nursing

1. PREECLAMP
SIA
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2. Hypertension is one of the most common
disorders of pregnancy and contributes
significantly to the maternal and perinatal
morbidity.
Hypertension may appear for the first time
during pregnancy as a direct result of the
gravid state or a sign of underlying
pathology , which maybe pre-existing
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4. Classification of hypertension in
pregnancy
A. PREGNANCY INDUCED HYPERTENSION
(PIH)
 With proteinuria and or oedema
 Preeclampsia
 Eclampsia
 Without gross oedema or proteinuria
 Gestational hypertension
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5. B. CHRONICHYPERTENSION IN
PREGNANCY
1. Essential hypertension
2. Reno vascular hypertension
3. Pheochromocytoma
4. Coaction of aorta
5. Thyrotoxicosis
6. Connective tissue disease systemic lupus
erythematous
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6. C. HYPERTENSION
WORSENEDBY PREGNANCY
 Superimposed preeclampsia
 Superimposed eclampsia
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7. DEFINITION
Preeclampsia is a multisystem disorder of
unknown aetiology characterized by
development of hypertension to the extent
of 140/90 mm of hg or more with proteinuria
induced by pregnancy after the 20thweek in
a previously normotensive and proteinuric
woman.
(International society for study of
hypertension in pregnancy, 1998)
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9. INCIDENCE
According to the new guidelines given
by American Congress Of Obstetricians
and Gynaecologist (ACOG) in 2013.
In INDIA, the incidence of preeclampsia
is reported to be 8-10%.
It occurs more frequently in young
primigravidae and in mothers over 35yrs
of age.
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10. It is known to be associated with
HYDATIFORM MOLE, MULTIPLE
PREGNANCY AND MATERNAL DIABETES.
The incidence in primigravidae is about 10%
and in multigravidae 5%.
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11. AETIOLOGY
Failure of trophoblastic invasion mediators
(abnormal placentation).
Vascular endothelial damage.
Inflammatory mediators.
Immunological intolerance between
maternal and foetal tissues.
Coagulation abnormalties.
Increased oxygen free radicals.
Genetic pre disposition.
Dietary deficiency or excess.
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12. Other Factors
Abnormal lipid metabolism (results in
more oxidative stress).
Mutation of factor V Leiden increase
risk.
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13. PATHOPHYSIOLOGY
• UTEROPLACENTAL BED
• KIDNEY
• BLOOD VESSELS
• LIVER
• HEART
• LUNGS
• HAEMATOLOGICAL CHANGES
• HORMONES
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15. CLINICAL TYPES
The clinical classification of preeclampsia is
arbitrary and in principally dependent on the
level of blood pressure for management
purpose.
1) MILD
2) SEVERE
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16. MILD
This includes cases of sustained rise of
blood pressure of more than 140/90 mm of
hg but less than systoloic or 110 diastolic
without significant proteinuria.
SEVERE:
A systolic blood pressure of more than 160
mm of hg or diastolic more than 110 mm
of hg.
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17. CLINICAL FEATURES
The clinical manifestation appears
usually after the 20th week.
ONSET: The onset is usually insidious
and the syndrome runs a slow course.
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19. MILD SYMPTOMS
 Slight swelling over the ankles (on
rising from bed in morning).
 Tightness of the ring on the finger.
 Swelling may extend to face
abdominal wall, vulva and even the
whole body.
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20. ALARMING SYMPTOMS
 Headache( occipital or frontal region).
 Disturbed sleep
 Diminished urinary output
 Epigastric pain
 Eye symptoms
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21. INVESTIGATION
 History collection
 Physical examination
 Urine analysis: proteinuria is the last feature of
preeclampsia to be appear.(there may be few
hyaline cysts, epithelial cells or even few red
cells).
 Opthalmoscopic examination
 Blood values or CBCs
 Liver Function Test
 Non stress test or biophysical profile
 Renal Function Test
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23. MANAGEMENT
So, As long as the aetiology of
preeclampsia remains obscure,
the treatment is mostly
empirical and symptomatic.
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24. PHARMACOLOGICAL MANAGEMENT
1. ANTIHYPERTENSIVE AGENTS
 Methyl Dopa: central and peripheral
anti adrenergic
action:250/500mg/tid/qid.
 Labetalol: adrenoceptor antagonist
(alpha and beta blockers):250mg
tid/qid. 24

25.  Nifedipine : calcium channel
blockers: 10-20mg/bid.
 Hydralazine: vascular smooth
muscle relaxant: 10-25mg bid.
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26. IN HYPERTENSIVE CRISIS:
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DIURETICS:
The diuretics should not be used
injudiciously as they cause harm to
the baby by diminishing placental
perfusion.
FRUSEMIDE (LASIX) 40 MG give orally
after breakfast for 5days in a week.

27. SEDATIVES:
To cut down the emotional
factors mild sedatives may be
given orally as
PHINOBARBITONE 60mg or
DIAZEPAM 5mg at bed time.
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28. Monitoring of a patient with severe preeclampsia on
MgSo4.
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 Pulse, blood pressure,
respiratory rate, SaO2
 Temperature, lung sounds
 Deep tendon reflexes,
level of consciousness,
assessment of headache,
visual disturbances,
epigastric pain
 Intake and output record
 Foetal wellbeing (ante
and intrapartum)
 Every 10 to 30 minutes
 Every 2 hour
 every 4 hour
 Intake IV crystalloids
(normal saline), colloids
(albumin, blood), total less
than or equal to 125 mL/h
 Continuous EFM

29. SURGICAL MANAGEMENT
Depending on the response to the treatment, the
patients are grouped into the following.
GROUP A: Preeclampsia features completely
subside.
GROUP B: Partial control of the preeclampsia
features but the blood pressure maintains a steady
high level.
GROUP C: Persistently increasing BP to severe
level.
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30. METHODS OF TERMINATION
1. Induction of labor
2. Caesarean section
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31. MANAGEMENT DURING LABOR
1) Blood pressure tends to rise during labor and
convulsions may occur.
2) The patient should be in bed
3) Antihypertensive drugs may be given.
4) Blood pressure should be monitored along
with urinary output.
5) Careful monitoring of Foetus also.
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32. PUERPERIUM:
The patient is to be watched closely
for at least 48 hours, the period
during which convulsions usually
occur.
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33. NURSING MANAGEMENT
1. Continue monitoring of vitals
sings.
2. Rest
3. Position
4. Diet
5. Fluids
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34. PREDICTION AND PREVENTION
Screening tests for prediction and prevention of
preeclampsia are not helpful.
The following steps that helps are:
1. Regular antenatal check-up for early detection.
2. Anti thrombotic agents
3. Calcium supplementations
4. Antioxidants
5. Nutritional supplements34

35. COMPLICATIONS
The complications may be considered are more
likely to occur if the patients are left untreated
from the following points of view;
1. IMMEDIATE
a. Maternal
b. Foetal
2. Remote 35

36. IMMEDIATE
(Maternal)
 Eclampsia
 Accidental haemorrhage
 Oliguria and anuria
 Dimness of vision even blindness
 Preterm labor
 HELLP syndrome
 Shock
 Sepsis 36

37. (Foetal)
 Intra uterine death
 Intra uterine growth restriction
 Asphyxia
 Prematurity
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38. REMOTE
 Residual hypertension
 Recurrent preeclampsia
 Chronic renal disease
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40. the end
special thanks to:
mrs. Snehlata parashar(lecturer)
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