GOVT COLLEGE OF NURSIG

MBS HOSPITAL,KOTA

A CASE STUDY ON
ECLAMPSIA

SUB-OBSTETRICS & GYNECOLOGY

SUBMITTED TO- SUBMITTED BY-

MR.MANISH SHARMA MS.POOJA PAREEK
LECTURER M.SC NURSING FINAL
GCON,MBS HOSPITAL (2019-20)
KOTA

SUBMITTED ON-
 IDENTIFICATION DATA OF PATIENT
NAME Sunita
HUSBAND NAME Mahesh
AGE / SEX 21 yrs. /HF
RELIGION HINDU
WARD / UNIT 3RD / SLR
DOA 11/12/20 at 5:55 P M
REG NO 31246
CONSULTANT NAME Dr R P KHUTETA SIR
HOSPITAL NAME MAHILA CHIKITSALYA SAGANERI GATE JAIPUR
ADDRESS VILL – SIRSALI, THE – BAMNWAS,
SAWAIMADHOPUR (RAJ.)
PROVISIONAL DIAGNOSIS – HYPERTENSION WITH FITS.
DIAGNOSIS – PRIMI WITH APE.

Present complaints – Patient complaining of headache, Edema, fits, lethargy and

irritable behavior.
Present medical history – Mrs. Sunita Meena 21 yrs. old. She has pregnancy of 34
weeks with labour pain. She was being taken to the Govertment hospital Dausa and
developed fits on the way with muscles rigidty, facial twitching and serection
coming from mouth. After primary treatment she was referred to Mahila
Chikitasalya Saganeri gate Jaipur and admitted in Dr. R. P. KHUTETA SIR
medical unit 3RD and treatment started.
Past medical history -No significant h/o T B, D M, Asthma and Hypertension. Pt
was taking medicine of antihypertensive drug (amlodepine 5 mg) about from last 1
month.
Past surgical history – No significant h/o of any surgery .
Family history - Her husband is about 30 years old and he is farmer. She is 21
years old. She got married last year.
Personal history / life habit - Non smoker, non alcoholic, vegetarian.
Sleep and rest – normal ,810 hours sleep
Habits – not significant
Allergy – no h/o allergy
Immunization history – She got two dose of T T during antenataperiod.
Menstrutal history Menarche at 14 yrs age . Duration of menstrution is 34 days
and flow is normal. Length and regularity of interval between cycle is 28 to 30
days. Colour and volume of flow is red pinkish with normal flow . First day of LMP
– 20/08/20 and EDD IS 27/O5/21.
Obstetrical history – G1 P0 L0 A0
Antenatal history – Mother was antenatally registered at health center. During
pregnancy she was not suffered from any infection / disease (HTN,
DM,ASTHMA)etc. She took IFA tabelts for 3 months and received two dose of T
T.
Intranatal history –
Duration of 1st stage labour – 5 hours
Duration of 2nd stage labour – 30 minutes
Duration of 3rd stage labour – 15 minutes .
Socioeconomic /cultural history –
Occupation of mother household work
Occupation of husband – carpenter
Education of husband – 10th
Education of mother – 6th
Housing condition – family has pacca house but sanitary conditions are not so
good . There is no sanitary latrine and open air. Family uses woods for cooking
food. They use Handpump water to bathe, wash, cook and drink.
Psychological status – Pt has mentally stress by poor contion and stress of having
no male child.
Vital signs –
Date 11/12/20 12/12 /20
BP 180/100 mm/hg 170 /110 mm/hg
Pulse 84/minute 80 /minute
Respiration 20/minute 19/minute
Temp 100 F 99 F

PHYSICAL EXAMINATION –
General appearance – lethargy ,edema, pallor skin ,weakness ,anxious and
comatose .
Anthropometry – wt – 46 kg
Ht – 5”3
Examination of head ,neck and face –

 Head spherical, head normal in size, no any injury and no any scar on head.

 Neck – erect and midline . Nuchal rigidity absent.

  Face – Dull facial expression ,anxious look with pallor colour .
Examination of eye ,ear and nose –

 Eye – sclera clear ,cornea clear and transparent pupil. Blinking reflex, corneal
reflex and papillary reflex present. Swelling on eye lids.

 Ear – ear alignment normal, stratle reflex elicited by loud, sudden noise. No
h/o of any drainage and any infection .

 Nose – nasal flaring absent . No h/o of cold drainage and any infection
Skin – skin dull and dry. Pallor and edematous. Skin texture normal. Examination
of mouth and throat – mucous membrane – pink and dry ,gums are normal in size,
mobility of tounge are normal , dry lips.
Chest and abdomen –

 Chest – clear and h/o chest pain at epigastric region.

 Abdomen – tenderness and bowel sound are present. Size of abdomen is

normal with normal body texture.
SYSTEMIC EXAMINATION –
[1] Cardiovascular system – B P 170 /110 mm/hg, Hypertension present,
tachycardia, palpitation, chest pain at epigastric region.
[2] Respiratory system – respiratory rate 20/minute, respiratory pattern rapid ,cough
reflex normal.
[3] CNS – oriented, no coordination of body movement due to convulsion
headache, visual disturbance due to convulsion (blurred vision)
[4]Musculoskeletal system – normal muscle tone, muscular tenderness and
stretching ability is increased at the time of convulsuon. Both the shoulders are at
normal level and spine are straight.
[5] Digestive system – No diarrhoea and vomitting slight tenderness of
abdomen ,bowel sound is present and loss of appetite.
[6]Integumentery system – oedematous skin ,loss of skin integrity, pallor skin .
[7]Urinary system – oligouria, proteinuria, urine out put is maintained 30 ml /hour
and folleys catheterisation is done .
DISEASE ABSTRACT
Introduction Eclampsia, a lifethreatening complicatio of pregnancy, results when a
pregnant woman previously diagnosed with preeclampsia (high blood pressure and
protein in the urine) develops seizures or coma.
 Approximately 57% of all pregnancies are complicated by preeclampsia.
 Preeclampsia usually occurs in a woman's first pregnancy but may occur for
the first time in a subsequent pregnancy.
 Less than one in 100 women with preeclampsia will develop eclampsia or
(convulsions or seizures) or coma.
 Up to 20% of all pregnancies are complicated by high blood pressure.
Complications resulting from high blood pressure, preeclampsia, and
eclampsia may account for up to 20% of all deaths that occur in pregnant
women.
Gestational hypertension or pregnancyinduced hypertension (pih) is defined as the
development of newarterial hypertension in a pregnant woman after 20 weeks
gestation without the presence of protein in the urine.
. There exist several hypertensive states of pregnancy:
Gestational hypertension
Gestational hypertension is usually defined as having a blood pressure higher than
140/90 without the presence of protein in the urine and diagnosed after 20 weeks of
gestation.
Preeclampsia
Preeclampsia is gestational hypertension (blood pressure greater than 140/90) plus
proteinuria (>300 mg of protein in a 24hour urine sample). Severe preeclampsia
involves a blood pressure greater than 160/110, with additional medical signs and
symptoms.
Eclampsia
This is when tonicclonic seizures appear in a pregnant woman with high blood
pressure and proteinuria.
Hellp syndrome
This is a dangerous combination of three medical conditions: hemolytic anemia,
elevated liver enzymes and low platelet count.
Acute fatty liver of pregnancy
This is sometimes included in the preeclamptic spectrum.
Preeclampsia and eclampsia are sometimes treated as components of a common
syndrome.
DEFINITION- Eclampsia (greek, "shining forth"), an acute and lifethreatening
complication of pregnancy, is characterized by the appearance of tonicclonic
seizures, usually in a patient who had developed preeclampsia. (preeclampsia and
eclampsia are collectively called hypertensive disorder of pregnancy and toxemia of
pregnancy.)
SIGNS AND SYMPTOMS

 Typically patients show signs of pregnancyinduced hypertension and

proteinuria prior to the onset of eclampsia, the eclamptic convulsion.

 Other cerebral signs may precede the convulsion such as nausea, vomiting,
headaches, and cortical blindness.

 other organ symptoms may be present including abdominal pain, liver failure,
signs of the hellp syndrome, pulmonary oedema, and oliguria.

 Iintrauterine growth retardation.

 foetal distress.
  placental bleeding and placental abruption may occur.
The eclamptic seizure four stages of an eclamptic event:

 In the stage of invasion facial twitching can be observed around the mouth.

 In the stage of contraction tonic contractions render the body rigid; this stage
may last about 15 to 20 seconds.

 the next stage is 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.

 The final stage is a more or less prolonged 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 .
During a seizure, the foetus may experience bradycardia.
RISK FACTORS

 Eclampsia, like preeclampsia, tends to occur more commonly in first

pregnancies and young mothers where it is thought that novel exposure to
paternal antigens is involved.

 women with preexisting vascular diseases (hypertension, diabetes, and

nephropathy) or thrombophilic diseases such as the antiphospholipid
syndrome are at higher risk to develop preeclampsia and eclampsia.

 having a large placenta (multiple gestation, hydatiform mole) also

predisposes women to toxaemia.

 Genetic component; patients whose mother or sister had the condition are at
higher risk.
  patients who've experienced eclampsia are at increased risk for
preeclampsia/eclampsia in a later pregnancy.
PATHOPHYSIOLOGY
While multiple theories have been proposed to explain preeclampsia and eclampsia,
it occurs only in the presence of a placenta and is resolved by its removal. Placental
hypoperfusion is a key feature of the process. It is accompanied by increased
sensitivity of the maternal vasculature to pressor agents leading to vasospasm and
hypoperfusion of multiple organs. Further, an activation of the coagulation cascade
leads to microthrombi formation and aggravates the perfusion problem. Loss of
plasma from the vascular tree with the resulting oedema additionally compromises
the situation. These events lead to signs and symptoms of toxemia including
hypertension, renal, pulmonary, and hepatic dysfunction, and in eclampsia
specifically cerebral dysfunction. Preclinical markers of the disease process are
signs of increased platelet and endothelial activation.
Placental hypoperfusion is linked to abnormal modelling of the foetalmaternal
interface that may be immunologically mediated. The invasion of the trophoblast
appears to be incomplete. Adrenomedullin, a potent vasodilator, is produced in
diminished quantities by the placenta in preeclampsia. Other vasoactive agents are
at play including prostacyclin, thromboxane a2, nitric oxide, and endothelins
leading to vasoconstriction. Many studies have suggested the importance of a
woman's immunological tolerance to her baby's father, whose genes are present in
the young foetus and its placenta and which may pose a challenge to her immune
system.
Eclampsia is seen as a form of hypertensive encephalopathy in the context of those
pathological events that lead to preeclampsia. It is thought that cerebral vascular
resistance is reduced, leading to increased blood flow to the brain. In addition to
abnormal function of the endothelium, this leads to cerebral oedema. Typically an
eclamptic seizure will not lead to lasting brain damage; however, intracranial
haemorrhage may occur.
DIAGNOSIS
Seizures during pregnancy that are unrelated to preeclampsia need to be
distinguished from eclampsia. Such disorders include seizure disorders as well as
brain tumor, aneurysm of the brain, medication or drugrelated seizures. Usually the
presence of the signs of severe preeclampsia that precede and accompany eclampsia
facilitate the diagnosis.

INVESTIGATIONS
Cbc, rft (renal function test), lft (liver function test), coagulation profile, plasma rate
concentration, 24 hour urine analysis, ultrasound
PREVENTION
Detection and management of preeclampsia is critical to reduce the risk of
eclampsia. Appropriate management of patients with preeclampsia generally
involves the use of magnesium sulphate as an agent to prevent convulsions, and
thus preventing eclampsia.
TREATMENT
The treatment of eclampsia requires prompt intervention and aims to prevent further
convulsions, control the elevated blood pressure and immediately terminate the
pregnancy.
PREVENTION OF CONVULSIONS
Prevention of seizureconvulsion is usually done using magnesium sulphate. The
idea to use mg2+ for the management of eclamptogenic toxemia dates from before
1955 when it was tested and published—the serum mg2+ therapeutic range for the
prevention of the eclampsic uterine contractions is still considered: 4.07.0 meq/l.
Even with therapeutic serum mg2+ concentrations, recurrent convulsions and
seizures may occur—patients would receive additional mgso4 but under close
monitoring for respiratory, cardiac and neurological depression:

 4–6 g loading dose in 100 ml iv fluid over 15–20 min.,

 then 2 g/hr as a continuous infusion.

ANTIHYPERTENSIVE MANAGEMENT
Antihypertensive management at this stage in pregnancy may consist of hydralazine
(5–10 mg iv every 1520 min until desired response is achieved) or labetalol (20 mg
bolus iv followed by 40 mg if necessary in 10 minutes; then 80 mg every 10 up to
maximum of 220 mg).
DELIVERY
If the baby has not yet been delivered, steps need to be taken to stabilise the patient
and deliver her speedily. This needs to be done even if the foetus is immature as the
eclamptic condition is unsafe for foetus and mother. As eclampsia is a manifestation
of a multiorgan failure, other organs (liver, kidney, clotting, lungs, and
cardiovascular system) need to be assessed in preparation for a delivery, often a
caesarean section, unless the patient is already in advanced labour. Regional
anaesthesia for caesarean section is contraindicated when a coagulopathy has
developed.
INVASIVE HAEMODYNAMIC MONITORING
Invasive haemodynamic monitoring may be useful in eclamptic patients with severe
cardiac disease, renal disease, refractory hypertension, pulmonary oedema, and
oliguria.
INVESTIGATION
S.NO NAME OF THE PATIENT NORMAL VALUE REMARK
. INVESTIGATION VALUE
CBC
1 HB 11.1GM/DL 1418GM/DL ANAEMIC
2 TLC 20.06 4.310.0 INCREASED
1000/CUMM
3 TRBC 5.79 4.56.3MILL/ NORMAL
CUMM
4 MCV 63.7 7793FEMTO DECREASED
 LITER
5 MCH 19.2 2632PICOGRAM DECREASED
6 MCHC 30.1 3236 GM/DL DECREASED
7 RDW – CV 23.3 12.8+1 – 1.2 INCREASED
8 PLATELET 3.49 1.44.4 LAKHS/ML NORMAL
COUNT
9 PACK CELL 36.9 40.54% DECREASED
VOLUME
10 B. SUGAR 95.O MG/DL 60 – 100 MG/DL NORMAL
11 S UREA 72.0 15 – 45 MG/DL INCREASED
12 S. CREATINE 1.2 0.6 1.6 MG/DL NORMAL
13 S.ELECTROLYTE
SODIUM 136 135 145MMOL/L NORMAL
POTASSIUM 3.62 3.5 5.5 MMOL/L NORMAL
CHLORIDE 100 95 105MMOL/L NORMAL
14 S. TOTAL 0.7 0 – 1.0MG/DL NORMAL
BILIRUBIN
DIRECT O.3 MG/DL NORMAL
INDIRECT 0.4MG/DL NORMAL
15 SGOT 36.O 040 U/L NORMAL
16 SGPT 26.0 536 U /L NORMAL
17 DLC
NEUTROPHILLS 88.5% 40 80% INCREASED
 LYMPHOCYTES 0.6 20 40% DECREASED
MONOCYTES 2.8 210% NORMAL
EOSINOPHILLS 0.1 1 6% DECREASED
18 U.ALBUMIN +3DIPSTIK INCREASED

MEDICAL MANAGEMENT –
S. Name of Dose ROUTE ACTION SIDE NURSING
N drug EFFECT RESPONS
O. IBILITIES
1 INJ. 20 MG I .V ANTIHYPE SUDDEN , OBSERVE
LABETAL RTENSIVE SEVERE SIX
OL DRUG HYPOTEN RIGHTS
SIONCAN GIVE
OCCUR SLOWLY
CHECK
VITAL
SIGNS
AVOID
GIVING
WOMEN
WITH
ASTHMA
OR
ASTHMA
2 12INJ.MA 4 MG IV ANTICONV RESPIRAT DONOT
GENSIUM MGSO4 ULSENT ORY GIVE
SULPHAT +20 ML DRUG RATE WHEN
E(I V FLUID2 FALLS TO KNEE
 LOADING 0% LESS JERKS
DOSE) IV SOLUTI THAN ARE
MAINTEN ON 16/MIN ABSENT .
CE DOSE ADMIN HYPERSE URINE
IM ISTRED STIVITY OUT
LOADING SLOWL OF THE BOUT IS
DOSE Y1 DRUG LESS
MG THAN 30
/H/24 ML/HOUR
HOURS . DO NOT
10 MG ADMINIS
IN 10 TRED IN
ML THE
FLUID CASE OF
50% HEART
SOLUTI BLOCK
ON AND
GIVEN MYOCAR
AS 5 DIAL
MG IN DAMAGE.
EACH SEVERE
BUTTO HEPATITI
CK S.
3 BLOOD 1 UNIT IV INCREASE REDNESS OBSERVE
TRANSFU HB LEVEL AND VITAL
SION AND ITICHING SIGNS
HEMATOC ON SKIN . AND SIX
RIT , NAUSEA RIGHTS .
PREVENT AND GIVE
HYPOVOL VOMITTI SLOWLY
EMIA NG .RESPI IN
RATORY ANEAMI
DISTRESS C
 PATIENT
4 INJ 100 ML OSMETIC
MANITTO DIURETIC
L DECREASE
IOP FLUID
MAINTEN
CE
5 INJ GDW 500 ML IV FLUID
5% MAINTENC
E
6 CAP 500 MG ORALLY ANTIBIOTI OBSERVE
AMOXILL C DRUG SIX
IN 500MG RIGHTS
CHECK
VITAL
SIGNS
7 TAB 100 MG ORALLY IRON NAUSEA TAB
FOLIC SUPPLEME AND FOLIC
ACID NT DRUG VOMITTI TABLETS
(FERROU NG NOT
S DIARRHO GIVEN
SULPHAT EA AND WITH
E) TACHYCA MILK
RDIA PRODUC
TS.
8 TAB .BRU 400 MG ORALLY ANALGESI TACHYCA
FEN C RDIA
9 TAB 300 MG ORALLY CALCIUM
CALCIUM SUPPLIME
LACTATE NT DRUG
10 TAB 5MG ORALLY ANTIHYPE HYPOTEN CHECK
AMLODE RTENSION SION BP TIME
PINE TO
TIMETO
PREVENT
HYPOTE
NSION.
11 SYP. 2TSF ORALLY LAXATIVE NAUSEA ASK FOR
CREMAFF AND LOOSE
INE DIARRHO MOTION
EA
12 TAB 10 MG SUBLINGU ANTIHYPE HYPOTEN CHECK
NIFEDIPI ALES RTENSIVE SION BP TIME
NE TO TOME

NURSING CARE PLAN OF ECLAMPSIA

A THROUGH ASSESSMENT OF THE PATIENT IS DONE AND THE PT.
HAVE THE FOLLOWING COMPLAINTS
S. NURSING NURSING NURSING NSG EVALUA
N DIAGNOS GOAL INTERVENTIO IMPLEMENTIO TION
O. IS N N
1 DIFFICUL TO ASSES PT CONDITION PT FEEL
TY IN RESPIRATO RESPIRATORY AND COMFOR
BREATHI RY STATUS STATUS OF RESPIRATORY T IN
NG DUE AIRWAY THE PATIENT STATUS BREATHI
LACK OF CLEARANC GIVE SIDE CHECKED. NG AND
AIRWAY E LYING SIDE LYING MAINTAI
CLEARAN POSITION TO POSITION N
CE AND PREVENT GIVEN.SUCTIO PATENT
INCREAS ASPIRATION NING IS DONE . AIRWAY.
DE OF VOMITUS O2
SECRETI AFTER THE INHALATION
ONS CONVULSION STARTED.CLO
DURING ENDOTREACH THES ARE
FITS EAL AND LOOSEN
NASOGASTRI
C
SUCTIONING
IS DONE
START O2
INHALATION
BY MASK
LOOSEN THE
PT CLOTH.
2 RISK OF TO REMOVE HARMFUL CONVUL
INJURY PREVENT HARMFULL OBJECTS ARE SION
DUE TO RISK OF OBJECTS REMOVED. ARE
CONVULS INJURY FROM THE MOUTH GAG IS CONTRO
ION AND ENVIRONMEN IMMLEMENTE LLED
CONTROL T USE MOUTH D. AND
OF GAG DURING ANTICONVULS PATIENT
CONVULSI FITS. ANT PREVENT
ON OBSERVE MEDICATION ED FROM
JERKING IS INJURY.
 REFLEXES OF GIVEN .PEDDE
ELBOW.GIVE D SIDERALLS
ANTICONVUL IS USED.
SION
MEDICATION.
USE PADDED
SIDE RALLS
TO PREVENT
INJURY.
3 INCREAS TO MAINTAIN VITAL SIGNS PATIENT
E MAINTAIN HYPERTENSIO CHECKED . RELIVED
CARDIAC HYPERYTE N PEACEFUL FROM
OUT PUT NSION REGULARLY. ENVIRONMENT HEADAC
DUE TO GIVE PROVIDED. HE AND
DISEASE ANTIHYPERTE ANTIHYPEWRT HT.
CONDIYI NSIVE DRUGS. ENSIVE DRUG
ON . PROVIDE 20 MG
CALMFUL SDTARTED.
ENVIRONMEN
T.
4 ANXIETY TO EXPLAIN Explation the Pt and her
R/T REMOVE ABOUT THE disease process. family
KNOPWL ANXIETY. DISEASE. Answer all member
EDGE EXPLAIN THE queries. Reassure feel
DEFICIET PTY AND the pt and family relaxed .
ABOUT RELATIVES members. help in all
DISEASE ALL the
PROCEDURE diagnostic
MADICATION procedure.
S AND I
nVESTIGAtion..
support to the
patient and
 family. Tell to
the patient and
family members
about preventive
measures of
hypotension.
5 Decrease Maintain Insertion of Catheterization is Urine
urine urine output folleys catheter . done . maintain i/o output
output due and kidney four hourly chart. I v fluid maintained
to mgso4 function urine out put started as .
affected on monitoring . prescribed.
kidney start I v flow
function. patency .MAIN
TAIN I/O
Chart.

HEALTH EDUCATION :
1. EDUCATE TO MAINTAIN PERSONAL HYGIENE.
2. TELL ABOUT THE PUERPERIUM CARE.
3. TELL ABOUT THE EXCLUSIVE BREAST FEEDING AND ITS
IMPORTANCE.
4. PATIENT SHOULD TAKE MEDICINE ON RIGHT TIME, RIGHT DOSE
AND AND RIGHT ROUTE OF DRUG.
5. TELL ABOUT NEW BORN CARE AND TO PREVENT FURTHER
COMPLICATION.
6. DIET SHOULD BE ADVISED SALT RESTRICATED AND SEMISOLID
WITH ROUGHLY DIET..
7. ABOUT EXERCISE ACTIVE AND PASSIVE TO MAINTAIN ABDOMEN
MUSCLES
 8. COME HOSPITAL TO REGULAR ROUTIK –UP.NE CHEC
9. GIVE PSYCHOLOGICAL SUPPORT TO HER AND FAMILY MEMBERS.
10. ADVICE TO PREVENT COMPLICATION TO FURTHER
PREGNANCY.
11. FAMILY PLANNING METHODS SHOULD BE TOLD.
12. SLEEPING PATTERN SHOOULD BE DONE 6 TO 8 HOURS /24
HOURS.

CONCLUSION: The pt. age 21 years is admitted in medical unit 3rd SLR ward
by Dr R P Khuteta. The pt was suffering from eclampsia. Her all the investigation
was done and mother was provided supportive and symptomatic treatment.her
condition is improving.
BIBLIOGRAPHY –
A. DIANE M FRASER ,MYLES TEXT BOOK FOR MIDWIVES 14
EDITION EDINBURGH LONDON NEWYORK OXFORD PHLIA
DELPHIA SYLOUIS TORNTO 2005 P NO
B. D C DUTTA TEXT BOOK FOR OBSTERIC ,6 EDITION 2004 P NO
C. SAUNDERS “COMPREHENSIVE REVIEW FOR THE NCLEX RN
EXAMINATION 5 EDITION ELSIEVERS PUBLICATION P NO
D. WWW.GOOGLE .COM