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 1
it is a case study report on PIH and Severe Pre eclampsia I did when I was posted on Kist Medical TEaching Hospital for Midwifery Practicum Prepared by: Rashmi Regmi B Sc Nursing Manmohan Memorial Institute Of health Sciences
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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
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
18
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
28
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)
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
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
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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
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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
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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