BIOGRAPHIC DATA

 NAME : Shazia
 AGE : 22 years
 MRD NO. : 0942478
 MARITAL STATUS : Married
 EDUCATION OF WIFE : Matriculated
 EDUCATION OF HUSBAND : Graduate
 OCCUPATION OF WIFE : Housewife
 OCCUPATION OF HUSBAND : Sales Manager
 LMP :18/12/2015
 E.D.D :25/09/2016
 INCOME : 30,000/-
 RELIGION :Muslim
 LANGUAGE KNOWN : Hindi
 ADDRESS : A-189/2, Sarojini Nagar, New Delhi.
 DIAGNOSIS : G2P2L1A0 with POG 35 weeks +6days with
pre- eclampsia
 DATE OF ADMISSION :2/9/2016
 DATE OF DISCHARGE :Not yet
 DATE OF CARE STARTED : 5/09/2016
 DATE OF CARE ENDED :7/09/2016
 INFORMANT : Self and husband
INTRODUCTION OF PATIENT

My patient Shazia , a 22 yrs old female with POG 35+2 wks & gestational diabetes
mellitus came to gynae OPD on 22.08.2016 with the complaints of deranged B.S.
profile, excessive thirst (polydypsia), increased volume of urine ( polyuria) , increased
frequency of micturation.

No C/o B.P.V, L.P.V, epigastric pain

C/o blurring vision (occasional),lathargy, restlessness, weakness, oedema (ankles).

Her general condition was poor. She looked not adequately hydrated.

On examination- T- 37.2°C
P- 88/ min
BP- 130/80 mm/Hg
R- 20/min
RBS stat- 136mg/dl

On Fundal examination- Soft

Cephalic
NTNT ʘ ( non-tender, non-tensed)
Liquor adequate
FHS ＋/ R/ 144/min

A series of diagnostic tests were carried out and patient was diagnosed & admitted in
Gynae ward under Unit IV.

Mrs Shazia 22 yrs old female was admitted in HAHC Hospital . Primigravida with POG
35 weeks +6days with severe pre eclampsia with complaints of abdominal pain she had a
history of pregnancy induced hypertension (PIH) and having Tab. Eltroxin and udiliv
since 11/8/16.

On admission BP was 170/110 mmhg conscious oriented ,facial puffiness positive.

SOCIOECONOMIC BACKGROUND
Mrs Shazia W/O Yasir lives in a city in her concrete house. Water and electricity facility
is adequate and her house is well ventilated. Her house has toilet constructed. Her husband
is the one of earning member the family she live in a joint family. No pet animals are there in
her house.

FAMILY HEALTH HISTORY

a) Family composition
S.No Name Relationship Age Sex Educati Occupation Heal
to the on th
patient statu
s
1. Zaroon Husband 25 Male Graduate Sales Goo
yrs Manager d
2. Shazia Self 22 Female 10 th Housewife Poor
yrs

3. Arifa Daughter 2 Female N/A N/A Healt

yrs hy &
immu
nized

b) Family medical history

There is a history of diabetes, hypertension T.B in her family.
IV. HISTORY OF PRESENT ILLNESS
Present Obstetric History
 Mrs. Shazia was admitted to HAH Centenary Hospital on 2 september 2016 having 35
weeks +6 days of gestation with complaints of pain abdomen since morning and
generalized weakness.

1st Trimester
The mother had bouts of nausea and vomiting and food craving for fried foods and aversion
for milk and milk products. She had increased urination, constipation and fatigue.

2nd Trimester
During the second trimester her nausea subsided but she started feeling pain in the lower
abdomen and groin. She observed changes in her skin and leg cramps and occasional
dizziness. She felt difficulty in lying in supine position and experienced comfort after
elevating her head with the help of pillows. Quickening start at 5 th month.

3rd Trimester
During the third trimester she is having increased fatigue, constipation, increased frequency
of mituration and vomiting and increase BP.

labour Notes:

FTNVD with left mediolateral episiotomy.

Under all aseptic precautions parts painted and draped. Patient given a lithotomy positioned
with good uterine contractions and good bearing efforts. Left mediolateral episiotomy given
under local anesthesia .A single live female baby with 2.649 kg on 6/09/16 at 12:42 Pm
delivered by vertex presentation no loop of cord around the neck liquor clear cord clamped
and cut . placenta delivered with complete membranes episiotomy stitched back in layers no
PPH . Vitals are checked

The client was having pain at suture line. Breast is secretory. Nipples are cracked and painful
while feeding. Baby given expressed milk. Baby is tolerating feeds well. The blood pressure
is under monitoring , edema has reduced considerably.
Present Medical History:
Mrs Shazia developed high blood pressure and abdominal pain with vomiting for which she
was admitted to the hospital.

Present Surgical History

No significant present surgical history.

Menstrual history:
She has regular cycles with duration of 4-5 days. She had mild dysmenorrhea.

V.HISTORY OF PAST ILLNESS

PAST OBSTETRICAL HISTORY

Mrs.Manju is a primigravida mother. Admitted with the complains 35wks+6days of
amenorrhea. No history of any abortion or pregnancy.

History of Past Medical Illness

No any significant history

History of Past Surgical Illness

No past surgical history
PERSONAL HISTORY

1. Personal habit : She is non-alcoholic and non-smoker

2. Diet : She is a non-vegetarian
3. Sleep and rest : She usually sleeps 8 hours at night. She has no
difficulty falling asleep
4. Activities of daily living : before the pregnancy she had no difficulty in
ADL
5. Elimination : bowel habits – once a day
6. Bladder habits : no problem in bladder habits. She has normal
Micturition.
7. Hobbies and interest : gossiping with others.
8. Marital status : she is married since 10 months
9. Sexual history : no history of any sexually transmitted disease
10. Drug history : no history of any drug allergy
11. Obstetric history : LMP: 18/12/15
EDD: 25/09/16
12.Psychiatric history : no history of any psychiatric illness
PRE ECLAMPSIA
Definition :- Pre -eclampsia is a multi system disorder of unknown characterized by
development of hypertension to the extent of 140/90 mmhg or more with proteinuria and
edema or both induced by pregnancy after the 20th week in a previously normotensive and
non proteinuria patient. The pre-eclamptic features cases of hydatidiform mole and acute
polydramnios.

Pre-eclampsia (PE) is a disorder of pregnancy characterized by high blood pressure and a

large amount of protein in the urine.The disorder usually occurs in the third trimester of
pregnancy and worsens over time.In severe disease there may be red blood cell breakdown,
a low blood platelet count, impaired liver function, kidney dysfunction, swelling, shortness
of breath due to fluid in the lungs, or visual disturbances

.Pre-eclampsia increases the risk of poor outcomes for both the mother and the baby. If left
untreated, it may result inseizures at which point it is known as eclampsia.
preeclampsia is a condition that pregnant women develop. It is marked by high blood pressurein
women who have previously not experienced high blood pressure before. Preeclamptic women
will have a high level of protein in their urine and often also have swelling in the feet, legs, and
hands. This condition usually appears late inpregnancy, generally after the 20 week mark,
although it can occur earlier.
If undiagnosed, preeclampsia can lead to eclampsia, a serious condition that can put you and
your baby at risk, and in rare cases, cause death. Women with preeclampsia who
have seizures are considered to have eclampsia.

CLASSIFICATION

The classifications of hypertension in pregnancy , the two conditions are often incorporated
 Primary: 70 %
Preeclampsia
Eclampsia (with convulsion)
Secondary 30%
Pre-eclampsia -- Eclampsia superimposed on chronic hypertension (25%)
Pre-eclampsia-- Eclampsia superimposed on chronic nephritis (5%)

DIAGNOSTIC CRITERIA FOR PRE-ECLAMPSIA

Onset of symptoms after 20 weeks’ gestation with remission by 6–12 weeks

postpartum.Mild pre-eclampsia:

 Hypertension (SBP ≥ 140 mmHg or DBP ≥ 90 mmHg), may be superimposed on

chronic hypertension
 Proteinuria (proteinuria ≥ 300 mg/24 hours, or significant increase from baseline)

Severe pre-eclampsia if one or more of the following:

 Sustained SBP ≥ 160 mmHg or DPB ≥ 110 mmHg (measured twice, at least six hours
apart)
 Evidence of other end-organ damage
 Deteriorating renal function including nephrotic range proteinuria ≥ 3 g/24
hours or 3+ on urine dipstick or sudden oliguria, especially with elevated
creatinine
 CNS disturbance (altered vision, headache)
 Pulmonary edema (3% of patients)
 Liver dysfunction
 Epigastric/right upper quadrant pain (stretching of hepatic capsule)
 Thrombocytopenia (15%–30% of patients)
 HELLP (may occur without proteinuria)
 Evidence of fetal compromise (IUGR, oligohydramnios, nonreassuring fetal
testing)

Causes
There is no definitive known cause of preeclampsia, though it is likely related to a number of
factors. Some of these factors include:

 Abnormal placentation (formation and development of the placenta)

 Immunologic factors
 Prior or existing maternal pathology – preeclampsia is seen more at a higher incidence
in individuals with preexisting hypertension, obesity, antiphospholipid antibody
syndrome, and those with history of preeclampsia
 Dietary factors, e.g. calcium supplementation in areas where dietary calcium intake is
low has been shown to reduce the risk of preeclampsia
 Environmental factors, e.g. air pollution
Those with long term high blood pressure have a risk 7 to 8 times higher than those without.
Physiologically, research has linked preeclampsia to the following physiologic changes:
alterations in the interaction between the maternal immune response and the placenta,
placental injury, endothelial cell injury, altered vascular reactivity, oxidative stress,
imbalance among vasoactive substances, decreased intravascular volume, and disseminated
intravascular coagulation.
While the exact cause of preeclampsia remains unclear, there is strong evidence that a major
cause predisposing a susceptible woman to preeclampsia is an abnormally implanted
placenta.This abnormally implanted placenta may result in poor uterine and placental
perfusion, yielding a state of hypoxia and increased oxidative stress and the release of anti-
angiogenic proteins along with inflammatory mediators into the maternal plasma.A major
consequence of this sequence of events is generalized endothelial dysfunction. The abnormal
implantation may stem from the maternal immune system's response to the placenta,
specifically a lack of established immunological tolerance in pregnancy. Endothelial
dysfunction results in hypertension and many of the other symptoms and complications
associated with preclampsia.Those with preeclampsia may have a lower risk of breast cancer.

Risk factors

Known risk factors for preeclampsia include:

 Nulliparity (never given birth)

 Diabetes mellitus
 Kidney disease
 Chronic hypertension
 Prior history of preeclampsia
 Family history of preeclampsia
 Advanced maternal age (>35 years)
 Obesity
 Antiphospholipid antibody syndrome
 Multiple gestation
 Having donated a kidney.
 Having sub-clinical hypothyroidism or thyroid antibodies
 Placental abnormalities such as placental ischemia.

Pathogenesis

Although much research into mechanism of preeclampsia has taken place, its exact
pathogenesis remains uncertain. Preeclampsia is thought to result from an abnormal placenta,
the removal of which ends the disease in most cases. During normal pregnancy, the placenta
vascularizes to allow for the exchange of water, gases, and solutes, including nutrients and
wastes, between maternal and fetal circulations. Abnormal development of the placenta leads
to poor placental perfusion. The placenta of women with preeclampsia is abnormal and
characterized by poor trophoblastic invasion. It is thought that this results in oxidative stress,
hypoxia, and the release of factors that promote endothelial dysfunction, inflammation, and
other possible reactions.
The clinical manifestations of preeclampsia are associated with general endothelial
dysfunction, including vasoconstriction and end-organ ischemia. Implicit in this generalized
endothelial dysfunction may be an imbalance of angiogenic and anti-angiogenic factors.Both
circulating and placental levels of soluble fms-like tyrosine kinase-1 (sFlt-1) are higher in
women with preeclampsia than in women with normal pregnancy.Flt-1 is an anti-angiogenic
protein that antagonizes vascular endothelial growth factor (VEGF) and placental growth
factor (PIGF), both of which are proangiogenic factors. Solubleendoglin has also been
shown to be elevated in women with preeclampsia and has anti-angiogenic properties, much
like sFlt-1 does.
Both sFlt-1 and sEng are upregulated in all pregnant women to some extent, supporting the
idea that hypertensive disease in pregnancy is a normal pregnancy adaptation gone awry. As
natural killer cells are intimately involved in placentation and placentation involves a degree
of maternal immune tolerance for a foreign placenta, it is not surprising that the maternal
immune system might respond more negatively to the arrival of some placentae under certain
circumstances, such as a placenta which is more invasive than normal. Initial maternal
rejection of the placental cytotrophoblasts may be the cause of the inadequately
remodeled spiral arteries in those cases of pre-eclampsia associated with shallow
implantation, leading to downstream hypoxia and the appearance of maternal symptoms in
response to upregulated sFlt-1 and sEng.
Oxidative stress may also play an important part in the pathogenesis of pre-eclampsia. The
main source of reactive oxygen species (ROS) is the enzyme xanthine oxidase (XO) and this
enzyme mainly occurs in the liver. One hypothesis is that the increased purine catabolism
from placental hypoxia results in increased ROS production in the maternal liver and release
into the maternal circulation that causes endothelial cell damage.
Abnormalities in the maternal immune system and insufficiency of gestational immune
tolerance seem to play major roles in pre-eclampsia. One of the main differences found in
pre-eclampsia is a shift towardTh1 responses and the production of IFN-γ. The origin of
IFN-γ is not clearly identified and could be the natural killer cells of the uterus, the placental
dendritic cells modulating responses of T helper cells, alterations in synthesis of or response
to regulatory molecules, or changes in the function of regulatory T cells in
pregnancy. Aberrant immune responses promoting pre-eclampsia may also be due to an
altered fetal allorecognition or to inflammatory triggers.It has been documented that fetal
cells such as fetal erythroblasts as well as cell-free fetal DNA are increased in the maternal
circulation in women who develop pre-eclampsia. These findings have given rise to the
hypothesis that pre-eclampsia is a disease process by which a placental lesion such as
hypoxia allows increased fetal material into maternal circulation, that in turn leads to
an immune response and endothelial damage, and that ultimately results in pre-eclampsia
and eclampsia.

One hypothesis for vulnerability to preeclampsia is the maternal-fetal conflict between the
maternal organism and fetus.After the first trimester trophoblasts enter the spiral arteries of
the mother to alter the spiral arteries and thereby gain more access to maternal
nutrients.Occasionally there is impaired trophoblast invasion that results in inadequate
alterations to the uterine spiral arteries.It is hypothesized that the developing embryo releases
biochemical signals that result in the woman developing hypertension and pre-eclampsia so
that the fetus can benefit from a greater amount of maternal circulation of nutrients due to
increased blood flow to the impaired placenta.This results in a conflict between maternal and
fetal fitness and survival because the fetus is invested in only its survival and fitness while
the mother is invested in this and subsequent pregnancies.

Another evolutionary hypothesis for vulnerability to pre-eclampsia is the idea of ensuring

pair-bonding between the mother and father and paternal investment in the
fetus. Researchers posit that preeclampsia is an adaptation for the mother to terminate
investment in a fetus that might have an unavailable paternal donor, as determined by
repeated semen exposure of the paternal donor to the mother.Various studies have shown
that women who frequently had exposure to partners’ semen before conception had a
reduced risk of pre-eclampsia. Also, subsequent pregnancies by the same paternal donor had
a reduced risk of pre-eclampsia while subsequent pregnancies by a different paternal donor
had a higher risk of developing pre-eclampsia.
Diagnosis

Preeclampsia laboratory values

Diagnostics

LDH=Lactate dehydrogenase,
Uric acid=Uric acid,
AST=Aspartate aminotransferase,
ALT=Alanine aminotransferase,
Plt=Platelets,
Cr=Creatinine.

Reference LDH: 105–333 IU/L

range Uric Acid: 2.4–6.0 mg/dL
AST: 5–40 U/L
ALT: 7–56 U/L
Plt: 140–450 x 109/L
Cr: 0.6–1.2 mg/dL

Diagnostic criteria
Pre-eclampsia is diagnosed when a pregnant woman develops:

 Blood pressure ≥ 140 mm Hg systolic or ≥ 90 mm Hg diastolic on two separate

readings taken at least four to six hours apart after 20 weeks gestation in an individual
with previously normal blood pressure.
 In a woman with essential hypertension beginning before 20 weeks gestational age,
the diagnostic criteria are: an increase in systolic blood pressure (SBP) of ≥30mmHg or
an increase in diastolic blood pressure (DBP) of ≥15mmHg.
 Proteinuria ≥ 0.3 grams (300 mg) or more of protein in a 24-hour urine sample or a
SPOT urinary protein to creatinine ratio ≥ 0.3 or a urine dipstick reading of 1+ or greater
(dipstick reading should only be used if other quantitative methods are not available).
Suspicion for pre-eclampsia should be maintained in any pregnancy complicated by elevated
blood pressure, even in the absence of proteinuria. Ten percent of individuals with other
signs and symptoms of pre-eclampsia and 20% of individuals diagnosed with eclampsia
show no evidence of proteinuria.In the absence of proteinuria, the presence of new-onset.

Hypertension (elevated blood pressure) and the new onset of one or more of the following is
suggestive of the diagnosis of pre-eclampsia

 Evidence of kidney dysfunction (oliguria, elevated creatinine levels)

 Impaired liver function (noted by liver function tests)
 Thrombocytopenia (platelet count <100,000/microliter)
 Pulmonary edema
 Ankle edema (pitting type)
 Cerebral or visual disturbances
Pre-eclampsia is a progressive disorder and these signs of organ dysfunction are indicative of
severe pre-eclampsia. A systolic blood pressure ≥160 or diastolic blood pressure ≥110 and/or
proteinuria >5g in a 24-hour period is also indicative of severe pre-eclampsia. Clinically,
individuals with severe pre-eclampsia may also present epigastric/right upper quadrant
abdominal pain, headaches, and vomiting.Severe pre-eclampsia is a significant risk factor for
intrauterine fetal death.
A rise in baseline blood pressure (BP) of 30 mmHg systolic or 15 mmHg diastolic, while not
meeting the absolute criteria of 140/90, is important to note but is not considered diagnostic
Complications

Complications of pre-eclampsia can affect both the mother and the fetus. Acutely, pre-
eclampsia can be complicated by eclampsia, the development of HELLP syndrome,
hemorrhagic or ischemic stroke, liver damage and dysfunction, acute kidney injury,
and acute respiratory distress syndrome (ARDS).
Pre-eclampsia is also associated with increased frequency of Caesarian section, preterm
delivery, and placental abruption. Furthermore, an elevation in blood pressure can occur in
some individuals in the first week postpartum attributable to volume expansion and fluid
mobilization. Fetal complications include fetal growth restriction and potential fetal or
perinatal death.
Long-term, an individual with preeclampsia is at increased risk for recurrence of pre-
eclampsia in subsequent pregnancies.

Eclampsia
Eclampsia is the development of new convulsions in a pre-eclamptic patient that may not be
attributed to other cause. Eclampsia is a serious complication of pre-eclampsia and results in
high rates of perinatal and maternal morbidity and mortality. Warning symptoms for
eclampsia in an individual with current pre-eclampsia may include headaches, visual
disturbances, and right upper quadrant or epigastric abdominal pain, with headache being the
most consistent symptom.Magnesium sulfate is used to prevent convulsions in cases of
severe pre-eclampsia.

HELLP Syndrome

HELLP syndrome is defined as hemolysis (microangiopathic), elevated liver enzymes (liver

dysfunction), and low platelets (thrombocytopenia). This condition may occur in 10–20% of
patients with severe pre-eclampsia and eclampsia and is associated with increased maternal
and fetal morbidity and mortality. In 50% of instances, HELLP syndrome develops preterm,
while 20% of cases develop in late gestation and 30% during the post-partum period.

Long term

There is also an increased risk for cardiovascular complications, including hypertension and
ischemic heart disease, and kidney disease.Other risks include stroke and venous
thromboembolism. It seems pre-eclampsia does not increase the risk of cancer.

INCIDENCE
The incidence in primigravidae is about 10% and multigravidae 5%

RISK FACTORS FOR PRE-ECLAMPSIA

 Maternal obstetric factors: nulliparity, history of pre-eclampsia, multiple gestation

pregnancy, gestational hypertension, molar pregnancy

 Maternal comorbid conditions: chronic hypertension, pregestational

vascular/endothelial/renal disease, pregestational diabetes

 Maternal genetic factors: antiphospholipid antibody, Factor V Leiden mutation (protein

C resistance), first-degree relative with a pre-eclamptic pregnancy

 Maternal lifestyle factors: obesity, smoking

 Other maternal factors: African-American race, age >40 years

ETIOLOGY OF PRE – ECLAMPSIA

1) There is an imbalance of different components of prostaglandins- relative or

absolute deficiency of vasodilators prostaglandin (PGI2) synthesized in vascular
endothelium and increased synthesis of thromboxane, a potent vasoconstrictor
in platelets.
2) There is increased vascular sensitivity to the pressor agent angiotensin-II.
3) Nitric oxide (NO) :- it is synthesized in the vascular endothelium and
syscytiotrophoblast from L- arginine .it significantly relaxes vascular smooth
muscle, inhibits platelet aggregation and prevents intervillous thrombosis.
Deficiency of nitric oxide contributes to the development of hypertension.
4) Endothelin- I is synthesized by endothelial cells and it is a potent
vasoconstrictor
5) It has been suggested that abnormality is due to a single recessive immune
response gene of homozygous in nature . lupus anticoagulant (LA) and
anticardiolipin antibodies (ACAs) also have been associated with pre-
eclampsia
6) Angiotensinase activity is depressed, more so following proteinuria with
elimination of alpha globulin
CLINICAL MANIFESTATIONS
These are usually associated with acute onset of the syndrome

1) Head ache
2) Disturbed sleep
3) Diminished urinary output
4) Epigastric pain
5) Eye symptoms

BOOK PICTURE PATIENT PICTURE

Signs & symptoms
 Abnormal weight gain . Present
 Raise blood pressure Present
 Oedema in legs Present
 Varicosities in legs Present
 Varicosities in vulva. Absent
 Protenuria Present
 Headache Present
 Disturb sleep Present
 Puffiness of face Present
 seizures Absent

ABDOMINAL EXAMINATION
BOOK PICTURE PATIENT PICTURE

ABDOMINAL EXAMINATION

Inspection:

 may reveal evidences of chronic placental Absent

insufficiency scanty liquor or growth retardation
of the fetus
 Palpation:. 35wks 6 days
 Term abdomen. 75cm
 Girth of the abdomen round the umbilicus is less
than the gestation period

INVESTIGATIONS
 Sonography
 Radiography
 Blood investigations
 Fundoscopy

INVESTIGATIONS DONE IN PATIENT

S TEST NAME RESULT NORMAL RANGE

N
O
 HAEMATOLOGY
1 Haemoglobin 11.7gm/dl 13-18gm/dl
2 Total leukocyte count 11000/cumm 4000-11000
3 Neutrophils 69% 45-70
4 Lymphocytes 30% 20-45
5 Eosinophils 01% Upto 6
6 Monocytes 02% 2-10
7 RBC 4.4mill/cumm 4.5-5.4
8 Haematocrit 28.9% 40-54
9 Platelet count 2.66lacs/cumm 1.5-4

LFT

1 S. Bil(/total) 0.7mg/dl 0.2-1.0

2 S. Bil (Direct) 0.3mg/dl 0.0-0.2
3 S. Bil(Indirect) 0.4mg/dl 0.2-0.8
4 SGOT 20IU/L 5-40
5 SGPT 26IU/L 5-40
6 S. Alk Phosphatase 110IU/L 25-90
7 AST 32(IU/L) 11-30(IU/L)
8 ALT 34(IU/L) 6-32(IU/L)

KFT

1 Blood urea 48mg/dl 15-45

2 S. Creatinine 1.8mg/dl 0.5-1.4
3 S. Protein 7mg/dl 6-8
4 S. Albumin 2.9mg/dl 3.7-5
5 S. Globulin 3.5mg/dl 1.5-3.0
6 S. Na 148meq/L 136-145
7 S. K 4.1meq/L 3.5-5.4
8 S. C 114meq/L 98-108
9 TSH 1.2Miu/l 0.3-3.04 mIU/L
VDRL negative negative
HIV negative negative
URINE:
 color: yellowish light yellow
 ph 5.6 4.5-7.2
 reaction acidic acidic
 pus cells 6-7 pus cells nil
 RBCs 2-3 0-3
 epithelial cells trace 0-trace
 urine protein 75-76 >80
trace negative
 urine ketone
 1) SONOGRAPHY:
MANAGEMENT:
Objectives are

1) To correct /stabilize the altered physiology

2) Prevention of complications
3) Prevention of eclampsia
4) Delivery of a healthy baby,in optimal time with minimum maternal morbidity

GENERAL MANAGEMENT:
 Patient is placed in a bed with side rails.( rest increases the renal blood flow diuresis )
 Detailed history is taken
 BP monitoring hourly
 Quick general, abdominal and vaginal examinations are done
 Catheterization and urine analysis
 Checking vitals half hourly
 Pulse oxymetry (<92%- O 2 administration)
 Fetal Heart Rate (FHR) monitoring
 Maintaining fluid balance
 NBM / NPO
 Continue to care for the woman in a quiet, single room
 MANAGEMENT

So long as the etiology of pre-eclampsia remains obscure, the treatment is mostly

empirical and symptomatic .while measures are directed to relieve oedema and
hypertension. There is no specific therapy to proteinuria which automatically subsides
with the control of hypertension

Scheme of management of pre-eclampsia

Pre-Eclampsia

Rest BP check (4 Platelet count, Uric acid Fetal well-being

times/day ) assessment
Creatinine , Wt. record

Intake/output
DFMC
24 hrs for protein
USG Doppler

Cardiotocography

Antihypertensive, Sedative

Complete control BP persistently

Aggravation of the
high
manifestations

preterm term Try to continue

the pregnancy till
37 completed
weeks
Discharge To stay in
hospital till EDD
To attend the
antenatal clinic
 Urgent delivery may need
prophylactic
termination termination
anticonvulsant therapy

Induction
PGE2,ARM.oxytocin C .S.

NURSING MANAGEMENT
Nursing Management:

 Monitor BP hourly
 Check vitals hourly
 Maintain fluid intake and output chart
 Monitor fetal well being
 Place patient in left lateral position
 Loosen clothes of patient
 Prevent aspiration by suctioning
 Do not leave patient alone

COMPLICATIONS OF PRE- ECLAMPSIA

Maternal:
1) During pregnancy: there is incidence of -

a) Elampsia.(2%)
b) Accidental haemorrhage .
c) Oliguria and anuria
d) Dimness of vision
e) HELLP syndrome
f) Preterm labour either spontaneous labour or induced.
g) Accidental hemorrhage.

2) During labour
 a) Elampsia.
b) Increased operative delivery hypertension
c) Retained placenta.
d) PPH due to coagulation failure
e) Shock.

3 ) Pueperium:

a) Elampsia.
b) Shock
c) Sepsis
d) Sub involution.
e) Increased puerperal morbidity.

Fetal:
a) Intrauterine death
b) IUGR
c) Asphyxia
d) Prematurity

Others:

a) Increased operative delivery.

b) Accidental hemorrhage.

PROGNOSIS

The prognosis of pre eclampia depends of period of gestation, severity of disease and response to treatment

IMMEDIATE: - if the pre eclampsia is detected early with prompt and effective treatment the pre
eclamptic features subside completely and the prognosis is not unfavorable both mother and the baby

Maternal mortality: increased with mainly related to eclampia ,accidental haemorrhage ,acute renal failure
,pulmonary oedema ,DIC and HELLP syndrome

Prenatal mortality: - stillborn is about 20% to 50%

REMOTE :- there is no evidence to suggest that severity of pre-eclampsia or its duration has got an effect on
the development of residual hypertension (50%) or recurrent pre eclampsia

TREATMENT MODALITIES
BOOK PICTURE PATIENT PICTURE
 1) Rest- admission in hospital Rest- admission in hospital
2) Diet –diet should contain adequate Present
amount of protein ,fluids restricted
3) Sedative – to cut down emotional factor Inj tramadol 100mg stat given
orally phenobarbitone 60mg or diazepam
5mg at bed time
4) Diuretics – commonly used frusemide
40 mg orally after breakfast for 5 days in
a week in acute condition IV route is
preferred Inj Lobet 100mg stat given at 2.30 pm on
5) Antihypertensive –commonly used 25/08/16 then 100 mg tds
a) Methyl dopa -250-500mg tid or qid
b) Labetalol – 250 mg tid or qid Tab Amlodipine 5mg bd
c) Nifedipine 10-25 mg bid
d) Hydralazine – 10-25mg bid
SPECIFIC TREATMENT
SPECIFIC TREATMENT Magnesium sulphate
Magnesium sulphate Loading dose -4mg IV over 3-5 min
Loading dose -4mg IV over 3-5 min followed followed by 10mg deep IM given at
by 10mg deep IM 2.30pm
Maintenance dose – 5 gm IM 4 hourly in Maintenance dose – 5 gm IM 4 hourly in
alternate buttock alternate buttock given at 7 pm

 Bloob 1point PCV

 2 point FFP

BP MONITORING HOURLY RECORDED DURING PATIENT CARE

NURSING CARE PLAN

1. Acute pain due to episiotomy and cracked nipples as evidenced by facial expressions

Interventions

a. Assess the intensity of pain

b. Provide comfortable position to the client
c. Provide hot application over perineal region to reduce pain
d. Administer prescribed medications
e. Provide psychological support.
f. Advice mother for breast care and exposing of breast to air
g. Advice to give expressed breast milk till nipples are cracked

2. Risk for infection due to episiotomy and pre-eclampsia as evidence by disease condition

Interventions:
a. Assess for infection.
 b. Assess vital signs.
c. Check temperature accurately because this may indicate infection & immediately inform the
physician.
d. Check orthostatic hypotension, due to release of excess of fluid and blood loss.
e. Provide perineal care and catheter care as in situ.

3. Impaired mobility related to pre- eclampsia evidenced by reduced activity level

Interventions
a. Assess the mobility of the client.
b. Assist client in activities of daily living
c. Encourage patient’s relatives in participation of patient care
d. Encourage early ambulation

4. Knowledge deficit related to the disease condition and breastfeeding

Interventions
a. Assess the knowledge level of the patient.
b. Advice client to have nutritious diet like green vegetables, milk, etc and ensure she is getting
enough extra calories and fluids.
c. Advice mother to breastfeed the baby after proper hand washing and breast care.
d. Advice mother to avoid accidental pregnancy by taking family planning measures.
e. Teach mother kegel exercises.
f. Advice client to maintain personal hygiene.

5. Anxiety related to the disease condition as evidence by patient verbal report

Interventions
a. Assess the anxiety level of the client
b. Clear the doubts of the client.
c. Provide psychological support to the client
d. Encourage mother to vent out her feelings.
e. To have a friendly and empathetic approach with the client

CONCLUSION

Hypertension is one of the common complications met with in pregnancy and contributes
significantly to maternal and perinatal morbidity and mortality hypertension is a sign of an
underlying pathology and effective management play a significant role in the outcome of
pregnancy. The identification of this clinical entity and effective management play a
significant role in the outcome of pregnancy. Both mother and the baby.

RESEARCH ARTICLE
Tessemma A .G.,Tekeste A.,Ayale A.T.,The prevalence and factors associated with preeclampsia among
pregnant women, BMC Pregnancy Childbirth. 2015, 15,( 73). DOI: 10.1186/s12884-015-0502-7
A study to assess the prevalence and factors associated with preeclampsia among pregnant
women attending antenatal care in Dessie referral hospital, Northeast Ethiopia. A hospital-
based cross-sectional study was conducted between August and September 2013. A total of
490 pregnant women were enrolled in the study. Pretested and structured questionnaire via
face-to-face interview technique was used for data collection. Results were found that 8.4%.
Women having family history of hypertension, chronic hypertension age ≥35 years, family
history of diabetes mellitus and being unmarried were found to be associated with
preeclampsia.

BIBLIOGRAPHY

1. Dutta .D.C. Textbook of Obstetrics. Sixth edition. 2004. Pg no221-230

2. Marie Elizabeth ,Midwifery for nurses ,2nd edition .2013.pg no. 206-215
3. Diagnosis and management of pre-eclampsia: an update Judi A Turner Published
online 2010 Sep 30. doi: 10.2147/IJWH.S8550 PMCID: PMC2990902
 CASE
PRESENTATION
On
PRIMIGRAVIDA WITH POG 35
WEEKS +6DAYS WITH
SEVERE
PRE – ECLAMPSIA

Submitted TO SUBMITTED BY
MS. ASHIN ms sneha sehrawat
tutor msc nursing 1 yr
Student