HYPERTENSIVE DISORDER OF PREGNANCY

1
HYPERTENSIVE DISORDER OF PREGNANCY
DR. SUMAIYA KHARODIA

• FIRST YEAR STUDENT
• JIVANYOG NURSING HOME
• VISNAGAR

2
Introduction

• Disease of many theories, known from
  centuries back, PIH is an enigmatic condition of
  pregnancy, cant predict, cant prevent, cant
  treat absolutely.

3
Introduction

• World wide each year
• 1,500,000 to 1,800,000 women develop Preeclampsia
• Upto 1,50,000 women have eclamptic convulsions
• 90 of these women are from developing countries
• Hypertensive disorders particularly severe
  hypertension of preeclampsia is the leading cause
  of maternal and perinatal mortality and
  morbidity.
• 
  Lewis G et al RCOG Press 2001

4
Incidence

• Preelampsia 5 to
  10
• Eclampsia (Developed countries) 1 2000
• In India
  130 to 1500
• Maternal Mortality in US 17.6
• In India
  25.5
• 
  Walker JJ, Lancet20003561260-65
• 
  Sawhney H et al, JOGR 2000
• Three fold increase in Perinatal Mortality

5
Perinatal Outcome
UK India
Overall Perinatal Mortality (per 1000 live births) 15 34
Proportion due to Hypertensive disease 18 18
Increased risk with Hypertensive disease 2.3 4.76

Douglas KA et
al, BMJ 1994 Shah DS, FOGSI
Perinatal Survey, 1994
Sardesai Jr Obstet Gynecol 2003
6
The most common definitions

• Hypertension that develops de novo as a
  consequence of pregnancy after 20th week of
  gestation, returning to normal after 6 weeks of
  delivery.
• PIH is present when diastolic BPgt 90 mmHg or
  Systolic gt140 or a systolic BP rises at least 30
  mm Hg over base line values or diastolic BP rises
  at least 15 mm Hg over base line value at least
  at two different occasions and at least 6 hours
  apart (ACOG)

7
National High Blood Pressure Education Program
Classification ( NHEP) 2000

• Gestational hypertension.
• Preeclampsia (mild, severe).
• Eclampsia.
• Superimposed preeclampsia upon chronic
  hypertension.
• Chronic hypertension with pregnancy.

8
Definitions

• Gestational hypertension
• Hypertension for first time after 20 w, without
  Proteinuria. BP returns to normal before 12 weeks
  postpartum.
• Chronic hypertension with pregnancy
• Hypertension antedates pregnancy and detected
  before 20 w, lasts more than 12 weeks
  postpartum.

9
Definitions

• Preeclampsia
• The development of hypertension and Proteinuria
  after 20 w
• May occur earlier in vesicular mole or twins.
• Eclampsia (in Greek Flash of light)
• The occurrence of tonic-clonic convulsions
  (without any neurological disease) in a woman
  with pre-eclampsia.

10
Definitions

• Superimposed pre-eclampsia
• It is the new development of Proteinuria after
  20 weeks gestation in a patient with chronic
  hypertension

11
Definitions

• Proteinuria
• 300mg/24 hours urine.
• 1 dipstick.
• Heavy Proteinuria
• 2gm/24 hours
• or 2 in dipstick.

12
Preeclampsia
13
Epidemiology of preeclampsia

• Incidence
• Is a disease of humans only.
• Is the most common medical disorder complicating
  pregnancy 5-15
• Is the most common hypertensive disorder in
  pregnancy.
• More common in primigravidas and elderly
  multipara.
• More common in winter.
• More in black races.

14
Etiology

• Basic concepts
• Exposed to chorionic villi for the first time
• Exposed to a superabundance of chorionic villi,
  as with twins or hydatidiform mole
• Have preexisting vascular disease
• Genetically predisposed to hypertension
  developing during pregnancy

15

• Vascular endothelial damage with vasospasm,
  transudation of plasma, and ischemic and
  thrombotic sequelae.
• Currently plausible potential cause (2003, Sibai)
• Abnormal trophoblastic invasion of Uterine
  vessels
• Immunological intolerance between maternal and
  fetoplacental tissues
• Maternal maladaptation to cardiovascular or
  inflammatory changes of normal pregnancy
• Diatary deficiencies
• Genetic influences

16
Abnormal Trophoblastic Invasion

• In normal implantation, endovascular trophoblasts
  invade the uterine spiral arteries.

17
(No Transcript)
18
Abnormal Trophoblastic Invasion

• In preeclampsia
• Incomplete trophoblastic invasion
• The magnitude of defective trophoblastic invasion
  of the spiral arteries correlated with the
  severity of the hypertensive disorder (2000,
  Madazli)
• Using electron micorscopy
• Endothelial damage
• Insudation of plasma constituents into vessel
  walls
• Proliferation of myointimal cells
• Medial necrosis
• Lipid and macrophage accumulates in myointimal
  cells

19
Etiology theories

• Genetic Predisposition.
• Free Radicals Theory
• In pre-eclampsia the levels of free radicals are
  higher than normotensive women leading to
  endothelial damage.

20
Oxidative stress
Vitamin C SOD
O2._ H2O2 ONOO_
Antioxidant capacity
ROS synthesis
21
Etiology theories

• Endothelial injury
• Endothelin 1(potent vasoconstrictors).
• Nitric Oxide ( vasodilator action).
• Vascular Endothelial Growth Factor (VEGF).

22
Etiology theories

• Prostaglandins
• There is decrease in prostacyclin /TX A2 ratio
  leading to
• vasoconstriction and tendency to thrombosis.

23
Etiology theories

• Inflammatory Factors
• Pre-eclampsia is considered an inflammatory
  disease due to increased number of activated
  leukocytes in the maternal circulation.
• Immunological Factor
• primigravidas
• Multipara with 1st pregnancy from a new husband.
  
• Abundant trophoblast ( vesicular mole and
  multiple pregnancy.

24
The Central Players (Hemostats) in PET

• The Endothelium
• Neutrophils
• 3. Platelets
• 4. Coagulation system.
• Once one is triggered
• Co- Workers are released (NO, PGs, ROS,
  Homosystein, etc)

25
The Constant Pathophysiological Changes

• Is
• Vascular endothelial
• Damage Dysfunction
• Spasm

26
Pathology

• PET is the clinical ice-berg tip manifestation of
  the disturbances in the maternal homeostasis,
  involving many systems and organs.

27
Multisystem Features Of Preeclampsia
28
PATHOPHYSIOLOGY

• MULTIPLE ORGAN SYSTEM INVOLVMENT

29
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

30
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

31
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

32
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

33
3-CVS

• High systemic vascular resistance hyperdynamic
  ventricular function ?avoid aggressive fluid
  adminstration
• Loss of the normal refractoriness to angiotensin
  II

34
4-BLOOD

• Hemoconcentration
• Thrombocytopenia lt 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 gt 600 U/L
• -T bilirubin gt1.2 mg/dl
• -AST gt 70U/L
• -Plt lt 100 000/mm³
• Found in 10 of the Pt with severe PET

35

• 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

36
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

37
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

38
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

39
High Risk Factors
Primigravida Extremes of reproductive age
(young
and elderly) Socio
economic (status) Disadvantaged
Ethnicity African American Family
history Hypertension, pre-eclampsia, (First
degree relatives) eclampsia
Placental abnormalities Molar pregnancy
Hyperplacentosis multiple
pregnancy Placental
ischaemia Associated medical conditions
Obesity, Diabetes, Renal disease,
Collagen vascular disease Thrombophilias
Anti-phospholipid syndrome, Protein

C, S deficiency, Factor V
Leiden Genetic History of
pre-eclampsia in sister,
mother
(Multi-factorial inheritance) Immunological
40
Prediction

• Roll-over Test
• Second Trimester Mean Arterial Pressure
• Urinary Calcium
• Uric acid
• Fibronectin
• Homocysteine level
• Cytokines
• Coagulation factors
• Placental peptides
• Doppler Ultrasound
• Fetal DNA

41
Tests for Prediction

• Roll over test is positive (rise of diastolic
  blood pressure 20 mmHg or more after turning from
  left lateral to dorsal position).
• Increased pressor response.
• Uric acid is elevated.
• Hypercalciuria.
• Doppler velocimetry to detect Uteroplacental hypo
  perfusion.

42
Diagnosis Of PET

• Hypertension Proteinuria
• Two facets of a complex pathophysiological
  process

43
A) Signs

• it is a disease of signs
• 2 cardinal signs or - Edema
• Hypertension
• usually precedes Proteinuria,
• Proteinuria detected by
• Boiling test.
• Quantitative assay.
• Dipstick test.

44
or - Edema

• occult or manifest
• The lower extremities.
• Abdominal wall, vulva or may be generalized
  anasarca.
• usually after hypertension.

45
Peripheral edema is not a useful diagnostic
criterion

•   1) it is common in normal pregnancy.
• 2) PET can occur without edema (dry type).
• so its presence does not ensure a poor prognosis
  and its absence not ensure a favorable outcome.

46
B) Symptoms (non specific)

• Headache.
• Blurring of vision.
• Nausea and vomiting.
• Epigastric pain (distension of the liver capsule)
• Oliguria or anuria

47
Severity Of Pre-eclampsia

• The severity of pre-eclampsia is assessed by
• The frequency and intensity of the signs and
  symptoms.
• The more the severity of PET, the more likely is
  the need to terminate pregnancy.

48
DD ,mild severe PET
Severe Mild Abnormality
110 mm Hg or higher lt 100 mg Hg Diastolic blood pressure
Persistent 2 or more Trace to 1 Proteinuria
Present Absent Headache
Present Absent Visual disturbances
Present Absent Upper abdominal pain
Present Absent Oliguria
Present (eclampsia) Absent Convulsion
Elevated Normal Serum creatinine
Present Absent Thrombocytopenia
Marked Minimal Liver enzyme elevation
Obvious Absent Fetal growth restriction
Present Absent Pulmonary edema
49
4) Diagnosis Of Eclampsia

• Eclamptic fit stages ( 4 stages)
• Premonitory stage (1/2 minute)
• Eye rolled up.
• Twitches of the face and hands.
• Tonic stage (1/2 minute)
• Generalized tonic spasm with episthotonus.
• Cyanosis.
• Tongue may be bitten between the clenched teeth.

50
4) Diagnosis Of Eclampsia

• Clonic stage (1-2 minutes)
• Convulsions .
• Tongue may be bitten.
• face is congested and cyanosed.
• conjunctival congestion.
• blood stained froth from the mouth,
• Stertorous breathing,
• temperature may rise.
• involuntary passage of urine or stool.
• Gradually convulsions stop.

51
4) Diagnosis Of Eclampsia

• Coma
• Variable duration due to respiratory and
  metabolic acidosis.
• Deep coma may occurs (cerebral hemorrhage).
• Labor usually starts shortly after the fit.
• Sometimes labor does not start and convulsions
  recur again the so called intercurrent
  eclampsia and carries a bad prognosis.

52
Classifications of Eclampsia

• Intercurrent Eclampsia eclampsia in which the
  eclamptic fits recur in the same pregnancy.
• Recurrent Eclampsia eclampsia that recurs in
  subsequent pregnancy.

53
Classifications of Eclampsia

• 1)Mild
• 2) Severe (Eden's criteria)
• Coma gt 6 hours.
• Temperature gt 39 (pneumonia or pontine hge)
• Systolic Bp gt 200 (risk of cerebral hge)
• Pulse gt 120/min ( acute heart failure).
• Anuria or Oliguria( renal failure).
• Respiratory rate gt 40/min( pneumonia)
• More than 10 fits (status eclampticus).

54
Prevention

• Aspirin
• -19 reduction in risk of PE.
• -16 reduction in fetal and neonatal
• death.
• - 8 reduction in the incidence of small
• for gestational age infants.
• Updated
  chrochane review-2000.
• 
  Systemic review 2003.
• The controversy is when to start treatment.

55
Prevention

• Calcium
• Protective effect in women with low calcium
  intake.
• 
  Cochrane data base 2005
• Supplementation with 1.5 gm calcium /day did not
  result in statistically significant decrease in
  the overall incidence of PE, but there is
  significant decrease risk of the more serious
  complications which included maternal and
  neonatal morbidity and mortality and preterm
  delivery .
• 
  WHO-2006

56
Prevention

• Antioxidants
• Antioxidants like Vit C, E, and lycopene found
  to be effective in smaller trials but VIP Trial
  demonstrated no decrease in risk of PE.
• 
  Lancet-2006, 367,1145-54.
• In the other large multicentric trial, the
  supplementation did not decrease the incidence of
  preeclampsia, IUGR or the risk of death or other
  serious outcomes.
• N. Eng. J .of Med.
  2006, 354, 1796-806

57
Criteria for diagnosis of Preeclampsia

• Blood pressure of 140 mm Hg systolic or higher or
  90 mm Hg diastolic or higher that occurs after 20
  wks of pregnancy in a woman with previously
  normal BP
• Proteinuria as urinary excretion of 0.3 g
  protein or higher in a 24 hrs specimen
• Am J Obstet
  Gynecol 2000183S1-S22

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PROTEINURIA
Develops late in the disease process Influenced
by exercise and posture 24 hour estimation is
better than random Hypertension with proteinuria
is a reliable indicator of fetal
jeopardy Proteinuria alone PNM unchanged HT
alone PNM 3 fold rise HT proteinuria PNM 8
fold rise (PNM perinatal mortality rate)
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EDEMA

• Early but non specific sign
• Rapid weight gain
• Edema of PIH is due to sodium retention and thus
  not limited to dependent edema
• Edema of hands and face more reliable than
  dependent edema
• Parasthesia due to medial or ulnar nerve
  compression

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Management

• AIMS
• Control of hypertension
• Prevention of eclampsia
• Prevention of accidental hemorrhage and DIC
• Prevention of renal damage
• Maintenance of placental perfusion
• Monitoring of fetal growth and well-being
• Planning timely delivery
• Care in puerperium
• Follow up.

61
Out Patient Management

• Gestational Hypertension less than
• 160/100 mm Hg
• Bed rest at home (controversial)
• Home BP monitoring, weight and urine protein.
• Referred for Day Assessment Unit (DAU) for
  evaluation like NST and USG

62
DAU management

• 4 to 6 hourly BP recording.
• Mid stream urine analysis.
• Proteinuria, protein creatinine ratio.
• CTG
• Hb, platelets, creatinine, liver function tests
  (enzymes, AST/ALT), uric acid.
• Review.

63
Indications for Hospitalization from Day Care
Unit (Severe Preeclampsia)

• BP equal to or more than 160/100 mm Hg
• Uric acid equal to or more than 450 mmol/L
• Platelets less than 1,50,000
• Proteinuria equal to or more than 5 gm in 24 hrs
• Oliguria
• S creatinine more than 1 mg
• Cerebral or visual disturbances
• Impaired liver function
• Non reactive CTG
• IUGR/Oligohydramnios

64
Maternal SURVEILLANCE
Bed rest Vital parameters BP measurement 6 hourly
Daily weight Input /output charting Urine
protein estimation daily Premonitory
symptoms Deep tendon reflexes Fundoscopy
65
BIOCHEMICAL MONITORING
CBC Urine routine and microscopy 24 hour
urine RFT, BUN, Creatinine, uric acid, creatinine
cleareance LFT enzymes, bilirubin,
proteins Platelet count Coagulation profile
66
Fetal Well-being

• Delay the delivery if mother is safe
• Prematurity is the most important
• determinant of perinatal outcome
• Antenatal Corticosteroids
• Fetal Surveillance
• - Daily Fetal Movement Count
• - Fetal growth clinically and by USG
• - Amount of liquor
• - Cardiotocogram
• - Doppler velocimetry of the
• umbilical artery

67
Control of Hypertension

• Aims of antihypertensive therapy
• - To increase renal perfusion
• - To increase uteroplacental perfusion
• - To prevent intracranial bleeding
• - To prevent Left ventricular failure
• - To prevent the selective cerebral
• arterial vasospasm that causes
• eclamptic seizures

68
Indications for Antihypertensive Therapy

• Role of antihypertensive therapy in Mild to
  Moderate Hypertension is unclear.
• Drugs and therapy Perceptive
  2001,17(18),11-15
• Persistent rise of BP in mild to moderate cases
• Severe preeclampsia
• Hypertensive crisis
• Chronic hypertension

69
Oral Antihypertensive for Control of Mild to
Moderate Hypertension in Pregnancy

• Methyldopa A drug of First Choice
• Labetalol A reasonable Alternative
• Atenolol To be avoided
• Nifedipine Calcium channel blocker in
  late
• pregnancy
• Propranolol can be used in late pregnancy
• Hydralazine add on therapy to Methyldopa
• ACE inhibitors To be avoided
• Diuretics not to be used as
• antihypertensive

70
Antihypertensive for Control of Acute or Severe
Hypertension in Pregnancy

• Short Acting Antihypertensive agents
• Hydralazine 5 mg IV repeated after 20 min
• Labetalol 20 mg IV, repeated every 30 min
  can be doubled maximum upto 80 mg
• Nifedipine 5 to 10 mg every 15 min to
• maximum upto 30 mg
• Other Antihypertensive agents
• Diazoxide 30 to 50 mg IV, repeated every 10
• to 15 min or by continuous infusion.
• Sodium Nitroprusside IV infusion 0.5 to 10
• mg/kg/min

71
Drugs used to lower blood pressure during
pregnancy
72
Planning Delivery
Place Multidisciplinary team and high dependency
care available Neonatal care facilities Route Aim
for vaginal delivery LSCS required for obstetric
indication or maternal or fetal compromise To
avoid general anaesthesia Time Conservative v/s
Early intervention
73
Decision making in severe preeclampsia
Gestational Age Course
More than 34 weeks Delivery
Less than 26 weeks Delivery
26 to 34 weeks Expectant management v/s Delivery
74
Criteria for delivering patient with Severe
Preeclampsia

• BP persistently 160/110 or more inspite of
  treatment
• Urine output lt 400 ml in 24 hrs
• Platelet count lt 50,000/mm3
• Progressive increase in S. Creatinine
• LDH gt 1000 IU/L
• Repetitive late decelaration with poor
  variability
• Severe IUGR with Oligohydramnios
• Reversed umbilical diastolic blood flow

75
Labour Management

• IV access
• Repeat haematological investigations
• Fluid management
• Seizure prophylaxis and anti hypertensives
• Electronic fetal monitoring
• Analgesia and Anaesthesia
• No ergometrine

76
Period of gestation convulsions occur In 50 of
cases gt36 wks of gestation Antepartum
- 46.3 Intrapartum - 16.4 Postparum
- 37.3 usually within 48 hrs
of delivery
Sibai BM et al Obstet Gynaecol 1981, 58
609.
77
Differential Diagnosis

• Eclampsia
• Epilepsy
• Cerebral malaria in tropics
• Encephalitis
• Meningitis
• Intracranial tumors
• Peripheral cerebral thrombosis
• Poisoning
• Hysteria

78
Complications of eclampsia

• Injuries
• Pulmonary edema
• Pneumonia
• Acute LVF
• Cerebral hemorrhage
• Renal failure
• Pulmonary embolism

• Hyperpyrexia
• Hepatic necrosis
• DIC
• Postpartum shock
• Puerperal sepsis
• Disturbed vision
• Psychosis

79
Causes of maternal / Perinatal mortality

• Cerebral haemorrhage
• Anoxia
• Cardiac failure
• Pulmonary oedema

• Aspiration pneumonia
• Pulmonary embolism
• Postpartum shock
• Puerperal sepsis

• Causes of perinatal mortality
• Prematurity
• Intrauterine asphyxia
• Effects of drugs used to control convulsion
• Trauma during delivery
• Perinatal mortality 30 to 50
• Sibai BM et al American Journal of Obstet
  Gynaecol 1983 146 307.

80
Principles of Management of Eclampsia

• General management
• To control convulsions using MgSO4
• To control Hypertension
• To avoid Diuretics
• To limit IV fluids unless excessive fluid loss
• To investigate
• To terminate the pregnancy
• Care in puerperium
• Follow up.

81
Management of Eclampsia

• General management
• To place in a railed cot in an isolated place
• To maintain airway
• To administer oxygen
• To take detail history from relatives
• After proper sedation quick examination
• Catheterization and check for proteinuria
• ½ an hourly Pulse, Temp, RR, BP, uterine
  contraction, FHS.
• 1 hrly urine output
• Maintain fluid balance with CVP monitoring
• To administer antibiotics

82

• Specific management
• To control seizures and to prevent its recurrence
• Magnesium sulfate the drug of choice

Regimens Loading dose
Maintenance dose Pritchard 4gm IV over 3
to 4 min 5gm buttock 4 hrly
10gm deep IM Zuspan 4gm IV
over 5 to 10 min 1-2gm hrly IV infu Sibai
6gm IV over 20 min 2gm hrly IV
infusion Sardesai 4 gm IV or IM
2 gm 3 hrly IV or IM
Therapeutic level of MgSO4 4 to
7mRQ/litre Monitor Presence of patellar reflex
(8 to 10mEQ/litre ? diagnose) Respiratory rate
gt16 (gt12mEQ /litre ? depression) Urinary output
30ml/hr Continuation for 24 hrs after the last
seizure M.M. 0.4
83
Lytic cocktail regimen
On admission 25mg chlorpromazine 100mg
pethidine in 20ml of 5 solution iv followed by
50mg chlorpromazine 25 mg promethazine im.
Later on Promethazine 25mg and chlorpromazine
50mg given alternately lM till 24 hr of last fit
or IV 500ml containing 100mg pethidine drip rate
adjusted to 20-30 drops/min till 24 hrs of last
fit and not to exceed 300 mg /day. Maternal
Mortality (MM) 2.2
84
Diazepam regimen Initial drug of 100mg iv
further 40mg in 500ml of Ringer lactate i. v. at
30 drops/min M.M. 5 Phenytoin therapy 10mg/kg
IV followed by 5mg/kg 2 hrs later Sedatives can
be used with above regimen
85

• To control hypertension
• Inspite of sedative if BP gt160/110mg then
  antihypertensive drugs are administered
• Hydralazine
• 5mg iv slowly
• rate 10mg every 20 minutes
• Monitoring BP every 5 minutes
• Repeat the dose when diastolic BP gt110mmHg
• labetalol - 20 mg i.v., repeated every 30 min
  can
• be doubled maximum upto 80 mg
• Nifedepine 5 to 10 mg every 15 min to
• maximum upto 30 mg

86

• Status eclampticus
• Phenytoin sodium 0.5gm dissolve in 20mg of 5
  dextose iv given slowly
• If no response then complete anesthesia, muscle
  relaxant, assisted ventilation and C. Section is
  done.

87
Planning the delivery

• Delivery is the ultimate cure

• Vaginal.
• LSCS is done for obstetric reasons, or before 32
  weeks of gestation.
• Anesthesia
• General to be avoided, as it increases blood
  pressure during intubation and extubation.
• Epidural is better than spinal.

88
Route of delivery

• Probability of achieving vaginal delivery after
  induction through an unripe cervix are below 20
• Hall DR et al, BJOG 2000
• Haddad B et al, AJOG 2004
• Prolonged labor can be detrimental for mother and
  fetus
• Caesarean delivery is preferable
• Sibai BM et al, COG 2005

89
Diagnosis of HELLP Syndrome

• Hemolysis
• Schistocytes in the blood smear
• S.Bilirubin gt or equal to 1.2 mg
• Absent Plasma hapatoglobin
• Elevated Liver Enzymes
• SGOT gt 72 IU/L
• LDH gt 600 IU/L
• Low Platelet Count

90
HELLP Syndrome.

• Prompt delivery , if it develops beyond 34 weeks.
• Dilemma- Before 34 weeks, administrations of
  corticosteroid for 48 hrs for both maternal and
  fetal benefits. But the results are variable in
  different studies.

91
Post Partum Care

• Over 40 of maternal deaths occur postpartum
• Post delivery a relative oliguria is not
  uncommon, occuring in 30 of patients with severe
  disease
• Continued close monitoring is required in a
  suitable environment
• Taper antihypertensive agents
• Contraception Counseling and Follow up

92
Long term prognosis.

• PE and Eclampsia is a forerunner of later life
  cardiovascular risk
• It is more in early onset PE.
• Does not affect long term renal function.
• No long term residual hepatic disease.
• Recurrence Risk-20 to 50 .
• HELLP-2 to 6 .

93
Conclusion.

• PIH is the leading cause of Maternal and
  Perinatal Mortality and Morbidity
• Maternal and neonatal outcome is good in
  gestational hypertension and with
  antihypertensive drugs they can go up to term.
• But PE is enigmatic, an unique syndrome,
  dangerous for both mother and fetus, no absolute
  preventive measure are available and does not
  respond well to treatment.
• Multidisciplinary approach with close medical
  supervision, timely delivery and management at
  tertiary center are the corner stones for good
  maternal and fetal outcomes.

94
Motherhood .
.. A dream of every woman
TOGETHER WE CAN MAKE IT A REALITY
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