preterm labour seminar

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PRETERM LABOUR Dr SNEHA JADHAV Dr JYOSTNA POTDAR Unit 3

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Page 1: Preterm labour seminar

PRETERM LABOURDr SNEHA JADHAV Dr JYOSTNA POTDARUnit 3

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PRETERM LABOR • DEFINITION :

Preterm labor (PTL) is defined as the onset of labor after the gestation of viability i.e.20 weeks, and before 37 completed weeks of pregnancy.

Williams 23rd edition

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INCIDENCE Preterm birth occurs in 7-12% of all deliveries.

Europe : 5–9% USA : 12–13%

India : 10-15%

studd

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INCIDENCE• Preterm birth occurs in 5-12% of all pregnancies and accounts for

majority of neonatal deaths and nearly half of all cases of congenital neurological disability, including cerebral palsy.

• A neonate weighing 1000- 1500 g today has ten times greater chance of surival then what it had in 1960s.

• The focus is hence shifting to early preterm births(<32 weeks) which account for 1-2% of all births but contribute to 60% of perinatal mortality and nearly all neurological morbidity.

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SKNMC STATISTICS

April may june51 60 60

378 361 395

% of preterm deliveries in sknmc 2016

preterm deliveries total deliveries

13% 16.6%15.1%

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PRETERM DELIVERIES IN SKNMC 2016

April May June0

10

20

30

40

50

60

70

4655 55

55 5

preterm labour patients delivered vaginally delivered by c section

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INTRODUCTION• Half of all neonatal morbidity occurs in preterm infants.• Inspite of all major advances in obstetric and neonatal care,

there has been no decrease in incidence of preterm labour over half a century.

• On the contrary , it has been increasing in the developed countries as more and more high risk mothers get pregnant.

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CLASSIFICATION OF PRETERM BIRTH

• Term 39- 40 wks 6 days• Early term – 37- 39 weeks• Late preterm birth - 34 - <37 weeks• Very preterm birth - 28 -<32 weeks• Extremely preterm birth - <28 weeks

NRHM guidelines june 2014

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BIRTH WEIGHTS• LOW BIRTH WEIGHT – 1500- 2500 gms• VERY LOW BIRTH WEIGHT – 500 – 1500 gms• EXTREMELY LOW BIRTH WEIGHT – 500 – 1000 gms.

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• One of the major reasons for increase in incidence of premature births is the increase in numbers of multiple pregnancies , particularly higher order pregnancies, resulting from the use of fertility drugs and assisted reproduction.

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BURDEN OF ILLNESS: SIGNIFICANCE

Accounts for over 85% of perinatal morbidity and mortality.

Major short term problems in preterm infants include:

• Respiratory distress syndrome• Bronchopulmonary dysplasia • Necrotizing enterocolitis• Hospital acquired infections• Intra ventricular hemorrhage • Retinopathy of prematurity• Patent ductus arteriosus • Hypoglycemia etc.

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LONG TERM PROBLEMS INCLUDE :

Reactive airway disease• Asthma• Bronchiolitis• Cerebral palsy, Cerebral atrophy• Hydrocephalus• Neurodevelopmental delay• Hearing loss• Blindness, Retinal detachment• Pulmonary hypertension• Hypertension in adulthood• Increased insulin resistance etc.

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PERINATAL SURVIVAL AND MORBIDITY BY BIRTH WEIGHT

Birth weight (GM)

Survival % RDS % Sepsis % IVH % NEC %

500-749 65.4 100 34.6 23.4 23.1750-999 87.3 92.9 14.3 9.8 3.61000-1499 98.6 86.3 15.1 3.6 9.61500-1999 99 36.6 3.0 0.8 4.02000-2499 97.6 27.8 1.6 0 02500-2999 99.2 28.0 3.0 0 0>3000 99.6 11.4 3.1 0 0

National neonatal database

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THRESHOLD OF VIABILITY• BIRTHS BEFORE 26 WEEKS ARE GENERALLY CONSIDERED AT THE

CURRENT THRESHOLD OF VIABILITY (22, 23, 24, OR 25 ACOG)• THESE PRETERM INFANTS POSE VARIOUS COMPLEX MEDICAL , SOCIAL,

ETHICAL CONSIDERATIONS .• SIDNEY MILLER CHILD BORN AT 23 WEEKS WEIGHED 615 gms

DEVELOPED SEVERE PHYSICAL AND MENTAL IMPAIRMENTS .• THEY ARE VULNERABLE AND FRAGILE AS THEY HAVE IMMATURE ORGAN

SYSTEMS AND AT A HIGH RISK FOR BRAIN INJURY FROM HYPOXIC-ISCHEMIC INJURY AND SEPSIS LEADING TO NEURODEVLOPMENTAL IMPAIRMENT.

Williams 23rd edition

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ETIOPATHOGENESIS

• The exact cause of preterm birth is unsolved.

• The cause of 50% of preterm births is never determined i.e Idiopathic

• Four different pathways have been identified that can result in preterm birth.

• One or more than one pathway can be activated at the same time.

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PATHOGENESIS• CAUSES OF PRETERM BIRTHSTHERE ARE 4 MAIN CAUSES WHICH INCLUDE :1. SPONTANEOUS UNEXPLAINED PRETERM LABOR WITH INTACT

MEMBRANES2. PPROM3. DELIVERY FOR MATERNAL OR FETAL INDICATIONS 4. TWINS AND HIGHER ORDER MULTIFETAL BIRTHS.

Williams 23rd edition

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SPONTANEOUS PRETERM LABOR• 4 MAJOR CAUSES-1. UTERINE DISTENTION- EARLY UTERINE DISTENTION ACTS TO INITIATE EXPRESSION OF CONTRACTION ASSOCIATED PROTEINS (CAPs) IN THE MYOMETRIUM WHICH CODES FOR GAP JUNCTIONS PROTEINS SUCH AS CONNEXIN 43 FOR OXYTOCIN RECEPTORS AND FOR PROSTAGLANDIN SYNTHASE. EXCESSIVE UTERINE STRECH ALSO LEADS TO EARLY ACTIVATION OF THE PLACENTAL FETAL ENDOCRINE CASCADE RESULTING IN EARLY RISE IN METERNAL CORTICOTROPIN RELEASING HORMONE AND ESTROGEN LEVELS

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Source: Lockwood CJ, Kuczynski E. Markers of risk for preterm delivery. J Perinat Med 1999;27:5-20. Copyright 1999 by Walter de Gruyter and Company. Reproduced with permission of Walter de Gruyter and Company

via Copyright Clearance Center.

ABNORMAL UTERINE DISTENSIONUterine distentionUterine expansile capacity

Myometrial activation

Fetal membrane cytokine activation

contractions rupture of membranescervical change

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2.MATERNAL-FETAL STRESS• MATERNAL PSYCHOLOGICAL STRESS

• INCRESED MATERNAL ESTRIOL AND CORTISOL

• LOSS OF UTERINE QUIESCENCE

• ACCELERATE CERVICAL RIPENING

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3.INFECTION• Bacteria can gain access to intrauterine tissues through1. Transplacental transfer of maternal systemic infection 2. Ascending infection with bacteria from vagina and cervix 3. Retrograde flow of infection from peritoneal cavity via fallopian tubes.

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DEGREES OF INFECTION# Potential degrees of intrauterine infections by Goncalves Stage 1 – bacterial vaginosisStage 2 - Decidual infection Stage 3 – Amniotic infection Stage 4 – fetal systemic infection

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PATHOGENESIS• Ascending microorganisms colonize cervix decidua and membranes

• Lipopolysaccharide or other toxins released by bacteria

• Immune cell recruitment in to the reproductive tract

• Cytokine production by immune cells

• Prostaglandin release from decidua , membranes or cervix

• Cervical ripening and loss of myometrial quiescence

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• Most common microbe associated with preterm birth are 1. Gardnerella vaginalis 2. Fusobacterium3. Mycoplasma hominis4. Ureaplasma urealyticum

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PRETERM PREMATURE RUPTURE OF MEMBRANES

(PPROM)

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DEFINITION:• Rupture of fetal membranes occuring before 37 wks of gestation.• It complicates about 3 % of pregnancies and contributes to one third of

preterm births• Risk factors are same as that of preterm labour.

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MOLECULAR CHANGES• Increased concerntrations of matrix metalloproteinase (MMP-

1 ,MMP-2, MMP-3, and MMP-9) in amniotic fluid Which cause collagen degradation.

• There is also decrease in levels tissue inhibitors of matrix metalloproteinases – TIMPs which alters the amniotic tensile strength

• Recently , bacterial endotoxins or TNF-alpha elicits release of FFN which binds to toll like receptors 4 and activate cascades .

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• Which results in release of prostaglandin E and elevated activity of MMP1 , MMP2 and MMP9

• PGs promote cervical ripening and uterine contractions and MMPs allow collagen breakdown in fetal membranes

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DIAGNOSIS OF PPROM• History of sudden escape of watery amnoitic fluid.• It needs to be differentiated from stress urinary incontinence and profuse

normal vaginal discharge.• A sterile speculum examination confirms that the fluid is coming through the

os.• Nitrazine test: turns blue from yellow if amniotic fluid leak.• Fern test• Ultrasound examination shows oligohydramnios• Amnisure test(immunochromatographic method) detects trace amounts of

placental alpha microglobulin 1 (PAMG-1)

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COMPLICATIONS OF PPROM• Maternal complications:

• Preterm delivery• Chorioamnoinitis• Placental abruption• Retained placenta• PPH• Endometritis

• Neonatal complications:• Prematurity• Pneumonia and early neonatal sepsis• Pulmonary hypoplasia

• Foetal death

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MULTFETAL GESTATION• The increased rates of multifetal births is due to increased

no of women having babies after the age of 30 , at which time the risk to conceive multiple rises .

• In addition use of fertility treatments has contributed to the elevated rates of multifetal pregnancies .

• The effects of uterine stretch are obvious in these pregnancies .

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ANTECEDENT AND CONTRIBUTING FACTORS

• Threatened abortion – vaginal bleeding in early pregnancy• Lifestyle – cigarette smoking inadequate maternal weight gain overweight and obese mothers young or advanced maternal age <18 or>40 yrs Low socioeconomic status short statured Ht <145 cm vit C deficiency physical or mental stress.

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CONT..• Genetic factors- recurrent , familial , and racial nature of

preterm birth has led to the suggestion that genetics may play a causal role.

• Birth defects – associated with preterm labor.• Short interval pregnancies – increased risk of preterm and small

for gestation age newborns• Prior preterm births- Major risk factor risk increased 3 times

compared to first term birth • Infections

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DIAGNOSIS

• WARNING SIGNALS In addition to painfull uterine contractions symptoms such as pelvic pressure or heaviness in vagina menstrual like cramps Abdominal cramps watery/ changed vaginal discharge : glairy mucoid or bloody lower back pain Uterine contractions less than 10 mins apart

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PREDICTION1. Assessment of risk factors 2. Per vaginum examination to assess the cervical status 3. Ultrasound examination: Trans vaginal usg4. Detection of fetal fibronectin in cervico vaginal secretions.5. Home uterine monitoring. 6. Salivary estriol ,IL-6 ,IL-8 ,TNF

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PER SPECULUM EXAMINATION

Any leakage PV/ Any abnormal discharge PVCervical length/Dilatation of cervix

DIGITAL EXAMINATION:

• Cervical length • Cervical dilatation• Status of the membrane

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VAGINAL U/S

• Cervical length (<3cm)• Internal os diameter• Presence or absence of funelling or widening (Y, V,

U shape)• Bulging of membranes in cervical canal • Thinning of lower uterine segment.

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SONOGRAPHIC CERVICAL LENGTH

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• Cervical length at 28 weeks and risk of PTL

• Cervical length - RR• <40 mm - 2.80• <35 mm - 3.52• <30 mm - 5.39• <26 mm - 9.57• <22 mm - 13.88• <13 mm - 24.94

• After 20 weeks gestation the cervix appears to shorten with median values falling from 35-40 mm at 24-28 weeks to 30-35 mm after 32 weeks

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FETAL FIBRONECTIN• Fetal Fibronectin (FFN)- it is a glue like protein (polypeptide) binding

choriodecidual membrane. • Normally present before 22 weeks and after 37 weeks.

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FETAL FIBRONECTIN

• Present in vaginal secretions between 23-34 weeks and signifies onset of labor.

• Bedside test can be done – if negative it rules out preterm labor in next two weeks.

• False positives can result from manipulation of the cervix--digital or ultrasound exam, or coitus within 24 hrs--or from vaginal lubricants or medications.

• Poor predictive value in low risk women.

• FFN > 50ng/ml + cervical length of 25 mm shows significant risk .

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INVESTIGATIONS:

• Full blood count

• Urine for routine analysis, culture and senstivity

• Cervico vaginal swab for culture and fibronectin

• Ultrasonography for fetal well being, cervical length and placental localisation.

• Serum electrolytes and glucose levels when tocolytic agents are to be used

• CRP

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MANAGEMENT OF PRETERM LABOUR

• PREVENTION OF PRETERM LABOUR IF POSSIBLE

• TO ARREST PRETRM LABOUR IF NOT CONTRA INDICATED

• APPROPRIATE MANAGEMENT OF LABOUR

• EFFECTIVE NEONATAL CARE

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Prevention of preterm labor

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Primary prevention

Public Educational Interventions:

• Greater awareness of the increased risk of preterm in ART could affect attitudes and choices made in fertility care.

• Reduction in prevalence of smoking.• Use of condoms to prevent STIs.• Recognition and early treatment of Depression.• Promotion of long acting reversible contraceptives.• Control of medical diseases.

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PROGESTERONE• Progesterone is a hormone that inhibits the uterus from contracting. • It is involved in maintaining pregnancy, especially early in gestation.• Progesterone has been recommended for pregnant women with prior preterm

birth.• This use is based on reviews of clinical research that indicated that

progesterone can prolong pregnancy for women at risk of preterm birth, based on having a prior spontaneous preterm birth.

• 17 hydroxyl progesterone caproate 500mg IM weekly or 200 mg NMP oral or vaginal recommemded from 24-34wks

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CONT…• Coitus should be avoided in late pregnancy as the seminal prostaglandis

and female orgasm increase the uterine contractions .• Treatment of vaginal and cervical infections . Bacterial vaginosis

increases the risk of preterm labour• Treatment of asymptomatic bacteriuria should be adequately done

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MEASURES TO ARREST PRETERM

LABOUR

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• As majority of preterm is associated with maternal and/or fetal complicating factor where early expulsion of fetus may be beneficial.

• About 10-20% of cases where fetus is not compromised ,maternal condition remains good and membranes are intact the following regime may be instituted in an Attempt to arrest preterm labour.

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REGIME• Admission and detailed history

• Bed rest – left lateral position

• Hydration and sedation to relieve anxiety

• Investigations like CBC, high vaginal swab, urine analysis. • Tocolytics after electrolytes and baseline ECG

• Cervical encerclage

• Prophylactic antibiotics

• Glucocorticoid therapy

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MAIN DRUG THERAPY IN PTL• TOCOLYSIS

• STEROIDS

• ANTIBIOTICS

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TOCOLYSIS

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• It is reasonable not to use tocolytic drugs, as there is no clear evidence that they improve outcome.

• However, tocolysis should be considered if the few days gained would be put to good use, such as completing a course of corticosteroids, or in utero transfer.

• Not associated with a clear reduction in perinatal or neonatal mortality, or neonatal morbidity.

• Most authorities do not recommend use of tocolytics at or after 34 weeks' .

• There is no consensus on a lower gestational age limit for the use of tocolytic agents.

RCOG Guideline Grade A recommendation 2011

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COTRAINDICATIONS TO TOCOLYSIS

ABSOLUTE • Choriamnionitis • Intra uterine demise • Severe IUGR• Lethal malformation• Severe PIH , Eclampsia

• Cardiac disease• Sever anaemia• Hyperthyroidism • Uncontrolled diabetes

RELATIVE • Mild PIH• Nonlethal anomaly• Mild IUGR• Advanced labour >4cm dilatation• Maturity > 34 wks • APH• fetal distress

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TOCOLYTIC AGENTS• Betamimetics • MgSO4• Calcium channel blockers• Prostaglandin synthase inhibitors• Nitroglycerine• Diazoxide• Oxytocin receptor antagonist – Atosiban• Potassiun channel openers- Aprikalim pinacidil

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MECHANISM OF ACTION OF TOCOLYTICS

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MAGNESIUM SULPHATE

• Acts by competitive inhibition to calcium ion either at motor end plate or at cell membrane.

• Decreases acetylcholine release and its sensitivity at motor end plate.

• Direct depressant action on uterine muscle

• In addition it hasA) anti oxidant propertiesB) anti inflammatory properties

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B- SYMPATHOMIMETIC AGENTS• MOA: Convert ATP into cAMP in the cell causing decrease of the free

calcium ion.

• Commonly used drugs are • Ritodrine• Terbutaline• Isoxsuprine

• Only ritodrine has been approved by FDA

• Beta-agonists reduce the risk of giving birth within 48 hours but there is no clear evidence that they are any more effective at preventing preterm birth than other tocolytic drugs.

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Side effects

• Maternal:palpitation, tremors, headache, chest pain, pulmonary edema, myocardial ischemia, arrhythmia, and even maternal death.

• Fetal : arrhythmia, cardiac septal hypertrophy, hydrops, pulmonary edema, and cardiac failure. hypoglycemia, hypocalcemia, periventricular-intraventricular hemorrhage, and fetal and neonatal death.

• Contraindications Diabetes, cardiac disease, hypertension.

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CALCIUM CHANNEL BLOCKERS• The use of CCBs compared with other Tocolytic agents was

associated with reduction in number of women giving birth within 7 days of receiving treatment and before 34 weeks of gestation.

• Decreased incidence of neonatal RDS, NEC, IVH than other Tocolytic drugs.

• When compared with other tocolytic agents associated with fewer adverse effects and less need to stop treatment because of adverse effect.

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INDOMETHACIN• COX-2 inhibitors compared with magnesium sulphate-no difference

between oral COX-2 inhibitor and intravenous magnesium sulphate in delaying preterm labour.

• Fetal risk:

• Premature closure of the ductus.• Renal and cerebral vasoconstriction.• Necrotising enterocolitis• Neonatal pulmonary hypertension• Common with high dose and prolonged exposure. RCOG 2012

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ATOSIBAN

• Oxytocin antagonist• Blocks myometrial oxytocin receptors.• Inhibits intracellular calcium release, PG’s release, inhibiting myometrial

contraction.• Half life is 12 mts

• Side-effects

• Nausea• Vomiting • Chest Pain

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MOA of steroids. 1. Enzyme induction for responsible for synthesis of pulmonary surfactant 2. Release of surfactant stored in type 2 pnemocytes. 3. Structural development of lungs 4. Accelerated maturation of fetal intestines (Prevent NEC). effect on myocardium (Prevent IVH) Repeated Dose Increased sepsis in PPROM Restricted fetal body and brain growth Adrenal Suppresssion.

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ANTIBIOTICS • Treats subclinical intrauterine infection• Prevents ascending infection from vaginal flora • Delays clinical chorioamnionitis in patients with PROM .• Broad spectrum antibiotics , particularly which covers bacterial vaginosis

are prescribed e.g Ampicillin / cephalosporins + metronidazole.

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MANAGEMENT DURING LABOUR • DURING FIRST STAGE

• The patient is put to bed• Ensure adequate oxygenation • Strong sedatives to be avoided• Epidural analgesia is of choice• Labour should be watched by intensive clinical monitoring• Continuous electronic monitoring of the labour• In case of delay or anticipating a traumatic vaginal

delivery Cesarean Section is to be performed

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MANAGEMENT CONTD…• DURING SECOND STAGE

• The birth should gentle and slow• Liberal Episiotomy may be done under LA to minimise

head compression• No instrumentation . Foetal distress is curtailed by low

forceps• Cord is clamped immediately at birth to prevent

hypervolaemia and hyperbilirubinaemia• Neonatologist should be present. if required shift the

baby to ICU.•

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MANAGEMENT CONTD…• 3rd stage of labour – there can be late separation of placenta and delivery

of the placenta.

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CARE OF PRETERM NEONATE• The cord is to be clamped quickly.• The cord length is kept long.• The air passage should be cleared of mucus promptly and gently.• Adequate oxygenation.• Maintainance of temp to prevent hypothermia.• Inj.vit k 1mg im

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SURVIVAL IN PREMATURE INFANTSSURVIVAL CHANCE IS DIRECTLY PROPORTIONAL TO THE MATURITY

• 26 wks – 80%• 27 wks – 90%• 28-31 wks – 90 to 95%• 32-33 wks – 95%• 34-36 wks – approaches

term survival rates Williams

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THANK YOU