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1. Hypertensive disorders in
pregnancy
(Recognition, pathophysiology and management)
Presented By:
Sunil Kumar Daha

2. • common medical complications of pregnancy and contributes significantly to
maternal and perinatal morbidity and mortality
• Sometimes there are no records of previous hypertension because the woman
has never presented to medical care until after 20 weeks of gestation
• In such situation, it is not possible to classify the hypertension in pregnancy
• In such condition, it is important to exclude underlying renal disease

4. Figure: Schematic shows normal reference ranges for blood pressure changes across pregnancy.
Patient A (blue) has blood pressures near the 20th percentile throughout pregnancy.
Patient B (red) has a similar pattern with pressures at about the 25th percentile until about 36
weeks when blood pressure begins to increase.
By term, it is substantively higher and in the 75th percentile, but she is still considered
“normotensive‘’ because her pressures are still < 140/90 mm Hg.

5. Pre-existing hypertension
• Is defined as the hypertension in a women diagnosed either before pregnancy or
before 20 weeks of pregnancy or persisting 12 weeks postpartum.
• Blood pressure normally decreases during the second and early third trimesters
in both normotensive and chronically hypertensive women.
• During the third trimester, blood pressures return to their originally hypertensive
levels.
• Therefore, it may be difficult to determine whether hypertension is chronic or
induced by pregnancy.

6. Pre-existing hypertension
• It can be
• Pre-existing hypertension (chronic hypertension) without proteinuria
• Pre-existing hypertension (chronic hypertension) with proteinuria
• Pre-existing hypertension (chronic hypertension) with superimposed pre-eclampsia.
• Pre-existing hypertension increases the risk of a woman developing pre-
eclampsia.

7. Pregnancy-induced hypertension (PIH)
“hypertension that develops as a direct result of the gravid state”
• includes—
(i) Gestational hypertension,
(ii) Pre-eclampsia, and
(iii) Eclampsia

8. Gestational hypertension
• New onset of hypertension during pregnancy which resolves by 12 weeks
postpartum but in whom proteinuria is not identified.
• BP > 140/90 mmHg after 20 weeks of pregnancy in previously normotensive non-
proteinuric women.
• Women who have a rise in pressure of 30 mm Hg systolic or 15 mm Hg diastolic
should be observed more closely because there is more likely to develop
eclamptic seizures in some of these women.

9. •There may be 3 conditions:
• Gestational hypertension (pregnancy induced hypertension) without
proteinuria.
• Gestational (pregnancy induced hypertension) proteinuria without
hypertension and
• Gestational hypertension (pregnancy induced hypertension) with
proteinuria: pre-eclampsia.

10. Delta Hypertension
• A sudden rise in mean arterial pressure later in pregnancy also signify
preeclampsia even if blood pressure is < 140/90 mm Hg.
• These women will develop eclamptic seizures or HELLP (hemolysis,
elevated liver enzyme levels, low platelet count) syndrome while still
normotensive.

11. PRE-ECLAMPSIA
“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 normotensive and nonproteinuric woman”
• Edema has been excluded from diagnostic criteria unless it is pathological.
• The preeclamptic features may appear even before the 20th week as in cases of
hydatidiform mole and acute polyhydramnios

12. DIAGNOSTIC CRITERIA OF PRE-ECLAMPSIA
1. Hypertension: An absolute rise of blood pressure of at least 140/90 mm Hg,
• Calculation based on mean arterial pressure (MAP) as advocated by Page
• (Systolic pressure + (diastolic pressure × 2))/3 = MAP
• A rise of 20 mm Hg MAP over the previous reading, or when the MAP is 105 mm Hg or
more should be considered as significant.
• The rise of blood pressure should be evident at least on two occasions at least 6 hours
apart. The level is arbitrary and is based on the observation, that complications are
likely to be more beyond this level.
• Blood pressure is measured on the right arm, with the patient lying on her side at 45° to
the horizontal. In the outpatient,
• sitting posture is preferred. In either case, the occluded brachial artery should be kept
at the level of the heart.

13. DIAGNOSTIC CRITERIA OF PRE-ECLAMPSIA
2. Edema: Demonstration of pitting edema over the ankles after 12 hours bed
rest or rapid gain in weight of more than 1 lb a week or more than 5 lb a month in
the later months of pregnancy may be the earliest evidence of pre-eclampsia
3. Proteinuria: Presence of total protein in 24 hours urine of more than 0.3 gm
or >2+ (1.0 gm/L) on at least two random clean-catch urine samples tested > 4
hours apart in the absence of urinary tract infection is considered significant.

14. Risk factors
• Primigravida: Young or elderly (first time exposure to chorionic villi)
• Family history of hypertension, pre-eclampsia
• Placental abnormalities:
• Hyperplacentosis: Excessive exposure to chorionic villi (molar pregnancy twins, diabetes)
• Placental ischemia.
• Obesity: BMI >35 kg/M2, Insulin resistance.
• Pre-existing vascular disease
• New paternity
• Thrombophilias (antiphospholipid syndrome, protein C, S deficiency, Factor V
Leiden).

15. Etiology
1. Placental implantation with abnormal trophoblastic invasion of uterine vessels
2. Vascular endothelial damage
3. Immunological maladaptive tolerance between maternal, paternal (placental),
and fetal tissues
-Coagulation abnormalities
4. Inflammatory mediators(cytokines)
5. Increased oxygen free radicals
6. Imbalance of angiogenic and antiangiogenic proteins
7. Maternal maladaptation to cardiovascular or inflammatory changes of normal
pregnancy
8. Genetic factors including inherited predisposing genes and epigenetic influences.

16. • Incidence in primigravidae is about 10% and in multigravidae 5%

17. Pathogenesis
• Basically involved pathology are
• Vasospasm and
• Endothelial dysfunction
• 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). Both are in a vicious cycle

19. Abnormal Trophoblastic Invasion
• Normal implantation is characterized by extensive remodeling of the spiral arterioles
within the decidua basalis.
• first trimester (10–12 weeks) endovascular trophoblasts invades up to decidual
segments and in the second trimester (16–18 weeks) another wave of trophoblasts
invades upto the myometrial segments.
• This process replaces the endothelial lining and the muscular arterial wall by fibrinoid
formation. The spiral arterioles thereby become distended, tortuous, and funnel-
shaped. This physiological change transforms the spiral arterioles into a low
resistance, low pressure, high flow system.
• In pre-eclampsia, there is failure of the second wave of endovascular trophoblast
migration and there is reduction of blood supply to the fetoplacental unit.

21. • In case of preeclampsia, there may be incomplete trophoblastic invasion.
• Decidual vessels, but not myometrial vessels, become lined with endovascular
trophoblasts.
• Their mean external diameter is only half that of corresponding vessels in normal
placentas.
• Also, there is changes like endothelial damage, insudation of plasma constituents
into vessel walls, proliferation of myointimal cells, and medial necrosis, lipid-
laden cell changes.
• These all causes spiral arteriole narrowing, atherosis, and infarcts in placentas.

22. Immunological Factor
• Normally there is maternal immune tolerance to paternally derived placental and
fetal antigens.
• Loss of this tolerance, or perhaps its dysregulation, account for preeclampsia
syndrome.
• Dysregulation include “immunization” from a previous pregnancy, some inherited
human leukocyte antigen (HLA) and natural killer (NK)-cell receptor haplotypes,
and possibly shared susceptibility genes with diabetes and hypertension

23. • Normally, placenta liberates angiotensinase which degrade angiotensin II.
• Vascular synthesis of prostaglandin I2 and NO neutralizes the vasoconstrictive
effect of angiotensin II.
• Increased level of VEGF restores the uteroplacental blood flow to normal.
• All these maintain blood pressure in normal state during pregnancy.

24. • But in pre-eclampsia, there are
• Imbalance of prostaglandin I2
• Increases synthesis of thromboxane A2
• Depressed activity of angiotensinase thereby increasing vascular sensitivity of
angiotensin II.
• Deficiency of NO.
• Increased synthesis of endothelin-1 (which is a potent vasoconstrictor)
• Cytokines (TNF-α, IL-6) elevated
• Oxidative stress
• All these contribute to vasospasm resulting in hypertension.

25. Endothelial Cell Activation
• Endothelial cell dysfunction may result from an extreme activated state of
leukocytes in the maternal circulation.
• Cytokines such as tumor necrosis factor-α (TNF-α) and the interleukins (IL) may
contribute to the oxidative stress.
• This is characterized by reactive oxygen species and free radicals that lead to
formation of self-propagating lipid peroxides.
• These in turn generate highly toxic radicals that injure endothelial cells, modify
their nitric oxide production, and interfere with prostaglandin balance.
• Other consequences of oxidative stress include production of the lipid-laden
macrophage foam cells seen in atherosis activation of microvascular coagulation
manifest by thrombocytopenia; and increased capillary permeability manifest by
edema and proteinuria.

26. Pathophysiology of proteinuria
Spasm of the afferent glomerular arterioles → anoxic change to the endothelium
of the glomerular tuft → glomerular endotheliosis → increased capillary
permeability → increased leakage of proteins.
• Tubular reabsorption is simultaneously depressed.
• Albumin constitutes 50–60% and alpha globulin constitutes 10–15% of the total
proteins excreted in the urine.

27. Pathophysiology of edema
• Not clear
• Probable explanation:
Increased oxidative stress → endothelial injury → increased capillary
permeability.

28. Pathological changes in severe pre-eclampsia and in
eclampsia
• Uteroplacental bed: Areas of occasional acute red infarcts and white infarcts are
visible on the maternal surface of the placenta.
• Villi: Syncitial degeneration, increased syncitial knots, marked proliferation of
cytotrophoblast, thickening of the basement layer, and proliferative endarteritis
are evident in varying degrees.
• Kidney: glomerular endotheliosis, Patchy areas of damage of the tubular
epithelium due to anoxia are evident
-severe cases, intense anoxia may produce extensive arterial thrombosis leading to
bilateral renal cortical necrosis.

30. • 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 hemorrhage. Hepatic insufficiency seldom occurs because of the
reserve capacity and regenerative ability of liver cells. Liver function tests are
specially abnormal in women with HELLP syndrome.

31. Clinical types
• Non-severe (mild and moderate)
• Severe

32. Abnormality Non-severe Severe
Diastolic BP <110 mm Hg ≥ 110 mm Hg
Systolic BP <160 mm Hg ≥ 160 mm Hg
Proteinuria None topositive None topositive
Headache Absent Present
Visual disturbances Absent Presnt
Upper abdominal pain Absent Present
Oliguria Absent Present
Convulsion (eclampsia) Absent present
Serum creatinine Normal Eleveted
Thrombocytopenia
(<10000/μL)
Absent Present
Serum transaminase
elevation
Absent Present
Fetal growth restriction Absent Present
Pulmonary edema Absent Present

33. Clinical features
Symptoms:
• Headache
• Eye symptoms: blurring, scotomata, dimness of vision or at times complete
blindness
• Epigastric or right upper quadrant pain: frequently accompanies
hepatocellular necrosis, ischemia, and edema that ostensibly stretches
Glisson capsule.
• Disturbed sleep
• Diminished urinary output: Urinary output of less than 400 ml in 24 hours

34. • 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 pre-eclampsia edema.
• Gradually, the swelling may extend to the face, abdominal wall, vulva and even the whole body
• Alarming symptoms: The following are the ominous symptoms, which may be evident either
singly or in combination.
(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.

35. Signs:
• Abnormal weight gain:
A rapid gain in weight of more than 5 lb a month or more than 1 lb a week in later months
of pregnancy is significant.
• Rise of blood pressure
• Edema

36. Complications
• Immediate complications
• Maternal
• Fetal
• Remote complications

37. Immediate complications
Maternal:
• During pregnancy:
• Eclampsia
• Accidental hemorrhage
• Oliguria and anuria
• Dimness of vision and even blindness
• Preterm labor
• HELLP syndrome
• ARDS

38. Immediate complications contd.
• During labor:
• Eclampsia
• PPH: may be related with coagulation failure
• Puerperium:
• Eclampsia (usually within 48 hrs)
• Shock (puerperal vasomotor collapse due to reduced concentration of
Na+ and cl- due to sudden fall in corticosteroid level.
• sepsis

39. Fetal complications
• Intrauterine deaths (due to spasm of uteroplacental circulation)
• Intrauterine growth restriction (due to chronic placental insufficiency)
• Asphyxia
• Prematurity

40. Remote complications
• Residual hypertension
• Recurrent preeclampsia
• Chronic renal disease
• Risk of placental abruption

41. MANAGEMENT

43. Prevention
• Dietary and lifestyle modification
• Low salt diet
• Calcium supplement
• Fish oil supplement
• Exercise
• Antihypertensive drugs
• Antioxidants
• Antithrombotic agents
• Low dose aspirin (50-150 daily)
• Low dose aspirin plus low molecular weight heparin

44. PROGNOSIS:
depends on the period of gestation, severity of disease and
response to treatment.

45. Management
• Objectives are:
(1) To stabilise hypertension and to prevent its progression to severe pre-
eclampsia.
(2) To prevent the complications
(3) To prevent eclampsia.
(4) Delivery of a healthy baby in optimal time.
(5) Restoration of the health of the mother in puerperium.

46. Management
The basic management objectives for any pregnancy complicated by preeclampsia are:
(1) Termination of pregnancy with the least possible trauma to mother and fetus,
(2) Birth of an infant who subsequently thrives, and
(3) Complete restoration of health to the mother
(4) Administration of corticosteroids improves perinatal (↑ pulmonary maturity, ↓ IVH
and ↓necrotizing enterocolitis) and maternal (↑ thrombocyte count, ↑ urinary
output) outcome

48. Hospital vs outpatient management
• Ideally, all patients of pre-eclampsia are to be admitted in the hospital
for effective supervision and treatment.
• However, in some centers cases of pre-eclampsia are managed in the
day care unit.
• Those who are receiving treatment as outpatient should be
counselled for ominous sign of pre-eclampsia.

49. Hospital management
• Rest
• Diet
• Diuretics
• Antihypertensive

50. Rest
• In left-lateral position as much as possible.
• It lessen the effects of vena caval compression.
• Increases the renal blood flow → diuresis
• Increases the uterine blood flow → improves the placental perfusion
• Reduces the blood pressure.

51. Diet
• Should contain adequate amount of daily protein (about 100 gm).
• Total calorie approximate 1600 cal/day.
• Usual salt intake is permitted.
• Fluids need not be restricted.

52. Diuretics
• Should not be used injudiciously as they can harm to the baby by
diminishing placental perfusion and by electrolyte imbalance.
• Indications for diuretics use are:
• Cardiac failure
• Pulmonary edema
• Along with selective antihypertensive drug therapy (diazoxide group) where blood
pressure reduction is associated with fluid retention
• Massive edema, not relieved by rest and producing discomfort to the patient.
• commonly used is furosemide (Lasix) 40 mg, given orally after breakfast for
5 days in a week.
• In acute condition, intravenous route is preferred

53. Antihypertensive
• The indications are:
• Persistent rise of blood pressure specially where the diastolic pressure
is over 110 mm Hg. The use is more urgent if associated with
proteinuria.
• In severe pre-eclampsia to bring down the blood pressure during
continued pregnancy and during the period of induction of labor

54. Management of Severe Pre-eclampsia
• Hypertensive crisis (BP≥160/110mmHg or MAP ≥125mmHg)
• Use any of the following drugs
• Labetalol
• (10-20 mg IV every 10 min)  max. 300 mg IV
• Hydralazine
• (5 mg IV every 30 min)  max. 30 mg IV
• Nifedipine
• (10-20 mg PO every 30 min)  max. 240 mg/24hr
• Short term (when others have failed)
• Nitroglycerin (5 μg/min IV)
• Sodium nitroprusside (0.25 – 5 μg/kg/min IV)

55. Methyldopa
MOA:
• α -methylnorepinephrine acts in the CNS to inhibit adrenergic
neuronal outflow from the brainstem.
• Methylnorepinephrine acts as an agonist at presynaptic α2 adrenergic
receptors in the brainstem, attenuating NE release and thereby
reducing the output of vasoconstrictor adrenergic signals to the
peripheral sympathetic nervous system.

56. Methyldopa
Side effects:
• Sedation, particularly at the onset of treatment.
• Nightmares, mental depression, vertigo
• Lactation, associated with increased prolactin secretion, can occur
both in men and in women treated with methyldopa.
• Discontinuation of the drug usually results in prompt reversal of these
abnormalities.
• Hepatotoxicity
• Hemolytic anemia

57. Labetalol
MOA:
Both beta- and alpha-blocking activity.
Side effects:
• Postural hypotension
• Rash
• Lever damage

58. Hydralazine
MOA:
• Directly acting arteriolar vasodilator.
• Involve generation of NO and stimulation of cGMP.
Contraindication:
• Elderly and in those with IHD.

59. Hydrazine
Side effects:
• Flushing, headache, dizziness, nasal stuffiness, fluid retention, edema.
• Angina, myocardial infarction can be precipitated in coronary artery disease.
• Parasthesias, tremor, muscle cramps, edema
• Lupus like syndrome
• Occurs mainly due to vasodilation.

60. Nefedipine
MOA:
• Vascular smooth muscle selective Ca+ channel blocker.
• The overriding action of nifedipine is arteriolar dilatation.
• The direct depressant action on heart requires much higher dose.

61. Nefedipine
Side effects:
• Palpitaion
• Flushing
• Ankle edema
• Hypotension
• Headache
• Drowsiness
• Ankle edema is not due to fluid retention, but because of greater
dilatation of precapillary than postcapillary vessels.

62. Consideration for Delivery
• Termination of pregnancy is the only cure for preeclampsia.
• With moderate or severe preeclampsia that does not improve after
hospitalization, delivery is usually advisable for the welfare of both
mother and fetus.
• Depends on
• severity of pre-eclampsia
• duration of pregnancy
• response to treatment
• condition of the cervix

63. Methods of delivery
• Induction of labor
• Cesarean section

64. Indications for induction of labour
• Aggravation of the preeclamptic features in spite of medical
treatment and/or appearance of newer symptoms
• Hypertension persists in spite of medical treatment with pregnancy
reaching 37 weeks or more.
• Acute fulminating pre-eclampsia irrespective of the period of
gestation
• Tendency of pregnancy to overrun the expected date.

65. Indications for cesarean section
• When an urgent termination is indicated and the cervix is unfavorable
(unripe and closed).
• Severe pre-eclampsia with a tendency to prolong the induction
(delivery interval).
• Associated complicating factors, such as elderly primigravidae,
contracted pelvis, malpresentation, etc

66. Acute Fulminant Preeclampsia
Treatment
• If detected at home adequately sedate by
• Pethidine 75-100 mg
• Diazepam 10 mg IM
• Shift gently to hospital setting
• Start prophylactic anticonvulsant therapy
• Start parenteral anti-HTNs
• Monitor BP, Urine output, Blood parameters, Proteinuria
• If condition fails to improve within 6-8 hrs  plan delivery

67. Improvements
• As with severe preeclampsia, an increase in urinary output after
delivery is usually an early sign of improvement.
• Proteinuria and edema ordinarily disappear within a week
postpartum.
• In most cases, blood pressure returns to normal within a few days to
2 weeks after delivery.

68. Eclampsia
“Preeclampsia with generalized tonic-clonic seizure is called eclampsia”
• Labor and delivery is a more likely time for convulsions to develop.

69. Stages of eclamptic convulsion
• Premonitory stage:
• Patient becomes unconscious
• Twitching of the muscle of the face, tongue, and limbs
• Eyeball roll or are turned to one side and become fixed
• Lasts for 30 seconds.
• Tonic stage:
• Whole body goes into tonic spasm
• Trunk: opisthotonus
• Limbs are flexed
• Hands are clenched
• Respiration ceases
• Tongue protrude between the teeth
• Cyanosis appears
• Eyeballs fixed
• Lasts for 30 seconds.

70. • Clonic stage:
• All voluntary muscles goes alternate contraction and relaxation
• Twitching start in the face
• Then involve one side of the extremities and ultimately the whole body is
involved in convulsion
• Biting of tongue occurs
• Breathing is stertorous
• Blood stained frothy secretion fill the mouth
• Cyanosis gradually disappears
• Lasts for 1-4 minutes.

71. • Stage of coma:
• Follows the convulsion
• Lasts for brief period or persists till another convulsion
• Patient in stage of confusion following the convulsion
• Do not remember the event

72. Physiological changes following convulsion
• Body temperature rises
• Pulse and respiration rates are increased
• Blood pressure increased
• Urinary output diminished
• Proteinuria is pronounced
• Blood uric acid is raised

73. Complications

74. PROGNOSIS
MATERNAL: Immediate: Once the convulsion occurs, the prognosis becomes uncertain.
• Prognosis depends on many factors and the ominous features are:
(1) Long interval between the onset of fit and commencement of treatment (late referral).
(2) Antepartum eclampsia specially with long delivery interval.
(3) Number of fits more than 10.
(4) Coma in between fits.
(5) Temperature over 102°F with pulse rate above 120/minute.
(6) Blood pressure over 200 mm Hg systolic.
(7) Oliguria (< 400 mL/24 hours) with proteinuria > 5 gm/24 hours.
(8) Nonresponse to treatment. (9) Jaundice.

75. PROGNOSIS contd..
FETAL: The perinatal mortality is very high to the extent of about 30–50%.
• The causes are:
(1) Prematurity— spontaneous or induced,
(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

76. Prevention
• Early detection and treatment of preeclampsia
• Use of antihypertensive drugs, Prophylactic anticonvulsants, timely delivery-
important steps in preeclamptic state (as majority of the eclampsia are preceded
by preeclampsia ).
• Close monitoring during labour and 24 hours postpartum.
• Eclampsia bypassing the preeclampsia: unpreventable (unfortunately 30-85% of
eclampsia case are unpreventable).

77. General management
• Ask for help
• Keep the patient in left lateral decubitus position
• Ensure airway
• Check pulse, RR, BP and blood glucose (dextrostrix)
• Secure IV access

78. • Send blood for
• Glucose
• Urea
• Elecrolytes
• Ca and Mg
• CBC
• LFT
• Coagulation profile
• Concentration of antiepileptic drugs
Investigations

79. First aid Treatment outside hospital
• Urgent referral to the tertiary care hospital.
• Monitor vitals regularly
• All the records in summary should be sent with referral
• BP should be stablished and convulsion should be arrested
• MgSO4 should be started (4gm IV lording dose and 10gm IM).

80. Principles of Hospital management
• Maintain ABCDE
• O2 administration 8-10L/min.
• Arrest convulsion
• Ventilatory support
• Prevention of injury
• Hemodynamic stabilization/control BP
• Organize necessary investigations
• Deliver by 6-8 hours
• Prevention of complications
• Intensive post partum care.

81. General treatment of eclampsia
1. Supportive care: prevent serious maternal injury from fall and trauma, prevent
aspiration, maintain airway, O2 inhalation
2. Detailed history and examination
3. Half hourly maternal vital and the FHS monitoring.
4. Fluid balance: RL as a first choice 1ml/kg/hr.
• Total fluid should not exceed the previous 24 hour urine + 1000 mL (insensible
loss).
• Careful monitoring of fluid therapy is necessary: may cause pulmonary
oedema, ARDS, and tissue overload.
5. Antibiotic treatment: Ceftriaxone 1gm IV twice daily is given

82. Immediate measures
• Call for extra help (communication)
• To put patient in left lateral recumbent position
• Maintain oral airway
• O2 inhalation- non breather mask (10L/Min)
• Commence IV line: 2 wide bore cannulas, Crystalloids (saline/RL) or colloid (albumin/blood)
≤125mL/hr
• Foley’s catheter with urometer
• Monitor O2 saturation
• Control of seizure: MgSO4 (IM/IV)
• Monitor vitals; foetal status; magnesium toxicity
• Control of HTN: Labetolol, Hydralazine
• Oropharyngeal suction
• Diuretics to prevent Odema

83. Specific management of Eclampsia
1. Anticonvulsant therapy:
• MgSO4 is drug of choice
• Repeated injection: if knee jerk are still present, urine output exceeds 30mL/hr and RR>12/min
• Monitor the magnesium level (4-7mEq/L), if toxicity present then manage accordingly.
• Alternative therapy are:
• Lytic Coctail: Clorpromazine + Promithazine + Pethidine
• Diazepam
• Phenytoin.
Advantages of MgSO4
• Controls fits effectively without any depression to mother and fetus
• Reduce risk of recurrent convulsion
• Significant decrease in maternal and foetal death
• Reduces perinatal mortality

84. Anti-HTN and Diuretics: Same regimen as in the preeclampsia
3. Management during Fits: ABC, prevent tongue bite, prevent aspiration, suction, elevate legs, O2
inhalation.
4. Status Eclampticus:
• Thiopentone 0.5 gm in 20 mL of D5 IV slowly,
• if fails give complete anaesthesia, muscle relaxants, assisted ventilation.
• In unresponsive case: Caesarean section (life saving)
5. Treatment of complications:
• Pulmonary oedema: Furosemide 40mg IV followed by 20 mg mannitol IV
• HF: O2 inhalation, parenteral Furosemide, Digitalis.
• Anuria management
• Hyperpyrxia: antipyrectis and cold sponging
• Psychosis: Clorpromazine
• Intensive care monitoring: Multidisciplinary approach.

85. Obstetric management of Eclampsia
DURING PREGNANCY
(Labour starts as soon as the convulsion starts, but if it failed to start, then management
depends upon whether fits controlled or not with anticonvulsant therapy)
• Fits controlled
• Mature foetus
• Delivery as soon as possible:
• cervix is favorable and the vaginal delivery is not contraindicate
• Induction of labour: ARM, Oxytocin drip if needed.
• Cervix is not favorable but cervical ripening:
• PGE2 gel or pessary before ARM.
• Cervix is unfavorable &/or there is obstetric CI of vaginal delivery:
• CS delivery
• Immature foetus (<37 weeks)
• Delivery in a NICU set up.
• Eclampsia persists until delivery
• Conservative treatment may prevent the complications
• If the foetus <34 weeks steroid therapy to mother

86. Fits uncontrolled (6-8 hrs. of Anticonvulsant
therapy)
Termination of pregnancy as soon as
possible:
• If PV examination indicates the
quick response to induction : low
RM, Oxytocin drip if needed.
During labour if VD is contraindicated:
• Low RM, dose of Anti HTN and ACT
should be increased
• 2nd stage labour should be curtailed:
instrumental delivery (forceps or
ventouse or craniotomy if the foetus
is dead)
• 10 IU Oxytocin IM/IV slowly
• Prevent/manage the PPH and shock

87. • Indication of CS in Preeclampsia
• Unc
• ontrolled fits in spite therapy
• Unconscious patient and poor protect of vaginal delivery
• Obstetric indications (malpresentation)
• Follow up and prognosis:
• Follow up till 6 weeks of post natal period
• HTN, proteinuria, abnormal blood biochemistry need further investigation and
consultation.
• Recurrent rate:
• Recurrence rate in next pregnancy varies from 2-25%
• Daughter of eclamptic mother: 25 % risk of preeclampsia and 3% risk of eclampsia

88. Figure: Comparison of serum magnesium levels in mEq/L following a 4-g intravenous loading dose of
magnesium sulfate and then maintained by either an intramuscular or continuing infusion.
Multiply by 1.2 to convert mEq/L to mg/dL.

89. • Eclamptic convulsions are almost always prevented or arrested by plasma
magnesium levels maintained at 4 to 7 mEq/L.

90. Magnesium Toxicity
• Magnesium sulfate USP is MgSO4·7H2O and not simple MgSO4.
• It contains 8.12 mEq per 1 g.
• Parenterally administered magnesium is cleared almost totally by renal
excretion.
• Therefore, magnesium intoxication is unusual when the glomerular filtration rate
is normal or only slightly decreased.
• Thus, serum creatinine levels must be measured to detect a decreased
glomerular filtration rate.

91. Magnesium Toxicity
• Patellar reflexes disappear when the plasma magnesium level reaches 10
mEq/L—about 12 mg/Dl
• This sign serves to warn of impending magnesium toxicity.
• When plasma levels rise above 10 mEq/L, breathing becomes weakened.
• At 12 mEq/L or higher levels, respiratory paralysis and respiratory arrest follow.

92. Reversal of magnesium toxicity
• Calcium gluconate or calcium chloride, 1 g intravenously, along with
withholding further magnesium sulfate, usually reverses mild to
moderate respiratory depression.

95. References
• Cunningham F. G. et al. Williams obstetrics, 24th edition
• DC Dutta’s Textbook of OBSTETRICS, 8th edition
• Obstetrics by Ten Teachers

96. Thank you