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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.

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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

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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.

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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.

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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

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INTRODUCTION

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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

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AIM OF THE STUDY

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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.

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REVIEW OF

LITERATURE

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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.

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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

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,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.

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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

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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

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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

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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

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ETIO PATHO GENESIS

CLINICAL FEATURES OF PRE ECLAMPSIA

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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.

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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.

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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.

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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 .

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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.

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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

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 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.

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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.

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 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

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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.

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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

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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.

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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 .

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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.

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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

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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 ,

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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.

(39)

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.

(40)

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.

(41)

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

(42)

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

(43)

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.

(44)

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.

(45)

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.

(46)

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

(47)

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.

(48)

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.

(49)

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.

(50)

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.

(51)

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.

(52)

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

(53)

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.

(54)

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

(55)

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.

(56)

MATERIALS AND

METHODS

(57)

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

(58)

(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

(59)

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

(60)

RESULTS AND

ANALYSIS

(61)

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

(62)

46

54

42 44 46 48 50 52 54 56

Primi Multi

Obstetric _ code

(63)

BOOKING STATUS

CATEGORY FREQUENCY

No 9

Yes 91

Total 100

In this study 9 were unbooked and 91 were booked.

(64)

9

91

0 10 20 30 40 50 60 70 80 90 100

No Yes

Booking status

(65)

HYPERTENSION- STATUS

CATEGORY FREQUENCY

Severe 32

Mild 68

Total 100

In this study 32 were severe hypertensive and 68 were mild hypertensive.

(66)

32

68

0 10 20 30 40 50 60 70 80

Severe Mild

Hypertension_ status

(67)

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.

(68)

6

64

9

21

0 10 20 30 40 50 60 70

No anti hypertensive

Labetalol Nifedipine Combined

ANTI HYPERTENSIVE DRUGS

(69)

"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.

(70)

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

(71)

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.

References

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