblast invasion Vascular endothelial damage Inflammatory mediators Immunological intolerance between maternal and fetal tissues Increased oxygen free radical Im balance of angiogenic and antiangiogenic protein Genetic predisposition Dietary deficiency or excess .

10. Etiopathogenesis The underlying basic pathology is endothelial dysfunction and intense vasospasm, affecting almost all the vessels, particularly those of uterus, kidney, placental bed and brain. preeclampsia is characterized by endothelial dysfunction and vasospasm. Endothelial dysfunction is due to oxidative stress and the inflammatory mediators. Vasospasm results from the imbalance of vasodilators (PGI2, NO) and vasoconstrictors (Angiotensin-II, TXA2, Endothelin 1).

11. Normally Spiral arteries open in intervillous space C y totrophoblast (extravilous) replaces lining ot spiral artery, Trophoblastic invasion They are converted from high resista nt vessels to low resistant vessels

12. In PlH , T he trophoblastic invasion is incomplėte( Vascular remodeling i s incomplete ) Anti-Angiogenic factor Increase SFLT 1, S-endoglin Vasoconstrictor Increases Thromboxane A2 A ngiogenic factor Decrease VEGF Placental Growth Factor Vasodilator Decrease
No

13. Resistance in the vessels remains high Due to vasoconstriction, volume of blood comingto intervillous space decreases. Placental ischaemia (placenta is small and pale ) Intlammatory mediators released Cont.....

14. Cont.... Makes Capillary Endothelium Leak Collection Of Fluid In Third Space Edema Hemoconcentration Thrombosis In Blood Vessels MultiOrgan Failure

15. In Pre-Eclampsia,Hemoconcentration Less Blood Goes To Brain Of The Mother Cerebral Hypoxia Convulsions Kidney Of The Mother RBF Decrease GFR Decrease Increase Serum Urea ,Uric Acid , Creatinin Decrease Fetal Blood Flow IUGR Decrease In RBF In Foetus Oliguria Oligohydramios

16. PathoPhysiology Uteroplacental bed: There is increased evidences of premature aging of the placenta. Areas of occasional acute red infarcts and white infarcts are visible on the maternal surface of the placenta. In preeclampsia, the normal endovascular invasion of cytotrophoblast into the spiral arteries fails to occur beyond decidua-myometrial junction Kidney : The changes are conspicuous in the glomerulus which becomes enlarged (glomerular endotheliosis). Endothelial cells swell up and fibrin-like deposits occur in the basement membrane

17. The net effects are reduced renal blood flow and glomerular filtration rate (25%), and impaired tubular reabsorption or secretory function Blood vessels: There is intense vasospasm. Circulation in the vasa vasorum is impaired leading to damage of the vascular walls, including the endothelial integrity. Liver : Periportal hemorrhagic necrosis of the liver occurs due to thrombosis of the arterioles. The necrosis starts at the periphery of the lobule. There may be subcapsular hematoma

18. Brain : Neuroimaging (CT, MRI) studies revealed: hypodense areas in the cortex, cerebral edema, capillary thrombosis, infarction, intraventricular and parenchymal hemorrhages, and necrosis. Posterior reversible encephalopathy syndrome: Posterior (Occipital and Posterior Parietal Lobes) Reversible Encephalopathy Syndrome (PRES) is a transient neuroradiological entity characterized by the features of hypertension, generalized seizures, altered mental status, headache and vision changes. The hallmark of diagnosis is bilateral symmetrical vasogenic edema in the occipital and posterior parietal lobes

19. Heart : Subendothelial hemorrhages may occur. Focal necrosis and hemorrhage in the myocardium may affect the conducting system leading to heart failure. Lungs : There is evidence of edema or hemorrhagic bronchopneumonia and ARDS. This is due to low oncotic pressure and leaky capillaries. Water and electrolyte balance: The net effect is intravascular dehydration and extravascular overhydration. Thus, there is hemoconcentration and rise in hematocrit value.

20. Hematological changes: there is hemoconcentration with increased hematocrit values. Coagulation — There is evidence of disseminated intravascular coagulopathy (DIC) affecting widespread organs of the body as opposed to selective DIC only at the placental site in normal pregnancy. There is reduction of platelets, fibrinogen, antithrombin-III, and plasminogen level in the blood

21. HELLP Syndrome: The acronym for Hemolysis (H), Elevated Liver enzymes (EL) and Low Platelet count ) (<100,000/mm3). HELLP syndrome may develop even without maternal hypertension. Clinical Features : nausea, vomiting, epigastric or right upper quadrant pain, along with biochemical, and hematological changes. Laboratory Observation : Hemolysis Is Characterised by : PeripheraL Smear(Schistocytes,Burr Cells) Elevated Liver Enzymes :AST &ALT >70 IU/L ,LDH,>600 IU/L Platelet Count <100,000/mm3

22. Complications Of HELLP Maternal : Abruptio placenta, DIC, acute renal failure, severe ascites, pulmonary edema, pleural effusions, cerebral edema, laryngeal edema, retinal detachment, subcapsular liver hematoma, ARDS, sepsis, and death. Perinatal : Morbidity and mortality are significantly increased. This is due to preterm delivery, prematurity, RDS and sepsis

23. Clinical Types Non-Severe : This includes cases of sustained rise of blood pressure of more than 140/90 mm Hg but less than 160 mm Hg systolic or 110 mm Hg diastolic without significant proteinuria. Severe : A persistent systolic blood pressure above or equal to 160 mm Hg or diastolic pressure above 110 mm Hg. Protein excretion of more than 5 g/24 h O liguria (<400 mL/24 h) Platelet count less than 100,000/mm3 HELLP syndrome

24. C erebral or visual disturbances P ersistent severe epigastric pain. Retinal hemorrhages, exudates or papilledema Intrauterine growth restriction of the fetus Pulmonary edema S erum Creatinine >1.1 mg/dl

25. Clinical Features ONSET: The onset is usually insidious and the syndrome runs a slow course. SYMPTOMS : Mild symptoms: Slight swelling over the ankles which persists on rising from the bed in the morning or tightness of the ring on the finger is the early manifestation of edema due to preeclampsia. Gradually, the swelling may extend to the face, abdominal wall, vulva and even the whole bod y .

26. Alarming symptoms : These are usually associated with acute onset of the syndrome. (1) Headache — either located over the occipital or frontal region, ( 2) Disturbed sleep, (3) Diminished urinary output— Urinary output of less than 400 mL in 24 hours is very ominous, (4) Epigastric pain—acute pain in the epigastric region associated with vomiting, at times coffee color, is due to hemorrhagic gastritis or due to subcapsular hemorrhage in the liver, (5) Eye symptoms—there may be blurring, scotomata, dimness of vision or at times complete blindness.

27. SIGNS 1. Abnormal weight gain: A rapid gain in weight of more than 4 lb a week in later months of pregnancy is significant. 2. Rise of blood pressure: The rise of blood pressure is usually insidious but may be abrupt. The diastolic pressure usually tends to rise first followed by the systolic pressure. 3. Edema: Visible edema over the ankles on rising from the bed in the morning is pathological. 4. There is no manifestation of chronic cardiovascular or renal pathology. 5. Pulmonary edema—due to leaky capillaries and low oncotic press u re

28. 6. Abdominal examination may reveal evidences of chronic placental insufficiency, such as scanty liquor or growth retardation of the fetus. T he manifestations of preeclampsia usually appear in the following order—rapid gain in weight → visible edema and/or hypertension → proteinuria.

29. Complications Of Pre-eclampsia IMMEDIATE : Maternal D uring pregnancy: (a) Eclampsia (2%) — more in acute than in subacute cases, (b) Accidental hemorrhage, (c) Oliguria and anuria, (d) Dimness of vision and even blindness, (e) Preterm labor, (f) HELLP syndrome ( g) Cerebral hemorrhage, (h) Acute respiratory distress syndrome (ARDS)

30. During labor: (a) Eclampsia, ( b) Postpartum hemorrhage — may be related with coagulation failure Puerperium: (a) Eclampsia — usually occurs within 48 hours, ( b) Shock (c ) Sepsis

31. Fetal: (a) Intrauterine death—due to spasm of uteroplacental circulation leading to accidental hemorrhage or acute red infarction ( b) Intrauterine growth restriction— due to chronic placental insufficiency, (c) Asphyxia, (d) Prematurity—either due to spontaneous preterm onset of labor or due to preterm induction. REMOTE : (a) Residual Hypertension (b) Recurrent Pre-Eclampsia (c) Chronic Renal Disease

32. Investigation Urine : Proteinuria is the last feature of preeclampsia to appear24 hours urine collection for protein measurement is done Ophthalmoscopic examination Blood values:The blood changes are not specific and often inconsistent. - A serum uric acid level (biochemical marker of preeclampsia) of more than 4.5 mg/dL indicates the presence of preeclampsia. - Blood urea level remains normal or slightly raised. Serum creatinine level may be more than 1 mg/dL. Antenatal fetal monitoring

33. Screening Test For Prediction & Prevention Uterine Artery Doppler Development of renal dysfunction: Rise in the level of serum uric acid and appearance of microalbuinuria are observed to be the predictors of preeclampsia. Average mean arterial pressure (MAP) in second trimester > 90 mm Hg may predict the onset. Fetal DNA—Detection of free fetal DNA (ff DNA) in maternal plasma in early pregnancy may be predictive of preeclampsia. Roll Over Test

34. Prophylactic Measures For Prevention Regular Antenatal Checkup Exercise
Anti platelet Agents Heparin or Low molecular Weight Heparin Calcium Supplementation
Antioxidans

35. Management Of Gestational Hypertension & Pre-Eclampsia Hospital Management : Rest — (1) increases renal blood flow → diuresis, (2) increases uterine blood flow → improves placental perfusion, and (3) reduces the blood pressure Diet : The diet should contain adequate amount of daily protein (about 100 g). Usual salt intake is permitted. Fluids need not be restricted. Total calorie approximate 16,00 cal/day

36. Diuretics : The diuretics should not be used injudiciously, as they cause harm to the baby by diminishing placental perfusion and by electrolyte imbalance. Antihypertensives : Indications are: (1) Persistent rise of blood pressure especially where the diastolic pressure is over 110 mm Hg. The use is more urgent if associated with proteinuria. (2) In severe preeclampsia, to bring down the blood pressure during pregnancy and labor .

37. Drugs Used in Management Of Pre-Eclampsia Labetalol : Mode Of Action : Adreniceptor Antagonist ( Alpha & Beta Blocker) Produces Vasodilation & Decrease In Systemic Vascular Resistance Dose: 100mg tid or qid Side Effects : Postural Hypotension Hepatotoxicity

38. Nifedipine : Mode Of Action: Calcium Channel Blocker It is a potent vasodilator, rapid onset of action ,safe and effective Dose: 10-20 mg bid Side Effects: Severe Headache , Hypotension, flushing

39. Methyl-dopa Mode of action : central and peripheral anti adrenergic action Dose 250-500 mg tid or qid Side effects : Fetal bradycardia Maternal Hypotension Headache Depression Vomiting Palpitation

40. Hydralazine Mode of action: vascular smooth muscle relaxant Dose : 10-25 mg bid Side effects Headache Flushing Peripheral Edema Overshoot Hypotension

41. Hypertensives Crisis when the BP is >160/110 mm Hg or the mean arterial pressure (MAP) is >125 mm Hg

42. Methods Of Delivery Induction Of Labour: Indications: (1) Aggravation of the preeclamptic features in spite of medical treatment and/or appearance of newer symptoms such as epigastric pain. (2) Hypertension persists in spite of medical treatment with pregnancy reaching 37 weeks or more. (3) Acute fulminating preeclampsia irrespective of the period of gestation (4) Tendency of pregnancy to overrun the expected date.

43. Methods: If the cervix is ripe, surgical induction by low rupture of the membranes is the method of choice. Oxytocin infusion may be added. If the cervix is unripe, prostaglandin (PGE2) gel 500 µg intracervical or 1–2 mg in the posterior fornix is inserted to make the cervix ripe when low rupture of the membranes can be performed. In severe preeclampsia, antihypertensive drugs should be used during induction.

44. Cesarean section : Indications: (1) When an urgent termination is indicated and the cervix is unfavorable (unripe and closed). (2) Severe preeclampsia with a tendency of prolonged induction—delivery interval. (3) Associated complicating factors, such as elderly primigravidae, contracted pelvis, malpresentation, etc . (4) Epidural anesthesia is preferred, unless there is coagulopathy.

45. ECLAMPSIA Pre-eclampsia when complicated with grand mal seizures (generalized tonic-clonic convulsions) and/or coma is called eclampsia. O ccur s in patients with pre-eclampsia or in patients who have pre-eclampsia superimposed on essential hypertension or chronic nephritis INCIDENCE India ranges from 1 in 500 to 1 in 30. It is more common in primigravidae (75%), five times more common in twins Occurs between the 36 th week & Term in more than 50%Cases

46. Incomplete Trophoblastic Invasion Of Spiral Arterioles Spiral Artery Remodeling is defective Spiral Arteries remain narrow Placental Ischaemia Release Of Inflammatory mediators Endothellial Dysfunction PathoPhysiology

47. Loss Of Cerebral Autoregulation Cerebral Hyperperfusion Endothellial Damage Cerebral Edema Release Of Excitatory Neurotransmitters in the brain Convulsions

48. PathoPhysiology

49. CAUSE OF CONVULSION : The cause of cerebral irritation leading to convulsion is not clear. The irritation may be provoked by: 1. Anoxia- spasm of the cerebral vessels -> increased cerebral vascular resistance ->Fall in cerebral oxygen consumption-> anoxia, 2. Cerebral edema 3. Cerebral dysrhythmia increases following anoxia or edema. 4. Excessive release of excitatory neurotransmitars (glutamate). 5. Loss of cerebrovascular autoregulation with forced dilatation and vasospasm

50. ONSET OF FITS: It occurs more commonly in the third trimester (> 50%). On rare occasions, convulsion may Occur in early months as in hydatidiform mole. Antepartum (50%): Fits occur before the onset of labour I ntrapartum (30%): Fits occur for the first time during delivery Pos tpartum (20%): Fits occur for the first time in puerperium, usually within 48-72 hours of delivery Late Pregnancy Eclampsia: Fits occurring beyond 48 hours but less than 4 weeks after delivery . Intercurrent(Antenatal ) : When the patient becomes conscious after recovery from convulsions and the pregnancy continues beyond 48 hours. The time limit is arbitrary as a period of 7 - 10 days .

51. Eclamptic convulsion or fit: The fits are epileptiform and consist of four stages. Premonitory stage: • The patient becomes unconscious. • There is twitching of the muscles of the face, tongue, and limbs • Eyeballs roll or are turned to one side and become fixed. • This stage lasts for about 30 seconds. Clinical Features

52. Tonic stage: • The whole body goes into a tonic spasm — the trunk-opisthotonus, limbs are flexed and hands clenched • Respiration ceases and the tongue protrudes between the teeth. • Cyanosis appears. • Eyeballs become fixed. • This stage lasts for about 30 seconds

53. Clonic stage : • All the voluntary muscles undergo alternate contraction and relaxation. • The twitchings start in the face then involve one side of the extremities and ultimately the whole body is involved in the convulsion. • Biting of the tongue occurs • Breathing is stertorous and blood stained frothy secretions fill the mouth; cyanosis gradually disappears. • This stage lasts for 1–4 minutes. Stage of coma: Following the fit, the patient passes on to the stage of coma. On occasion, the patient appears to be in a confused state following the fit and fails to remember the happenings.

54. Differential Diagnosis (1) Epilepsy (2) Hysteria, (3) Encephalitis, (4) Meningitis, (5) Puerperal cerebral thrombosis, (6) Poisoning, (7) Cerebral malaria in tropics, (8) Intracranial tumors. Absence of previous history of convulsion with presence of edema, hypertension and proteinuria along with fits or coma during pregnancy or soon after, points to the diagnosis of ECLAMPSIA .

55. Prognostic Risk Factors For Eclampsia MATERNAL : (1) Long interval between the onset of fit and commencement of treatment (late referral). (2) Antepartum eclampsia especially with long delivery interval. (3) Number of fits more than ten. (4) Coma in between fits. (5) Temperature over 102°F with pulse rate above 120/minute. (6) Blood pressure over 200 mm Hg systolic.

56. (7) Oliguria (< 400 mL/24 hours) with proteinuria > 5 g/24 hours. (8) Nonresponse to treatment. (9) Jaundice. FETAL : (1) Prematurity (2) Intrauterine asphyxia due to placental insufficiency arising out of infarction, retroplacental hemorrhage and spasm of uteroplacental vasculature, (3) Effects of the drugs used to control convulsions, (4) Trauma during operative delivery.

57. Complications Of Eclampsia

58. Prevention E arly detection and effective institutional treatment with judicious termination of pregnancy during preeclampsia Use of antihypertensive drugs, Prophylactic anticonvulsant therapy Close monitoring during labor and 24 hours’ postpartum is also important in prevention of eclampsia. Magpie trial (2002) showed prophylactic use of magnesium sulfate lowers the risk of eclampsia. Management

59. General Management First Aid Treatment Outside The Hospital The patient, either at home or in the peripheral health centers should be shifted urgently to the tertiary referral care hospitals. BP should be stabilized and convulsions should be arrested Magnesium sulfate [4 g IV loading dose with 10 g IM is given. Labetalol 20 mg IV is given to control hypertension Diuretic is given if there is pulmonary edema. Diazepam, if used, should be given 5 mg slowly over 1 minute period to avoid apnea or cardiac arrest

60. Supportive care : (i) To prevent serious maternal injury from fall (ii) Prevent aspiration, (iii) to maintain airway and (iv) to ensure oxygenation. Detailed History To Be Taken Examination

61. Monitoring : Half hourly pulse, respiration rate and blood pressure are recorded. Hourly urinary output is to be noted,fetal heart rate is to be monitored as Immediately after a convulsion, fetal bradycardia is common Fluid balance : Crystalloid solution (Ringer’s solution) is started as a first choice. Total fluids should not exceed the previous 24 hours urinary output plus 1000 mL Infusion of balanced salt solution should be at the rate of 1 mL/kg/h. Antibiotic : To prevent infection, Ceftriaxone 1 g IV twice daily is given.

62. Specific Management Management Of Fits: (a) In the premonitory stage, a mouth gag is placed in between the teeth to prevent tongue bite and should be removed after the clonic phase is over. (b) The air passage is to be cleared off the mucus with a mucus sucker. (c) Patient head is to be turned to one side to prevent aspiration .Raising The Foot end of bed ,facilitates postural drainage of the upper Respiratory Tract . (c) Oxygen is given until cyanosis disappears.

63. Anticonvulsant Regime : Magnesium Sulphate Is Drug Of Choice Mechanism Of Action : Acts on NMDA receptors In brain Blocks them Central Vasodilation Reduced Central Hypoxia & Treats Convulsion

64. Regimens Of MgSo4 For Management Of Pre-Eclampsia & Eclampsia IV rate of Infusion not to exceed 1g/min

65. Magnesium sulfate is continued for 24 hours after the last seizure or delivery whichever Occurs later. For recurrence of fits, further 2 g IV bolus is given over 5 minute . If the patient seizes, despite magnesium therapy, midazolam 1–2 mg IV is given . Therapeutic Range For MgSo4 To Control Fits ,Optimum Serum Magnesium level is 4.8-8.4 mg/dl (4-7mEq/L ) (or) 2-3.5 mmol/L to be maintained.

66. Magnesium Toxicity Loss Of Knee Jerk :when Serum Magnesium levels cross 10mEq/L Respiratory Paralysis :when Serum Magnesium levels cross 12mEq/L Cardiac Arrest :when Serum Magnesium levels cross 15mEq/ L

67. Detection of Magnesium Toxicity

68. Other Regimens 1) Lytic cocktail (Menon 1961) using chlorpromazine, promethazine and pethidine. (2) Diazepam (Lean) and (3) Phenytoin Compared To Other Regimens Benefits Of Magnesium Sulphate Are: (i) It controls fits effectively without any depression effect to the mother or the infant. (ii) Reduced risk of recurrent convulsions (9%) (iii) Significantly reduced maternal death rate (3%) and (iv) reduced perinatal mortality rate

69. Antihypertensives : Inspite of anticonvulsant regime, if the blood pressure remains more than 160/110 mm Hg, antihypertensive drugs should be administered. First line of antihypertensive drugs are: labetalol and hydralazine (ACOG-2011). Labetalol 20 mg IV is given. Repeat doses may be needed after an interval of 10 minute. Alternatively hydralazine 5 or 10 mg IV is given. Repeat dose may be needed if no response occurs after 20 minutes time.

70. Treatment Of Complications Pulmonary Edema: Furosemide 40 mg IV followed by 20 g of mannitol IV reduces pulmonary edema and also prevents adult respiratory distress syndrome. Heart failure: Oxygen inhalation, parenteral lasix and digitalis are used. Hyperpyrexia : cold sponging and antipyretics Psychosis: Chlorpromazine or Eskazine (trifluoperazine) is quite effective.

71. Status Epileptics: The fits are usually multiple, recurring at varying intervals. When it occurs in quick succession, it is called status eclampticus. Thiopentone sodium 0.5 g dissolved in 20 mL of 5% dextrose is given intravenously very slowly. If the procedure fails, use of complete anesthesia, muscle relaxant and assisted ventilation may be employed. In unresponsive cases, cesarean section in ideal .

72. INDICATIONS OF INTUBATION : Patient remains unconscious in post seizure period Seizures not controlled Signs of aspiration Persistent hypoxia

73. Obstetric Management During pregnancy : In majority of cases with antepartum eclampsia, labor starts soon after convulsions. But when labor fails to start, the management depends on—(i) whether the fits are controlled or not and (ii) the maturity of the fetus. The decision to deliver is made once the woman is stable. Epidural Anaesthesia can be used during Labour & delivery

74. Fits Controlled Baby Mature Baby Premature Baby dead Fits Not Controlled Termination Of Pregnancy If Vaginal examination indicates a quick induction,Low rupture of membrane is to be done .Oxytocin Infusion may be added

75. During Labour: In the absence of any contraindication to vaginal delivery, as soon as the labor is well established, low rupture of the membranes is to be done to accelerate the labor. The dose schedule of antihypertensive and anticonvulsant drugs may be increased to quieten the patient. Second stage should be curtailed by forceps, ventouse or craniotomy, if the baby is dead. Prophylactic intravenous ergometrine or syntometrine following the delivery of the anterior shoulder should not be given as it may produce further rise of blood pressure. Instead, 10 units of oxytocin IM or IV slowly should be given. One should remain vigilant about postpartum hemorrhage and shock.

76. Indications of cesarean section: Eclampsia before 30 weeks gestation with unfavourable cervix (i i) Uncontrolled fits in spite of therapy. ( iii ) Unconscious patient and poor prospect of vaginal delivery. ( iv) Obstetric indications (malpresentation).

77. Follow up Patient should be followed up in the postnatal clinic by 6 weeks time. Persistence of hypertension, proteinuria and abnormal blood biochemistry necessitates further investion & Consultation . Further pregnancy should be deferred till they are controlled.

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