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
 The 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
 Imbalance 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).

12.  Normally
Spiral arteries open in intervillous space
Cytotrophoblast (extravilous) replaces lining ot spiral
artery,
Trophoblastic invasion
They are converted from high resistant vessels to low
resistant vessels

13.  In PlH,
 The trophoblastic invasion is incomplėte(Vascular
remodeling is incomplete)
Anti-Angiogenic factor
Increase
SFLT 1, S-endoglin
Vasoconstrictor
Increases
Thromboxane A2
Angiogenic factor
Decrease
VEGF
Placental Growth Factor
Vasodilator Decrease
No

14. 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.....

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

16.  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

17. 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

19.  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

20.  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

21.  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.

22.  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

23. 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

24. 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

25. 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
 Oliguria (<400 mL/24 h)
 Platelet count less than 100,000/mm3
 HELLP syndrome

26.  Cerebral or visual disturbances
 Persistent severe epigastric pain.
 Retinal hemorrhages, exudates or
papilledema
 Intrauterine growth restriction of the fetus
 Pulmonary edema
 Serum Creatinine >1.1 mg/dl

27. 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 body.

29.  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.

30.  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 pressure

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

32. Complications Of Pre-eclampsia
 IMMEDIATE: Maternal
 During 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)

33.  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

34.  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

35. 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

36. 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

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

38. 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

39.  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.

40. 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

41.  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

42.  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

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

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

45. 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.

46.  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.

47.  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.

48. ECLAMPSIA
 Pre-eclampsia when complicated with grand mal seizures
(generalized tonic-clonic convulsions) and/or coma is called
eclampsia.
 Occurs 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 36th week & Term in more than
50%Cases

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

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

51. PathoPhysiology

52. 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

53. 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
 Intrapartum (30%): Fits occur for the first time during delivery
 Postpartum (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.

54. 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

55.  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

56. 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.

57. 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.

58. 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.

59. (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.

60. Complications Of Eclampsia

61. Prevention
 Early 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

62. 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

63. 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

64. 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.

65. 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.

66. 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

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

68.  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.

69. 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

70. Detection of Magnesium Toxicity

71. 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

72.  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.

73. 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.

74.  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 .

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

76. 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

77.  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

78.  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

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

81. 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.

82. Thank you