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DEFINITION
 Pre eclampsia is a multi system disorder
of unknown etiology characterised by
development of hypertension to the
extent of 140/90 mm Hg or more with
proteinuria after 20th week in a
previously normotensive &
nonproteinuric patient .
Contd..
 MILD–
 This includes
cases of
sustained rise
of blood
pressure of
more than
140/90 mm Hg
but less than
160 systolic or
110 diastolic
without
proteinuria
SEVERE-
This includes
1. Persistant systolic BP of > 160 mm Hg or
diastolic of >110 mm Hg .
2. Persistant severe epigastric pain.
3. Cerebral or visual disturbances .
4. Oliguria ( <400ml /24 hr).
5. Protein excretion of > 5 gm /day .
6. Platelet count <100,000/mm3.
7. HELLP syndrome.
8. IUGR , Pulmonary edema.
Path physiology
The path physiological changes that
distinguish pre-eclampsia from normal
pregnancy are:
Intense
vasospasm
Plasma
volume
contraction
Intravascular
coagulation
Intense vasospasm
In pregnancies complicated
by pre-eclampsia, the blood
vessels constrict, leading
to vasospasm and a
reduction in blood flow
leading to maternal organ
damage.
Intravasular coagulation
Platelets are used to repair
the damaged vessel wall
caused by vasospasm
resulting in platelet
consumption which led's to
intravascular coagulation.
Plasma volume contraction
In normal pregnancy, plasma volume increases
dramatically resulting in a 50% increase in
total blood volume.
Women with pre-eclampsia have a slight or
unchanged total extracellular fluid volume,
plasma volume is reduced leading to
haemoconcentration
 The net result of vasospasm,
intravascular coagulation and plasma
contraction is decreased blood flow
resulting in organ hypo perfusion.
 Organ hypo perfusion is detrimental not
only to the mother, but to the fetus if
the placenta is similarly affected
 Primigravida ( young & elderly).
 Family history.
 Genetic disorder
 New paternity .
 Pre existing vascular or renal disease .
 Thrombophilias – antiphospholipid syndrome
, protein c , s deficiency .
 Placental abnormalities.( poor placentation ,
hyperplacentosis – multiple pregnancy , Rh
incompatibility , diabetes , placental ischaemia
).
Signs
Oligohydr
omnios
MILD SYMPTOMS –
Slight swelling over
ankles . This swelling
may extend to the
face , abdominal wall ,
vulva & even whole
body .
Symptoms
mild severe
SEVERE SYMPTOMS –
1. Headache ( occipital or frontal ).
2. Disturbed sleep .
3. Diminished urinary output .
4. Epigastric pain .
5. Eye symptoms ( blurring or dimness of
vision ).vision is usually regained in 4-6
weeks after delivery .
 Urine for presence of protein.
 Opthalmoscopic examination for retinal
oedema and constriction of arterioles.
 Blood values
-Serum uric acid level more than 4.5mg/dl
-Serum creatinine level more than 1 mg/dl.
-Thromobocytopenia and abnormal
coagulation
profile.
 Antenatal fetal monitoring.
Investigations
Complications
Immediate
Maternal Fetal
Remote
During pregnancy During labour Puerperium
Eclampsia Eclampsia Eclampsia
Accidental
haemorrhage
Postpartum
haemorrhage
Shock
Oliguria & anuria Sepsis
Dimness of vision &
even blindness.
Preterm labour
HELLP syndrome
1).Maternal
 Intrauterine death .
 Intrauterine growth
restriction ( due to chronic
placental insufficiency).
 Asphyxia .
 Prematurity ( either due to
spontaneous preterm onset
of labour or induction
2). Fetal
 Residual hypertension .
In this hypertension may persist even after 6
months following delivery in about 50 % cases.
 Recurrent pre eclampsia
25% chance of preeclampsia to reccur in
subsequent pregnancies.
 Chronic renal disease
High incidence of glomerulonephritis in women
with pre eclampsia
3).Remote
PREVENTION
 Reduce dietary salt intake
 Supplementation 1g of calcium a day
 Supplementation antioxidants: such as
vitamin C, vitamin E
 Nutritional supplementation with Mg , Zn,
fish oil , high protein .
 Regular antenatal check up .
 Antithrombotic agents.
Objectives –
1. To correct / stabilize the
altered physiology .
2. Prevention of
complications
3. Prevention of eclampsia.
4. Delivery of healthy baby
with minimal maternal
morbidity .
Management
TREATMENT MODALITIES
Rest
Diet
Drugs
Contd..
Rest
While in bed patient
should be in left lateral
position . It increases the
1. Increases the renal
blood flow >diuresis.
2. Increases the
uterine blood flow >
improves the
placental perfusion .
3. Reduces the blood
pressure
Diet
Diet should contain
adequate amount of
proteins (about
100gms),
with no restriction
over
salt n fluids
DRUGS
 SEDATIVE
Mild sedative like phenobarbitone 60 mg or diazepam
5mg orally at bedtime.
 DIURETICS
Compelling reasons to use it are-
 Cardiac failure
 Pulmonary oedema
 Massive oedema not relieved by rest
 Along with antihypertensive drug therapy to treat
fluid retention.
Mostly frusedamide 40mg given for 5 days in a week.
ANTI HYPERTENSIVES
Labetalol Hydralazine Nitroprusside Nitroglycerine
Adrenoreptor
antagonist
Vascular smooth
muscle relaxant
Calcium channel
blocker
Calcium channel
blocker
200 mg in 200
ml NS at the
rate of 20 mg
/hr to be
doubled every
30 mins
5 mg iv bolus to
be followed by
infusion 25 mg in
200 ml NS , the
rate being 2.5mg
to be doubled
every 30 mins
0.25-5
micrograms/kg/mi
n
5
micrograms/mins
PROGRESS CHART
 The effect of treatment should be
evaluated by maintaining a chart which
records the following –
1. Blood pressure – at least 4 times a day.
2. State of edema & daily weight.
3. Fluid intake n urinary output
Contd..
4. Urine examination – for
proteins daily.
5. Blood for- cbc, platelet
count,uric acid ,creatinine &
LFT .
6. Opthalmoscopic examination.
7. Fetal well being assessment .
SCHEME OF MANGMENT
Rest
BP checking
4 hourly
•Plt count
•RFT
•LFT
•24 hour
urine
opthalmosc
opy
Fetal
assessment
Antihypertensive if
DBP>110mm Hg
Complete
control
BP
persistently
high
Increased
BP inspite
use of
antihyperte
nsive
Addition of
omnious
symptoms
Couple
counselling
preter
m
Term
To continue
pregnancy till
37 completed
discharge
Stay in
hospital
Termination
Termination
Induction
•PGE2 gel
•ARM
•Oxytocin
C.S.
METHODS OF TERMINATION
Induction
of labour
Caesarean
section
1. Aggravation of pre eclamptic features inspite of
medical treatment & / appearance of newer
symptoms such as epigastric pain.
2. If hypertension persists inspite of medical
treatment.
3. Tendency of pregnancy to overrun the expected
date.
4. Acute fulminating preeclampsia irrespective
of period of gestation.
Indications for IOL
 If the cervix is ripe , surgical induction by low
rupture of membranes is the method choice .Oxytocin
infusion may be added to accelerate the process.
 If the cervix is unripe & termination is not the urgent
one , than prostaglandin (PGE2)gel 500microgm
intracervical or 1-2 mg in posterior fornix to make
cervix ripe. In severe preeclampsia , antihypertensive
should be used.
METHODS
CAESAREAN SECTION
 When urgent termination is indicated & the cervix is
unfavorable .
 Severe preeclampsia with tendency to prolong the
induction –delivery interval.
 Associated complicating factors such as elderly
primigravida , contracted pelvis malpresentation.
Toxemia of pregnancy: pre-eclampsia

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Toxemia of pregnancy: pre-eclampsia

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  • 3. DEFINITION  Pre eclampsia is a multi system disorder of unknown etiology characterised by development of hypertension to the extent of 140/90 mm Hg or more with proteinuria after 20th week in a previously normotensive & nonproteinuric patient .
  • 4. Contd..  MILD–  This includes cases of sustained rise of blood pressure of more than 140/90 mm Hg but less than 160 systolic or 110 diastolic without proteinuria
  • 5. SEVERE- This includes 1. Persistant systolic BP of > 160 mm Hg or diastolic of >110 mm Hg . 2. Persistant severe epigastric pain. 3. Cerebral or visual disturbances . 4. Oliguria ( <400ml /24 hr). 5. Protein excretion of > 5 gm /day . 6. Platelet count <100,000/mm3. 7. HELLP syndrome. 8. IUGR , Pulmonary edema.
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  • 7. Path physiology The path physiological changes that distinguish pre-eclampsia from normal pregnancy are: Intense vasospasm Plasma volume contraction Intravascular coagulation
  • 8. Intense vasospasm In pregnancies complicated by pre-eclampsia, the blood vessels constrict, leading to vasospasm and a reduction in blood flow leading to maternal organ damage.
  • 9. Intravasular coagulation Platelets are used to repair the damaged vessel wall caused by vasospasm resulting in platelet consumption which led's to intravascular coagulation.
  • 10. Plasma volume contraction In normal pregnancy, plasma volume increases dramatically resulting in a 50% increase in total blood volume. Women with pre-eclampsia have a slight or unchanged total extracellular fluid volume, plasma volume is reduced leading to haemoconcentration
  • 11.  The net result of vasospasm, intravascular coagulation and plasma contraction is decreased blood flow resulting in organ hypo perfusion.  Organ hypo perfusion is detrimental not only to the mother, but to the fetus if the placenta is similarly affected
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  • 14.  Primigravida ( young & elderly).  Family history.  Genetic disorder  New paternity .  Pre existing vascular or renal disease .  Thrombophilias – antiphospholipid syndrome , protein c , s deficiency .  Placental abnormalities.( poor placentation , hyperplacentosis – multiple pregnancy , Rh incompatibility , diabetes , placental ischaemia ).
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  • 17. MILD SYMPTOMS – Slight swelling over ankles . This swelling may extend to the face , abdominal wall , vulva & even whole body . Symptoms mild severe
  • 18. SEVERE SYMPTOMS – 1. Headache ( occipital or frontal ). 2. Disturbed sleep . 3. Diminished urinary output . 4. Epigastric pain . 5. Eye symptoms ( blurring or dimness of vision ).vision is usually regained in 4-6 weeks after delivery .
  • 19.  Urine for presence of protein.  Opthalmoscopic examination for retinal oedema and constriction of arterioles.  Blood values -Serum uric acid level more than 4.5mg/dl -Serum creatinine level more than 1 mg/dl. -Thromobocytopenia and abnormal coagulation profile.  Antenatal fetal monitoring. Investigations
  • 21. During pregnancy During labour Puerperium Eclampsia Eclampsia Eclampsia Accidental haemorrhage Postpartum haemorrhage Shock Oliguria & anuria Sepsis Dimness of vision & even blindness. Preterm labour HELLP syndrome 1).Maternal
  • 22.  Intrauterine death .  Intrauterine growth restriction ( due to chronic placental insufficiency).  Asphyxia .  Prematurity ( either due to spontaneous preterm onset of labour or induction 2). Fetal
  • 23.  Residual hypertension . In this hypertension may persist even after 6 months following delivery in about 50 % cases.  Recurrent pre eclampsia 25% chance of preeclampsia to reccur in subsequent pregnancies.  Chronic renal disease High incidence of glomerulonephritis in women with pre eclampsia 3).Remote
  • 24. PREVENTION  Reduce dietary salt intake  Supplementation 1g of calcium a day  Supplementation antioxidants: such as vitamin C, vitamin E  Nutritional supplementation with Mg , Zn, fish oil , high protein .  Regular antenatal check up .  Antithrombotic agents.
  • 25. Objectives – 1. To correct / stabilize the altered physiology . 2. Prevention of complications 3. Prevention of eclampsia. 4. Delivery of healthy baby with minimal maternal morbidity . Management
  • 27. Contd.. Rest While in bed patient should be in left lateral position . It increases the 1. Increases the renal blood flow >diuresis. 2. Increases the uterine blood flow > improves the placental perfusion . 3. Reduces the blood pressure Diet Diet should contain adequate amount of proteins (about 100gms), with no restriction over salt n fluids
  • 28. DRUGS  SEDATIVE Mild sedative like phenobarbitone 60 mg or diazepam 5mg orally at bedtime.  DIURETICS Compelling reasons to use it are-  Cardiac failure  Pulmonary oedema  Massive oedema not relieved by rest  Along with antihypertensive drug therapy to treat fluid retention. Mostly frusedamide 40mg given for 5 days in a week.
  • 29. ANTI HYPERTENSIVES Labetalol Hydralazine Nitroprusside Nitroglycerine Adrenoreptor antagonist Vascular smooth muscle relaxant Calcium channel blocker Calcium channel blocker 200 mg in 200 ml NS at the rate of 20 mg /hr to be doubled every 30 mins 5 mg iv bolus to be followed by infusion 25 mg in 200 ml NS , the rate being 2.5mg to be doubled every 30 mins 0.25-5 micrograms/kg/mi n 5 micrograms/mins
  • 30. PROGRESS CHART  The effect of treatment should be evaluated by maintaining a chart which records the following – 1. Blood pressure – at least 4 times a day. 2. State of edema & daily weight. 3. Fluid intake n urinary output
  • 31. Contd.. 4. Urine examination – for proteins daily. 5. Blood for- cbc, platelet count,uric acid ,creatinine & LFT . 6. Opthalmoscopic examination. 7. Fetal well being assessment .
  • 32. SCHEME OF MANGMENT Rest BP checking 4 hourly •Plt count •RFT •LFT •24 hour urine opthalmosc opy Fetal assessment
  • 33. Antihypertensive if DBP>110mm Hg Complete control BP persistently high Increased BP inspite use of antihyperte nsive Addition of omnious symptoms Couple counselling preter m Term To continue pregnancy till 37 completed discharge Stay in hospital Termination
  • 35. METHODS OF TERMINATION Induction of labour Caesarean section
  • 36. 1. Aggravation of pre eclamptic features inspite of medical treatment & / appearance of newer symptoms such as epigastric pain. 2. If hypertension persists inspite of medical treatment. 3. Tendency of pregnancy to overrun the expected date. 4. Acute fulminating preeclampsia irrespective of period of gestation. Indications for IOL
  • 37.  If the cervix is ripe , surgical induction by low rupture of membranes is the method choice .Oxytocin infusion may be added to accelerate the process.  If the cervix is unripe & termination is not the urgent one , than prostaglandin (PGE2)gel 500microgm intracervical or 1-2 mg in posterior fornix to make cervix ripe. In severe preeclampsia , antihypertensive should be used. METHODS
  • 38. CAESAREAN SECTION  When urgent termination is indicated & the cervix is unfavorable .  Severe preeclampsia with tendency to prolong the induction –delivery interval.  Associated complicating factors such as elderly primigravida , contracted pelvis malpresentation.