Prepared by:

Rashmi Regmi
B. Sc Nursing
Manmohan Memorial Institute of Health Sciences

OBJECTIVES
The main objective of this case study is enabling students to develop knowledge regarding
the normal reproductive process, and skill and practice in providing nursing care, provide
advices, health teaching to patient and family for management of the disease.
During this process I got opportunities to learn about disease condition, its complications and
other potential gynecological and obstetric abnormalities and complication that arise due to
the disease.
General Objectives:
To obtain detail obstetric and gynecological history of patient
To perform physical assessment of a woman with gynecological and obstetric problem
To provide advices, health teaching to patient and family for management of the disease,
medications and complications
To identify minor and major discomfort and advice the woman relieving measures
To apply nursing process to care the client with obstetric and gynecological problems
as per her need
To identify the different modern technologies to treat the disease for overcoming the
problem regarding reproductive health (RH) and educate them about RH.

1
2
PATIENT’s HISTORY
1. Demographic Data
Name of Patient: Bimala Gurung
Age: 29 years Sex: Female
Caste: Gurung
Religion: Hindu
Marital status: Married No. of Children: 1
Address:
permanent: Lumjung
Temporary: Harisiddhi, Lalitpur
Name of Guardian: Som Gurung (husband)
Date Of Admission: 2070/1/19 Inpatient number: 19381
Date of Discharge:
Medical Diagnosis:
Provisional Diagnosis: G3P2L1 at 26+4 WOG with PIH
Final Diagnosis: Pre-eclamsia with HELLP syndrome
Economic Status: Medium Occupation: Business

2. Chief Presenting Complaints

1. Epigastric pain X 1-2 hour
2. Vomiting (2 episodes)
3. Headache absent
4. Blurring of vision absent
5. Perceiving good fetal movement

3. History Of Present Illness

Past history of Intra Uterine Fetal Death (IUFD) 3 years back at Prasuti Griha, Thapathali
due to PIH
Sudden onset of severe Epigastric pain accompanied by vomiting, no symptoms perceived
earlier

3
 4. Elaboration Of Patient Chief Complaints In Detail
Amenorrhea X 6 months
Patient was pregnant with 26+4 weeks of Gestation
Patient complained severe heartburn which occurred suddenly before 1-2 hours accompanied
by two episodes of vomiting
No history of blurring of vision and headache
Patient was perceiving good Fetal movement
S.N Problem Onset Frequency Severity Alleviating Aggravating
factors factors
1. Epigastric pain Sudden (1- continuous Severe Not -
2 hours relieved by
before) food
2. Vomiting sudden 2 times Mild - -

5. Obstetric History
Married for: 10 years Age of marriage: 16 years
Gravida: G3
Parity: P3
Living: 1

a. Abortions (Spontaneous, Induced, Duration Of Pregnancy):

Once
Induced second Trimester abortion (medical termination of pregnancy) on 2070/1/21 at Kist
Medical Teaching Hospital due to PIH complicated by Pre-eclampsia and HELLP syndrome
at 26+6 WOG

b. Type Of Previous Deliveries (Normal/ Instrumental/ LSCS)

Normal vaginal delivery of 1st child (daughter) on 2061/2/26 at Prasuti Griha
Thapathali
Induced Spontaneous Vaginal Delivery of Second child (son) IUFD 3 years back
(2066/4/27) at Thapathali due to IUFD secondary to PIH at 37 WOG

4
 Third child (daughter) medical termination of pregnancy on 2070/1/21 at Kist
Medical Teaching Hospital by spontaneous vaginal delivery as indicated by
deteriorating maternal fetal condition due to PIH complicated by Pre-eclampsia and
HELLP syndrome at 26+6 WOG

c. Significant Antenatal Problem/ 3rd Stage Puerperal Complications In Previous

Deliveries:
No any significant problem during pregnancy and delivery of first child
Antenatal period complicated by PIH on other two pregnancies

d. Year And Place Of Previous Deliveries, Sex Of Baby, Living Or Not, If Neonatal
Death (Age And Cause Of Death, Congenital Malformation)
2061/2/26 at Prasuti Griha, Thapathali, Female child, living
2066/4/27 at Prasuti Griha, Thapathali, Male child, dead (IUFD)
2070/1/21 at Medical Teaching Hospital, Female child, dead (premature baby)

e. Year Of Marriage, Gravida, Para, Abortion, Living Issues

No. Year ANC attendance/ Period of Type of Complications in
pregnancy gestation delivery/ puerperium
complication abortions
1 2061 4 visits/ no any 37+WOG SVD No any
significant significant
complications complications
2 2066 4 visits/ IUFD due to 37WOG Instrumental No any
PIH delivery (Forcep significant
delivery) complications
3 2070 2 visits / MTP due to 26+WOG SVD No any
PIH significant
complications

Age of last child birth/ year of last pregnancy: 3 years, 2066/4/27

5
 6. Menstrual History
Age of menarche: 14 years
Duration of flow: 6-7 days
Length of cycle (from 1st day of one cycle to 1st day of next cycle): 30 days
Regular/ irregular (range of shortest – longest cycle) : 28- 30 days
Amount of flow, passage of clots, no. of soaked pads/ day : normal, passage of some
clots, 2pads/day
Dysmenorrhea (severity, duration): No history of dysmenorrhea
Intermenstrual bleeding: Absent
Post coital bleeding: Absent
Last menstrual period (LMP): 2069/7/15

7. Contraceptive History
Type of contraception, duration, cause of discontinuation: Oral Contraceptive Pills, 3 years,
for conception

8. Past History: Pregnancy Induced Hypertension 3 years back

9. Medical History
Immunization: Done
Allergies (food, drug, environment): Absent
Previous hospitalizations ( if yes reasons): 22 days on 2nd pregnancy due PIH on third
trimester
Injuries/ accidents: Not any

6
 10. Chronic Illness
SN Diseases In patient In family
Yes No Yes No
1 Hypertension Yes No
2 Cardiovascular diseases No No
3 Diabetes No No
4 Tuberculosis No No
5 Asthma No No
6 Cancer No No
7 Malaria No No
8 Filarial No No
9 Others No No

11. Surgical History

Surgeries/ operations (minor/ major), year, type, indication: Not Any

12. Treatment History

Any treatment done for present illness or any medication which patient is taking
regularly? Not Any
Traditional healer prescription: Not Any
Medical practitioner’s prescription: treated for gestational hypertension on last
pregnancy 3 years back but as symptom subsided after delivery and blood pressure
returned to normal no any treatment continued at home
Self prescription: Not Any

13. Personal History

Smoking: Absent
Alcohol intake: Absent
Rest and sleep: adequate rest and sleep
Recreation habit: watching television
Elimination: normal bowel and bladder habit
Hygiene: hygienic

7
 Dietary habits: balanced diet supplemented by extra sources of vitamins, minerals and
proteins like meat, milk, fruits and vegetables

14. Miscellaneous
a. For Antenatal Cases:
Duration of cessation of menses: approximately 4 months
LMP: 2069/7/15
EDD: 2070/4/22
Gestation in weeks (by date): 26+4 WOG
Fetal movements: date of perception and whether normal or not: date of perception
not known, around 16 WOG, perceiving normal fetal movements
ANC attendance (place, regularity and starting): Regular, Health post Harisiddhi
starting 1st trimester
TT immunization: Once
Taking iron/calcium or any other drugs: under regular Iron and Calcium
supplementation

b. Any Problems In Each Trimester (e.g. severe vomiting, pain abdomen, fever,
urinary problems, vaginal bleeding or abnormal discharge, severe headache, swelling,
any conditions requiring hospital admissions during this pregnancy)
Second Trimester presented with Severe Epigastric Pain and vomiting, and generalized
edema

15. Family History

Tuberculosis, diabetes mellitus, hypertension, female genital tract malignancies: Absent
In antenatal cases: multiple pregnancies, congenital malignancies (esp. Down ’s syndrome):
Absent

8
 16. Family tree

87 years 64yrs
92yrs (Unknown) 82yrs alive (fall injury)

68 yrs 66yrs 63yrs 58yrs 56yrs 52yrs 50yrs 60yrs 57yrs 54yrs 50yrs 48

34yrs 33yrs 29yrs 27yrs 24yrs

Healthy Healthy PIH Healthy Healthy

Key:
Alive healthy male

Alive healthy female

P Patient

Dead male

Dead female

9
PHYSICAL EXAMINATION FINDINGS
Examination Findings
A. General examination
INSPECTION
1. Observe client’s ability to respond to The client is confused and disoriented,
verbal commands inappropriate responses
2. Observe client’s LOC (level of Lowered LOC
consciousness)
3. Observe facial expression and mood Eyes are closed
Client was frowning
Client was unable to answer questions
4. Observe general appearance; posture, Patient needed support to stand and
gait, movement walk
Decreased movement
Even gait
5. General state of health Weak appearance
6. Nutritional status Well nourished
7. Behavior Inappropriate reaction to situation,
disoriented
8. Responses Not responding well
9. Cleanliness Hygiene maintained but not well
groomed
10. Speech Clear, adequate pace
VITALS Normal temperature
Temperature: 97º f Normal pulse rate
Pulse Rate: 82/min Hypertension (high blood pressure)
Blood Pressure: 140/110 and 150/110 in right
and left hand Normal respiratory rate
Respiratory Rate: 20/min
Height : 156cm
Weight: 56kg
B. Skin Assessment
INSPECTION AND PALPATION
1. Inspect skin from head to toe Slightly pale and yellowish skin color
Erythema present on skin of hip
2. Palpate skin for moisture and texture Slightly moist, no excessive moisture
or dryness
Firm, smooth, soft, elastic skin
3. Palpate skin for temperature Warmth
4. Palpate skin for hydration and turgor Pinched skin promptly returns to it’s

10
 previous state when released
No sign of dehydration
5. Press suspected edematous areas with Presence of pitting edema in ankle
the edge of the finger for 10 seconds
and observe for the depression
6. Inspect skin for lesions, cut and Skin is intact
surgical incision No variation in pigmentation and
texture
Freckles, moles and warts are normal
C. Nail
1. Inspect and palpate the fingernails Pink colour
and toenails
note color, shape and any lesion
2. Check capillary refill by pressing the Normal return of color <3 sec
nail edge to blanch and then release No discoloration, ridges, pitting,
pressure quickly, noting the return of thickening or separation from the
color edge
D. Hair and Scalp
1. Inspect hair for color, texture, growth, Color Black, fine texture, wavy hair
distribution
2. Inspect scales, lumps, nevi or other No lumps, lesions, scales and nevi
lesions
E. Head
1. Observe the skull for size, shape and Skull symmetrical, round and erect on
symmetry midline
2. Palpate skull for deformities, No depression, lumps, tenderness and
depression, lump or tenderness any deformities
F. Face
1. Inspect for abnormal facial Normal facial expression
expression, gestures and involuntary No any involuntary movements
movements, swelling and masses Swelled face
2. Palpate face for edema, tenderness Peri- orbital edema present around
and depression eyes
G. Sinuses
1. Palpate sinuses for tenderness No tenderness in frontal, maxillary
and ethmoid sinuses
H. Eye
1. Inspect both eyes for position and No deviation from normal condition
alignment
2. Eye brows inspected for distribution Uniform distribution and no scaliness
and any scaliness

11
3. Eyelashes inspected for infection and No infection or sty
sty
4. Conjunctiva inspected for redness, No redness, paleness, discharge,
paleness, discharge, foreign body, foreign body, dryness or tearing
dryness or tearing
5. Inspect sclera for color change, injury Slightly yellowish sclera
and dilated blood vessels
6. Cornea for color, abrasion and white Transparent , no abrasion or white
spots spots
7. Pupil for size, shape and symmetry Pupil round, symmetrical and uniform
comparison
8. Co-ordination of eye movement Good eye movement and co-
ordination
9. Papillary reaction to light Normal papillary
10. Lens inspected for opacity Lens transparent
11. Convergence test Normal (positive)
I. Ear
1. Location and size The top of pinna cross the occiput
line
Equal size bilaterally
2. Pinna for any lump or lesion No lump or lesion
3. The external auditory canal for ear No discharge, redness, masses or
discharge, mass foreign body and foreign body, small amount of
crumen crumen present
4. Palpate for tenderness No pain while moving pinna or
palpating mastoid process
5. Weber test Sound heard equally on both ear
6. Rinne Test Air conduction of sound is greater
than bone conduction
J. Nose
1. Location of nose Centrally located
2. Nostrils for their size and Uniform in size and symmetrical
symmetry
3. Nasal septum for polyp No polyp
4. Nasal canal Pink mucosa, no discharge or foreign
body
K. Mouth And Throat
1. Lip for color, moisture, cracks or Lip pink in color, moist, no
ulcer discoloration, cracks or ulcer

12
 2. The mucous membrane of the mouth Pink, moist, mucous membrane, no
for color, ulcer, nodules and amount ulcer, nodules, adequate saliva
of saliva

3. Gum for inflammation, swelling, Pink gum, no inflammation, swelling,

redness and bleeding redness and bleeding present
4. Teeth for color, cavities and missing White color, No missing teeth,
teeth cavities present
5. Tongue for symmetry, color and Pink, moist, symmetrical, papillae
papillae normal
6. Pharynx and tonsils observed No inflammation and swelling and
difficulty swelling
L. Neck
INSPECTION
a. Ask patient to sit straight No tilting of neck
b. Observe for masses, congenital No masses, congenital goiters, scars
goiters, scars, distended jugular vein or distended jugular vein
c. Thyroid gland No enlargement of thyroid gland
d. Ability to move neck No neck stiffness, smooth range of
motion and no tenderness
Palpation
1. Thyroid gland palpated to exclude No goiter, , masses and enlargement
goiter, masses and enlargement
2. The back of neck along the spine and No abnormal alignment of spine
back
M. Lymph nodes
1. Inspection and palpation of lymph No tenderness or enlargement
nodes for enlargement and tenderness
N. Chest and lungs
INSPECTION
1. Shape, size and symmetry Lateral diameter wider than antero
posterior diameter
Symmetrical, sternum located at
midline
2. Bilateral expansion of lungs Equal expansion of both lungs
PALPATION
1. Chest for expansion, lumps, Equal Bilateral expansion of lungs,
tenderness and depression along ribs no lumps, tenderness or depression
noted

13
PECUSSION
1. The front and back of chest from apex Resonant sound heard over the entire
to base chest, anteriorly and posteriorly
AUSCULTATION
1. The front and back of the chest to Vesicular sound heard all over the
evaluate breath sound using lungs
stethoscope
2. Compare duration of inspiration and Inspiration longer than expiration
expiation
3. Check for abnormal breathe sound No rales, rhonchi or wheezes present
like rales, fine crackles, rhonchi and Breathing sound clear
wheezing
O. Heart
INSPECTION
1. Enlargement of neck veins No enlargement of jugular veins
AUSCULTATION
1. Aortic area (2nd intercostals space just Clear regular heart rate 84/min
right of the sternum) No abnormal S3 heart sound present
2. Pulmonic area (2nd intercostals space
just left of the sternum)
3. Tricuspid area (5th intercostals space
just left of the sternum)
4. Mitral area (5th intercostals space at
midclavicular line)
5. Note the clarity and regularity of heart Regular, Normal heart sound S1 and
sound S2 present
No abnormal heat sound like gallop
and murmur present
P. Female Breast
INSPECTION
1. Size and shape of the breast, observe Breasts and nipples are uniform in
nipple condition shape and size, nipples are pointed in
same direction
Left breast slightly larger than right
breast
2. Look for swelling, dimpling or No swelling, dimpling or retraction of
retraction of breast breast
3. Nipples for cracks and discharge No cracks and discharge
PALPATION
1. Both breast were palpated in circular Soft, non tender, no masses, lumps
motion for masses, swelling and swelling were detected

14
 Q. Abdomen
INSPECTION
1. For shape, size, dilated veins, straie, Round shape, no distention, lesions,
previous incisional scars, lesions previous incisional scars or dilated
abdominal veins present
Linea nigra and striae gravidarum
present
AUSCULTATION
1. For bowel sound (increased bowel Bowel sound present in all areas in
sound or decreased bowel sound by every 20 seconds
placing stethoscope for 5 minutes) Gurgling sound present
2. Note type of sound
PECUSSION
1. Keep patient in supine position and Tympanic sounds heard over gas-
percuss abdomen in all four quadrants filled viscera and dull sound over
fluid filled viscera
Dull sounds were more prominent
PALPATION
1. Keep patient in supine position and No abdominal masses and tenderness
ask patient to relax abdomen, palpate
abdomen in all 9 parts
Feel for any masses and tenderness
2. Palpate liver, place left hand on 11th Liver not palpable, no tenderness or
and 12th rib and apply firm pressure to enlargement
push liver forward towards the right
hand
Note enlargement and tenderness
3. Spleen: keep patient in right lateral Spleen not palpable, no enlargement
position, place left hand on patient’s or tenderness
back under the left rib cage
4. Kidneys: keep patient in supine Kidneys non palpable and non tender
position, place left hand on the on
patient’s back between the lowest rib
and the pelvic bone. Ask patient to
take deep breath, press firmly with
right hand and try to palpate kidney.
Repeat same process for left side too
Note enlargement and tenderness
R. Anus
INSPECTION
1. Anus for irritation, hemorrhoids, No irritation, hemorrhoids, cracks,
cracks, fissure fissure

15
 S. Genital Area
INSPECTION
1. Vulval swelling, discharge, condition No discoloration, swelling, or redness
of perineum, labia for color, redness, No abnormal vaginal discharge
swelling of labia
2. Check for urethral orifice for redness No redness or discharge
or discharge
3. Vaginal discharge or bleeding from No abnormal Vaginal discharge or
vagina bleeding from vagina
T. Musculoskeletal System
INSPECTION
1. The muscles and joints Patient was unable to perform ROM
ask patient to perform range of exercises due to patients deteriorating
motion exercises, joint movement of condition and generalized body pain
neck, wrist, ankle, hip in all possible Patient was in no condition to
direction perform it
2. Patient’s supine, note placement and Spine is in midline;slightly curved out
curvature from neck inward at the waist
PALPATION
1. Palpate joints for swelling, tenderness No joint swelling, or tenderness,
and temperature normal temperature
2. Ask patient to perform range of Patient was in no condition to
motion exercises, joint movement of perform it
neck, wrist, ankle, hip in all possible
direction
U. Nervous System
1. Muscle strength, push against Weak muscle strength
patient’s hand and ask to resist push
2. Sensation Present
3. co-ordination of movements co-ordinated motor activities
V. Reflexes
1. Biceps reflex Contraction of the biceps muscle and
flexion of the forearm
2. Triceps reflex Normal response, extension of
forearm
3. Knee jerk Extension of lower leg
4. Plantar reflex Flexion of all toes and inversion and
flexion of the forefoot

16
SUMMARY OF FINDINGS
Physical examination was performed from head to toe OF Mrs. Bimala Gurung, 29 years
female with diagnosis of PIH with severe pre-eclampsia on 2070/1/19. The findings obtained
are listed below
Weight: 156cm
Height: 56kg

Vital Signs
Temperature: 97º f
Pulse: 82/m
Respiration: 20/m
Blood Pressure: 140/110mm Hg and 150/110 mm Hg

Findings:
General Appearance: weak appearance
Gait: Imbalanced
Nutritional Status: well built
Facial Expression: frowning
Skin: pale and yellowish
Bilateral pedal edema present, Peri- orbital edema present around eyes
Head: normal contour, no lesions were observed
Chest: no added murmur sounds were heard, no adventitious breathe sound heard
Abdomen: no organomegaly (hepatomegaly/ spleenomegaly), no dilated veins over abdomen,
straie gravidarum and linea nigra present, no masses and tenderness over abdomen present
Genitalia: No discoloration, swelling, or redness, No abnormal vaginal discharge present
Musculoskeletal: weak muscle strength
Reflexes: normal reflexes

17
DEVELOPMENTAL NEED AND TASK
As my patient is 29 years old female, she is at young adulthood stage (18-35years) in her life.

According to book
According to Diekelmann (1976) there are five developmental task of young adulthood and
they are:
The young adult achieve independence from parental control
They begin to develop strong friendships and intimate relationship outside the family
They establish personal set of values
They develop a sense of personal identity
They prepare for life work and develop the capacity for intimacy

In my patient
She achieved independence from parental control
She formed an intimate relationship with her husband
She has her own set of personal values
She has developed a sense of personal identity
She has prepared herself for life and has already built the capacity for intimacy

18
19
HYPERTENSIVE DISORDERS IN PREGNANCY

Introduction
Hypertensive disorders in Pregnancy is regarded as one of the most serious medical disorders
in pregnancy
It may complicate 5-15% of all pregnancies and is responsible for 15-20% of all
maternal mortality in developing and developed countries
There is a generalized vasospasm leading to systemic disorders involving the vital organs of
the body. Hence, any vital organ failure can lead to chronic illness

Classification of Hypertensive Disorders In Pregnancy

1. Gestational Hypertension or Pregnancy Induced Hypertension or Transient
Hypertension
2. Pre-eclampsia
3. Eclampsia
4. Superimposed Pre-eclampsia
5. Chronic Hypertension

Chronic Hypertension may be associated with:

Essential Hypertension
Chronic Renal Diseases
Co-arctation of Aorta
Pheochromocytoma
Thyrotoxicosis (hyperthyroidism)
Connective Tissue Disease
Systemic Lupus Erythematous

20
Definitions
1. Normal Blood Pressure
Normal Blood Pressure normally falls in pregnancy with no change in systolic blood
pressure but diastolic blood pressure is lowered by 10 mmHg with lowest recording at
14-20 weeks of pregnancy, before rising to pre-pregnancy value by term
the mid trimester fall in blood pressure is due to significant decrease in vascular tone
following the cardiovascular alterations leading to peripheral vasodilation

2. Gestational Hypertension
It is a condition in which systolic blood pressure is greater than 140mmHg and
diastolic blood pressure is greater than 90 mmHg or more on at least two occasions
four or more hours apart beyond 20th weeks of gestation or during 24 hours after
deliver in previously normotensive woman

3. Pre-eclampsia
Pre-eclampsia is Pregnancy Induced Hypertension in association with significant
Proteinuria

4. Eclampsia
Eclampsia is defined as seizures that cannot be attributed to any other cause in women
with pre-eclamsia

5. Chronic hypertension
Chronic Hypertension is hypertension antedating pregnancy or hypertension
diagnosed before 20 weeks of pregnancy but not attributable to gestational
trophoblastic disease
It is also known hypertension before pregnancy or hypertension.
Diagnosed in first trimester before 20 weeks of pregnancy and persisting 12 weeks of
postpartum is also considered as chronic hypertension

21
 6. Super-imposed Pre-eclampsia
It is the development of pre-eclampsia in a patient with chronic hypertensive vascular
or renal disease when hypertension antedates the pregnancy as established by
previous blood pressure recordings.

Criteria
A rise in systolic blood pressure by 30 mmHg or
A rise in diastolic blood pressure by 15 mmHg and
Development of proteinuria or edema or both

Above criteria should be fulfilled during pregnancy to establish the diagnosis of

Super-imposed Pre-eclampsia

PREGNANCY INDUCED HYPERTENSION

It is a condition in which systolic blood pressure is greater than 140mmHg and diastolic
blood pressure is greater than 90 mmHg or more on at least two occasions four or more hours
apart beyond 20th weeks of gestation or during 24 hours after deliver in previously
normotensive woman

Criteria for diagnosis of Pregnancy Induced Hypertension

Absence of any evidence for underlying causes of Hypertension
Unassociated with other evidences for pre-eclampsia (edema or proteinuria)
Not associated with haemoconcentration,, thrombocytopenia, raised serum uric acid
level and hepatic dysfunction

22
PRE-ECLAMPSIA
Pre-Eclampsia is a multisystem disorder of unknown etiology characterized by development
of hypertension to the extent of 140/90 mmHg or more with proteinuria after the 20th week of
pregnancy in previously normotensive and non proteinuric patient.
Some amount of edema is common in normal pregnancy thus edema has been
excluded from diagnostic criteria unless it is pathological.
The pre-eclamptic features may appear before 20th week of pregnancy as in case of H.mole
and polyhydraminous

Pre-Eclampsia is disease of unknown etiology occurring after 20th week of gestation

characterized by blood pressure more than 140/90mmHg (systolic blood pressure >30mmHg
and diastolic blood pressure >15mmHg) over previously documented blood pressure and
mean arterial pressure > 105 or >20mmHg over previously documented Mean arterial
pressure with significant proteinuria (>0.3g/ 24hours) and generalized edema

Criteria

Pre-eclampsia is diagnosed when a pregnant woman develops both:

Blood Pressure >140 systolic and/or >90 diastolic (two separate readings taken at least
six hours apart)
300 mg of protein in a 24-hour urine sample (proteinuria).

INCIDENCE
5-15% of all pregnancies, more common in primigravida and is about 10% and 5% in
multigravida
Increasing incidence in developing countries and if unrecognized, it is the most serious life
threatening condition to both mother and fetus

23
RISK FACTORS
Genetic factors
Family history: (hypertension, pre-eclampsia, eclampsia)
Genetic disorder

Obstetric factors
Primigravida: young or elderly (first time exposure to chorionic villi, <20/>40 years)
Obstetric complications e.g. H.mole, twins, diabetes
Rh incompatibility
Previous history of pre-eclampsia
Placental abnormalities:
i. hyperplacentosis: excessive exposure to chorionic villi- (molar pregnancy twins,
diabetes)
ii. placental ischaemia
iii. hydrops fetalis with large placenta
iv. poor placentation
New paternity

Medical factors
Obesity: BMI>35kg/M², insulin resistance
Pre-existing vascular disease or renal disease
Thrombophilias (antiphospholipid syndrome, protein C,S deficiency, Factor V leiden)
Immunological phenomenon
Chronic hypertension
Diabetes
Connective tissue diseases like SLE
Hyperhomocystinaemia
Polycystic ovarian disease

24
ETIOPATHOLOGICAL FACTORS FOR PRE-ECLAMSIA
1. Failure of trophoblastic invasion
2. Vascular endothelial damage
3. Inflammatory mediators
4. Immunological intolerance between maternal and fetal tissues
5. Coagulation abnormalities
6. Increased oxygen free radicals
7. Genetic predisposition (polygenic disorder)
8. Dietary deficiency of excess

ETIOPATHOGENESIS OF PRE-ECLAMPSIA
Pre-eclampsia has been described as a disease of theories, because the cause is unknown.
Some theories include
Endothelial cell injury,
Immunological phenomenon (insufficient production of blocking antibodies),
Placental pathology
Altered vascular reactivity,
Imbalance between prostacyclin and thromboxane,
Decreased glomerular filtration rate with retention of salt and water,
Decreased intravascular volume,
Increased central nervous system irritability,
Disseminated intravascular coagulation,
Uterine muscle ischemia
Dietary factors, and
Genetic factors.

25
 1. Placental Pathology:
pre-eclampsia and idiopathic IUGR are part of the same disease spectrum and both are
primarily due to abnormal placentation. In normal pregnancy, the spiral arteies of placenta
are invaded by the cytotroblast and the elastic and muscular coats are replaced by fibroid
tissues.
Early in second Trimester, a second wave of cytotrophoblast invasion transforms the
myometrial segments of the spiral arteries into wide mouthed vessels unresponsive to
vasomotor stimuli. Thus, the blood supply is transformed from a high resistance low flow
system to a low resistance high flow system in order to increase the uteroplacental flow and
meet the needs of fetus

In pre-eclampsia, the primary wave of trophoblastic invasion partly impaired and the second
wave fails to occur. This results in reduced uteroplacental flow which worsens as gestation
advances. In addition, the arteries remain very sensitive to vasomotor stimuli. These changes
are not specific to Pre-eclampsia and can occur in IUGR without pre-eclampsia.

2. Endothelial Cell Dysfunction and Vasospasm

It is the primary pathology of pre-eclampsia. The precise mechanism by which the ischaemic
placenta causes widespread endothelial cell damage in preeclampsia is not known. one theory
is that it is caused by lipid perioxidation stimulated by free oxygen radical because of
oxidative stress. Prostacyclin is a prostaglandin produced by vascular endothelium and is a
powerful vasodilator and inhibitor of platelet aggregation. Nitric oxide is another vasodilator
produced by the endothelium. Thromboxane is produced by the platelets and causes
vasoconstriction and platelet aggregation. In normal pregnancy, there is an increase in
prostacyclin resulting in vasodilation
In pre-eclampsia, due to the endothelial cell dysfunction between prostacyclin anion there is a
reduction in prostacyclin and nitric oxide, so overall, there is a shift in the balance between
prostacyclin and thromboxane in favors of thromboxane. Therefore, there is vasospasm,
platelet activation and activation of coagulation system. Apart from this, in normal pregnancy
the peripheral resistance and thus blood pressure, falls due to the acquired insensitivity to the
pressor effect of angiotensin II. In contrast, in pre-eclampsia there is loss of vascular
26
insensitivity. This results in vasospasm and thereby an increase in vascular resistance and
increase in blood pressur
3. Coagulation system and platelets
Endothelial dysfunction will lead to activation of platelets and coagulation system by the
tissue factor on the endothelium. This results in widespread DIC and hence platelets and
clotting factors are used up. The disturbance may range from subclinical to pathological DIC.
These results in consumption of clotting factors and platelets may manifest
thrombocytopenia. Tissue factors is increased in pre-eclampsia and stimulated by cytokines
like Tumor Necrosis Factor (TNF). So, activation of the coagulation system is also linked to
pro-inflammatory state. As a result of all these changes there are widespread multiple small
hemorrhages and fibrin deposition in many organs.

4. Metabolic factors
central obesity and insulin resistance are risk factors for pre-eclampsia. There is a dramatic
increase in free fatty acids and triglycerides in pre-eclampsia, which may be due to the insulin
resistance. The hyperlipidaemia may induce endothelial dysfunction directly. Alternatively,
oxidative stress can result in free oxygen radicals producing lipid perioxidation, which can
also result in endothelial dysfunction.
Therefore, pre-eclampsia may be the pregnancy as associated expression of the metabolic
syndrome.

5. Genotype and phenotype

There is definitely an inherited maternal component in pre-eclampsia. The placenta is
probably the trigger, but it is the maternal response that is critical. We know that there is a
familial tendency. The same problem of abnormal placentation causes both pre-eclampsia and
idiopathic IUGR. Hence, it is possibly those women who do not have susceptible genotype or
phenotype, which develop IUGR without pre-eclampsia.

27
PATHOPHYSIOLOGY

Primary cause unknown (genetic/ immunological)

Initial phase: vascular pathology

Failure of second wave of trophoblast invasion

Decrease blood flow in spiral artery

Decrease placental blood flow

Placental bed ischemia

Stimulation of macrophage system

Liberation of TNF α (trigger)

interleukins

oxygen free radicals

lipid peroxides

Endothelial damage/ dysfunction

28
a. Placenta: the placental changes are central to pre-eclampsia. The typical vascular lesion is
termed as acute atherosis. This is characterized by fibrinoid necrosis, macrophages and
mononuclear cell infiltration

b. Kidney: the main pathology of kidney is glomerular endotheliosis which narrows lumen.
This comprises swollen endothelial cells due to fibrin deposition. There is glomerular and
tubular dysfunction. The main pathology is glomerular dysfunction, the manifestation of
which is proteinuria. There is also a reduction in the glomerular filtration rate and creatinine
clearance, which in severe cases leads to an increase in the blood urea and serum creatinine.
Acute renal failure can rarely supervene and is usually due to acute tubular necrosis which is
reversible. Very rarely, it is due to irreversible acute cortical necrosis tubular dysfunction is
manifested as hyperuricaemia.

c. Liver: Periportal thrombosis and fibrin deposition, hemorrhages and necrosis seen in the
liver. There is an increase in the liver enzymes SGOT and SGPT and clinical jaundice can
occur. The liver changes are responsible for the nausea and vomiting in severe cases. The
small hemorrhages may coalesce to form a sub capsular hematoma, which may cause
stretching of the Gilson’s capsule and Epigastric pain. This is a very serious sign and seen in
impending eclampsia. These changes are responsible for HELLP syndrome, which is
described as an extremely rare but catastrophic complication and may lead to liver rupture.

d. Brain: The main finding in brain is the cerebral vasospasm. Small cerebral hemorrhages,
thrombosis and fibrinoid necrosis can occur especially in eclampsia and are secondary to
endothelial dysfunction. Cerebral edema is also usual in eclampsia. Massive cerebral
haemorrhages are a rare complication of severe hypertension. Visual disturbances are
common and are usually due to edema of the occipital lobe. Cortical blindness can rarely
occur due to occipital edema which is usually temporary.

e. Eyes: localized retinal vasospasm is the commonest finding. Hemorrhages and

papilloedema may be seen rarely in severe hypertension. Blindness could rarely be due to
retinal artery ischemia or infraction. Another complication is retinal detachment, which
usually improves with time.

29
CLINICAL TYPES
The clinical classification of Pre-eclampsia is principally dependent on the level of the blood
pressure. It is classified into
a. Mild Pre-eclampsia
b.Severe Pre-eclampsia

a. Mild Pre-eclampsia:
It includes cases of sustained rise of blood pressure of more than 140/90 mmHg but less than
160mmHg systolic or diastolic without significant proteinuria.

b. Severe Pre-eclampsia:
It comprises of
A persistent systolic blood pressure of ≥160mmHg or diastolic pressure of
>100mmHg
Proteinuria excretion of >5gm/24hrs
Oliguria (<400ml/24hr)
Platelet count <100,000/mm³
HELLP syndrome
Cerebral or visual disturbances
Persistent severe Epigastric pain
Retinal hemorrhages, exudates or papilloedema
Intrauterine growth restriction of the fetus
Pulmonary edema

30
 Indicators of mild to moderate and severe preeclampsia

Site Indicator Mild to Severe

Moderate
Central nervous Symptoms and Hyperreflexia Blurred vision
system signs Headache Headache
Irritability
Kidney Proteinuria 0.3-5 g/24 h > 5 g/24 h or catheterized urine
with 4+ protein
Urinary output > 20-30 mL/h < 20-30 mL/h
Liver AST, ALT, LDH Normal Elevated LFTs
Epigastric pain
Ruptured liver
Hematologic Platelets > 100,000/uL < 100,000/uL
Hemoglobin Normal range Elevated
Vascular Blood pressure < 160/110 mm >160/110 mm Hg
Hg
Retina Arteriolar spasm Retinal hemorrhages
Fetal- placental Growth retardation Absent Present
unit
Oligohydramnios May be present Present
Fetal distress Absent Present

Key:
AST = aspartate aminotransferase;
ALT = alanine aminotransferase;
LDH = lactate dehydrogenase;
LFTs = liver function tests.

 My patient was presented with severe Pre-eclampsia.

31
ECLAMPSIA
Eclampsia is an acute and life-threatening complication of pregnancy, characterized by the
appearance of tonic–clonic seizures, usually in a patient who has developed pre-eclampsia.
Eclampsia includes seizures and coma that happen during pregnancy but are not due to
preexisting or organic brain disorders

Sign and Symptoms

- Patients show signs of pregnancy-induced hypertension and proteinuria before the onset of
the eclamptic convulsion.
- Other cerebral signs may precede the convulsion such as nausea, vomiting, headaches,
and cortical blindness
- With the advancement of the pathophysiological process, other organ symptoms may be
present including abdominal pain, liver failure, signs of the HELLP syndrome, pulmonary
edema, and Oliguria
- The fetus may be compromised by intrauterine growth retardation, and with the toxemic
changes during eclampsia may suffer fetal distress
- Placental bleeding and placental abruption may occur.

Seizures
It is divided into following 4 stages:
1. The stage of invasion facial twitching can be observed around the mouth.
2. The stage of contraction tonic contractions, or sustained muscular contractions without
intervals of relaxation, render the body rigid; this stage may last about 15 to 20 seconds.
(Tonic contractions are also known as tetanic contractions).
3. The stage of convulsion when involuntary and forceful muscular movements occur, the
tongue may be bitten, foam appears at the mouth. The patient stops breathing and
becomes cyanotic; this stage lasts about one minute.

4. Coma. When the patient awakens, she is unlikely to remember the event.
In some rare cases there are no convulsions and the patient falls directly into a coma. Some
patients may experience temporary blindness upon waking from the coma.

32
CLINICAL FEATURES
According To Book In My Patient
Onset
Usually insidious onset but on rare occasions Onset acute and rapid
onset may be acute and rapid

Symptoms
Mild symptoms

Slight swelling over ankles which persists on Swelling over ankles present
rising from bed in morning and tightness of
the ring finger

Swelling gradually extending to face, body, Generalized edema present with peri-orbital
abdominal wall, vulva and whole body edema around eyes and face

Alarming symptoms (usually associated with acute onset)

Headache – either located in occipital or Headache present

frontal region

Disturbed sleep pattern Absent

Diminished urinary output – urinary output Diminished urinary output present

less than 400ml in 24 hours

Epigastric pain- acute pain in the Epigastric Acute Epigastric pain with vomiting
region associated with vomiting, coffee color
vomitus due to sub capsular haemorrhage in
the liver

33
Eye symptoms- blurring, scotomata, dimness Blurring of eye initially absent but present as
of vision or at times complete blindness disease progressed
vision regained within 4-6 weeks

Signs
Abnormal Weight Gain- within short span of Absent
time. A rapid weight gain of more than 5lbs
or more than 1lbs a week

Rise of blood pressure: the rise of blood Present blood pressure raised up to 160/120
pressure may be insidious or abrupt. Diastolic mm Hg
pressure rises followed by systolic pressure

Edema: visible edema over the ankles on Generalized edema present

rising from bed in morning, generalized
edema in severe cases.

No manifestation of chronic cardiovascular No manifestation of chronic cardiovascular

and renal pathology and renal pathology

Pulmonary edema: due to leaky capillaries Absent

and low oncotic pressure

Abdominal examination: reveals evidences of Absent, IUFD occurred due to induction of

chronic placental insufficiency such as labour
Oligohydramnios, IUGR

34
INVESTIGATIONS
According to Book In my Patient
Blood Pressure measurement ✓
CBC (Hb, TC, DC, ESR) ✓
Blood Grouping and Cross Matching ✓

Coagulation Profile (PT, CT, BT, APPT) ✓

Hematocrit ✓

Liver Function Test:

Serum Alanine Aminotransferase (ALT) ✓
Aspartate Aminotransferase (AST) levels
Indirect Bilirubin
Renal Function Test:
Serum creatinine
BUN ✓
Creatinine Clearance
Creatinine urine
24-hour urine collection for protein
Urine Dipstick Test ✓

Urine analysis ✓
Peripheral blood smear ✓

Serum lactate dehydrogenase (LDH) level X

Ultrasonography: Trans abdominal, to assess
the status of the fetus and evaluate for growth ✓
restriction; umbilical artery Doppler
ultrasonography, to assess blood flow
Fundoscopy ✓

35
INVESTIGATIONS RESULTS
Investigations Findings in my patient Normal values
Blood Pressure 160/110 – 150/90mmHg 120/80 mmHg
TLC 12,800/mm³ 4,000-12,000
DLC:
Neutrophils 60 54-62%
Lymphocytes 38 25-30%
Eosinophils 02 1-3%
HB 9mg/dl 12-15mg/dl
Platelets 86,000/cumm 1,50,000-4,50,000/cumm
Blood Grouping and cross A Negative
matching
Coagulation Profile:
BT- 10min 1-6min
CT- 14min 1-10min
INR- 9.0 0.8-1.2
Biochemistry:
Urea 25mg/dl 10-40mg/dl
Creatinine 1.1mg/dl 0.4-1.4mg/dl
Sodium 142mmol/l 135-146mmol/L
Potassium 2.9mmol/dl 3.5-5.2mmol/L
Bilirubin total 4.76 mg/dl Up to 1.0mg/dl
Bilirubin direct 3.2 mg/dl Up to 0.2mg/dl
SGOT (AST) 1837U/L 0-40U/L
SGPT (ALT) 913U/L 0-40U/L
Total Protein 7.2 gm/dl 6-8gm/dl
Albumin 4.8 gm/dl 3.5-5.5gm/dl
LDH 2057IU/L <480 IU/L
RBS 83mg/dl Up to 140mg/dl
Uric Acid 4.7mg/dl 2.4-5.7mg/dl
Urinalysis: Reaction: alkaline
Colour: yellow
Epi cells: 16-18/hpf
RBC: 10-12/hpf
WBC: 14-16/hpf
Albumin: 3+
24 hour urine Protein Positive
Fundoscopy No retinal detachment seen
USG Singleton preganancy of 25
WOG

36
COMPLICATIONS

Complications can be classified as immediate and remote

Immediate:
1. Maternal
During pregnancy:
a. Eclampsia
b. Accidental hemorrhages
c. Dimness of vision and even blindness
d. Preterm Labour
e. HELLP syndrome
f. Oliguria and Anuria
g. Cerebral Hemorrhages
h. Acute Respiratory Distress Syndromes (ARDS)
i. Disseminated intravascular coagulation (DIC)
j. Acute fatty liver of pregnancy
k. Acute renal failure
l. Placental abruption

During labour
a. Eclampsia
b. Postpartum hemorrhages- related with coagulation failure

Puerperium
a. Eclampsia- usually occurs within 48 hours
b. Shock- Puerperal vasomotor collapse
c. Sepsis

2. Fetal
The fetal risk is related to the severity of the pre-eclampsia
Prematurity
Intrauterine growth retardation (IUGR)
Intrauterine Fetal Death (IUFD)

37
MANAGEMENT
Mild Pre-eclampsia
Mild pre-eclampsia can be managed in OPD basis, especially those without proteinuria.
Monitoring maternal and fetal condition is essential.
Bed rest in left lateral position is suggested.
No sedatives, salt restrictions and diuretics are suggested as they further reduce
uteroplacental flow and worsen IUGR, the only indication of diuretics is pulmonary edema

Anti-hypertensives
The effect of anti hypertensive in Mild pre-eclampsia is controversial. It is prescribed only
when diastolic blood pressure is more than 100 mm Hg and systolic blood pressure is more
than 160 mm Hg.
The main objective is to reduce the risk of severe hypertension and cerebral hemorrhage,
once the Mean Arterial Pressure is more than 150, there is loss of cerebral auto regulation and
high risk of cerebral hemorrhage. The use of anti hypertensive may help in prolongation of
pregnancy.
The drug of choice in pregnancy is α-methyldopa. Other commonly used first line drugs are
nifedipine and labetalol.
labetalol should be avoided in woman with known asthma. Beta blockers like Atenolol can
cause IUGR and thus avoided. ACE inhibitors are absolutely contraindicated in Pregnancy as
they can impair renal function causing fetal Oliguria and oligohydraminous.

Blood pressure and urine albumin daily

Twice weekly Peripheral Blood Smear, platelet count, coagulation profile, uric acid, renal
and liver functions tests

Fetal

Daily fetal movement count

Ultrasound to assess fetal growth and well-being
NST and amniotic fluid volume assessment
Doppler velocimetry in IUGR

38
The frequency of monitoring should be individualized depending upon the severity and
presence of IUGR.

Delivery
Delivery is the only definitive treatment for pre-eclampsia and usually labour is induced at 38
weeks. Early termination may be needed if there is progression to severe eclampsia and
eclampsia with worsening of either maternal or fetal condition. Antenatal corticosteroid to
accelerate lung maturity in preterm. If there are no obstetric indication for caesarean section
labour can be induced If the cervix is favorable with bishop’s score labour can be induced by
ARM followed by oxytocin infusion. If cervix is not favourable PGE2 gel can be used to
ripen cervix. Continuous CTZ monitoring is preferred during labour. Prophylactic
Ergometrine is avoided as it leads to sudden rise in blood pressure

Common anti hypertensive drugs

Name Mode of action Dosage Side effects

α methydopa Central action 1000-2000mg/day Postural hypotension, CNS
3-4 divided doses depression, Hemolytic
anemia
Nifedipine Ca channel 20-40mg/day Headache, flushing,
blocker 2-4 divided doses palpitation
Hydralazine Peripheral 50-300mg.day Headache, flushing,
vasodilation 2-3 doses tachycardia, lupus
Labetalol Combined α and 200-400mg/day Postural hypotension, tremors
β blocker 2 doses
Atenolol β blocker 50-200mg.day Bradycardia, hypotension,
1-2 doses hypoglycaemia, fatigue,
IUGR

*Note: Methyldopa is drug of choice

ACE inhibitors absolutely contraindicated

39
Severe Pre eclampsia Management
In Severe Pre eclampsia, there is deterioration of either maternal or fetal condition or both
and the definitive treatment is delivery after 34 weeks, severe pre eclampsia is best treated
with termination especially if there is worsening of biochemical parameters. In cases before
34 weeks if the initial condition stabilizes there may be place for management. Severe Pre
eclampsia before 24 weeks is best managed with termination of pregnancy.

Antepartum Management
The aim of expectant management is to protect mother and fetus from the consequences of
the disease and at the same time prolong pregnancy if possible to avoid the dangers to the
fetus of prematurity. The expectant management is abandoned if immediate termination uis
decided

1. Anti hypertensive: Indicated to prevent cerebral hemorrhages, α methydopa and nifedipine

are commonly used. Hydralazine and labetalol can also be used.

2. Close monitoring: Close monitoring of materal and fetal condition is performed

Blood pressure and urine albumin daily

Peripheral Blood Smear, platelet count, coagulation profile, uric acid, renal and liver
functions tests on alternate days and in fulminant cases twice daily

Fetal

Daily fetal movement count

Ultrasound to assess fetal growth and well-being
NST and amniotic fluid volume assessment
Doppler velocimetry in IUGR

.poor oxygen saturation can occur in pulmonary edema and so continuous measurement of
oxygen saturation using pulse oximetry is indicated in such cases

3. Antenal Corticosteroids: to accelerate lung maturity of fetus

40
 Criteria for Immediate Termination of pregnancy

No reassuring fetal heart status

Ruptured membrane
Uncontrollable BP
Oligohydramnios, with amniotic fluid index (AFI) of less than 5 cm
Severe intrauterine growth restriction in which the estimated fetal weight is less than 5%
Oliguria (< 500 mL/24 hr)
Serum creatinine level of at least 1.5 mg/dL
Pulmonary edema
Shortness of breath or chest pain with pulse oximetry of < 94% on room air
Headache that is persistent and severe
Right upper quadrant tenderness
Development of HELLP syndrome

Intrapartum Management

1. Control of blood pressure : The diastolic pressure should not cross 100 mm Hg. Labetalol
can be used as IV infusion 2mg over 2 min or bolus over 2 min. Hydralizine 5 mg bolus Iv
injestion can also be given for acute control of blood pressure. Sublingual nifedine can be given
but side effect is sudden drop of blood pressure. Rapid fall of blood pressure should be avoided
as it may affect fetus.

If diastolic blood pressure is 110mmHg, antihypertensive drugs are given

Goal of antihypertensive therapy is to manage blood pressure up to 90-100 mmHg to prevent
cerebral hemorrhage.
Drug of choice Hydralazine 5 mg slowly over 5 min
Nifedipine 12.5mg IM every two hourly as needed
Labetelol and Nifedipine 10 mg IV after 10 mins (diastolic blood pressure increase 110mmHg)
Labetelol 20 mg IV given
Dose can be increased up to 40 mg and then 80 mg if not maintained after 10 minutes
Nifedipine 5mg sublingually after 10 minutes 5 mg sublingually if BP not lowered

41
2. Anticonvulsants: Prophylactic Magnesium sulphate can be given to prevent eclampsia in
severe Pre eclampsia as MAGPIE trial.

Dose of MgSO4
- Loading dose
4gm 20% MgSO4 IV over 5 minutes

- follow
10gm 50% MgSO4, 5gm in each buttock as deep IM injection with 1 ml of 2% lignocaine in
same syringe
Apply aseptic technique while administering MgSO4 deep IM
Patient may feel warm and flushing after administration of MgSO4

If convulsant reoccur
2gm of 50% MgSO4 IV over 5 minutes

Maintenance Dose
- 5gm of 50% MgSO4 in 1ml 2% lignocaine by same syringe four hourly in alternate buttocks
- Continue treatment with MgSO4 for 24 hours after delivery or last convulsion

Adverse Effects of MgSO4

Flushing
Sweating
Hypotension
Depressed reflexes
Flaccid paralysis
Hypothermia
Circulatory collapse
CNS depression
hypocalcaemia with tetany

Contraindication
Decreased blood pressure

42
Respiratory arrest
Disappearance of patellar reflex

Precaution
Respiratory rate < 16/ min
Platellar Reflex present
Urinary output at least 30ml/hr over 4 hours (if urinary output decreases MgSO4 absorption
increases in blood and results increased toxic effects)

Antidote (if toxic effect presents)

- Assist ventilation (emergency drugs and intubation)
- 10 ml 10%, 1 gm calcium gluconate IV slowly until respiratory rate returns to normal

Diazepam
If MgSO4 absent, diazepam can be used
Diazepam is not a safe drug as it causes neonatal respiratory depression as it passed through
placenta
Long term IV use may cause respiratory depression in babies suffering from ischaemia due to
placental compression and preterm birth.
Loading dose
10mg IV slowly over 2 min
convulsion reoccurs Repeat dose again
Maintenance dose
40mg in 500ml IV in NS/RL
If dose exceeds 30 mg / hr maternal respiratory depression occurs
Dose should not exceed 100mg in 24 hours
Ventilation should be assessed and assisted while administering diazepam.

Rectal dose when IV not accessible

Loading dose: 20mg in 10 ml syringe.
if convulsions not controlled within 10 minutes 10mg/hr or more

43
3. Fluid management
Despite the presence of peripheral edema, patients with preeclampsia are intravascularly
volume depleted, with high peripheral vascular resistance. Diuretics should be avoided.

Aggressive volume resuscitation may lead to pulmonary edema, which is a common cause of
maternal morbidity and mortality. Pulmonary edema occurs most frequently 48-72 hours
postpartum, probably due to mobilization of extravascular fluid.

Central venous or pulmonary artery pressure monitoring may be indicated in critical cases. A
central venous pressure (CVP) of 5 mm Hg in women with no heart disease indicates sufficient
intravascular volume, and maintenance fluids alone are sufficient. Total fluids should generally
be limited to 80 mL/h or 1 mL/kg/h.

Careful measurement of fluid input and output is advisable, particularly in the immediate
postpartum period. Many patients will have a brief (up to 6 h) period of oliguria following
delivery; this should be anticipated and not overcorrected.

4. Corticosteroids:
Corticosteroids are indicated in HELLP syndrome. The other indication is to accelerate lung
maturity of fetus.

Obstetric Management
Delivery is the only specific management of severe eclampsia and eclampsia Delivery should
be conducted regardless of week of gestation if maternal or fetal condition worsens. Woman’s
condition re establishes to normal within few hours after delivery and after 24 hours most of
the symptoms regress.
In severe eclampsia delivery should be conducted within 24 hours and in eclampsia within 12
hours.
Assess cervix, if unfavorable induce (prostaglandin, misoprostol to ripen cervix)
If favorable membrane rupture, augmentation
Caesarean Section
If FHR abnormal (less than 100 or more than 180b/min), Caesarean section is done

44
Cervix is unfavorable and fetal is alive, Caesarean section is done, IUFD, too premature for
survival, dead baby or absence of safe anesthetic drugs vaginal delivery is planned

Indication of Caesarean Section

Associated obstetric indications
Failure induction
Rapid worsening of maternal condition and delivery not imminent
Fetal distress or severe IUGR

Postpartum Management

Prophylactic ergometrine and methargin are contraindicated and instead oxytocin or PGF2α can
be used. These patients have contracted blood volume and there are more chances of PPH and
shock so fluid management should be done. Cross matched blood should be kept ready.
Oliguria is common after delivery but usually subsides, aggressive fluid replacement is avoided.
the post partum period is crucial and continuous monitoring of biochemical and hematological
parameters are required. This is because HELLP syndrome can occur in Postpartum period as
well.
Magnesium Sulphate is continued for another 24 hours. Antihypertensive drugs are continued
in postpartum period as well. Methyldopa is avoided in post partum as it may cause depression
Nifedipine and beta blockers like atenolol are prescribed.
Medicines are stopped after 6 weeks. If hypertension persists cause is ruled out and woman is
counseled for re occurrence of PIH and pre-eclampsia in next pregnancy and prophylaxis with
low dose aspirin is considered in next pregnancy.

45
Management done in my patient
My patient was admitted with diagnosis of PIH but later she developed severe eclampsia
followed by HELLP syndrome.
Antenal Management
Initially she was managed with methyldopa but when blood pressure was not controlled and
patient’s condition progressively deteriorate MgSO4 and depin were added to course of
treatment for blood pressure regulation and prevent impending eclampsia along with fluid
management.

Intranatal Mangement
Though my patient had 26 WOG she wanted to continue pregnancy but later her condition
worsened and she developed HELLP syndrome thus, medical termination of pregnancy was
done at 26+5 WOG by inducing labour with misoprostol and oxytocin.

Postnatal Management
Daily hematological and biochemical parameters were monitored to evaluate HELLP
syndrome, patient had Oliguria thus, fluid management was continued in postpartum along with
anti hypertensives and MgSO4. Two pint blood was transfused to treat anemia as her Hb level
dropped to 7 mg/dl
Injection Rhogam was administered for prophylaxis
All symptoms subsided 5 days after MTP and patient was discharged

HELLP Syndrome
It is acronym for hemolysis (H), Elevated Liver Enzymes (EL) and Low Platelet count (LP)
(<100,000/mm³) this is a rare complication of pre eclampsia (10-15%). HELLP syndrome may
develop even without maternal hypertension. This syndrome is manifested by nausea,
vomiting, Epigastric pain or right upper quadrant pain along with biochemical and
hematological changes. Parenchymal necrosis of liver causes elevation of hepatic enzymes
(AST and ALT >70 IU/L, LDH>600 IU/L) and Bilirubin (>12 mg/dl). There may be
subcapsular haematoma formation (which is diagnosed by CT scanning) and abnormal
peripheral blood smear. Eventually liver may rupture to cause sudden hypotnsion, due to
hemoperitoneum.
46
Management
Principle of management same as severe pre eclampsia and eclampsia. Anti seizure prophylaxis
with magnesium sulphate is started. Assessment of maternal and fetal condition followed by
delivery is done. Corticosteroids are administered as it improves perinatal ( increase pulmonary
maturity, decrease IVF and necrotizing enterocolitis) and maternal (increase thrombocyte count
and increase urinary output) outcome.
Caesarean section is the most common mode of delivery. Epidural anesthesia can be used if
platelet count is >1,00,000/ mm³. Platelet transfusion is done if the count is <50,000/mm³.
patient should be managed at ICU until there is improvement in platelet count, urine output, BP
and liver enzymes.
recurrent risk of HELLP syndrome is 3-19%

Expectant Management: it has been carried out selectively when pregnancy is <34 weeks, with
bed rest, plasma volume expansion (infusion of 5-25% albumin),, antithrombotic agents
(dipyridamole), immunosuppressive agents (steroids) and others ( fresh frozen plasma). In
HELLP syndrome perinatal mortality ranges between 5-60% and maternal mortality up to 25%

Complications
Maternal: abruption placenta, DIC, acute renal failure, severe ascites, pulmonary edema,pleural
effusions, cerebral edema, laryngeal edema, retinal detachment, subcapsular hematoma, ARDs,
sepsis and death
Perinatal: morbidity and mortality are significantly increased this is due to pre term delivery,
prematurity, RDS and sepsis

47
PROGNOSIS

Pre-eclampsia is usually insidious in onset and runs a slow course. Rarely onset may be acute
and follows a rapid course of events. The prognosis of pre-eclampsia depends on the period
of gestation, severity of disease and response to treatment

The following courses may occur:

If detected early: with prompt and effective treatment the pre-eclamptic features may subside
completely

If left untreated:
a. The Pre-eclamptic features remain stationary at varying degrees till delivery

b. Aggravation of the pre-eclamptic features with appearance of symptoms of acute

fulminating pre-eclampsia. Most commonly occurs in cases with acute onset

c. Eclampsia

d. Spontaneous remission of Pre-eclamptic features

48
49
NURSING MANAGEMENT
Assessment
a. History Taking: including patient’s chief complain, present health status, birth history,
family history, onset of sign and symptoms (increased blood pressure, edema, headache,
epigastric pain, nausea and vomiting, blurred vision).
Previous History of Preganacy: Previous history of pregnancy with preeclampsia or
eclampsia before.

b. Physical Examination: Skin pale and yellowish, Bilateral pedal edema present, Peri- orbital
edema present around eyes, no hepatomegaly and spleenomegaly, increased blood pressure
monitor fetal heart rate to determine fetal distress, assess patellar reflex

c. Investigations:
vital signs: blood pressure every two hourly in both arm
laboratory: urine protein increased to +3, decreased Hematocrit , increased serum creatinine,
BUN, SGOT, SGPT, platelets
Level of consciousness: reduced GCS
Ultrasound: to evaluate fetus condition

Nursing diagnosis

Ineffective Cerebral Tissue Perfusion related to decreased cardiac output secondary to

vascular vasopasm.

Impaired Gas Exchange related to accumulation of fluid in the lungs pulmonary

edema.

Activity Intolerance related to weakness.

Self care deficit related to decreased strength and endurance as evidenced by inability
to ambulate independently

Impaired Urinary Elimination related to impaired glomerular filtration as evidenced

by anuria and oliguria

Risk for Injury related to diplopia and increased intra-cranial pressure, seizures.

50
 Risk for impaired skin integrity related to impaired physical mobility and invasive
procedure (deep IM injections)

Knowledge Deficit related to the management and treatment of disease

Planning/ Goal
The major goals are to maintain adequate cerebral tissue perfusion by lowering blood
pressure, maintain effective gas exchange, increase activity tolerance, encourage and assist
patient on Activities Of Daily Livings (ADLS), maintain fluid status, prevent patient from
potential injuries caused by seizure activities, maintain skin integrity and provide education
regarding management of disease

Interventions
1. Ineffective cerebral tissue perfusion

Monitor neurological status and compare it to normal state.

Monitor vital signs.
Record changes such as the blindness of vision, or visual field disturbances in
perception.
Assess the higher functions, such as speech function.
Put head slightly elevated position.
Maintain a state of bed rest,
Create peaceful environment;
limit the activities of visitors or patients as indicated.
Provide oxygen therapy as indicated

2. Impaired gas exchange

Encourage deep breathing and coughing exercise
Elevate head of bed to semi-fowler’s position
Avoid restrains
Administer oxygen therapy as indicated
Stop MgSO4 immediately if sings of respiratory occurs

51
3. Activity Intolerance

Assess patient's level of mobility

Assess potential for physical injury with activity (falls or overexertion)
Assess patient's cardiopulmonary status before activity
Assist for ambulation and short range of motion exercises as tolerant by patient

4. Self care deficit

Assess client level to perform ADLS

Assist client with daily activities
Provide positive reinforcement during activity.
Allow patient to perform tasks at his or her own rate
Encourage independent activity as able and safe

5. Impaired Urinary output

Assess the signs of fluid volume excess, respiratory distress due to pulmonary edema
Monitor input output strictly
Avoid over resuscitation of fluid
Change patients position frequently
Administer IV fluids as prescribed

6. Risk for Injury

Monitor blood pressure every 2 hourly

Record the patient's level of consciousness
Assess signs of eclampsia (hyper active, the patellar reflexes, decreased pulse and
respiration, epigastric pain and oliguria)
Monitor for signs and symptoms of labor or uterine contractions.
Administer antihypertensive as prescribed to reduced blood pressure

52
7. Risk for impaired skin integrity

Maintain adequate fluid intake

Elevate lower extremities to decrease edema
Keep bed sheets clean and dry, tug bed sheets properly and avoid wrinkles
Inspect skin surfaces to assess skin breakdowns
Change position every two hourly
Provide back care

8. Knowledge Deficit

Give education regarding home based management of disease

Provide health education regarding diet modifications
Provide information’s regarding drug dosage and it’s adverse effects

53
APPLICATION OF NURSING THEORY
While providing care to my patient, I applied Orem’s Theory of Nursing.
Orem’s Theory consists of
1. Theory of self care
2. Theory of self care deficit
3. Theory of Nursing System
My patient Bimala Gurung, 29years female was admitted on
Gynaecology ward of Kist Medical Teaching Hospital with diagnosis of Pregnancy induced
Hypertension with Severe Pre-eclampsia with HELLP syndrome.
Before termination of pregnancy my patient’s condition was critical, and was partly
conscious, she was pale, weak and was in need of assistance to meet her needs but after
pregnancy her condition gradually progressed and she was able to carry out activities of daily
living by herself and needed no assistance to meet her needs. Thus, I applied Orem’s theory
as it appeared to be the best possible theory to meet my client’s need while providing nursing
care.
Orem’s Theory of Nursing Care
Orem’s theory of nursing has three related theories
1. Theory of self care
2. Theory of self care deficit and
3. Theory of nursing system

By assessing condition of my patient I figured out theory of nursing system as most suitable
theory for caring my patient

Theory of nursing system.

It describes how the patients self care needs will be met by the nurse, patient and both
It identifies three classifications of nursing system to meet the self care requisites of the
patient
- Wholly compensatory system
- Partly compensatory system
- Supportive- educative system

54
Wholly compensatory nursing system is represented by a situation in which the individual is
unable to engage in self care actions requiring self directed and controlled ambulation and
manipulative movement or the medical prescription to refrain from such activities
Person with these limitations are socially dependent on others for their continued existence
and wellbeing. Example patient in coma

Partly compensatory nursing system represented by a situation in which both nurse and
patient perform care measures or other action involving manipulative tasks or ambulation.
Either patient or nurse may have major role in performance of self care measures. Examples a
person who recently had surgery

Supportive- educative system: in this system the person is able to perform or can and should
learn to form required measures of externally or internally oriented therapeutic self care but
cannot do so without assistance. This is also known a supportive developmental system.
In this system patient is doing all of his self care. The patient’s requirements for help are
confined to decision makings behavior control, and acquiring knowledge and skills.
The nurse’s role is to promote the patient as a self care agent. Example chronic disease
patients like hypertension

I applied Partly compensatory by

- By providing all self care activities like mouth care, back care when my patient was
partly conscious
- Her elimination need was fulfilled by catheterization
- Medication
- Providing safe environment

And I applied supportive educative theory by

- Providing information about disease condition
- Medication
- Complication and it’s prognosis
- Home based management of disease and possible risks
- Diet
- Follow up

55
 NURSING CARE PLAN
Demographic Data
Name of patient: Bimala Gurung
Age: 29 years Sex: Female
Caste: Gurung Religion: Hindu
Marital status: Married No. of Children: 1
Date Of Admission: 2070/1/19 Inpatient number: 19381
Medical Diagnosis:
Provisional Diagnosis: G3P2L1 at 26+4 WOG with PIH
Final Diagnosis: Pre-eclamsia with HELLP syndrome

Assessment
My patient presented with chief complain of amenorrhea for last six months, Epigastric pain
for 1-2 hours, vomiting two episodes and headache on emergency and was admitted with
diagnosis of PIH but later she developed severe eclampsia followed by HELLP syndrome.
My patient had fetus with 26 WOG she wanted to continue pregnancy but later her condition
worsened and she developed HELLP syndrome thus, medical termination of pregnancy was
done at 26+5 WOG by inducing labour on 2070/1/21
All symptoms subsided 5 days after MTP and patient was discharged

Nursing Diagnosis
Ineffective Cerebral Tissue Perfusion related to decreased cardiac output secondary to
vascular vasopasm.
Impaired Gas Exchange related to accumulation of fluid in the lungs pulmonary
edema.
Activity Intolerance related to weakness.
Self care deficit related to decreased strength and endurance as evidenced by inability
to ambulate independently
Impaired Urinary Elimination related to impaired glomerular filtration as evidenced
by anuria and oliguria
Risk for Injury related to diplopia and increased intra-cranial pressure, seizures.
Risk for impaired skin integrity related to impaired physical mobility and invasive
procedure (deep IM injections)
Knowledge Deficit related to the management and treatment of disease

56
S.N. Assesment Nursing Nursing Goal Nursing intervention Rationale Evaluation
Diagnosis
1 Subjective data: Ineffective Maintain Monitor neurological status To detect early signs
I feel dizziness Cerebral Tissue effective and compare it to normal of impaired cerebral Goal met patient’s
Perfusion related cerebral tissue state. tissue perfusion condition was
Objective data: to decreased perfusion with stabilized after
- Partly cardiac output no signs of Monitor vital signs. Assess condition of intervention as
conscious secondary to impaired GCS patient. evidenced by
- No response to vascular within 4 hours increase verbal
verbal vasopasm. of intervention Indicates communication
Record changes such as the
command neurological and regain of
blindness of vision, or
- Impaired impairment and consicousness
visual field disturbances in
communication impaired tissue
perception.
- Not oriented perfusion
to time place
and person Assess the higher functions, To assess
such as speech function. neurological status
and plan early
intervention

Put head slightly elevated To improve blood

position. circulation and
decrease blood flow
resistance

Maintain a state of bed rest To prevent potential

57
 Create peaceful injuries
environment To provide rest to
patient
Limit the activities of
visitors or patients as To eliminate fatigue
indicated. and agitation

Provide oxygen therapy as

To improve tissue
indicated
perfusion
2 Subjective Impaired Gas Maintain gas Encourage deep breathing Promotes chest
Data: Exchange related exchange and and coughing exercise expansion Goal met oxygen
I have chest to accumulation of oxygen saturation was
saturation with
pain while fluid in the lungs Elevate head of bed to semi- Facilitates maintained at
in 3 hour
breathing pulmonary edema. fowler’s position respiratory function 96% with oxygen
by use of gravity at 2l/min
Objective Data:
Respiratory It may cause
Avoid restrains
Rate: 32/m agitation with
SpO2 86% Administer oxygen therapy increased cardiac
without oxygen as indicated workload
sign of
cyanosis: Stop MgSO4 immediately if MgSO4 toxicity
bluish lips seen sings of respiratory occurs causes depression of
respiratory centre
To maintain oxygen

58
 Administer oxygen at saturation
2l/min
3 Subjective data: Activity Increase Assess patient's level of To assess patient’s
I can’t do it, I Intolerance related tolerance to mobility condition Goal met as
feel weak to weakness. simple activity patient did short
after 2 hour Assess potential for physical To prevent potential range of motion
Objective data: injury with activity (falls or hazards exercises and
Decreased overexertion) tolerated the
activity exertion after
Weak To assess patients encouraging her
Assess patient's
appearance ability to carry out
cardiopulmonary status
activities
before activity

To gradually
Assist for ambulation and
increase tolerance to
short range of motion
activities and make
exercises as tolerated
patient independent
4 Subjective data Self care deficit Provide and Assess client level to To obtain baseline Goal met ,
I have difficulty related to assist in self perform ADLS data and evaluate patient’s hygiene
doing works decreased strength care activities patient’s ability was maintained
and endurance as after assisting her
evidenced by Assist client with daily To maintain hygiene and encouraging
inability to activities and promote comfort her it perform it
ambulate by herself
independently Provide positive To encourage client

59
 Objective data: reinforcement during and build up positive
Patient cannot activity. attitude
mobilize and Allow patient to perform To maintain client’s
carry out tasks at his or her own rate self esteem
activities by
herself Encourage independent To promote client’s
activity as able and safe ability
5 Subjective data: Impaired Urinary Maintain fluid Assess the signs of fluid Intravascular fluid is
- Elimination related volume and volume excess, respiratory contracted and Gal was met as
to impaired increase urine distress due to pulmonary sudden shift of fluid Oliguria subsided
Objective data: glomerular output to edema into intravascular 24 hour after
urine output filtration as 30ml/hour compartment causes MTP
less than evidenced by within 24 hour fluid volume excess
30ml/hour anuria and oliguria
Generalized Monitor input output strictly To monitor Oliguria
edema and maintain fluid
balance

To avoid
Avoid over resuscitation of
complication like
fluid
pulmonary edema

Change patients position

To maintain fluid
frequently
volume with gravity
To manage
Administer IV fluids persistent Oliguria

60
6 Subjective data: Risk for Injury Patients Monitor blood The pressure over Goal met as
- related to diplopia remains free of pressure every 2 hourly 110 mmHg diastole patient didn’t had
and increased injury and systole 160 or any seizure
Objective data: intra-cranial more an indication episodes and
Diplopia and pressure, seizures. of PIH. remained free
blurring of from injuries
vision due to Record the patient's level of The decline of
pressure caused consciousness consciousness as an
on small indication of
capillaries of decreased cerebral
eye blood flow.
Increased blood
pressure Assess signs of eclampsia The symptoms are a
(hyper active, the patellar manifestation of
reflexes, decreased pulse changes in the brain,
and respiration, epigastric kidney, heart and
pain and oliguria) lung that precedes
seizure status.

Monitor for signs and Seizures will

symptoms of labor or increase the
uterine contractions. sensitivity of the
uterus which will
allow the delivery.

61
 Administer antihypertensive Anti-hypertension
as prescribed to reduced to lower blood
blood pressure pressure.

7 Subjective data: Risk for impaired Maintain skin Maintain adequate fluid To maintain turgor Goal met patient
- skin integrity integrity intake of skin showed no signs
related to impaired of skin
Objective data: physical mobility To decrease fluid breakdown and
Elevate lower extremities
prolonged and invasive volume in pressure sores
immobilization procedure (deep Extracellular
redness on back IM injections) compartment and
sacral area decrease edema
Ecchymosis on
Keep bed sheets clean and
buttocks due to To reduce shearing
dry, tug bed sheets properly
IM injection force of linen and
and avoid wrinkles
given prevent skin
breakdown

Inspect skin surfaces to To detect early signs

assess skin breakdowns of skin breakdown

Change position every two To prevent bed sore

hourly and maintain skin
Provide back care integrity

62
8 Subjective data: Knowledge Deficit Provide Give education regarding To manage disease Goal met, patients
We don’t know related to the knowledge home based management of at home and visitors were
what precaution management and regarding disease given teching
we should take treatment of home based regarding home
after being disease management of Provide health education To prevent based
discharged disease regarding diet modifications complications and management of
lead a healthy life PIH and pre
Objective data: style eclampsia
-
Provide informations To maintain drug
regarding drug dosage and compliance and
it’s adverse effects manage side effects
of drugs

63
Diversional Therapy
Diversional therapy is a kind of therapy which is used to distract the mind of the patient.
hospital environment causes stress and anxiety to both patient and family. Hospital is new
environment for both patient and family. Hospital stay might be more frustrating to patient as
she has to undergo through various investigations and medicine on daily basis it may make
patient more anxious thus, to divert mind from such anxiety diversional therapy is used to
reduce stress and maintain mental health of patient and it is very useful for the full recovery
of patient. My patient was anxious about the disease condition especially regarding condition
of fetus thus I applied talk therapy, distraction therapy and deep breathing therapy.

Talk Therapy:
It is the best way to verbalize patient feeling, sharing and communicating one’s feeling and
anxiety. I used talk therapy to divert her mind and express her anxiety regarding disease
prognosis it’s re occurrence and fetal condition. She shared her feelings and I reassured that
she might be able to recover fully and disease have very good prognosis after delivery

Distraction therapy
To distract patient’s mind I asked visitors to talk with her and provide her support, talk about
her interest and her daughter.

Deep breathing and relaxation therapy

This is the most simple and beneficial relaxation therapy, in this therapy client is asked to
take deep breaths and relax all abdominal and respiratory muscles, it improves respiratory
function of body as well as distracts client.

64
65
DRUGS USED IN MY PATIENT

SN Drugs Dose Route Frequency

1. Tab Iron 500mg PO OD

2. Tab Calcium 400mg PO OD

3. Tab Methyldopa 500mg PO TDS

4. Inj Magnesium Sulphate 4gm (20%) IV Stat

followed by
5gm (50%) Deep IM on 4 hourly over
alternate buttocks 24 hours

5. Tab Aciloc 150mg PO BD

6. Tab Pentodac 40mg PO OD

7. Tab Depin 50mg PO OD

8. Tab Miso 100mg PV Stat

50mg 4 hourly

9. Inj Syntocin 5U in RL IV Starting from

10 drops/min
upto 40 drops

10. Tab Amlodipine 5mg PO OD

11. Syrup Lactulose 10ml PO TDS

12. Inj. Durataz 4.5gm IV BD

13. Tab B-long 2Tab PO TDS

14. Inj Rhogam 1 amp IV Stat

15. Tab Cefexime 400 mg PO BD

66
Iron
Trade name: E-fol
Generic name: Ferrous Suphate
Group: Minerals
Iron is a micronutrient, it is essential for formation of haemoglobin.

Mechanism of action
It is essential micronutrient for formation of haemoglobin. It’s product haem combines with
globulin to produce hemoglobin

Indication
Anemia, pregnancy and puerperim

Preparation
tablet and iron dextran

Usual Dose
100-200 mg of iron in divided doses
can be given parenterally where oral therapy cannot be taken as iron dextran
Treatment should be continued until haemoglobin reach normal
citric acid and ascorbic acid increase its absorption

Contraindication
During 1st trimester of pregnancy, patient under tetracycline and antacids

Side effect
GIT: abdominal discomfort, constipation, black stool

Nursing consideration

Ascorbic acid increases absorption of iron. Consuming citrus fruit or tomato juice
with iron preparation may increase its absorption.

67
 Milk, eggs, or caffeine beverages inhibit absorption.
Increase fluid intake
Iron preparations cause dark green or black stools.
Report constipation or diarrhea
Encourage fiber and roughage containing diet

Calcium
Trade name: Calvit
Generic name: Calcium phosphate
Group: Minerals

Mechanism of action
It helps in contraction of muscles and transmission of nerve impulses from nerve endings to
muscle fibers and in clotting of blood. It is important component of teeth and bones. Vitamin
D and some hormones controls absorption and excretion of calcium from kidney, parathyroid
hormone and calcitonin control the regulation of calcium

Indication
Hypocalcaemia in tetany, rickets, hyperkalemia, osteomalacia, pregnancy, cardiac arrest,
chronic renal disease

Preparation
Calcium Sachet
Calcium Tablet
Calcium Chewable Tablet

Usual Dose
Adult: 800mg/Day
Pregnancy Lactation: 1200 Mg/Day

68
Contraindication
Renal Stone

Side Effect
Respiratory: Bronchospasm
Skin: Rash, Itching
GIT: Constipation
CVS: Bradycardia, Cardiac Arrhythmias

Nursing Consideration
Increase fluid intake

Methyldopa
Trade name: Dopamet
Generic name: α-methyl-L-dopa
Group: Centrally acting anti hypertensives

Mechanism of action
Although the mechanism of action has yet to be conclusive , the resultant hypotensive effect
is due to the drug's action on the CNS. Methyldopa is converted into the metabolite, alpha-
methylnorepinephrine, in the CNS, where it stimulates the central inhibitory alpha-adrenergic
receptors, leading to a reduction in sympathetic tone, total peripheral resistance, and blood
pressure. Reduction in plasma renin activity, as well as the inhibition of both central and
peripheral norepinephrine and serotonine production may also contribute to the drug's
antihypertensive effect, although this is not a major mechanism of action. This is done
through the inhibition of the decarboxylation of dihydroxyphenylalanine (dopa)—the
precursor of norepinephrine—and of 5-hydroxytryptophan (5-HTP)—the precursor of
serotonin—in the CNS and in most peripheral tissues.

69
Indication
For use in the treatment of hypertension.

Preparation
Tablet 125mg, 250mg, 500mg

Usual Dose
Initially: 250mg orally 2 to 3 times a day increased gradually at intervals of at least 2 days
(maximum 3gm/day) initially 125mg twice daily in the elderly

Contraindication
Active Liver Disease, Phaecochromocytoma Depression

Side effect
Sedation, Depression, Nightmare, Headache, Fever, Dry Mouth, GI Upset, Hemolytic
Anemia, Hepatitis, Nasal Stiffness, Edema, Parkinsonism, Gynaecomastia, Lactation,Rashes,
Blood Dycariasis, Positive Coomb’s Test

Nursing consideration
- If sign of orthostatic hypotension and other adeverse effect develop, give medicine at -
bedtime
- Warn patient to avoid hazardous activities that require mental alertness until sedative effect
subside
- Weight patient daily, salt and water retention may occur but can be relieved by diuretics

70
Magnesium sulphate
Trade name: Magnesuim Sulphate
Generic name: Magnesuim Sulphate
Group: Anti convulsant

Mechanism of action
It increases cerebral blood flow as established by Doppler studies. It reduces cerebral
vasospastic ischemia. Elevated concentration of circulatory magnesium decreases the
acetylcholine release and reduces the motor plate sensitivity to acetylcholine. This therapy
reduces neuromuscular irritability It also decreases intracranial edema and helps in dieresis. Its
peripheral vasodilation effect improves the uterine blood supply

Indication
Severe Pre eclampsia
Eclampsia

Preparation
Injection (50%) 2mmol Mg++/ml ampoule 10ml (5gm)

Usual Dose
- Loading dose
4gm 20% MgSO4 IV over 5 minutes
- follow
10gm 50% MgSO4, 5gm in each buttock as deep IM injection with 1 ml of 2% lignocaine in
same syringe
Apply aseptic technique while administering MgSO4 deep IM
Patient may feel warm and flushing after administration of MgSO4
If convulsant reoccur
2gm of 50% MgSO4 IV over 5 minutes
Maintenance Dose
- 5gm of 50% MgSO4 in 1ml 2% lignocaine by same syringe four hourly in alternate buttocks
- Continue treatment with MgSO4 for 24 hours after delivery or last convulsion

71
Adverse Effects of MgSO4
Flushing, Sweating, Hypotension, Depressed reflexes, Flaccid paralysis, Hypothermia,
Circulatory collapse, CNS depression, hypocalcaemia with tetany

Contraindication
Decreased blood pressure
Respiratory arrest
Disappearance of patellar reflex

Precaution
Respiratory rate < 16/ min
Platellar Reflex present
Urinary output at least 30ml/hr over 4 hours (if urinary output decreases MgSO4 absorption
increases in blood and results increased toxic effects)

Nursing consideration
- Monitor and assess respiratory status, depth and rate
- Assess patellar reflex (knee jerk) as high dose leads to muscular paresis in this case medicine
should be withheld
- Assess vital sign strictly
- Maintain input output chart, urine output should be more than 30ml/hr
- Renal function must be monitored
- Inj calcium gluconate should be at hand in case of high dose

72
Aciloc
Trade name: Aciloc
Generic name: Ranitidine
Group: H2 receptor antagonist

Mechanism of action
It inhibits action of histamine at H2 receptor by blocking the receptor. This prevents histamine
from combining to H2 receptors. Thus, histamine will be unable to stimulate the secretion of
proton (H+) which combines with chloride in stomach and produce HCL. This leads to
reduction of acidity and increase pH.

Indication
Used in the treatment of peptic ulcer disease (PUD), dyspepsia, stress ulcer prophylaxis, and
gastroesophageal reflux disease (GERD).

Preparation
Ranitidine Tablet 150mg, 300mg
Ranitidine Injection 25mg/dl

Usual Dose
150 Mg BD For 4-6 Weeks
Beningn Gastric Ulcer Or Duodenal Ulcer 300mg Orally At Night For 4-8 Weeks
Maintenance 150mg Orally At Night
IV 50mg 6-8 Hourly

Contraindication
hypersensitivity, lactation, preganancy, renal/hepatic disease

Side effects
CNS: headache, dizziness, confusion, malaise, drowsiness
CVS: bradycardia or tachycardia, hypertension

73
GIT: nausea, vomiting, diarrhea, hepatitis, abdominal pain
Genitourinary: impotence
Eye: ocular pain, blurred vision

Nursing consideration
- Administer Iv slowly, if possible dilute with distilled water over 5 minutes
- Dosage adjustment for patients with impaired Renal function
- Instruct patient to take drugs as directed, even after pain subsides to ensure proper healing
-If patient is taking single dose advice to take at bed time

Pentodac
Trade name: Pentodac, Pantop
Generic name: Pantoprazole
Group: Proton Pump Inhibitor

Mechanism of action
Pantoprazole is a proton pump inhibitor (PPI) that suppresses the final step in gastric acid
production by forming a covalent bond to two sites of the (H+,K+ )- ATPase enzyme system at
the secretory surface of the gastric parietal cell. This effect is dose- related and leads to
inhibition of both basal and stimulated gastric acid secretion irrespective of the stimulus.

Indication
Used in the treatment of peptic ulcer disease (PUD), dyspepsia, stress ulcer prophylaxis, and
gastroesophageal reflux disease (GERD).

Preparation
Tablet delayed releasing 20 mg, 40mg
Powdered Injection 40 mg/vial
Usual Dose
40mg/day for 8 weeks for erosive esophagitis if not healed continued for another 8 weeks

74
Contraindication
None

Side effects
Rare diarrhea, headache, dizziness, pruritus, skin rash

Nursing consideration
- Give tablet without regards to meal, tablet should not be chewed
- Refrigerate vial, protect from sun
- For reconstitution mix 40mg vial with 10ml 0.9% NaCl then further dilute with 100 ml 5%
dextrose or NS or RL to have concentration of 0.4mg/ml
- Do not refrigerate reconstituted once diluted, solution I stable for 12 hours

Depin
Trade name: Depin
Generic name: Nifedipine
Group: Calcium Channel Blockers

Mechanism of action
Nifedipine decreases arterial smooth muscle contractility and subsequent vasoconstriction by
inhibiting the influx of calcium ions through L-type calcium channels. Inhibition of the initial
influx of calcium inhibits the contractile processes of smooth muscle cells, causing dilation of
the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue,
decreased total peripheral resistance, decreased systemic blood pressure, and decreased
afterload. The vasodilatory effects of nifedipine result in an overall decrease in blood pressure.

Indication
For the management of vasospastic angina, chronic stable angina, hypertension, and Raynaud's
phenomenon. May be used as a first line agent for left ventricular hypertrophy and isolated
systolic hypertension (long-acting agents).

75
Preparation
Capsules (5mg, 10mg)
tablet depin retard (10mg, 20mg)

Usual Dose
5-20mg 3 times a day with or after meals, 10-20mg BD as sustained release (SR) with or after
meals

Contraindication
Cardiogenic Shock, Acute MI, Hypertension in Pregnancy

Side effect
Headache, dizziness, flushing, palpitation, edema, lethargy, gum hyperplasia

Precaution
Inheart failure, severe hypotension, diabetes mellitus, liver disease, lactation

Nursing consideration
- 4 hourly BP should be taken and recorded
- Drugs should be reduced slowly
- Tablet should not be chewed
- Tell patient about hypotensive effects during adjustments

Misoprostol
Trade name: Misoprostol
Generic name: Misoprostol
Group: Prostaglandin

Mechanism of action
It binds with prostaglandin receptors of uterus and help in uterine contration, frequency,
ripening of cervix

76
Indication
Pregnant women with unfavourable cervices. This indication is avoided in women with prior
uterine surgery or cesarean surgery due to an increased risk of possible uterine rupture.
Misoprostol is also used for the prevention or treatment of serious postpartum hemorrhage.

Preparation
In form of tablet
100mcg and 200mcg

Usual Dose
100-200mcg QID after meal at bed time
labor induction 25mcg 3-6 hourly vaginally or bucally

Contraindication
pregnancy, lactation

Side effect
diarrhea, abdominal pain, appetite change, headache, anxiety, dysmennohea, miscarriage

Nursing consideration
- Give with food to minimize GI adverse effects
- Store away from heat, light, and moisture.
- Monitor for diarrhea; may be minimized by giving drug after meals and at bedtime. Diarrhea
is a common adverse effect that is dose related and usually self-limiting

77
Syntocin
Trade name: Syntocin
Generic name: Oxytocin
Group: Anti-tocolytic Agents

Oxytocin is an octapeptide secreted by posterior pituitary along with ADH. Oxytocin is a

naturally occurring nanapeptide hormone. It has pronounced effects on uterine contraction and
for this purpose it is used clinically to induce labour.
Mechanism of action
Binds the oxytocin receptor which leads to an increase in intracellular calcium levels. The
oxytocin-oxytocin receptor system plays an important role as an inducer of uterine contractions
during parturition and of milk ejection. It induces hypotension at high dose and decrease urine
output

Indication
To assist in labor, elective labor induction, uterine contraction induction, reduction of postpartum
haemorrhage and expulsion of placenta, incomplete abortion, increase mill secretion

Preparation
Injection oxytocin 5IU/ml (1IU of oxytocin = 2mcg of pure hormone)

Usual Dose
Induction and augmention of labour start 1-4 milliunit/min increasing the rate every 15-20 min
to max of 20milliunit.min
Postpartum haemorrhage Prevention IM5-10 units
Treatment by slow IV injection 5 units, severe cases : by IV infusion 5-10 units in normal saline

Contraindication
hypersensitivity, pregnancy, severe toxaemia, obstructed labour, hypertonic uterus, placenta
previa, fetal distress

Side effect

78
CNS: subarachnoid hemorrahage
CVS: hypertension, tachycardia arrhthymias
Blood: afibrinogenemia
GIT: nausea, vomiting
Miscellaneous: hypersensitivity, hypertonic uterine contraction, abruption placenta, impaired
uterine blood flow, pelvic hematoma, increased uterine motility, uterine rupture and PPH

Nursing consideration
- Ensure continuous observation of patient receiving IV oxytocin for induction or stimulation of
labor; fetal monitoring is preferred. A physician should be immediately available to deal with
complications if they arise.
- Regulate rate of oxytocin delivery to establish uterine contractions that are similar to normal
labor; monitor rate and strength of contractions; discontinue drug and notify physician at any
sign of uterine hyperactivity or spasm.
- Ensure fetal position and size and absence of complications that are contraindicated with
oxytocin before therapy.
- Monitor maternal BP during oxytocin administration, discontinue drug and notify physician
with any sign of hypertensive emergency.
- Monitor neonate for the occurrence of jaundice.

AMLODIPINE
Trade name: Amlod
Generic name: Amlodipine
Group: Calcium channel blocker

Mechanism of action
Inhibits calcium movement across cell membrane of cardiac and vascular smooth muscles,
dilates coronary arteries, decreases total vascular resistancy by vasodilation.

Indication
Hypertension

79
Preparation
Tablet: 2.5mg, 5mg, 10mg.

Usual Dose
For hypertension: initially 5mg/day as single dose, maximum 10mg/day.
For angina: 5-10 mg:adult; 5mg:elderly

Contraindication
Severe hypotension, impaired hepatic function, aaortic stenosis, CFH.

Side effect
Peripheral edema, headache, flushing, dizziness, palpitation, nausea, asthenia.

Nursing consideration
Access BP, if systolic BO s below 90 mm Hg withhold medicine and inform to physician.
Access the peripheral edema behind medical malleolus for fluid retention.
Instruct patient as do not discontinue the medication abruptly.
Avoid concomitant ingestion of grapefruit juice.

Lactulose
Trade name: Cephulac
Generic name: lactulose
Group: hyperosmotic laxative

Mechanism of action
Lactulose is a synthetic sugar used in the treatment of constipation and liver disease. It consists
of the monosaccharides fructose and galactose. In the colon, lactulose is broken down primarily
to lactic acid, and also to small amounts of formic and acetic acids, by the action of via evolved-
beta galactosidase from colonic bacteria, which results in an increase in osmotic pressure and
slight acidification of the colonic contents. This in turn causes an increase in stool water content
and softens the stool. In treating heptic diseases (hepatic encephalopathy) lactulose draws out
ammonia from the body in the same way that it draws out water into the colon.

80
Indication
Treatment of constipation
Prevention and treatment of portal-systemic encephalopathy

Preparation
Syrup 10 g/15 ml

Usual Dose
Laxative:
15-30 ml/d PO; may be increased to 60 ml/d as needed.
Portal-systemic encephalopathy
30-45 ml TDS or QID

Contraindication
known allergy to lactulose, low-galactose diet.
Use cautiously with diabetes and lactation.

Side effect
GI: Transient flatulence, distension, intestinal cramps, belching, diarrhea, nausea
Hematologic: Acid---base imbalances

Nursing consideration

- Give laxative syrup orally with fruit juice, water or milk to increase palatability.
Do not freeze laxative form. Extremely dark or cloudy syrup may be unsafe; do not use
- Administer retention enema using a rectal balloon catheter. Do not use cleansing enemas
containing soap suds or other alkaline agents that counteract the effects of lactulose.
- Do not administer other laxatives while using lactulose.
- Monitor serum ammonia levels.
- Monitor with long-term therapy for potential electrolyte and acid---base imbalances.

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Durataz
It is active against betalactamase producing bacteria but not effective against pseudomonas,
poteus and enterococci. It is highly protein bound (85%-90%). It is very commonly used drug
in typhoid then switch over cefixime. It is administered parenterally only.

Trade name: Xone, Taxim, Accutaz Durataz

Generic name: Ceftriaxone
Group: Cephalosporin

Mechanism of action
Inhibits bacterial growth by interfering with a specific step in bacterial call wall synthesis,
probably by acylation of membrane bound transpeptidase enzyme.
This prevents the cross linkage of peptidoglycon chains, which is necessary for bacterial wall
synthesis.

Indication
salmonella typhi, gram negative infections resistant to usual antibiotics, endocarditis,
chancroid, gonorrhea, meningitis

Preparation
Available in injections
Ceftriaxone sodium injection 250mg, 500mg, 1gm

Dose
1-2 g/d IV TDS or QID or in equal divided doses BD. Do not exceed 4 g/d.

Adverse Effects
Gastrointestinal: nausea/ vomiting, diarrhea, taste perversion, constipation
Cardiovascular: vasodilatation
Respiratory: Dyspnea

Precaution
use with caution in infants under 6 weeks of age

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Contraindication
hypersensitivity

Nursing Implication

Use cautiously in patients with renal impairment, where dose adjustment is needed.
Make sure patient does not have cephalosporin and penicillin allergy
Patient are suggested to take a lot of water
Advice patient to inform doctor immediately if allergy occurs

B- long

Trade name: B- long

Generic name: Pyridonxine
Group: Vitamin

Mechanism of action
Pyridoxine is the 4-methanol form of vitamin B6 and is converted to pyridoxal 5-phosphate in the body.
Pyridoxal 5-phosphate is a coenzyme for synthesis of amino acids, neurotransmitters (serotonin,
norepinephrine), sphingolipids, aminolevulinic acid.

Indication
For the treatment of vitamin B6 deficiency and for the prophylaxis of isoniazid-induced peripheral
neuropathy.

Preparation
capsules, syrups and injection

Usual Dose
Pyridoxine deficiency: 10 to 25 mg/day orally, IM, or IV for 3 weeks followed by 2 to 5
mg/day from a multivitamin product.
anemia: 200 to 600 mg orally daily

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Contraindication
Hypersensitivity

Rhogam
Trade name:
Generic name:
Group: Immunoglobulin
Mechanism of action
Sterile nonpyrogenic gamma globulin solution containing immunoglobulins (IgG) of at least 90%
IgG, which provides passive immunity by suppressing active antibody response and formation of anti-
Rh (D) (isoimmunization) in Rh-negative individuals previously exposed to Rh-positive
Effective for exposure in Rh-negative women when Rh-positive fetal RBCs enter maternal circulation
during third stage of labor, fetal-maternal hemorrhage (as early as second trimester), amniocentesis, or
other trauma during pregnancy, termination of pregnancy, and following transfusion with Rh-positive
RBC, whole blood, or components (platelets, WBC) prepared from Rh-positive blood.

Indication
To prevent isoimmunization in Rh-negative individuals exposed to Rh-positive RBC Rh D immuno
globulin micro-dose is for use only after spontaneous or induced abortion or termination of ectopic
pregnancy up to and including 12 wk of gestation.

Preparation
Injection: single dose vial, 5% solution in prefilled syringes, 120 mcg, 300 mcg, 1000 mcg vials

Usual Dose
1. Antepartum Prophylaxis
Adult: IM/IV 1 vial or 300 mcg at approximately 28 wk; followed by 1 vial of mini-dose or
120 mcg within 72 h of delivery if infant is Rh-positive
2. Postpartum Prophylaxis
Adult: IM/IV 1 vial or 300 mcg within 72 h of delivery if infant is Rh-positive
3. Following Amniocentesis, Miscarriage, Abortion, Ectopic Pregnancy

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Adult: IM 1 vial of the microdose, preferably within 3 h but at least within 72 h
4. Transfusion Accident
Adult: IM/IV 1 vial or 300 mcg for each volume of RBCs infused divided by 15, given within
at least 72 h of accident

Contraindication
Rho(D)-positive patient;
person previously immunized against Rho(D) factor,
hypersensitivity , severe immune globulin hypersensitivity, bleeding disorders, pregnancy , neonates,
pediatric clients.

Side effect
Injection site irritation, slight fever, myalgia, lethargy.

Nursing consideration
- Obtain history of systemic allergic reactions to human immune globulin preparations prior
to drug administration.
- Send sample of newborn's cord blood to laboratory for cross-match and typing immediately
after delivery and before administration of Rho(D) immune globulin. Confirm that mother is
Rho(D) and Du-negative. Infant must be Rh-positive.

Cefexime
Trade name: Taxim
Generic name: Cefexime
Group: Cephalosporins

Mechanism of action
Like beta-lactam antibiotics, cefixime binds to specific penicillin-binding proteins (PBPs) located inside
the bacterial cell wall, causing the inhibition of the third and last stage of bacterial cell wall synthesis. Cell
lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that
cefixime interferes with an autolysin inhibitor.

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Indication
Effective against Streptococcus pyogenes, Streptococcus pneumoniae, and gram-negative
bacilli, including Haemophilus influenzae, Branhamella catarrhalis, and Neisseria
gonorrhoeae. Little activity againstStaphylococci, and no activity against Pseudomonas
aeruginosa; also uncomplicated UTI, otitis media, pharyngitis, tonsillitis, and bronchitis.

Preparation
200 mg, 400 mg tablets; 100 mg/5 mL suspension

Usual Dose
PO 400 mg/d in 1–2 divided doses

Contraindication
Patients with known allergy to the cephalosporin group of antibiotics.

Side effect
GIT: Diarrhea, loose stools, nausea, vomiting, dyspepsia, flatulence.
CNS: Drug fever, headache, dizziness.
Skin: Rash, pruritus,
Urogenital: Vaginitis, genital pruritus.

Nursing consideration
- Determine previous hypersensitivity reactions to cephalosporins, penicillins, and history of
other allergies
- Monitor I&O rates and pattern: Nephrotoxicity occurs more frequently in patients >50 y,
with impaired renal function
- Report loose stools or diarrhea during drug therapy and for several weeks after. Older adult
patients are especially susceptible to pseudomembranous colitis.
- Take this antibiotic for the full course of treatment.
- Do not miss any doses and take the doses at evenly spaced times, day and night.
- Do not breast feed while taking this drug without consulting physician.

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PROGRESS REPORT
Date Day Progress Report Remarks
2070/1/19 Day of Vitals:
admission T-97.6ºf
P-84/m
R-24/m
Blood Pressure: 150/110
Patient was admitted at 12 MN
Under oral anti hypertensive medicine
BP monitored every 2 hourly
I/O charting done
2070/1/20 1st day of Vitals: Albumin (3+)
admission T-97ºf WBC: 10-12/hpf
P-80/m Epithelial cells: 16-
R-20/m 18/hpf
Blood Pressure: 150/110 TLC: 12,800/mm³
BP monitored every one hourly Platelets:
CBC, Urine Analysis, Biochemistry, 1,55,000/cumm
Hematology and other investigations RBS:83mg/dl
sent and report collected Urea: 25mg/dl
Tab methyldopa 150mmg TDS and Creatinine: 1.1mg/dl
Tab depin 10mg TDS started Sodium: 142mmol/l
24 hour urine collection started Potassium: 2.9mmol/l
Catheterization done Uric Acid: 4.7mg/dl
MgSO4 started, maintenance dose was LDH:2057 IU/L
give every 4 hourly USG: singleton
urine measured every 2 hourly pregnancy with 25
IV drip started WOG
Tab Pantop 40mg OD added
Strict I/O charting done

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2070/1/21 2nd day of Vitals:
admission T-97ºf
P-92/m
R-32/m SPO2- 86% without O2
BP: 160/110
Oxygen started at 2l/min
RFT, LFT,LDH, BT, CT, PT, INR,
CBC, Peripheral Blood Smear,
Urinalysis sent
Inj RL continued slowly
Misoprostol 100mcg 1st dose kept per
vaginally
MgSO4 maintenance dose continue
Blood grouping and cross matching
done
24 hour urine protein sample sent
Male fetus 0.9kg expelled at 11pm
2070/1/22 3rd day of Vitals:
admission T-98ºf
P-88/m
R-28/m, SPO2- 96% without O2
BP: 140/90
first day following MTP
Catheter continued oxygen stopped,
SPO2 maintained
Depin holded
II pint whole blood+ II pint FFP and I
pint PFR collected
MgSO4 maintenance dose continue and
stopped after 24 hours following MTP
Strict I/O charting done

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2070/1/23 4th day of Vitals: Hb: 9.0 gm%
admission T-97ºf Pt: 86,000
P-80/m Urine RBC 14/hpf
R-20/m
BP: 150/100
Patient was in IV and Oral medicine
Catheter continued
IV drip stopped
Strict I/O charting done
BP monitored every two hourly
Patient diagnosed with HELLP
syndrome
2070/1/24 5th day of T-97ºf
admission P-80/m
R-20/m
BP:140/90
Vital Sign monitored
Medical consultation done
Opthalmological consultation done
Vital monitored
Catheter out done and self voiding
done by patient
Inj Rhogam given
2070/1/25 Day of Vitals:
discharge T-97ºf
P-84/m Patient was stable and
R-22/m platelet count at the
Blood Pressure: 140/90 time of discharge was
Medical consultation was done and 138,000
discharged patient on request

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DISCHARGE TEACHING
My Patient Bimala Gurung 28 years female was admitted on 2070/1/19 12 MN from
emergency with provisional diagnosis of G3P2L1 at 26+4 WOG with PIH and later
diagnosed with Severe pre eclampsia with HELLP syndrome. After six days of
hospitalization she was discharged on request on 2070/1/25. At the time of discharge, I gave
discharge teaching to patient and visitor focusing on

Medication:
Tab Iron 1tab PO BD for 2 months
Tab Calcium1tab PO OD for 45days
Tab Amlodipine 5 mg PO OD continue

Follow up:
Follow up in OPD after 1 week
Follow up in Medical OPD after 1 week (mon/wed/thur)
Follow up in eye OPD after 6 months

Management:
Continue Amlodipine until blood pressure drops to normal, stop on doctor’s advice only
home monitoring of BP

Diet:
Take high protein and carbohydrate diet, limit fatty food and intake low sodium diet

Health Teaching:
- Avoid heavy lifting and staining for 6 weeks
- Avoid sexual intercourse at least a month
- Adopt proper family planning method
- Maintain compliance to drug therapy
- Come regularly for follow up
- Before conception of another child take medical advice or do counseling

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LESSON LEARNT
My Patient Bimala Gurung 28 years female was admitted with provisional diagnosis of
G3P2L1 at 26+4 WOG with PIH on 2070/1/19 12 MN from emergency with chief
complain of Epigastric pain, vomiting and headache, she was admitted for 6 days and
during this period I provided nursing care to my patient based on a nursing theory. I got
opportunity to apply theoretical knowledge in practical setting beside that I also learnt how to
manage case, its medical treatment and protocols.

During this course I took history of my patient, which revealed she had history of IUFD 3
years back due to PIH, I performed physical examination and distinguished characteristic
features seen in PIH and sever pre eclampsia while comparing it with my patient and book.

I got opportunity to study my case side by side comparing with theory and practical, it helped
to broaden my knowledge regarding this disease. I also learnt its causes, clinical features,
pathology and complications.

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SUMMARY
During my clinical practicum for child Midwifery and Obstetric I and II , as per our
curriculum I did a case study on 28 years old female with diagnosis of PIH with severe pre
eclampsia with HELLP syndrome admitted on 2070/1/19 with chief complain of Epigastric
pain, vomiting, headache and blurring of vision. She also had history of IUFD 3 years back
due to PIH.
She was admitted for six days, at the time of admission she was well oriented to time place
and person however after 24 hours of hospitalization her condition deteriorated severely and
after sending investigations for urinalysis (for albumin) and biochemistry (LDH, LFT, RFT)
she was diagnosed with severe preeclampsia, her blood pressure were rising and was not
being controlled which created threat of developing eclampsia in patient thus medical
termination was planned as fetus was too small for survival and continuation of labour was
not possible for mother so labor was induced. A male fetus of 0.9 kg was delivered vaginally.
After delivery patient’s platelet counts decreased to 86,000 and liver enzymes SGOT and
SGPT were elevated thus was diagnosed with HELLP syndrome, with persistent rise in blood
pressure even after delivery, patient’s condition thought however improved but was not still
stable.
After blood transfusion her platelets counts were elevated, along with PIH and Pre eclampsia
my patient had Rh incompatibility as well, her blood group was A negative thus Injection
Rhogam was given for isoimmunization, medical consultation and opthalmological
consultation were done to evaluate complications of PIH and she was discharged on
2070/1/25 on patient’s request.

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REFERENCES
- Dutta D. C. ,Textbook of Obsterics, 7th edition , New Central Book agency (P) Ltd,
Kolkata
- Balakrishna Shiela, Text book of obstetrics, 1st edition, 2007, Parces Medical
Publishers, Hyderabad, India
- Tuitui R, manual of Midwifery I, 8th edition, 2012, Vidyarthi Pustak Bhandar,
Bhotahity, Kathmandu
- Gautam S, Subedi D, Midwifery Nursing Part, Edition 2nd, Medhavi Publication
- Tuitui R, Pocket books of dugs, 4th edition,2008, Makalu Publication

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