A STUDY OF MATERNAL AND PERINATAL
OUTCOME IN PREECLAMPSIA
Dissertation submitted to
The Tamilnadu Dr. M.G.R. Medical University,
Chennai – 600032
with partial fulfillment of the regulations
for the award of degree of
M.S – BRANCH - II
OBSTETRICS AND GYNAECOLOGY
K.A.P.Viswanatham Government Medical College
Tiruchirappalli
The Tamilnadu Dr.M.G.R.Medical University
Chennai.
April 2016.
CERTIFICATE
This is to certify that this dissertation titled “A STUDY OF
MATERNAL AND PERINATAL OUTCOME IN PREECLAMPSIA” IN
MAHATMA GANDHI MEMORIAL HOSPITAL, TIRUCHIRAPPALI”
is a bonafide work of DR.PADMA. K., Postgraduate M.S.Obstetrics and
Gynaecology, Department of Obstetrics and Gynaecology,
K.A.P.Viswanatham Government Medical College, Trichy and has been
prepared by her under our guidance. This has been submitted in partial
fulfillment of regulations of The Tamilnadu Dr. M.G.R. Medical University,
Chennai -32 for the award of M.S. Degree in Obstetrics and Gynaecology.
Prof.Dr.D.PARIMALADEVI,M.D.D.G.O
Professor & Head
Department of Obstetrics and Gynaecology
K.A.P.V. Govt.Medical College,
Trichy
Dr.D. UMA.,M.D., D.G.O.,
Associate Professor
Department of Obstetrics and
Gynaecology
K.A.P.V. Govt. Medical College,
Trichy
Prof.Dr.M.K .MURALIDHARAN,M.S.,M.ch (Neurosurgery)
Dean
K.A.P.Viswanatham Govt.Medical College, Trichy
DECLARATION
I Dr.Padma. K., solemnly declare that this dissertation titled, A STUDY
OF MATERNAL AND PERINATAL OUTCOME IN PREECLAMPSIA
IN MAHATMA GANDHI MEMORIAL HOSPITAL, TRICHY” is a
bonafide work done by me at K.A.P.Viswanatham Government Medical
College, Trichy, during 2012-2015 under the guidance and supervision of Head
of the Department , Department of Obstetrics and Gynaecology
PROF.Dr.D.PARIMALADEVI, M.D,D.G.O. The dissertation is submitted to
The Tamilnadu Dr. M.G.R. Medical University, towards the partial fulfillment
of university rules and regulations for the award of M.S.Degree(Branch-II) in
Obstetrics and Gynaecology.
PLACE : TRICHY.
DATE :
Dr. PADMA.K.
ACKNOWLEDGEMENT
I am extremely grateful to The Dean, Prof.Dr.B.MURALIDHARAN,
M.S.,M.ch. K.A.P.Viswanatham Government Medical College,
Tiruchiraappalli for granting me permission to undertake the study and to avail
the facilities needed for my dissertation work.
It gives me immense pleasure to express my gratitude and thanks to my
respected Prof. Dr. D. PARIMALA DEVI , M.D.,D.G.O. Professor and Head
of the Department, Obstetrics and Gynaecology who gave immense support
and encouragement and all the facilities to complete thiswork.
I sincerely express my gratitude and thanks to my respected
Prof. Dr. D.UMA, M.D.,D.G.O Associate Professor, Obstetrics and
Gynaecology Department.
I am particularly grateful for Prof. Dr. Vidhyaravi.M.D., D.G.O., and
Prof. Dr.S. Bama.,M.D.,D.G.O.,DNB.O.G., for their valuable guidance and
help during the study.
I sincerely thank my teacher, guide and mentor Senior Assistant Prof.
Dr. P.Backiavathy.M.D.,O.G.. for her valuable guidance and support.
My heartfelt thanks to all my assistant professors for their guidance in my
study.
I owe my thanks to Dr. Selvam.,M.D., Assistant Professor.,Department
of community Medicine.
I am grateful to the patients without whom the study would have not
been possible.
CONTENTS
S. NO.
TITLE
PAGE
NO.
1. INTRODUCTION 1
2. AIM OF THE STUDY 2
3. REVIEW OF LITERATURE 3
4. MATERIALS AND METHODS 45
5. RESULTS AND ANALYSIS 47
6. DISCUSSION 80
7. SUMMARY 82
8. CONCLUSION 84
9 BIBLIOGRAPHY 85
.
ANNEXURES
PROFORMA
CONSENT
MASTER CHART
ABBREVATIONS
INTRODUCTION
INTRODUCTION
Pre-eclampsia is a multisystem disorder specific to pregnancy and
puerperium, it manifests by onset of hypertension and proteinuria after
twenty weeks of gestation .It occur earlier with gestational trophoblastic
diseases or multiple pregnancies and resolves by twelve weeks postpartum.
Hypertension During pregnancy is diagnosed when the systolic pressure is
140mmHg or more and Diastolic pressure of 90mmHg or more measured
on two occasions at least 6 hours apart within seven days. A single
reading of diastolic above 110mmHg in a pregnant woman is considered as
hypertension.
In 1916, Zweifel first called the toxaemia ―the disease of
theories‖.1 This was recognised as clinical entity since time of Hippocrates.
Pre-eclampsia remained a significant public health threat in both developed
and developing countries, contributing to maternal and perinatal
morbidity and mortality globaly the incidence of preeclampsia among
hospital patients about 7 to 10% of antenataladmissions. The dangers of
Eclampsia, Intrauterine growth restriction & Intrauterine fetal death, etc.
dependent on the degree of pre-existing pre-eclampsia .They can be
mitigated by good obstetric care. In this study, an attempt has been made
to study effect of Preclampsia & the severity on pregnancy & on
maternal & fetal outcome.2
AIM OF THE STUDY
AIMS OF THE STUDY
To study about the prevalence of preeclampsia in relation to
1)age
2)parity
3)unregistered and registered
To study the incidence of various maternal complication of pre
eclampsia. To study the fetal outcome in pregnancies complicated by pre
eclampsia.
REVIEW
OF
LITERATURE
REVIEW OF LITERATURE
SIMILAR STUDIES:
1) Study of maternal and perinatal outcome in preeclampsia by Ankita
Gawde ,U. T. Bhosale dept of obs and gynae , Bharathi Vidhyapeeth ,
Deemed University, Medical college and hospital Sangli , Maharashtra
,INDIA.
2) Maternal and perinatal outcome associated with eclampsia in a teaching
hospital Sukkur, BY Aisha Abdullah , Altaf Ahmed Shakik ,
Bahawaldin Jamro , Dept of obs and gynaecol, medicine, and
paediatrics . Ghulam Mohamed mahar medical college sikkur.
3) Risk factors for preeclampsia and its perinatal outcome. By Sultana and
Aparna.j The Shadan institute of medical sciences , Himayatsagar,
Hyderabad.
4) Maternal and perinatal outcome in pregnancy induced hypertension –
Hospital based study .By Dr. P.Meshram , Dr. Y.H. Chavan G.M.C
Nanded India.
Hypertension is the most common medical problem encountered in
pregnancy .Incidence is seen around 5-10% of all pregnancies.Preeclampsia is
the second common cause of maternal mortality in India & major cause of
perinatal mortality & morbidity.According to International society for the study
of Hypertension in pregnancy(ISSHP).Hypertension is defined as a Systolic
blood pressure morethan 140 mmhg or Diastolic blood Pressure morethan 90
mmhg atleast 2 occations taken 6 hours apart.
MEAN ARTERIAL PRESSURE:
Mean arterial pressure calculated by following formula.
MAP=Diastolic pressure+1/3 Pulse pressure
MAP morethan 105 is significant.In normal pregnancy diastolic Blood
pressure begins to fall in early pregnancy and continues to fall in the second
trimester and reach a nadir at 22-24 weeks .The fall is Due to reduced vascular
tone .Blood pressure should be measured in Woman sitting at 45 degree angle,
cuff should be appropriate size placed at the level of Heart .Multiple readings
should be taken. Korotkoff sound phase 5 is the appropriate measurement of
diastolic blood pressure .Preferably Right arm should be used.
CLASSIFICATION OF HYPERTENSIVE DISORDERS IN
PREGNANCY:
GESTATIONAL HYPERTENSION Hypertension first time
during pregnancy.
No proteinuria
BP returns normal twelve
weeks postpartum.
PRE-ECLAMPSIA & ECLAMPSIA Hypertension diagnosed after
20 weeks of Gestation
Proteinuria
Associated with other signs
& symptoms of pre-eclampsia
Eclampsia associated with
seizures that cannot be
attributed to other causes like
space occupying lesions
,seizure disorders, head injury
and electrolyte imbalance.
PRE-ECLAMPSIA
SUPERIMPOSED ON CHRONIC
HYPERTENSION
New onset proteinuria in
hypertensive women after
twenty weeks gestation
CHRONIC HYPERTENSION Hypertension before
pregnancy
Hypertension diagnosed
before twenty weeks of
pregnancy not attributable to
trophoblastic disease or
multible pregnancy.
Hypertension diagnosed 1st
diagnosed after twenty weeks
gestation &persistent beyond
12 weeks postpartum.
CRITERIA FOR DIAGNOSIS OF PREECLAMPSIA;
Blood pressure of >140/90 mmhg occurring after 20 weeks of Gestation,
presence of proteinuria >300mg per day or 1+ in urine dipstick
examination.24 hours protein measurement is the best method to
quantify proteinuria3.Urinary protein creatinine ratio 0.3 or more is
significant. Edema is little value as an objective sign.
RISK FACTORS: 4
Couple
related
Primi parity
Limited
sperm
exposure
Paternal
Factors
Maternal risk
facors:
Extremes of age
Prior history of
pre eclampsia
Renal diseases
Infection
Susceptible
history
Pregnancy related
Multi fetal
gestation
Hydropic
degeneration of
placenta
Hydatidiform
mole& triploidy
Genesis of pre eclampsia as a two stage disorder
Maternal factors
1.genetic
2.underlying medical disorders
(thrombophilia ,diabetes,
hyperhomocysteinemia,
obesity,hypertension,etc.)
3.immune-maladaptations to
pregnancy.
Placental factors
1.shallow trophoblast invasion in
spiral arteries(abnormal
placentation)
2. placental ischaemia
Connecting
link
Endothelial dysfunction Stage 2
Pre-eclampsia
Good endothelium Bad endothelium
Mild disease Severe disease
Balanced tilted in
favour of oxidative
stress markers
OXIDATIVE STRESS
Free Radicals
Anti oxidants
AETIOPATHOGENESIS:
Exact aetiology of preeclampsia is unknown. Preeclampsia is a two
stage disorder.Theory was propounded by Redman and collegues. 4
According
to this stage one is preclinical and characterised by poor placentation or faulty
endovascular trophoblastic remodelling of Uterine arteries which cause
placental hypoxia. Stage two caused by oxidative stress which causes release
of placental factors into maternal circulation .This inturn causes systemic
inflammatory response and endothelial activation results in clinical syndromes
of preeclampsia and intra uterine growth restriction.
ABNORMAL TROPHOBLASTIC INVASION:
In normal pregnancy, spiral arteries of placenta are invaded by
cytotrophoblast and the elastic and muscular layers are replaced by fibrinoid .In
second trimester second wave of cytotrophoblastic invasion transforms the
myometrial segments of spiral arteries into wide mouthed vessels unresponsive
to vasomotor stimuli .Blood supply is transformed from high resistence low
flow system to low resistence high flow system inorder to increase
uteroplacental flow and meet the needs of the fetus. In preeclampsia primary
wave of trophoblastic invasion is impaired and secondary wave fails to occur.
ABNORMAL ANGIOGENESIS:
Angiogenesis and Antiangiogenesis factors5 involved in placental
vascular development .There is imbalance in these factors. There excess
antiangiogenic factors produced as a result of hypoxia. Trophoblast produces
atleast two antiangiogenic peptides in the circulation . Soluble fms like
tyrosinekinase [sflt -1] and soluble endoglobulin. Decrease in angiogenic
factors like vascular endothelial growth factor [VEGF].
Endothelial cell dysfunction and vasospasm
Endothelial cell dysfunction is the most important factor in
preeclampsia .AntiAngiogenic and metabolic factors and other inflammatory
factors provoke endothelial cell injury .Another one theory is lipid peroxidation
stimulated by Free oxygen radicals because of oxidative stress .Cytokines like
tumour necrosis factor and interleukins also contribute to preeclampsia .It
causes endothelial cell injury, modify the nitricoxide production and interfere
with prostaglandin balance.Increased capillary permeability manifests as
oedema and proteinuria. 4
ETIO PATHO GENESIS
CLINICAL FEATURES OF PRE ECLAMPSIA
ALTERATION IN NITRICOXIDE AND PROSTOGLANDINS:
Protacyclin is a Prostoglandin produced by the vascular endothelium 5. It
is a powerful vasodilator and inhibitor of platelet aggregation. Nitric oxide is
an another potent vasodilator produced by the endothelium .Thromboxane is
produced by platelets and causes vasoconstriction and platelet aggregation. In
normal pregnancy there is an increased production of prostacyclin resulting in
vasodilatation. 6
Damaged endothelial cell lead to reduced production of
nitricoxide. So in preeclampsia vasospasm and platelet activation and adhesion
occurs and activation of coagulation system also occurs.
COAGULATION SYSTEM AND PLATELETS:
Endothelial dysfunction will lead to activation of platelets and
coagulation system by the tissue factor on the endothelium .Results in
widespread disseminated intravascular coagulation . So clotting factors are
used. This results in subclinical to frank DIC. This results in consumption
coagulopathy lead to thrombocytopenia.
METABOLIC FACTORS :
Central obesity and insulin resistance are risk factors for preeclampsia.
Dramatic Increase in free fatty acids and triglycerides in preeclamsia. Calcium
deficiency also a risk factor for preeclampsia.
GENOTYPE AND PHENOTYPE:
There is a definite inherited maternal component in preeclampsia.
Phenotypes will differ among genotypes depending on interaction with
environmental factors.
IMMUNOLOGICAL FACTORS:
Invasion of trophoblast into myometrium and decidua is controlled by
the immune mechanism7. The decidua contains lymphoid tissue,
predominantly natural killers .The NK cells express KIR receptors ,which
recognise the LA class1 molecules. The NK cells VEGF, PLGF, and
Angiotensin 2 which bring about maternal placental bed vascular changes.
MOFFET KING and collegues studied the HLA C-NKcell receptor
Interaction. They state that each pregnancy is unique because of the NKcell
KIR –HLA C interaction .Mothers with absent or decreased KIRs which
interact with HLA C group have increased propensity towards preeclampsia6
PATHOPHYSIOLOGY
Changes because of vasospasm and endothelial dysfunction.
PLACENTA
The typical vascular lesion is termed acute atherosis of the decidual
arteries. Leads to fibrinoid necrosis, macrophages and mononuclear
infiltration. Result in intra uterine growth restriction oligohydraminios,
placental abruption and ultimately fetal demise.
KIDNEY
Main pathology in kidney is glomerular and tubular dysfunction and
glomerular endotheliosis Swollen endothelial cells due to fibrin
deposition.Glomerular dysfunction lead to reduced glomerularFiltration rate
and creatinine clearance. Acute renal failure usually due to acute tubular
necrosis which is reversible. Rarely it lead to irreversible due to acute cortical
necrosis. Tubular dysfunction manifest as hyperuricaemia. Proteinuria due to
increased capillary permeability.
LIVER
Periportal thrombosis and fibrin deposition, haemarrhages and necrosis
seen in liver. There is an increase in enzyme levels [SGOT,SGPT] and clinical
jaundice can occur. 7 Liver changes are responsible for nausea and vomiting.
Small haemorrhages may coalesce to form a sub scapsular haematoma. Which
cause stretching of Glisson’s capsule, and epigastric pain.Catastrophic rare
complication is liver rupture. The typical vascular lesion is termed acute
atherosis of the decidual arteries Lead to fibrinoid necrosis, macrophages and
mononuclear infiltration.
Result in intra uterine growth restriction,
oligohydraminios, placental abruption and uiltimately fetal demise.
PATHOPHYSIOLOGY :
CARDIOVASCULAR SYSTEM.
Three major changes in the cardio vascular system
1.Increased cardiac afterload caused by hypertension .
2Dimnished cardiac preload due to the diminished hypervolaemia of
pregnancy in preeclamsia .
3 Endothelial cell activation with increased capillary permeability Which
causes extravasation of fluid from the intravascular to extravascular space and
into The lungs resulting in pulmonary edema. Haemoconcentration is the
hallmark preeclamsia.so women with preeclamsia and eclampsia sensitive to
fluid therapy and easily can develop pulmonary edema .Also sensitive to even
normal blood loss at delivery.
BLOOD AND COAGULATION
Endothelial dysfunction lead to activation of platelets and the
coagulation System. By activation of tissue factor on the endothelium ,Results
in subclinical to frank DIC. Resulting in consumption coagulopathy result in
throbocytopaenia.This can be demonstrated by the presence of schistiocytes,
Burr cells and fragmented red cells in peripheral blood and also by elevated
lactate dehydrogenase levels.
BRAIN.
In the brain main pathology is cerebral vasospasm .Small cerebral
haemarrhages , thrombosis and fibrinoid necrosis can occur. 9
Cerebral edema
also occur8. Massive cerebral haemorrhage may be the rare complication in
severe hypertension .In CT imaging may show localised hyper intense lesions
are seen at the gray- white matter junction ,primarily in the occipital lobes. This
is known as PRES OR POSTERIOR REVERSIBLE ENCEPHALOPATHY
SYNDROME.
EYES
Retinal vasospasm is the most common finding .Haemorrhage and
Papilloedma Rarely seen in severe hypertension.Visual disturbances are
common and are due to edema of the occipital lobe. Cortical blindness rarely
due to occipital edema . It is temporary. Blindness can also occur due to
involvement of Lateral geniculate nuclei and retina.In Retina ischaemia
,infarction, or retinal detachment can occur. Prognosis is usually good and
reversible following delivery.
CLINICAL EVALUATION.
Most women with hypertension during pregnancy may or may not
present with symptoms and signs of hypertension and related disorders. Raised
blood pressure may be noticed during routine antenatal checkups.Detailed
history is important .
Blood pressure in early pregnancy or in the booking visit Blood
pressure in the prior pregnancy
Is there any palpitation, chestpain pallor?
Is there any history of Headache or epigastric pain orvisual
disturbances?
Is there any history of kidney disease?
Had she noticed any weakness of limbs?
Is there any history of nocturia, polyuria, ?
Is there any history of reduced urine output?
Is there any family history of hypertension
Is there any history of oral contraceptive pills prior to pregnancy?
CLINICAL MANIFESTATIONS :
Hypertension in pregnancy is generally asymptomatic and diagnosed
during antenatal check up.sudden onset and excessive weight gain ,generalized
edema affecting the face ,hands and ankles, particularly non-dependent
oedema, epigastric or right upper quadrant pain, headache and visual
complaints like scotomata,blurred vision or rarely,blindness in a woman with
hypertension are features of severe pre-eclampsia. Symptoms of blurred vision
and severe generalized or occipital headache are suggestive of accelerated
hypertension and impending eclampsia. Physical examination On physical
examination,particular attention should be paid to the apex beat; the second
sound at the aortic area may be accentuated .Ophthalmoscopic examination is
an essential part in the examination .In most women with mild and moderate
pre-eclampsia,fundus is normal.women with long standing pre-existing
hypertension, silver – wiring and tortuosity of the arterioles .In more severe
cases , arterio venous nipping is seen.The grave sign is the development of
papilledema.
Laboratory investigations:
In addition to the routine test in the pregnancy , platelet count ,liver
enzymes ,serum uric acid , lactate dehydrogenase level ,24 hour urine analysis
and culture ,Creatinine clearance should be done.patients with history of poor
compliance to blood pressure ,target organ damage must be detected by ECG ,
ECHO to rule out left ventricular hypertrophy.
Complete blood count and blood film:
Low haemoglobin with increased reticulocytes and abnormally shaped
red blood cells (schistocytes and spherocytes ) indicates microangiopathic
haemolytic anemia. Blood urea and serum creatitine levels are usually lower in
pregnancy due to increased glomerular filteration and hemodilution. Acute rise
may indicate acute renal injury . Serum uric acid is also lowered in pregnancy
due to increased renal clearance. It is more specific especially in women with
super imposed preeclampsia. A rising level in the last trimester indicates
impaired fetal prognosis.
URINE ANALYSIS:
It is usually examined by dip stick method on random sample of urine .if
positive , 24 hour urine collection is done for the quantification of the
albuminuria. Infection gives a false positive results. So culture and sensitivity
must be done to exclude it.
SEVERITY OF PRE-ECLAMPSIA
Pre-eclampsia is classified into mild and severe according to blood
pressure and Proteinuria.
SEVERITY OF PRE-ECLAMPSIA
Diastolic blood pressure 110mmhg and above .
Systolic blood pressure 160mmhg and above
Proteinuria 5gm in 24 hours or more [3+proteinuria or more]
Headache ,visual disturbances or epigastric pain
Oliguria or urine output <than 500ml in 24 hours.
Intra uterine growth restriction
Pulmonary edema
Thrombocytopaenia <than 1,00,000/mm3
Increased liver enzymes[>50IU/L]
PREDICTION OF PRE- ECLAMPSIA.
Previous h/o pre-eclampsia ,antiphospholipid antibodies, and pre-
existing medical conditions. Advanced maternal age in first pregnancy,
multiple pregnancy, interpregnancy interval>10years And booking blood
pressure 130≥systolic ,80mmhg ≥ diastolic historical markers .It will Help us to
screen the women for high risk of pre-eclampsia. At present no single
screening test That can be considered reliable and cost effective for predictive
of pre-eclampsia. BMI>than 35kg/m2, alfa fetoprotein , fibronectin , and
uterine artery Doppler [bilateral notching ]were all Found to have specificities
above 90%,but poor sensitivity.Uterine artery Doppler pulsatility Index
combined with bilateral notching shows the best predictive value.
UTERINE ARTERY DOPPLER VELOCIMETRY
In normal pregnancy, impedence to uterine artery blood flow is
markedly reduced. Failure to undergo physiological trophoblastic invasion
reflected by high impedence flow in the uterine arteries. Increased resistance
to flow and presence of a diastolic notch associated with pre-eclampsia.
PREVENTION.
Low dose aspirin in women at high risk for developing disease.Dietary
supplements like magnesium, antioxidants, marine oils ,and folic acid,do not
reduce the incidence of preeclampsia.Low Serum zinc levels may be
associated with suboptimal level of outcome of pregnancy.
COCHRANE REVIEW (2012) which included over 15,000 women
did not reveal any evi dence of improvement of pregnancy.L-arginine calcium
supplementation ,vitC ,vitE β carotene however the studies investigating
so far having conflicting results.
REST: COCHRANE REVIEW (2006) showed that there was a
significant reduction in the relative risk of pre-eclampsia.
EXERCISE AND PHYSICAL ACTIVITY
Prospective study failed to show the reduction in the relative risk of
pre-eclampsia.
REDUCED DIETARY SALT
Two trials conducted them showed no correlation was observed.
ASPIRIN AND PLATELET AGENTS
Aspirin is an antiplatelet aggregator so improves blood flow by
preventing the formation of micro thrombi within the vessels .A large
randomised control trial ,the Collaborative Low Dose Aspirin Study in
Pregnancy (CLASP) .It showed a non significant reduction of 12%in pre-
eclampsia. Significant reduction of proteinuric pre-eclampsia in a group of
women who were at high risk of Developing early onset pre-eclampsia
leading to preterm delivery, when aspirin was started early in the 2nd trimester.
The study showed that low dose aspirin was generally safe for the fetus and
neonate.
MANAGEMENT OF PRE-ECLAMPSIA.
Natural course of preeclampsia is blocked at the secondary and tertiary
level of prevention. Early detection and treatment according to severity
reduces the complications ,thereby reduce the morbidity and mortality, better
maternal and neonatal outcome9 .Evidence based practice and setting a
protocol in the management of acute onset, severe Hypertension in
preeclampsia and eclampsia improve an immense outcome.10
NICE
guidelines state that intravenous or oral labetalol,oral nifedipine and
intravenous hydralazine May be the 1st line of management of severe pre-
eclampsia. Magnesium sulphate regimen to be considered in case of eclampsia
and imminent eclampsia. 11
Incase of severe pre-eclampsia after 34 weeks of
gestation induction of labour shoud be Considered.The patient is delivered by
induction or caesarean section depending on the Obstetric and fetal indications
benefits of termination weighed against potential risk of continuation of
Pregnancy.
If pregnancy is less than 34 weeks betamethasone 12mg 2 doses 24hours
apart for the Benefit of baby.It will accelerate lung maturity , reduce the
incidence of intra ventricular haemorrhage Necrotising enterocolitis.12
Likewise patients with gestation of ≤34weeks with imminent symtoms, Signs
of multiorgan failure, non reassuring fetus, and eclampsia are delivered,
similarly. A recent review states expectant management in a patients with
pre-eclampsia at a gestational age between 24 and 33 weeks is a safe and a
better practice and is said to bring prolongation of pregnancy for 7 to 10
days. Criteria for termination of pregnancy for patients on expectant
management are as follows;
Uncontrolled blood pressure
Imminent signs and symptoms of pre –eclampsia
Nonreassuring fetal cardiac status
Oligohydraminios
Elevated liver enzymes
Oliguria
Elevated liver parameters especially serum creatinine concentration
Elevated liver enzymes
Development of Hellp syndrome
Pulmonary edema
Pre eclampsia is an unpredictable disorder, only definite cure is
termination of pregnancy. Management depends upon the severity of disease
and period of gestation.IF the pregnancy is 37 weeks are more elective
induction of labour may be performed when Particularly if association of
proteinuria. Time of delivery depends upon the gestational age ,fetal lung
maturity,and most importantly Severity of disease.
MANAGEMENT ACCORDING TO GESTATIONAL AGE
<Than 24weeks ;Stabilise the patient and terminate the pregnancy. 25 to
33 weeks ;Expectant management with intensive maternal and fetal
monitoring.
Indication>34 weeks ;Stabilise the patient with strict fetal surveillance
and deliver Surveillance, steroid therapy for fetal lung maturity, and deliver,if
maternal or fetal compromise.
MATERNAL SURVEILLANCE
Blood pressure should be checked at least 4 times a day. Urine
albumin once a day. Biochemical parameters including full blood count,
kidney function test ,electrolytes, Liver enzymes,and serum bilirubin two to
three times a day . ophthalmic examination to be done On admission to be
repeated if required.
FETAL SURVEILLANCE
Fetel well being by NST and BIOPHYSICAL PHYSICAL (BPP)
.NST is performed usually twice a week .In severe cases twice daily.BPP
can be done weekly.Fetal growth must be monitored by ultrasonagraphy and
sonography wise Amniotic fluid volume is assessed periodically. DOPPLER
studies are useful,in case of Intrauterine growth restriction .It helps in deciding
the frequency of monitoring and optimal time of delivery. DOPPLER is
velocimetery started at 28 and 30 weeks .Repeated at 2 to 4 weeks intervals.
MODE OF DELIVERY.
Preferred mode of delivery for pre eclampsia is vaginal. Caesarean
section may be indicated in Fetal distress , malpresentation, placental
abruption or placenta previa . In case of severe pre eclampsia Remote from
term , caesarean section may be advisable due to the chances of prolonged
and Unsuccessful induction and fetal compromise .
INTRA PARTUM MANAGEMENT.
Blood pressure should be measured every two hours. Aim is to maintain
the diastolic BP below 110mmhg and systolic BP below 160mmhg .Urine
output and signs of impending Eclampsia to be monitored
carefully.Eclampsia prophylaxis to be given in case of severe precclampsia
and Impending pre eclampsia. Continuous fetal monitoring should be
done.Adequate pain relief by Epidural anaesthesia avoids the risk of aspiration
and difficult intubation due to edema of the Airway.Ergometrine to be avoided
because it will cause intense vasoconstriction may lead to Hypertensive crisis.
MATERNAL COMPLICATIONS
Eclampsia
Cerebro vascular accident
Hemiplegia ,Dysphasia
Visual disturbances
Placental abruption
HELLP syndrome [Haemolytic anaemia,Elevated liver
enzymes,low platelets]
Pulmonary edema with or without left ventricular failure
Acute renal failure
Microangiopathic haemolytic anaemia
Side effects of drug therapy.
FETAL COMPLICATIONS
Intrauterine growth restriction related to duration of hypertension
Oligohydraminios
Prematurity
Ante partum and Intrapartum asphyxia
Intrauterine death
Fetal side effects of antihypertensive drugs.
HELLP SYNDROME
Hellp syndrome is an acronym which was coined by Louis Weinstein in
1982 .It includes Haemolysis ,Elevated liver enzymes, and Low platelets.Well
recognised complication of severe pre eclampsia, it can occur in the absence of
Hypertension and proteinuria.Incidence about 0.2 to o.6 % of all pregnancies
and in 10 to 20 %0f cases with severe pre eclampsia .About 2/3 of patients
present antepartumly and the rest in the postpartum period, usually within 48
hours of delivery.
DIAGNOSIS.
The syndrome generally presents in the third trimester. When it occurs
earlier ,particularly in association with early onset pre-eclampsia , Anti
phospholipid antibody syndrome. Symptoms of Malaise ,nausea, vomiting ,
epigastric pain and headache.Because of vague symtoms diagnosis May be
missed until laboratory investigations are performed.The diagnosis of Hellp
requires the Presence of elevated liver enzymes (ALT and AST), and low
platelet count Haemolysis can be documented by examination of a peripheral
blood smear (schistocytes ,echinocytes , and burr cells).Elevated indirect
bilirubin ,Low serum haptoglobulin level, a low haematocrit, and serum LDH
greater than 600IU/L.The coagulation profile is usually normal unless DIC
supervenes.Positive D –dimer test ,which indicates subclinical
coagulopathy.Differential diagnosis for hellp syndrome
1)Acute fatty liver of pregnancy
2)Thrombotic thrombocytopenic purpura
3)Haemolytic uremic syndrome.
CLASSIFICATION
Classified into three categories based on the platelet counts.
Class 1] ,<50,000/mm3.
Class2] _50,000 to <1,00,000/mm3.
Class 3}more than 1,00,000.
Another system of classification based on number of abnormalities
present , I,e. haemolysis, elevated liver enzymes and low platelets.when 2 or 3
present this known as Partial Hellp , When all are present this is known as
complete or full Hellp syndrome.
MANAGEMENT.
Maternal mortality and morbidity increase with increasing disease
severity and worsening laboratory parameters.Perinatal mortality and morbidity
depends on the gestational age associated complications like Intra uterine
growth restriction or placental abruption rather than the severity of Hellp
syndrome.LDH Platelet will be the best marker to follow the Hellp syndrome ,
disease progression, which start to normalize by 72 hours follow the
delivery.Anti hypertensive treatment and anticonvulsant trearment are
administered as indicated.High dose corticosteroid treatment has to be
proposed to improve maternal prognosis of HELLP Syndrome10
. COCHRANE
review, ELEVEN TRIALS were included comparing the corticosteroids with
placebo or no treatment . There was no difference in the risk of maternal
death or maternal morbidity . or perinatal morbidity. Therefore good evidence
to support corticosteroids therapy in the management of Hellp
syndrome.Termination of pregnancy is planned according to the gestational
age, the favorability of cervix and severity of condition. When gestational age
34 weeks or more , prompt delivery as soon as the maternal condition is
stabilised .
At 27 to 34 weeks , corticosteroid should be given to promote the fetal
lung maturity prior to delivery. Expectant management before 34 weeks
seems to be rational approach to increase fetal maturity and survival .There
is no clinical trials to compare with conservative management and immediate
delivery.The potential benefits have to be outweighed against the risks of
expectant management, which include abruption placentae, acute renal
failure, pulmonary edema DIC, perinatal and maternal morbidity and
mortality.Patients more than 34 weeks of gestational age may be induced
unless there is no other contraindication.Women have past history of HELLP
syndrome carry on increased risk of atleast 20% developing some form of
gestational hypertension in the future pregnancy.
ANTI HYPERTENSIVE THERAPY
A wide of variety drugs available with various modes of administration
.The most commonly used drugs are Labetalol, Nifedipine, Alpha methyl
dopa, and Hydralazine.Gradual and prompt reduction of blood pressure in
severe pre –eclampsia is warranted by administration of intermittent dosage of
drugs or by a continuous monitored infusion .Combination of drugs not
advisable because of their compound effect may lead to hypotensive episode.
Maintenance of Blood pressure at 140 to 160 mmhg systolic and 90 to 105 mhg
of Diastolic range during the treatment of hypertension in pregnancy .A
sudden decline of Blood pressure will compromise the uteroplacental flow
and thereby the fetus. The patient should be monitored for antihypertensive
effect of the drug and occurrence of adverse effect s in mother and the fetus.
The dosage to be monitored according to the response. Many studies
comparing the antihypertensive effect of Hydralazine with Labetalol in acute
blood pressure control.Hydralazine is associated with poor outcomes namely
increased caesarean sections , placental abruption , and fetal heart
abnormalities ,so the use of Hydralazine is not recommended . Many studies
show the efficacy and rapidity of action of oral and intravenous Labetalol in
mild to moderate hypertension and acute severe hypertension of pregnancy.
Use of intravenous Labetalol and oral nifedipine has found its place in the
Tertiary care protocol in the management of severe pre-eclampsia and
eclampsia in our India.
LABETALOL.
Labetalol is a alfa and beta adrenergic blocker. Chemical formulation
four sterioisomers With distinct action profiles on the receptor subtype. The
available commercial preparation is Racial mixture of two pairs of chiral
isomers. The ration of alfa to beta blockade is 1:7 following intravenous
administration .The systolic and diastolic fall in blood pressure is due to both
alfa 1 and beta1 blockade. Vasodilatation is due to beta2 weak agonistic
activity. The reduction in systemic vascular resistance with no change heart
rate and cardiac output is by alfa blockade. It reduces the Bood pressure
smoothly and rapidly. There is a decrease in cardiac index following both oral
and Intravenous administration .Labetalol is a category C drug .It crosses the
placenta small amounts secreted in the breast milk .Sibai in his study prefers
the use of Labetalol.The protocol by the NHBPEP Working group (2000) and
American College of Obstetricians and Gynaecologists (2002)Recommends
the usage of 20mg initial intravenous dose in the management of acute
severe hypertension in pregnancy.
The dose is doubled every ten minutes if there is no desired reduction
of blood pressure till the total dose infusion of 220mg per episode.The use of
20mg initial dose of labetalol is preferred since target concentration is reached
more rapidly.100% bioavailability following iv administration.Onset of action
following i.v is 2.5minutes .Peak action at 5minutes.Target concentration is
0.1mg/dl .Labetalol was about 50% plasma protein bound.T1/2 is
4.9hours.Metabolized in liver via conjugation to glucuronide metabolites.
Various studies conducted by Mabie and collegues12
and Vigil-De13
Gracia
and collegues high light the rapid action , better maternal and neonatal
outcomes and minimal side effect profile of intravenous labetalol in
comparison with hydralazine in antepartum and postpartum period
accordingly.Hydralazine needs lower dose to control but associated with higher
maternal and fetal adverse effects. Labetalol is a safe and effective
alternative drug ,when compared to Hydralazine.
ADVERSE EFFECTS.
Most common side effect is dizziness reported in 20% of the patients.
Nausea fatigue and light headedness .since postural hypotension is common
Left lateral position is advisable during Intravenous administration.
CONTRAINDICATIONS.
1] Patients with obstructive airway diseases including bronchial asthma
2] Cardiac failure and heart block
3] Impaired liver function
4] Diabetes mellitus and cardiac failure
The drug does not have any adverse impact on the maternal symptoms ,
neonatal outcome ,mode of Delivery ,and further complications disease per se.
NIFEDIPINE.
This drug was discovered as early as 1800 that calcium influx is an
essential part in smooth muscle contraction. L type calcium channel blockers
are used in various indications. Nifedipine , a prototype of dihydropyridine
group of calcium channel blocker12
has been studied for its utility in
hypertensive disorders of pregnancy. This drug has been used both in mild to
moderate hypertensive disorders of pregnancy and severe pre-eclampsia for
acute blood pressure control .Calcium channel had 4sub types of receptor ,
Nifedipine is said to block the α1 subtypes of receptor And thus reduce s the
transmembrane calcium current , thereby producing a long lasting smooth
muscle relaxation14
.
PHARMACOKINETICS OF NIFEDEPINE.
It has 45 t0 70% bioavailability .Metabolized in the liver.Onset of action
in 20 minutes .peak action in 0.5 to 1 hour.T1/2 is 4 hours duration is 4 to8
hours .excreted through renal 20% .No need for dose reduction in renal
disorders. Nifedipine effectively dilates the arterioles in preference to veins
thus producing an effective vasodilatation without producing postural
hypotension.It also reduces the total peripheral resistance so reduces the
afterload. It may produce inconsequential amount of reflex tachycardia. There
is a small increase in cardiac index . It has rapid onset of action by oral route.
The drug is available in immediate release, and extended release tablets and
capsules.The oral route provides an ease of administration without
compromising the efficacy. The site of absorption of oral Nifedipine is at the
duodenum and jejunum. The gastric emptying time of pregnant women is
found to be the same as in the non pregnant. However there is a delay in the
gastric emptying in labour most often due to the use of analgesics. The
elimination half life of Nifedipine is said to be shortened with pregnant women
implying a frequent dosing for a better Antihypertensive effect.so oral route of
administration is adequate enough to give a prompt onset of Action in the
Blood pressure control. Sublingual route is not recommended, since it produce
Rapid fall of blood pressure .
NICE guidelines recommends the use of oral nifedipine in blood
Pressure control in eclampsia and pre-eclampsia.The antihypertensive effect
was compared with Placebo in a trial by Ismail et al 15
. which shows that the
Mean arterial pressure was effectively reduced in nifidepine group and the
drug brought about the increased urine output because of vasodilatory effect.
This is a category C drug .The drug crosses the placenta. There in reported
change in the uteroplacental blood flow.About 5% of the drug secreted in
breast milk , producing little or no neonatal hypotension.
ADVERSE REACTIONS and CONTRAINDICATIONS.
a]Ankle edema 10 to 30%
b]Flushing 10 t0 20%
c]Dizziness25% Headache10 to 20%[34]
The only contraindication for this drug is hypersensitivity reactions.
Theoriticaly some interaction between magnesium sulphate has been
demonstrated.both the Drugs exhibit pharmacodynamic synergism when
administered together producing hypotension neuromuscular blockade and
warranted close monitoring. 16
Magpie trial involving 10141women with pre –
eclampsia had 3029 women with concominant magnesium sulphate and
ifidepine administration .There was no hypotension or neuromuscular blockade
reported in this study.
ALPHA METHYL DOPA.
Methyi dopa with an established long term safety, 17
is an effective drug
as a Monotherapy in mild to moderate hypertension reducing the progression to
severe Pre-eclampsia .This is not useful in severe hypertension.Mechanism of
action is by reduction of overall sympathetic flow. Onset of action is in 4 to 6
hours.It is metabolized in the liver and excreted through kidney.The most
common side effect is postural hypotension; excessive sedation and depression.
HYDRALAZINE.
It acts by direct peripheral vasodilatation.It was the drug of choice in
hypertensive Emergencies in the past. The onset of action is 10 to 20
minutes.It produces significant hypotension producing non reassuring fetal
cardiac status and fetal distress.18
DIAZOXIDE.
Diazoxide is a benzothiazine derivative that acts by direct vasodilataion
Producing arapid and long lasting effect.Since its usage is associated with
maternal cerebral Ischaemia , maternal death and fetal distress.Recently the use
of mini bolus doses of diazoxide Constituting 15mg has not associated with
profound maternal hypotension.
SODIUM NITROPRUSSIDE.
It has been used as a last resort in reducing high blood pressure. It acts
by release of nitric oxide .It has vasodilator effect. It has rapid onset of
action.Associated with rebound hypertension Cyanide toxicity is reported in the
fetus following its use.
NICARDIPINE.
A calcium channel blocker, nicardipine is evaluated as asecond line drug
antihypertensive agent in pregnancy. The drug needs monitoring for possible
renal shut down.
DIURETICS AND OTHER DRUGS.
Diuretics can compromise placental blood flow, 20
the usage is solely
limited to pulmonary edema. It reduces the already depleted intravascular
volume.19
FLUID MANAGEMENT.
Pre-eclampsia is intravascular fluid depleted condition .The knowledge
of fluid management comes from invasive hemodynamic monitoring in pre-
eclampsia and in compromised states such as pulmonary edema, cardiac
failure, and renal shut down. The state of volume depletion with decreased
cardiac output coupled with low oncotic pressure And capillary damage
predisposes to pulmonary edema. The condition is further deteriorated By the
injudicious use of volume expanders .The American College of Obstetrics and
gynaecologist recommends invasive hemodynamic monitoring in severe
cardiac diseases , renal disorders renal shut down, refractory hypertension and
pulmonary edema.Central venous pressure. Monitoring and Swan Ganz
catheter insertion provide information regarding right ventricular pressure
monitoring is validated in the correction of hypovolaemia prior to
antihypertensive therapy.
Crystalloids are recommended in comparison to 125ml per hour in
volume dpleted states. Swan Ganz catheter is useful in conditions like
pulmonary edema , uncontrolled hypertension ,Severe oliguria and multi organ
dysfuntion Both the procedure associated with risk of cardiac arrhythmias,
pulmonary infarction, and pulmonary haemorrhage.
ANASTHETIC CONSIDERATION.
General practice principles recommend early involvement of
anaesthetists in patients With pre –eclampsia the issues in consideration are
anaesthetic risk assessment control of blood Pressure, fluid management
,seizure prophylaxis and anasthetic or or analgesic considerations.
Patients with organ failure require high dependency setting .Epidural
anaesthesia serves as a good adjunct to vaginal delivery by improving the
renal and uteroplacental blood supply.
The drugs to be avoided are ergometrine ketamine and NSAIDS
.Regional anaesthesia is used in Preference to general anaesthesia.platelet count
of less than 50,000/cu.mm is a contraindication for regional anaesthesia .
POSTPARTUM MANAGEMENT.
Seizure prophylaxis should be considered for 24 hours post partum
period.Antihypertensives drugs should be continued in the post partum period
according to blood pressure .The dosage to the titrated according to the blood
pressure control.Fluid balance monitoring, evaluation of hepatic renal function
and neurological status is validated .Since preeclampsia Is a risk factor for
thrombosis ,throboprophylaxis is administered unless surgically
contraindicated. In hospital stay, obesity, nephritic range proteinuria and
operative delivery predispose to thrombosis.
FOLLOW UP.
Patients requiring medication for the control of blood pressure should be
frequently Reviewed .Since these patients are at an increased risk for adverse
cardiovascular events, They should be under surveillance.21
Preconception
counselling should be advised in the next pregnancy. Early onset severe
disease should be evaluated for the presence of Antiphospholipid . Antibody
syndrome and further screening for thrombophilia if indicated20
Contraceptive
advice Should also be provided.
ECLAMPSIA.
Eclampsia is defined as the development of seizures that cannot be
attributed to other Causes and unexplained coma during pregnancy or
puerperium in a women with pre-eclampsia.1 in 2000 deliveries in developed
countries21
, whereas the incidence in developing countries , varies from 1 in
100 to 1 in 1700 cases.Incidence and mortality and morbidity of maternal and
perinatal has come down because of better antenatal care.23
PATHOPHYSIOLOGY OF ECLAMPSIA.
Loss of cerebral vascular autoregulation lead to either overdilatation or
vasospasm. As part of the autoregulatory response to severe hypertension ,
cerebral vasoconstriction occurs which leads to ischaemia ,cytotoxic edema
and infarction. When the autoregulatory mechanism fails at some point ,
dilatation of vessels occurs resulting in hyper perfusion and vasogenic edema.
Autopsy studies showed edema, cortical and white matter microinfarcts
, pericapillary And parenchymal bleeding and vascular lesions predominantly
in the occipital and watershed Areas.
SYMTOMS AND SIGNS OF IMPENDING ECLAMPSIA.
1] Headache -Persistent occipital or Frontal
2]Visual disturbances - Blurred vision and photophobia
3Restless ness and Agitation
4Epigastric and or Right upper guardant pain
5]Nausea and vomiting
6]Oliguria
7]Laboratory evidence of disseminated intra vascular coagulation
CLINICAL COURSE OF ECLAMPSIA.
Stage of invasion:
(a)The patient become unconscious. There is twitching of muscles of the
face, tongue and limbs which lsats for about 30 seconds.
(b)Stage of contration: whole body goes into a tonic spasm . Cyanosis
appears .this last for about 30 seconds.
(c)Stage of convulsion: All voluntary muscles undergo alternate
contraction and Relaxation.Biting of the tongue occurs.This will last for 1 to 4
Minutes.
(d) Stage of coma: Following the convulsions , the patient passes on to
the stage of coma which usually lasts for a brief period.
DIFFERENTIAL DIAGNOSIS.
Epilepsy, Hysteria, Encephalitis, Meningitis, Puerperal cerebral
thrombosis, cerebral malaria in trophics, Cysticercosis , Intracranial tumour.
COMPLICATIONS OF ECLAMPSIA.
1]Maternal injuries
2]Placental abruption(10%)
3]Neurological deficit(7%)
4]Aspiration pneumonia(7%)
5]Pulmonary edema(5%)
6]Disseminated intravascular coagulation(3%)
7]Cardio pulmonary arrest(5%)
8]HELLP syndrome(4%)
9]Acute renal failure(4%)
10]Maternal death(1%)
FETAL COMPLICATIONS
The perinatal morbidity and mortality rate is very high to the extent of
about 30 to 50%.24
THE CAUSES ARE;
1]IUGR due to chronic placental insufficiency
2]Prematurity either spontaneous or induced.
3]Intra uterine asphyxia
4]Effects of the drugs used to control convulsions.
5]Increased operative deliveries.
GENERAL MANAGEMENT.
It plays on important role in the management of eclampsia. The patient
is nursed in a quiet room with a medical or nursing attendant always present .
Pulse rate, respiration, blood pressure , oxygen saturation, restlessness, urine
output, must be constantly observed . A mouth gag , airway ,and O2 must be
available .Patient is put in left lateral position in a railed cot .Throat is cleared
of secretions and vomitus by intermittent suctioning .A soft firm mouth gag
introduced in time will save injury to the Tongue. An indwelling catheter in
the bladder will give an accurate assessment of the urine output and will also
prevent restlessness due to a full bladder.Blood pressure is measured half
hourly till it is controlled and then second hourly .A record of grade of
consciousness is maintained.Nutrition and hydration are maintained
parenterally.
MEDICAL MANAGEMENT.
ANTICONVULSANT THERAPY.
The drug of choice for control and prevention of convulsions is
magnesium sulphate. PRITCHARD’S Regime.This has been conclusively
proven by the collaborative eclampsia trial in 1995.which was large
multicenteric trials comparing magnesium sulphate and phenytoin in
eclampsia.Previously used anticonvulsants for eclampsia include Krishna
Menon’s regime (lytic cocktail of pethidine chlorpromazine and Phenergan)
phenytoin sodium ,and diazepam.
MAGNESIUM SULPHATE(Mgso4).
In 1955 , Pritchard initiated a standardized treatment regimen at
Parkland hospital. In 1964 , Zuspan initiated the intravenous magnesium
sulphate regimen.
PHARMACOKINETICS OF MAGNESIUM SULPHATE.
Magnesium sulphate USP is Mgso4 .7H2O. Molecular weight about
24.3 1gm of magnesium sulphate has 98mg of elemental magnesium.
DISTRIBUTION AND PLASMA LEVELS.
40% of plasma magnesium is protein bound . Un bound magnesium ion
diffuses into the extra vascular , extracellular space , into bone and across the
placenta and fetal membrane and into the fetus and amniotic fluid . In pregnant
women , apparent volumes of distribution usually reach constant values
between the third and fourth hour after administration.
EXCRETION.
Magnesium is excreted by the kidneys. 50% of the infused dose is
excreted after 4 hours in urine .90% of the bolus intravenous dose is excreted
within 24 hours.
MECHANISM OF ACTION.
Mainly peripheral at the neuromuscular junction with minimal central
effects. Calcium entry into the neurons is regulated by specific excitatory
amino acid linked channels like L _ glutamate and L _ aspartate are the major
neurotransmitters in mammalian central nervous system.NMDA receptor has
its channel blocked by magnesium ion and thus blocking the calcium influx.
Magnesium sulphate is a potent vasodilator especially in cerebral vasculature
thus relieving cerebral vasospasm which is thought to be a cause for
eclampsia.
OTHER ACTIONS .
Increased uterine bood flow
Vasodilatation in vascular beds
Increased prostacyclin release by endothelial cells
Increased renal blood flow
Bronchodilatation
Attenuation of vascular response to pressor substances
Decreased angiotensin converting enzyme levels
Decreased plasma renin activity
Reduced platelet aggregation
PHARMACOLOGICAL EFFECTS .
Mild decrease in frequency of uterine contractions , no change in
the intensity of contractions.
Anticonvulsant action
Transient hypotensive action
No change in long term variability of fetal heart rate or fetal heart
rate acclerations.
Insignificant decrease in short term variability of fetal heart rate.
Duley et al .(1995 ) in his study he proved clinical evaluation alone is
enough , there is no need to check the serum magnesium levels routinely
PRITCHARD REGIMEN 33
Loading dose Maintenance Dose
4gm of 20% Mgso4 IV at a rate not
exceeding
1gm /minute
Every 4 hours there after , 5gm of
50%Mgso4 as
IM on alternate buttocks after ensuring
10gm of 50% Mgso4 as deep IM ,
5gm in each buttock through a 3inch
long _20 gauge needle
a)Patellar reflex is present
b)Respiration rate >16/minute
c)urine output >100ml in the
preceding 4 hours.
IF convulsions persists after 15 minutes ,2gm of Mgso4 IV is given at
a rate not exceeding 1gm/minute.Mgso4 is continued for 24 hours after
delivery or the last episode of convulsion Whichever is later.
Monitoring to be done .If there is any abnormality urine output less than
30ml/min or there is any abnormality in respiratory rate and patellar reflex
the next dose to be skipped. Loading dose. To be given to all cases irrespective
of urine output. If patellar reflex absent the blood level of Magnesium
sulphate is about 10MEq/L.IF there is respiratory arrest the level of Magnesium
sulphate is about 12MEq/L. The therapeutic range is about 4 to 8MEq/L. This
is the narrow therapeutic index drug.So close monitoring is needed.
TREATMENT FOR MAGNESIUM TOXICITY.
If there is magnesium toxicity respiratory depression will occur. In that
case infusion Should be discontinued.O2 should be given and 10ml of 10%
calcium gluconate to be given. If respiratory arrest cardio pulmonary
resuscitation should be started and the patient should be intubated. Recurrent
seizures. Further bolus of 2g magnesium sulphate to be considered.Midazolam
or lorazepam may be given.
FETAL EFFECTS OF MAGNESIUM.
Neonatal depression will occur it may be clinically insignificant. Beat to
beat variability may occur. Magnesium sulphate have a protective effect
against cerebral palsy in very low birth weight infants.
ABSOLUTE CONTRAINDICATIONS.
1]Myasthenia gravis
2]Recent myocardial infarction.
ANTIHYPERTENSIVE AND FLUID MANAGEMENT.
Like pre –eclampsia the antihypertensive drug should be given
according to blood Pressure. Strict fluid intake and output chart to be
maintained because these patients are more Prone for pulmonary edema.
OBSTETRIC MANAGEMENT.
Immediate termination of pregnancy after controlling of seizures and
stabilization of the patients. Principles of obstetric management and
postnatal care will be the same like pre-eclampsia There is contraindication for
vaginal delivery, delivery is not within 6 to 8 hours of induction from the
clampsia caesaerean section to be considered. The anaesthetist should be
informed about the magnesium sulphate and this drug should be continued
throughout labour and 24hours postpartum or occurrence of fits whichever is
later.
STATUS ECLAMPTICUS.
In these cases , Midazolam , lorazepam , or even Thiopentone sodium
may be given under supervision of anaesthetist. If it persist even after the
above measurement patient may be intubated and connected to ventilator in
intensive care unit.
MATERIALS AND
METHODS
MATERIALS AND METHODS
METHODS
This is a prospective observational study done from August 2013 to
August 2015 (22 months) at K.A.P.V. Medical College &
M.G.M.GOVERNMENT HOSPITAL, Tiruchirapalli . It consists of analysis
of maternal and fetal outcome in preeclampsia. pregnant women with more
than 20 weeks of pregnancy with systolic B.P >140 mmHg & diastolic
>90mmHg in two separate readings taken 6 hrs apart. any patient fulfilling the
inclusion criteria to be explained the type of study and after taking her
writtenconsent patients were assessed on the basis of history, clinical
examination, ultra sound & laboratory investigations were done according to
the severity of pre eclampsia
INCLUSION CRITERIA :
(i) BP Systolic >140mmHg and diastolic >90mmHg
(ii) Urine albumin>1+ on dipstick single test
(iii) Edema may or may not be present
EXCLUSION CRITERIA :
(i) Chronic hypertension diagnosed before 20 weeks of gestations,
(ii) Patients Having hepatitis
(iii) Heart disease
(iv) DM
(v) Reno vascular HT
(vi) Cushing syndrome
(vii) Pheochromocytoma
(viii) Thyrotoxicosis
(ix) SLE
(x) Glomerulonephritis
PROTOCOL
Patients having mild PE, with gestation age group >37 weeks were
induced & delivered, and <37 weeks were advised in patient or out patients
according to their Bloood pressure. Severe pre eclampsia patients were
admitted to hospital . Within 1st 24 hours of admissions all patients with GA
<34 wks should be received 2 doses of beta methasone 12 mg each 24 hrs
apart.noted and any NICU admissions indications and duration of admission
were recorded.
DATA COLLECTION AND METHODS
Detailed history is taken. Clinical evaluation of the patient is done.
Investigations are recorded. Patients with imminent ecclampsia should be
received mgso4 prophylactically as per criteria laid down in MAGPIE trial and
were intensively monitored. For Hypertension labetalol, nifedepine were
commonly used , dose was adjusted according to the severity of hypertension.
Monitoring to be done depending on severity and Gestational age. Mode of
termination depends on the periods of gestation, favourability of cervix &
urgency of termination. Fetal outcome assessed by APGAR SCORE at birth.
In preeclampsia. To study the prevalence of preeclampsia in relation to
A) Unregistered or registered age &parity
B) To study the incidence of various maternal complication of
preeclampsia.
C) To study the fetal outcome in pregnancies complicated by
preeclampsia
RESULTS AND
ANALYSIS
RESULTS AND ANALYSIS
OBSTETRIC-CODE
CATEGORY FREQUENCY
Primi 46
Multi 54
Total 100
In our study group 46 members belongs to Primi gravida
and 54 members belongs to Multi gravid.
*These cases are referal from Periphery
46
54
42
44
46
48
50
52
54
56
Primi Multi
Obstetric _ code
BOOKING STATUS
CATEGORY FREQUENCY
No 9
Yes 91
Total 100
In this study 9 were unbooked and 91 were booked.
9
91
0
10
20
30
40
50
60
70
80
90
100
No Yes
Booking status
HYPERTENSION- STATUS
CATEGORY FREQUENCY
Severe 32
Mild 68
Total 100
In this study 32 were severe hypertensive and 68 were mild
hypertensive.
32
68
0
10
20
30
40
50
60
70
80
Severe Mild
Hypertension_ status
ANTI HYPERTENSIVE DRUGS
CATEGORY FREQUENCY
No anti
hypertensive 6
Labetalol 64
Nifedipine 9
Combined 21
Total 100
IN our study 64 patients were on labetalol ,9 patients were on
nifedipine,21 patients on both drugs,
6 patients not started any drugs.
6
64
9
21
0
10
20
30
40
50
60
70
No anti hypertensive
Labetalol Nifedipine Combined
ANTI HYPERTENSIVE DRUGS
"LFT" AND "RFT" RESULTS
RESULTS LIVER FUNCTION
TEST
RENAL FUNCTION
TEST
Increased 29 17
Normal 71 83
Total 100 100
29% of patients had increased liver function test values and 17%
patients had renal function test values.71% of patients had normal liver
function tests,83% of patients had normal renal function tests.
29
17
71
83
0
10
20
30
40
50
60
70
80
90
LIVER FUNCTION TEST
RENAL FUNCTION TEST
Increased
Normal
"LFT & RFT " Results
CATEGORY FREQUENCY
Labour Natural 55
LSCS
Maternal Indication 30
Fetal Indication 15
Total 100
In our study 55% patients had labour natural,45% patients had lscs
among them 30% were maternal indication,15% were fetal indication.
LABOUR CATEGORY
55
30
15
0
10
20
30
40
50
60
Maternal Indication Fetal Indication
Labour Natural LSCS
ECLAMPSIA
CATEGORY FREQUENCY %
No 85 85.00
Antepartum 8 8.00
Intrapartum 3 3.00
Postpartum 4 4.00
Total 100 100
In our study in 100 patients 15 patients were developed eclampsia among them
8 patients were developed antepartum eclampsia&3 patients were developed
intrapartum& 4 patients developed Postpartum eclampsia.
85
8
3 4
0
10
20
30
40
50
60
70
80
90
No Antepartum Intrapartum Postpartum
ECLAMPSIA
ABRUPTION ,HELLP,CVT
CATEGORY
FREQUENCY
%
PRESENT ABSENT
Abruption 14 86 100
Hellp 15 85 100
CVT 10 90 100
Among 100% patients 14% were developed abruption,15% patients
developed HELLP,10% patients were developed CVT.
14 15
10
86 85
90
0
10
20
30
40
50
60
70
80
90
100
Abruption Hellp CVT
FREQUENCY PRESENT
FREQUENCY ABSENT
ABRUPTION HELLP CVT
RENAL FAILURE ,PULMONARY EDEMA & MATERNAL DEATH
CATEGORY
FREQUENCY
%
PRESENT ABSENT
Renal failure 8 92 100
Pulmonary Edema 13 87 100
Maternal death 2 98 100
8 % OF patients were developed renal failure,13% of patients were
developed pulmonary edema.2 % of patients were died and they were belongs
to severe preeclampsia category.
813
2
9287
98
0
20
40
60
80
100
120
Renal failure Pulmonary Edema Maternal death
FREQUENCY PRESENT
FREQUENCY ABSENT
RENAL FAILURE PAULMONARY EDEMA& MATERNAL DEATH
APGAR - NEW BORN AT 1 MINUTE
CATEGORY FREQUENCY
1[0 >3] 5
2[3 to5] 36
3[more than 6] 59
Total 100
APGAR new born at one minute,5%were under 0-3 ,36% were under3-
5,59% were under>6.
0
10
20
30
40
50
60
70
1[0 >3] 2[3 to5] 3[more than 6]
APGAR -NEW BORN AT 1MINUTE
PERINATAL OUTCOME
CATEGORY FREQUENCY %
NICU Admission 49 49
IUGR 20 20
IUD 3 3
Neonatal death 7 7
Normal Neonates 21 21
49% of new born admitted in NICU,20% of developed IUGR,3% died
inutero,7% died in neonatal period.
PERINATAL OUTCOME
49
20
3
7
21
0
10
20
30
40
50
60
NICU Admission IUGR IUD Neonatal death Normal Neonates
BOOKING STATUS vs ABRUPTION
Abruption %
Statistical
significance
Present Absent
No 4 5 9
0.006
44.40% 55.60% 100.00%
Yes 10 81 91
11.00% 89.00% 100.00%
Total 14 86 100
14.00% 86.00% 100.00%
9% were unbooked &91 were booked.P Value in this study is 0.006
which is highly significant.44.4% of unbooked cases developed Abruption.
4
44
.40
% 10
11
.00
%
14
14
.00
%
5
55
.60
%
81
89
.00
%
86
86
.00
%9
10
0.0
0%
91
10
0.0
0%
10
0
10
0.0
0%
0
20
40
60
80
100
120
No Yes Total
Abruption Present
Abruption Absent
%
BOOKING STATUS VS ABRUPTION
HYPERTENSION STATUS vs ECLAMPSIA
Hyper tension status Eclampsia
Absent Antepartum Intrapartum Postpartum
Severe 21
65.60%
7
21.90%
1
3.10%
3
9.40%
Mild 64
94.10%
1
1.50%
2
2.90%
1
1.50%
Total 85
85.00%
8
8.00%
3
3.00%
4
4.00%
Statistical
significance 0.001
In this study 32 patients were severe preeclamptic&68 patients were mild
preeclamptic.P Value between this group is 0.001 which is highly
significant.21.9% of severe preeclamptic group developed antepartum
eclampsia,94.1%of mild preeclamptic patients not developed any type of
eclampsia.so severity of hypertension highly influence the occurance of
eclampsia.
21
65
.60
%
64
94
.10
%
85
85
.00
%
7
21
.90
%
1 1.5
0% 8
8.0
0%
1 3.1
0%
2 2.9
0%
3
3.0
0%
3
9.4
0%
1 1.5
0%
4
4.0
0%
05
1015202530354045505560657075808590
1 2 3 4 5 6
Hyper tension status
Eclampsia Absent
Eclampsia Antepartum
Eclampsia Intrapartum
Eclampsia Postpartum
HYPERTENSION STATUS vs ECLAMPSIA
URINE ANALYSIS vs ABRUPTION
Category Abruption
% Present Absent
Nil 1 22 23
Trace 1 24 25
1+ 6 33 39
2+ 5 6 11
3+ 1 1 2
Total 14 86 100
Statistical significance 0.004
23% of patients with no proteinuria among them only 1% developed
abruption .Among 77%of patients with proteinuria 13% of patients developed
abruption.P value is highly significant.so proteinuria significantly differs
between this two groups.So severity of proteinuria significantly correlates with
occurrence of abruption.
1 1
6
5
1
22
24
33
6
1
0
5
10
15
20
25
30
35
Nil Trace 1+ 2+ 3+
Abruption Present
Abruption Absent
URINE ANALYSIS VS ABRUPTION
URINE ANALYSIS vs HELLP
Category Hellp
% Present Absent
Nil 2 21 23
Trace 2 23 25
1+ 3 36 39
2+ 6 5 11
3+ 2 0 2
Total 15 85 100
Statistical significance 0.000
Among 23% of patients with no proteinuria 2% developed HELLP.
Among 77% of patients with proteinuria 13% developed HELLP.P value in this
study is 0.000 which is highly significant. So severity of proteinuria has
significant impact on occurance of HELLP.
2 2
3
6
2
21
23
36
5
0
0
5
10
15
20
25
30
35
40
Nil Trace 1+ 2+ 3+
Hellp Present
Hellp Absent
URINE ANALYSIS VS HELLP
OBSTETRIC CODE vs COMPLICATION
Abruption %
Statistical
significance
Hellp %
Statistical
significance Present Absent Present Absent
Primigravida 5 41 46
0.405
3 43 46
0.028
10.90% 89.10% 100.00% 6.50% 93.50% 100.00%
Multigravida 5 45 54 12 42 54
10.90% 83.30% 100.00% 22.20% 77.80% 100.00%
Total 14 86 100 15 85 100
14.00% 86.00% 100.00% 14.00% 86.00% 100.00%
In comparison of parity and the occurance of abruption and HELLP ,P value is 0.4,which is not significant. 10.9 % of the
multi gravida developed abruption. 22.2 % of muti gravida developed HELLP.
5
10
.90
%
5
10
.90
%
14
14
.00
%
41
89
.10
%
45
83
.30
%
86
86
.00
%
46
10
0.0
0%
54
10
0.0
0%
10
0
10
0.0
0%
0
20
40
60
80
100
120
Abruption Present
Abruption Absent
%
OBSTETRIC CODE VS ABRUPTION
OBSTETRIC CODE vs HELLP
DISCUSSION
DISCUSSION
Pre-eclampsia is more prevalent in both developed and developing
countries contributing to maternal and and perinatal morbidity and mortality. It
will produce maternal syndrome.It includes Hypertension , proteinuria and
with or without edema.Fetal syndrome includes fetal growth restriction,reduced
amniotic fluid,and abnormal placentation.OUT of 100 cases 32 cases were
severe and 68 cases were mild pre –celampsia.Some patients had irregular
antenatal check up and followup. This is the reason why incidence of pre
eclampsia and related complications more in developing countries . In our
study 9% cases were unbooked and 91%of patients were booked .
Unbooked cases were developed more complication than booked cases. Study
cases are referral cases from the periphery.
In the study age < 20years 9 cases among them 3 cases had
eclampsia, and age 20 to 29 83 cases among them 10 patients had
eclampsia , and age more than 30 years 8 cases among them 2cases were
developed eclampsia .Similar incidence was found in SIBAI BH IN 1997.
Least incidence was found in age group above 30 years.It positively correlates
with vitthal Kulchake study in 2010. Out of 100 cases 46 patients were
primigravida, and 54 patients were multigravida.26
Urinary proteins are directly
correlates with severity of pre eclampsia .urinary protein also correlates with
severity of Maternal morbidity like onset of HELLP syndrome, and
abruptioplacenta. In our study 29% percentage of patients had
elevated liver enzymes and 71% of patients had normal liver parameter.17%
of patients had altered [elevated liver parameters]and 83% patients had normal
renal function. Out of 100 patients 54 patients had labour natural, 44 patients
had lscs. 1patient Had hystrotomy.Among lscs 30% had maternal indications
like mal presentation ,cephalo pelvic Disproportion and failure of
induction .15% had lscs because of fetal indications like fetal distress, Intra
uterine growth restriction.27
ECLAMPSIA.
Eclampsia is the preventable condition31
by means of regular ante natal
visits and control of Blood pressure.Eclampsia means flashes of light.It may
develop antepartum , intrapartum And postpartum. Postpartum eclampsia
unlikely to be after 4 days, but it may occur up to 6 weeks Postnatally.Out of
100 patients 85% patients didn’t had eclampsia episode. 8% had ante partum
Eclampsia, 3% had intrapartum eclampsia, and 4% patients had post partum
eclampsia. 5 patients belongs to primigravida and 10 patients belongs to
multigravida. Abruption is the one the dreadful complications of servere pre-
celampsia.14% of patients had Abruption.booking status had highly significant
relation with abruption .Among 9patients of Unbooked 4 had {44.4% }
developed abruption. Abruption strongly correlates with severity of
preeclampsia and severity of urine proteinuria.
A study done by Conde Agadelo A, 2000 and Noreen Akmal and Gul
E , Raanian 2006 revealed urinary protein levels are directly related to
severity of preeclampsia , in turn increase the morbidity and mortality. In this
study among 23% of patients with no proteinuria 2% were developed HELLP
among 77% of patients with proteinuria 13% developed HELLP.P value in
this study is 0.000. which is highly significant.so severity of proteinuria has
significant impact on Occurance of HELLP syndrome.
Mode of delivery depends on the severity of the disease .Induced
vaginal delivaries were higher in severe preeclampsia. Similar study by
Vitthal kuchake deliveries by caesarean section were around 61% . In this
study caesarean section rate was 45% . labour by induction by various
methods were about 55%.Incidence of maternal mortality 1% a study
conducted by who in2002. In this study the maternal mortality was 2% . , and
they were belong to severe preeclampsia and multigravida and they had
Irregular antenatal visit.
Acute renal failure. Study of maternal and fetal outcomes in pregnancy
induced hypertension A Hospital based study by Dr.D.P . Meshram ARF was
found in only 2 cases of preeclampsia .No case was found in
eclampsia.incidence found to be 2.2%. In this study 8%developed renal
failure. 2% were irreversible belongs to severe preeclampsia. 6% were
recovered from renal failure later.Leduc et al 1n 1992 reported significant
association between Thrombocytopenia and maternal complications and
reported that platelet nadir is the best predictor of maternal outcome. . 20%
had reduced platelet count In this study 15% patients developed HELLP. 80%
were normal platelet count.
Comparing the APGAR score at 1minute and severity of disease
there was statistically significant correlation .Study done by Odegard et al
showed pregnancies complicated by severe preeclampsia had infant birth
weight less than 12% lower than expected .
Doppler study, Study done by Sulthana and Aparna J, on Risk factors
for preeclampsia and its perinatal outcome28
showed increased resistance on
Doppler in 10 cases of preeclampsia when compared to without any high risk
cases. This data shows significance of abnormal Doppler finding sin relation to
perinatal morbidity and mortality in preeclampsia and need for early
termination of pregnancy in high risk cases managed through abnormal
Doppler. In this study Doppler abnormalities were found in 26 cases and those
cases were strictly followed and delivered accordingly.
IUGR29
babies were more common in severe Preeclampsia .study by
Attiya Ayaz, Taj Muhammad, neonatal outcome in preeclamptic patients
IUGR were about 10% .
APGAR new born at one minute,5%were under 0-3 ,36% were under3-
5,59% were under>6 49% of new born admitted in NICU,20% of developed
IUGR,3% died inutero,7% died in neonatal32
period. Main factor determining
the perinatal mortality was the lack of regular antenatal checkups,
complicated caes of preeclampsia and lack of awareness regarding significance
of symptoms like decreased fetal movements and late arrival at hospital, all
contributing to stillbirth and Intra uterine death and early neonatal death.
SUMMARY
SUMMARY
In this study, 46 were primi gravida and 54 were multi gravid In this
study 9 were unbooked and 91 were booked.In this study 32 were severe
hypertensive and 68 were mild hypertensive IN our study 64 patients were on
labetalol ,9 patients were on nifedipine,21 patients on both drugs,6 patients not
started any drugs In this study,29% of patients had increased liver function test
values and 17% patient had renal function test values.71% of patients had
normal liver function tests,83% of patients had normal renal function tests. In
our study 55% patients had labour natural,45% patients had lscs among them
30% were maternal indication,15% were fetal indication In our study in 100
patients 15 patients were developed eclampsia among them 8 patients Were
developed antepartum eclampsia&3 patients were developed intrapartum& 4
patients developed Postpartum eclampsia.
Among 100% patients 14% were developed abruption,15% patients
developed HELLP,10% patients were developed CVT.8 % OF patients were
developed renal failure,13% of patients were developed pulmonary edema.2 %
of patients were died and they were belongs to severe preeclampsia category.
APGAR new born at one minute,5%were under 0-3 ,36% were under3-
5,59% were under>6 49% of new born admitted in NICU,20% of developed
IUGR,3% died inutero,7% died in neonatal period 9% were unbooked &91
were booked.P Value in this study is 0.006 which is highly significant.44.4% of
unbooked cases developed Abruption.In this study 32 patients were severe
preeclamptic&68 patients were mild preeclamptic. P Value between this group
is 0.001 which is highly significant.21.9% of severe preeclamptic group
developed antepartum eclampsia,94.1%of mild preeclamptic patients not
developed any type of eclampsia.so severety of preeclampsia highly influence
the occurance of eclampsia. 23% of patients with no proteinuria among them
only 1% developed abruption .
Among 77%of patients with proteinuria 13% of patients developed
abruption.P value is highly significant.so proteinuria significantly differs
between this two groups Among 23% of patients with no proteinuria 2%
developed HELLP. Among 77% of patients with proteinuria 13% developed
HELLP.P value in this study is 0.000 which is highly significant. So severity of
proteinuria has significant impact on occurance of HELLP.
In comparison of parity and the occurance of abruption and HELLP ,P
value is 0.4,which is not significant. 10.9 % of the multi gravida developed
abruption. 22.2 % of muti gravida developed HELLP.
CONCLUSION
CONCLUSION
Life threatening complications like Eclampsia , Abruption, HELLP,
DIC, and pulmonary edema were more common in unbooked and Severe
preeclampsia category. 2% Maternal death occured in multigravida and
severe preeclampsia. Preterm deliveries and IUGR, more common in severe
pre eclampsia cases.The natural course of preeclampsia is blocked at the
secondary and tertiary levels of prevention.while early detection and prevention
of occurrence of the disease per se is called for,the allying of the severity of the
disease and thereby reducing the complications prompt the mainstay in the
present times.
The morbidity and mortality of the preeclamptic mother and the neonate
is considerably reduced with effective management. Evidence based practice
and setting up of a protocol in the management of acute onset ,severe
hypertension in preeclampsia and eclampsia bring about an immense
encouraging outcome.
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APPENDIX
PROFORMA
PROFORMA
MATERNAL AND PERINATAL OUTCOME IN PREECLAMPSIA
NAME: AGE: IP NO:
HUSBAND NAME: GRAVIDA: PARA:
MISCARRIAGE:
BOOKED/UNBOOKED:
PRESENTING COMPLAINTS:
MENSTRUAL HISTORY:
MARITAL HISTORY: OBSTETRICAL HISTORY:
LMP EDC
PAST SURICAL HISTORY: PAST MEDICAL HISTORY:
FAMILY HISTORY: PERSONAL HISTORY:
SOCIO-ECONOMIC HISTORY
GENERAL EXAMINATION:
BUILT : SENSORIUM: ANEMIA: ICTERUS:
EDEMA : BMI:
TEMPERATURE : PULSE : BP : RR :
SYSTEMIC EXAMINATION: CVS: RS: CNS:
OBSTETRICAL EXAMINATION:
Fundal height:
Acting
Presenting part
FETAL HEART SOUND
ESTIMATED FETAL WEIGHT:
PELVIC EXAMINATION:
ADMISSION CTG:
DIAGNOSIS:
INVESTIGATIONS: Urine albumin: Hb%: Blood Group and Rh typing :
Others :
Serum uric acid: clotting time: platelet count:
24hrs urine protein: RFT: LFT:
Fundus examination:
ULTRASOUND :
Previous USG
Malformation
AFI
LABOUR:
Induced / Spontaneous :
Induction-Delivery interval:
Appearance of amniotic fluid: Clear / Thick Meconium / Thin Meconium
Intrapartum CTG:
MATERNAL OUTCOME:
Mode of delivery:
Delivery notes:
Operative Notes:
Indication for LSCS:
Post op complications:
FETAL OUTCOME:
Apgar score : 1 min 5min
Birth weight :
Admission to neonatal ward:
Maternal morbidity :
Maternal mortality:
Perinatal morbidity:
Perinatal mortality :
MASTERCHART
CONSENT
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ABBREVIATIONS
ABBREVIATIONS
BMI : Body mass index.
Baby wt : Baby weight.
CPD : Cephalo pelvic disproportion.
DIC : Disseminated intra vascular coagulation.
F/D : Fetal distress
F/I : Failed induction.
Gel : Cerviprime gel.
IUGR : Intra uterine growth restriction.
IUD : Intra uterine death.
MSAF : Meconium stained amniotic fluid.
Nife : Nifedipine.
NICU : Neonatal intensive care unit
PROM : Premature rupture of membrane.
Pre lscs : Previous lower segment caesarean section.
RF : Renal failure.
RFT : Renal function test.
SSM : Sweeping and stipping of membrane.
SYS bp : Systolic blood pressure.
24 Hours UP : 24 H ours urine protein.
CVT : Cortical vein thrombosis.
DIA BP : Diastolic blood pressure.
LAB : Labetalol.
LFT : Liver function test.
OBST CODE : Obstetric code.
GA IN WKS : Gestational age in weeks.
CT BRAIN : COMPUTED TOMOGRAPHY.
HELLP : HAEMOLYSIS, ELEVATED LIVER ENZYMES,
LOW PLATELET COUNT.
DOP : DOPPLER STUDY OF UMBILICAL ARTERIES.
S/D ratio
ECLAMP : Eclampsia
ABRUP : Abruption
PUL EDEMA : Pulmonary Edema
MAT DEATH : Maternal death
HT : Hypetension
DM : Diabetes Mellitus
- : Absent
+ : Present
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