2. 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
4. 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.
5. SKNMC STATISTICS
51 60 60
378 361 395
APRIL MAY JUNE
% of preterm deliveries in sknmc 2016
preterm deliveries total deliveries
13% 16.6%
15.1%
6. PRETERM DELIVERIES IN SKNMC
2016
46
55 55
5
5 5
0
10
20
30
40
50
60
70
April May June
preterm labour patients delivered vaginally delivered by c section
7. 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.
8. 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
10. • 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.
11. 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.
12. 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.
14. 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
15. 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.
16. PATHOGENESIS
• CAUSES OF PRETERM BIRTHS
THERE ARE 4 MAIN CAUSES WHICH INCLUDE :
1. SPONTANEOUS UNEXPLAINED PRETERM LABOR WITH INTACT MEMBRANES
2. PPROM
3. DELIVERY FOR MATERNAL OR FETAL INDICATIONS
4. TWINS AND HIGHER ORDER MULTIFETAL BIRTHS.
Williams 23rd edition
17. 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
18. 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 DISTENSION
Uterine distention
Uterine expansile capacity
Myometrial
activation
Fetal membrane
cytokine activation
contractions rupture of membranescervical change
19. 2.MATERNAL-FETAL STRESS
• MATERNAL PSYCHOLOGICAL STRESS
• INCRESED MATERNAL ESTRIOL AND CORTISOL
• LOSS OF UTERINE QUIESCENCE
• ACCELERATE CERVICAL RIPENING
20. 3.INFECTION
• Bacteria can gain access to intrauterine tissues through
1. 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.
22. 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
23. • Most common microbe associated with preterm birth are
1. Gardnerella vaginalis
2. Fusobacterium
3. Mycoplasma hominis
4. Ureaplasma urealyticum
25. 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.
26. 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 .
27. • 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
28. 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)
29. 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
30. 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 .
31. 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.
32. 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
33. 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
34. PREDICTION
1. Assessment of risk factors
2. Per vaginum examination to assess the cervical status
3. Ultrasound examination: Trans vaginal usg
4. Detection of fetal fibronectin in cervico vaginal secretions.
5. Home uterine monitoring.
6. Salivary estriol ,IL-6 ,IL-8 ,TNF
35. PER SPECULUM EXAMINATION
Any leakage PV/ Any abnormal discharge PV
Cervical length/
Dilatation of cervix
DIGITAL EXAMINATION:
• Cervical length
• Cervical dilatation
• Status of the membrane
36. 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.
38. • 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
•
•
39. FETAL FIBRONECTIN
• Fetal Fibronectin (FFN)- it is a glue like protein (polypeptide) binding choriodecidual
membrane.
• Normally present before 22 weeks and after 37 weeks.
40. 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 .
41. 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
42. 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
44. 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.
45. 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
46. 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
48. • 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.
49. 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
52. • 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
53. 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
56. 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 has
A) anti oxidant properties
B) anti inflammatory properties
57. 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.
58. 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.
59. 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.
60. 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
62. 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.
63. 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.
64. 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
•
65. 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.
•
66. MANAGEMENT CONTD…
• 3rd stage of labour – there can be late separation of placenta and delivery of the placenta.
67. 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
68. SURVIVAL IN PREMATURE INFANTS
SURVIVAL 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
