1
Forth stage
Obstetric
Lec-6
.د
ا
سماء
1/1/2016
Preterm labour
The student by the end should be able to:
1. Predict high risk patients for preterm delivery.
2. Prevent preterm labor in patient at high risk.
3. Enumerate the neonatal risk of prematurity.
4. Evaluate the advantages of tocolytic therapy in improving neonatal outcome.
5. Describe the side effect of certain types of tocolytic drugs
6. Evaluate the advantages of steroid therapy in reducing neonatal complications.
7. Describe the essential steps during delivery of preterm fetus.
Preterm labour (PTL): is the onset of labour after the gestation of viability (20-28 weeks
depending on definition) and before 37 completed weeks.
PTL occurs in about 5-10 % of all pregnancy depending on the population studied.
Preterm labour could be :
Spontaneous PTL accounts for 72%.
Indicated PTL accounts for 28% as for:
1. Preeclampsia . 43%
2. Fetal distress . 27%
3. Fetal growth restriction . 10%
4. Abruptio placentae . 7%
5. Fetal death 7%
Risk factors and causes of preterm labour:
Wide spectrum of causes and demographic factors have been implicated in the birth of
preterm infant.
1.Ideopathic :often no cause can be identified for preterm labour during evaluation and at
least makes up 70% of PTL.
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2.Medical and obstetric causes:
Preeclampsia.
Placenta previa
abruptio placentae.
Multiple birth .
Polyhydramnia
Fetal anomaly
Fetal death.
Previous second trimester abortion or induced abortion.
Uterine causes : anomaly, fibroid .
Cervical incompetence
Drug intoxication
Trauma or surgery
Immunological disorder as antiphospholipid Ab syndrome
DES exposure
3.Genetic factors:
Genetic factor may have a role since PTL runs in families and there is tendency for
recurrence in subsequent pregnancy, and have different incidence in different races.
4.Infection:
-Chorioaminionitis : local infection following abnormal bacterial vaginal colonization
(bacterial vaginosis) cause local release of prostaglandin and stimulate uterine contractions
, it’s responsible for 10-20% of cases of preterm labour with intact membrane.
-Systemic infection ; as pyelonephritis is also implicated in preterm labour ,torches.
5.Lifestyle factors :
Age less than 20 years.
Poor nutrition.
Poor weight gain during pregnancy.
Low maternal prenatal weight gain .
Poverty.
Smoking.
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Short stature.
Occupational factors.
Psychological stress.
Risk and complications of PTL:
1.Maternal risk:
Risk of the underlying maternal disease which precipitate preterm delivery.
Risk of the treatment regimens used for PTL.
Risk of caesarean section : which is preferred for better immediate survival of the
very preterm infant. This will increase the risk of haemorrhage and infection in the
poorly formed lower segment.
Also the scar of the operation will compromise future uterine function without
documented improvement in the perinatal mortality and morbidity.
Psychological trauma to the parents.
2.Fetal risk :
1.The risk of underlying fetal condition which precipitate PTL as IUD , IUGR ,
congenital infection oranomalies , these will contribute to the increased perinatal
mortality and morbidity.
2.Gestational age at presentation affect the management and outcome.
3.Fetal intrapartum hypoxia and birth trauma associated with preterm infant and
very low birth weight infant.
3.Early neonatal risk of:
Difficulty in maintaining body temperature.
Difficulties in oral feeding.
Increased risk of infection.
Lung immaturity proportionate to the gestational age
Congestive heart failure (PDA).
Liver immaturity and sever neonatal jaundice with increased neurotoxic effects of
unconjucated bilirubin.
Intracranial haemorrhage.
Necrotizing enterocolitis.
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-These complication cause increased mortality , morbidity and costs of preterm delivery .
-All are higher at lower gestational age , 90 % mortality rate at 23 weeks gestation dropping
to 2% at 34 weeks.
-Babies who survive have high risk of short and long term morbidity and disability as
pulmonary disorder , cerebral palsy and neuro-developmental delay .
-These consequences of prematurity have lead to an attempt to improve outcome by
predicting , preventing and treating preterm labour.
Screening and prediction of PTL:
1. Maternal risk scoring.
2. Fetal fibronectin (FFN) testing:
Presence of FFN in the cervicovaginal secretion in the late second and early third
trimester indicate disruption of the choriodecidual interface which can be caused by
preterm labour ,infection , stress ,or haemorrhage .
Positive fetal fibronectin test increase the risk of preterm labour .
3. Cervical sonographic assessment:
cervical length of 15 mm or less predict preterm delivery in 26% of cases and >
30mm is unlikely to have PTL.
Prevention of preterm delivery:
Preventing the onset of labour is generally unrewarding:
1.Behavioural and life style modification coupled with optimal management can reduce
the incidence of preterm delivery (stop smoking , adequate nutrition).
2.Cervical cerculage : prophylactic cerculage in asymptomatic patient with short cervix
diagnosed by ultrasound or patient with history suggestive of cervical incompetence.
3.Progesterone: progesterone has many cellular functions which maintain pregnancy and
it’s withdrawal is a prerequisite for labour.
prophylactic treatment with 17-alpha hydroxy progesterone caproate given by weekly i.m.
injection reduce preterm delivery and reduce the complication rate of necrotising
enterocolitis, intraventricular haemorrhage and the need for oxygen supplementation.but
it should not be used before safety is confirmed .
4.Screening and treatment of bacterial vaginosis early in pregnancy in asymptomatic
patient and treatment of symptomatic patient could reduce the preterm labour.
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Management of preterm labour:
*History :
- proper estimation of the gestational age with the regard of the previous ultrasonic
assessment to confirm that the baby is preterm.
-symptoms of PTL/PROM:
Abdominal pain : not necessarily regular .
Backache.
Leaking liquor .
Vaginal discharge/Vaginal bleeding.
- Underlying condition predispose to PTL:
medical (UTI ,gastroenteritis)
obstetric (APH , previous PTL)
fetal (anomaly ,death)
*Examination :
1-General : to exclude maternal disease as systemic infection , dehydration , hypertention .
2-Abdominal examination:
-exclude underlying abdominal pathology as appendicitis, pyelonephritis .
-obstetric examination : palpable uterine contraction, fundal height , lie , presentation ,
fetal heart.
3-Pelvic examination : to exclude cervical dilatation and effacement, rupture of the
membrane, infection ,bleeding.
*Investigations:
1. GUE (mid stream)
2. HVS.
3. blood culture is indicated if pyrexia more than 38.5.
4. C-reactive protein and ESR in cases of rupture of membrane.
5. Abdominal ultrasound.
6. Tranvaginal ultrasound to predict preterm delivery.
7. Fetal fibronectin testing .
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*Treatment:
-Before we start treatment we should:
Establish the diagnosis of actual PTL.
Search for treatable causes that trigger preterm labour.
Exclude maternal and fetal contraindication for labour inhibition.
-Initial treatment :
Bed rest in lateral decubitus.
external cardiotocographic monitoring .
tocolysis.
steroid administration.
1.Tocolysis :
-These are disparate classes of drugs that are used to reduce uterine contractility , mostly
they act as smooth muscle relaxants.
-Currently these drugs are only recommended to gain time by delaying delivery to improve
neonatal outcome by transferring the women to a unit with appropriate neonatal facilities
and for administration of steroids.
-Maintenance tocolysis is not recommended for routine practice.
-Tocolytic drugs are contraindicated for obstetric and medical reasons:
a-Absolute:
1. Sever PIH.
2. Sever abruptio placentae.
3. Chorioaminionitis.
4. Fetal death.
5. Fetal anomaly incompatible with life.
6. Sever IUGR.
b-Relative :
1. Mild chronic hypertention.
2. Mild abruptio placentae.
3. Stable placenta previa.
4. Maternal cardiac disease.
5. Hyperthyroidism.
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6. Uncontrolled DM.
7. Fetal distress.
8. Fetal anomaly.
9. Mild IUGR.
10. Cervix > 5 cm dilated.
-Pharmacological treatments currently in use:
1. Beta- adrenergic agonists.
2. Mg sulphate .
3. NSAIDs.
4. Ca channel blockers.
5. Glyceryl trinitrate.
6. Oxytocin antagonists
Problems in these drug therapy:
These drugs have side effects .
Some are expensive.
There is no certainty that a drug prolong gestation more than others.
Combination of drugs only increase the side effect.
Beta- adrenergic agonists:
-In these drugs the dose should be individualized to each patient because of difference in
uterine activity and cervical changes and difference in plasma clearance, and there is
reduction in myometrial receptors with continuous treatment.
-These drugs can be given as i.v. infusion , i.m., s.c. and oral route.
-By i.v. infusion we start with the lowest recommended dose increase it till tocolysis is
achieved or side effect are noted , infusion continued for 24 hours then we can shift to oral
therapy.
-Ritodrine is the only drug approved by FDA .
Dose : 150 mg in 500 ml 5% dextrose (0.3 mg /ml) initial dose 0.05 mg increased by 0.05 mg
every 10 min.until contraction cease ,reaching max. dose of 0.35 mg/min. ,or maternal
pulse > 140 beats. Maintenance dose for 6 hours. Oral : 10 mg ½ hour before stopping
infusion and repeated every 2-4 hours . Titrate dose and frequency to maintain pulse > 100
b/min.
-Maternal side effect:
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Hypotention, palpitation, arrythmia, ischemia, pulmonary oedema ,maternal death in
patient with unrecognized cardiac disease , hyperglycaemia. Pulmonary oedema is the most
common serious adverseeffect , predisposing factors as :
Twin pregnancy .
Persistent heart rate above 130 beat /min.
Anaemia .
Fluid over load.
Corticosteroid ,Mg sulphate.
Mg sulphate:
-It suppress myometrial activity in a dose dependent manner (5-8 mg/dl) .
-Hypermagnesemia leading to loss of deep tendon reflex ,respiratory and cardiac
impairment , it decrease serum Ca leading to osteoporosison long term use.
NSAIDs:
-As indomethacin ,given orally or rectally
-it can cause fetal side effect as oligohydramnios ,intraventricular haemorrhage ,closure of
PDA. These side effect are uncommon if the drug is used for less than 24 hours.
Ca channel blocker:
As nifidipine. maternal side effect are generally mild, including headache and flushing.
Glyceryl trinitrate(GTN):
It’s relatively safe , yet to be assessed in trials.
Oxytocin antagonist’s :
Atosiban is as effective as beta agonist with markedly reduced side effects ,but follow up
of babies up to 2 years before wide use is established .
2.Antenatal corticosteroid:
-Betamethasone and dexamethasone given in single dose regimen,24 mg divided in 2-4
doses apart, they improve neonatal outcome by reducing respiratory distress syndrome ,
intraventricular haemorrhage , necrotising enterocolitis.
-Maximal beneficial effect is between 24 h and 7 days.
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-Steroids are recommended between 24-36 weeks gestation for single or multiple
pregnancies, includingthose with PROM and mothers with diabetes (careful control)
(risk/benefit should be considered in patients more than 34 weeks).
-Betamethasone is superior to dexamethasone as it reduce the incidence of cystic
periventricular leukomalasia more than the use of dexamethsone or no intake of steroid.
-Single coarse is recommended than multiple because of low risk of side effect as IUGR
,maternal osteoporosis, immunosuppression and impaired glucose tolerance.
*If labour become established certain point are differs from delivery of term
pregnancy:
1. Continuous CTG monitoring (more risk of fetal distress ).
2. Delivery of the fetus in their sac is better or to delay rupture of the membrane as
late as possible in labour to protect the fragile fetus from birth trauma.
3. caesarean section indicated in preterm breech presentation ,preterm twin or higher
order multiple pregnancy .
4. classical C.S. may be indicated in extreme prematurity.
5. Assisted delivery to shorten the second stage of labour by forceps not ventouse to
reduce the risk of I.C.trauma.