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

PATIENT’s HISTORY

2

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

factors

Aggravating

factors

1. Epigastric pain Sudden (1-

2 hours

before)

continuou

s

Severe Not

relieved by

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

Third child (daughter) medical termination of pregnancy on 2070/1/21 at Kist

Medical Teaching Hospital by spontaneous vaginal delivery as indicated by

4

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/

pregnancy

complication

Period of

gestation

Type of

delivery/

abortions

Complications in

puerperium

1 2061 4 visits/ no any

significant

complications

37+WOG SVD No any

significant

complications

2 2066 4 visits/ IUFD due to

PIH

37WOG Instrumental

delivery (Forcep

delivery)

No any

significant

complications

3 2070 2 visits / MTP due to

PIH

26+WOG SVD No any

significant

complications

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

6. Menstrual History

Age of menarche: 14 years

Duration of flow: 6-7 days

5

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

10. Chronic Illness

SN Diseases In patient In family

Yes No Yes No

6

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

Dietary habits: balanced diet supplemented by extra sources of vitamins, minerals and

proteins like meat, milk, fruits and vegetables

7

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

16. Family tree

87 years 64yrs

8

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

Patient

Dead male

Dead female

PHYSICAL EXAMINATION FINDINGS

9

P

P

Examination Findings

10

A. General examinationINSPECTION

1. Observe client’s ability to respond to verbal commands

The client is confused and disoriented, inappropriate responses

2. Observe client’s LOC (level of consciousness)

Lowered LOC

3. Observe facial expression and mood Eyes are closed Client was frowning Client was unable to answer questions

4. Observe general appearance; posture, gait, movement

Patient needed support to stand and walk

Decreased movement Even gait

5. General state of health Weak appearance6. Nutritional status Well nourished7. Behavior Inappropriate reaction to situation,

disoriented8. Responses Not responding well9. Cleanliness Hygiene maintained but not well

groomed10. Speech Clear, adequate pace

VITALSTemperature: 97º fPulse Rate: 82/minBlood Pressure: 140/110 and 150/110 in right and left handRespiratory Rate: 20/minHeight : 156cmWeight: 56kg

Normal temperature Normal pulse rate Hypertension (high blood pressure)

Normal respiratory rate

B. Skin AssessmentINSPECTION 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 skin3. Palpate skin for temperature Warmth4. Palpate skin for hydration and turgor Pinched skin promptly returns to it’s

previous state when released No sign of dehydration

5. Press suspected edematous areas with the edge of the finger for 10 seconds

Presence of pitting edema in ankle

11

and observe for the depression6. Inspect skin for lesions, cut and

surgical incision Skin is intact No variation in pigmentation and

texture Freckles, moles and warts are normal

C. Nail1. Inspect and palpate the fingernails

and toenailsnote color, shape and any lesion

Pink colour

2. Check capillary refill by pressing the nail edge to blanch and then release pressure quickly, noting the return of color

Normal return of color <3 sec No discoloration, ridges, pitting,

thickening or separation from the edge

D. Hair and Scalp1. Inspect hair for color, texture, growth,

distribution Color Black, fine texture, wavy hair

2. Inspect scales, lumps, nevi or other lesions

No lumps, lesions, scales and nevi

E. Head 1. Observe the skull for size, shape and

symmetry Skull symmetrical, round and erect on

midline2. Palpate skull for deformities,

depression, lump or tenderness No depression, lumps, tenderness and

any deformitiesF. Face 1. Inspect for abnormal facial

expression, gestures and involuntary movements, swelling and masses

Normal facial expression No any involuntary movements Swelled face

2. Palpate face for edema, tenderness and depression

Peri- orbital edema present around eyes

G. Sinuses1. Palpate sinuses for tenderness No tenderness in frontal, maxillary

and ethmoid sinuses H. Eye1. Inspect both eyes for position and

alignment No deviation from normal condition

2. Eye brows inspected for distribution and any scaliness

Uniform distribution and no scaliness

3. Eyelashes inspected for infection and sty

No infection or sty

4. Conjunctiva inspected for redness, paleness, discharge, foreign body, dryness or tearing

No redness, paleness, discharge, foreign body, dryness or tearing

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5. Inspect sclera for color change, injury and dilated blood vessels

Slightly yellowish sclera

6. Cornea for color, abrasion and white spots

Transparent , no abrasion or white spots

7. Pupil for size, shape and symmetry comparison

Pupil round, symmetrical and uniform

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 transparent11. Convergence test Normal (positive)I. Ear

1. Location and size The top of pinna cross the occiput line

Equal size bilaterally2. Pinna for any lump or lesion No lump or lesion3. The external auditory canal for ear

discharge, mass foreign body and crumen

No discharge, redness, masses or foreign body, small amount of 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. Nose1. Location of nose Centrally located2. Nostrils for their size and

symmetry Uniform in size and symmetrical

3. Nasal septum for polyp No polyp4. Nasal canal Pink mucosa, no discharge or foreign

bodyK. Mouth And Throat1. Lip for color, moisture, cracks or

ulcer Lip pink in color, moist, no

discoloration, cracks or ulcer2. The mucous membrane of the mouth

for color, ulcer, nodules and amount of saliva

Pink, moist, mucous membrane, no ulcer, nodules, adequate saliva

3. Gum for inflammation, swelling, redness and bleeding

Pink gum, no inflammation, swelling, redness and bleeding present

4. Teeth for color, cavities and missing teeth

White color, No missing teeth, cavities present

13

5. Tongue for symmetry, color and papillae

Pink, moist, symmetrical, papillae normal

6. Pharynx and tonsils observed No inflammation and swelling and difficulty swelling

L. NeckINSPECTION

a. Ask patient to sit straight No tilting of neckb. Observe for masses, congenital

goiters, scars, distended jugular vein No masses, congenital goiters, scars

or distended jugular veinc. Thyroid gland No enlargement of thyroid glandd. Ability to move neck No neck stiffness, smooth range of

motion and no tendernessPalpation

1. Thyroid gland palpated to exclude goiter, masses and enlargement

No goiter, , masses and enlargement

2. The back of neck along the spine and back

No abnormal alignment of spine

M. Lymph nodes1. Inspection and palpation of lymph

nodes for enlargement and tenderness No tenderness or enlargement

N. Chest and lungsINSPECTION

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 lungsPALPATION

1. Chest for expansion, lumps, tenderness and depression along ribs

Equal Bilateral expansion of lungs, no lumps, tenderness or depression noted

PECUSSION1. The front and back of chest from apex

to base Resonant sound heard over the entire

chest, anteriorly and posteriorlyAUSCULTATION

1. The front and back of the chest to evaluate breath sound using stethoscope

Vesicular sound heard all over the lungs

2. Compare duration of inspiration and expiation

Inspiration longer than expiration

14

3. Check for abnormal breathe sound like rales, fine crackles, rhonchi and wheezing

No rales, rhonchi or wheezes present Breathing sound clear

O. HeartINSPECTION

1. Enlargement of neck veins No enlargement of jugular veinsAUSCULTATION

1. Aortic area (2nd intercostals space just right of the sternum)

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)

Clear regular heart rate 84/min No abnormal S3 heart sound present

5. Note the clarity and regularity of heart sound

Regular, Normal heart sound S1 and S2 present

No abnormal heat sound like gallop and murmur present

P. Female BreastINSPECTION

1. Size and shape of the breast, observe nipple condition

Breasts and nipples are uniform in shape and size, nipples are pointed in same direction

Left breast slightly larger than right breast

2. Look for swelling, dimpling or retraction of breast

No swelling, dimpling or retraction of breast

3. Nipples for cracks and discharge No cracks and dischargePALPATION

1. Both breast were palpated in circular motion for masses, swelling

Soft, non tender, no masses, lumps and swelling were detected

Q. AbdomenINSPECTION

1. For shape, size, dilated veins, straie, previous incisional scars, lesions

Round shape, no distention, lesions, previous incisional scars or dilated abdominal veins present

Linea nigra and striae gravidarum present

AUSCULTATION1. For bowel sound (increased bowel

sound or decreased bowel sound by Bowel sound present in all areas in

every 20 seconds

15

placing stethoscope for 5 minutes)2. Note type of sound

Gurgling sound present

PECUSSION1. Keep patient in supine position and

percuss abdomen in all four quadrants Tympanic sounds heard over gas-

filled viscera and dull sound over fluid filled viscera

Dull sounds were more prominentPALPATION

1. Keep patient in supine position and ask patient to relax abdomen, palpate abdomen in all 9 partsFeel for any masses and tenderness

No abdominal masses and tenderness

2. Palpate liver, place left hand on 11th and 12th rib and apply firm pressure to push liver forward towards the right handNote enlargement and tenderness

Liver not palpable, no tenderness or enlargement

3. Spleen: keep patient in right lateral position, place left hand on patient’s back under the left rib cage

Spleen not palpable, no enlargement or tenderness

4. Kidneys: keep patient in supine 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 tooNote enlargement and tenderness

Kidneys non palpable and non tender

R. AnusINSPECTION

1. Anus for irritation, hemorrhoids, cracks, fissure

No irritation, hemorrhoids, cracks, fissure

S. Genital Area INSPECTION

1. Vulval swelling, discharge, condition of perineum, labia for color, redness, swelling of labia

No discoloration, swelling, or redness No abnormal vaginal discharge

2. Check for urethral orifice for redness or discharge

No redness or discharge

3. Vaginal discharge or bleeding from vagina

No abnormal Vaginal discharge or bleeding from vagina

T. Musculoskeletal System

16

INSPECTION1. The muscles and joints

ask patient to perform range of motion exercises, joint movement of neck, wrist, ankle, hip in all possible direction

Patient was unable to perform ROM exercises due to patients deteriorating condition and generalized body pain

Patient was in no condition to perform it

2. Patient’s supine, note placement and curvature

Spine is in midline;slightly curved out from neck inward at the waist

PALPATION1. Palpate joints for swelling, tenderness

and temperature No joint swelling, or tenderness,

normal temperature2. Ask patient to perform range of

motion exercises, joint movement of neck, wrist, ankle, hip in all possible direction

Patient was in no condition to perform it

U. Nervous System1. Muscle strength, push against

patient’s hand and ask to resist push Weak muscle strength

2. Sensation Present3. co-ordination of movements co-ordinated motor activitiesV. Reflexes1. Biceps reflex Contraction of the biceps muscle and

flexion of the forearm2. Triceps reflex Normal response, extension of

forearm

3. Knee jerk Extension of lower leg4. Plantar reflex Flexion of all toes and inversion and

flexion of the forefoot

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

17

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

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

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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

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

20

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

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

21

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

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

22

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

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

23

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

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

24

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

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

25

ETIOPATHOGENESIS OF PRE-ECLAMPSIAPre-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.

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

26

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

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

27

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.

PATHOPHYSIOLOGY

Primary cause unknown (genetic/ immunological)

Initial phase: vascular pathology

Failure of second wave of trophoblast invasion

Decrease blood flow in spiral artery

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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

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.

29

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.

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:

30

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

Indicators of mild to moderate and severe preeclampsia

Site Indicator Mild to Moderate

Severe

Central nervous system

Symptoms and signs

HyperreflexiaHeadache

Blurred visionHeadacheIrritability

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 LFTsEpigastric painRuptured liver

Hematologic Platelets > 100,000/uL < 100,000/uL

31

Hemoglobin Normal range Elevated

Vascular Blood pressure < 160/110 mm Hg

>160/110 mm Hg

Retina Arteriolar spasm Retinal hemorrhages

Fetal- placental unit

Growth retardation Absent Present

OligohydramniosFetal distress

May be presentAbsent

PresentPresent

    

Key:

AST = aspartate aminotransferase;

ALT = alanine aminotransferase;

LDH = lactate dehydrogenase;

LFTs = liver function tests.    

My patient was presented with severe Pre-eclampsia.

ECLAMPSIAEclampsia 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

32

- 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.

CLINICAL FEATURES

According To Book In My Patient

Onset

Usually insidious onset but on rare occasions

onset may be acute and rapid

Onset acute and rapid

Symptoms

Mild symptoms

Slight swelling over ankles which persists on

rising from bed in morning and tightness of

the ring finger

Swelling over ankles present

33

Swelling gradually extending to face, body,

abdominal wall, vulva and whole body

Generalized edema present with peri-orbital

edema around eyes and face

Alarming symptoms (usually associated with acute onset)

Headache – either located in occipital or

frontal region

Headache present

Disturbed sleep pattern Absent

Diminished urinary output – urinary output

less than 400ml in 24 hours

Diminished urinary output present

Epigastric pain- acute pain in the Epigastric

region associated with vomiting, coffee color

vomitus due to sub capsular haemorrhage in

the liver

Acute Epigastric pain with vomiting

Eye symptoms- blurring, scotomata, dimness

of vision or at times complete blindness

vision regained within 4-6 weeks

Blurring of eye initially absent but present as

disease progressed

Signs

Abnormal Weight Gain- within short span of

time. A rapid weight gain of more than 5lbs

or more than 1lbs a week

Absent

Rise of blood pressure: the rise of blood

pressure may be insidious or abrupt. Diastolic

pressure rises followed by systolic pressure

Present blood pressure raised up to 160/120

mm Hg

34

Edema: visible edema over the ankles on

rising from bed in morning, generalized

edema in severe cases.

Generalized edema present

No manifestation of chronic cardiovascular

and renal pathology

No manifestation of chronic cardiovascular

and renal pathology

Pulmonary edema: due to leaky capillaries

and low oncotic pressure

Absent

Abdominal examination: reveals evidences of

chronic placental insufficiency such as

Oligohydramnios, IUGR

Absent, IUFD occurred due to induction of

labour

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:

35

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 ✓

INVESTIGATIONS RESULTS

Investigations Findings in my patient Normal valuesBlood Pressure 160/110 – 150/90mmHg 120/80 mmHgTLCDLC: NeutrophilsLymphocytesEosinophils HBPlatelets

12,800/mm³

6038029mg/dl86,000/cumm

4,000-12,000

54-62%25-30%1-3%12-15mg/dl1,50,000-4,50,000/cumm

Blood Grouping and cross matching

A Negative

Coagulation Profile:BT-CT-INR-

10min14min9.0

1-6min1-10min0.8-1.2

36

Biochemistry: UreaCreatinineSodiumPotassiumBilirubin totalBilirubin directSGOT (AST)SGPT (ALT)Total ProteinAlbuminLDHRBSUric Acid

25mg/dl1.1mg/dl142mmol/l2.9mmol/dl4.76 mg/dl3.2 mg/dl1837U/L913U/L7.2 gm/dl4.8 gm/dl2057IU/L83mg/dl4.7mg/dl

10-40mg/dl0.4-1.4mg/dl135-146mmol/L3.5-5.2mmol/LUp to 1.0mg/dlUp to 0.2mg/dl0-40U/L0-40U/L6-8gm/dl3.5-5.5gm/dl<480 IU/LUp to 140mg/dl2.4-5.7mg/dl

Urinalysis: Reaction: alkalineColour: yellowEpi cells: 16-18/hpfRBC: 10-12/hpfWBC: 14-16/hpfAlbumin: 3+

24 hour urine Protein Positive Fundoscopy No retinal detachment seenUSG Singleton preganancy of 25

WOG

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

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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)

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.

38

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

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

39

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

3-4 divided doses

Postural hypotension, CNS

depression, Hemolytic

anemia

Nifedipine Ca channel

blocker

20-40mg/day

2-4 divided doses

Headache, flushing,

palpitation

Hydralazine Peripheral

vasodilation

50-300mg.day

2-3 doses

Headache, flushing,

tachycardia, lupus

Labetalol Combined α and

β blocker

200-400mg/day

2 doses

Postural hypotension, tremors

Atenolol β blocker 50-200mg.day

1-2 doses

Bradycardia, hypotension,

hypoglycaemia, fatigue,

IUGR

*Note: Methyldopa is drug of choice

ACE inhibitors absolutely contraindicated

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

40

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

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

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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

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

42

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

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)

43

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

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.

44

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

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

45

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.

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.

46

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.

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.

47

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

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:

48

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

49

NURSING MANAGEMENT

Assessmenta. 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.

50

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.

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

51

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

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

52

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

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

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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

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

54

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

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

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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

NURSING CARE PLANDemographic 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

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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 2070/1/21All 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

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58

Assesment Nursing Diagnosis

Nursing Goal Nursing intervention Rationale Evaluation

Subjective data:I feel dizziness

Objective data:- Partly conscious- No response to verbal command- Impaired communication- Not oriented to time place and person

Ineffective Cerebral Tissue Perfusion related to decreased cardiac output secondary to vascular vasopasm.

Maintain effective cerebral tissue perfusion with no signs of impaired GCS within 4 hours of intervention

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

To detect early signs of impaired cerebral tissue perfusion

Assess condition of patient.

Indicates neurological impairment and impaired tissue perfusion

To assess neurological status and plan early intervention

To improve blood circulation and decrease blood flow resistance

To prevent potential injuriesTo provide rest to patient

To eliminate fatigue and agitation

To improve tissue perfusion

Goal met patient’s condition was stabilized after intervention as evidenced by increase verbal communication and regain of consicousness

Subjective Data:I have chest pain while breathing

Objective Data:Respiratory Rate: 32/mSpO2 86% without oxygensign of cyanosis:bluish lips seen

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

Maintain gas exchange and oxygen saturation with in 3 hour

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

Administer oxygen at 2l/min

Promotes chest expansion

Facilitates respiratory function by use of gravity

It may cause agitation with increased cardiac workload

MgSO4 toxicity causes depression of respiratory centreTo maintain oxygen saturation

Goal met oxygen saturation was maintained at 96% with oxygen at 2l/min

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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.

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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%)followed by5gm (50%)

IV

Deep IM on alternate buttocks

Stat

4 hourly over 24 hours

5. Tab Aciloc 150mg PO BD

6. Tab Pentodac 40mg PO OD

7. Tab Depin 50mg PO OD

8. Tab Miso 100mg50mg

PV Stat4 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

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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.

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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

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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.

Indication

For use in the treatment of hypertension.

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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

Magnesium sulphate

Trade name: Magnesuim Sulphate

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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

Adverse Effects of MgSO4

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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

Aciloc

Trade name: Aciloc

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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

GIT: nausea, vomiting, diarrhea, hepatitis, abdominal pain

Genitourinary: impotence

Eye: ocular pain, blurred vision

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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

Contraindication

None

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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).

Preparation

Capsules (5mg, 10mg)

tablet depin retard (10mg, 20mg)

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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

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.

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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 

Syntocin

Trade name: Syntocin

Generic name: Oxytocin

Group: Anti-tocolytic Agents

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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

CNS: subarachnoid hemorrahage

CVS: hypertension, tachycardia arrhthymias

Blood: afibrinogenemia

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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

Preparation

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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.

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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.

81

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

2070/1/1

9

Day of

admission

Vitals:

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

2070/1/2

0

1st day of

admission

Vitals:

T-97ºf

P-80/m

R-20/m

Blood Pressure: 150/110

BP monitored every one hourly

CBC, Urine Analysis, Biochemistry,

Hematology and other investigations

sent and report collected

Tab methyldopa 150mmg TDS and

Tab depin 10mg TDS started

24 hour urine collection started

Catheterization done

MgSO4 started, maintenance dose was

give every 4 hourly

urine measured every 2 hourly

IV drip started

Tab Pantop 40mg OD added

Strict I/O charting done

Albumin (3+)

WBC: 10-12/hpf

Epithelial cells:

16-18/hpf

TLC: 12,800/mm³

Platelets:

1,55,000/cumm

RBS:83mg/dl

Urea: 25mg/dl

Creatinine: 1.1mg/dl

Sodium: 142mmol/l

Potassium: 2.9mmol/l

Uric Acid: 4.7mg/dl

LDH:2057 IU/L

USG: singleton

pregnancy with 25

WOG

83

2070/1/2

1

2nd day of

admission

Vitals:

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

2070/1/2

2

3rd day of

admission

Vitals:

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

2070/1/2 4th day of Vitals: Hb: 9.0 gm%

84

3 admission T-97ºf

P-80/m

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

Pt: 86,000

Urine RBC 14/hpf

2070/1/2

4

5th day of

admission

T-97ºf

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

2070/1/2

5

Day of

discharge

Vitals:

T-97ºf

P-84/m

R-22/m

Blood Pressure: 140/90

Medical consultation was done and

discharged patient on request

Patient was stable and

platelet count at the

time of discharge was

138,000

DISCHARGE TEACHING

85

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

LESSON LEARNTMy Patient Bimala Gurung 28 years female was admitted with provisional diagnosis of

86

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.

SUMMARY

87

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.

REFERENCES

88

- 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

89