Transcript Preterm labour

Preterm
labour
 The student by the end should be able to:
 Predict high risk patients for preterm delivery.
 Prevent preterm labor in patient at high risk.
 Enumerate the neonatal risk of prematurity.
 Evaluate the advantages of tocolytic therapy in
improving neonatal outcome.
 Describe the side effect of certain types of tocolytic
drugs
 Evaluate the advantages of steroid therapy in reducing
neonatal complications.
 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:
Preeclampsia .
43%
Fetal distress .
27%
Fetal growth restriction .
10%
Abruptio placentae .
7%
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.
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.
 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 or
anomalies , 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.
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:
 Maternal risk scoring.
 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 .
 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 un
rewarding:
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.
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) or fetal (anomaly ,death)
Examination :
General : to exclude maternal disease as systemic
infection , dehydration , hypertention .
Abdominal examination:
-exclude underlying abdominal pathology as appendicitis,
pyelonephritis .
-obstetric examination : palpable uterine contraction,
fundal height , lie , presentation , fetal heart.
Pelvic examination : to exclude cervical dilatation and
effacement, rupture of the membrane, infection ,
bleeding.
Investigation :
 GUE (mid stream)
 HVS.
 blood culture is indicated if pyrexia more than 38.5.
 C-reactive protein and ESR in cases of rupture of
membrane.
 Abdominal ultrasound.
 Tranvaginal ultrasound to predict preterm delivery.
 Fetal fibronectin testing .
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:
Absolute:
1. Sever PIH.
2. Sever abruptio placentae.
3. Chorioaminionitis.
4. Fetal death.
5. Fetal anomaly incompatible with life.
6. Sever IUGR.
Relative :
1. Mild chronic hypertention.
2. Mild abruptio placentae.
3. Stable placenta previa.
4. Maternal cardiac disease.
5. Hyperthyroidism.
6. Uncontrolled DM.
7. Fetal distress.
8. Fetal anomaly.
9. Mild IUGR.
10. Cervix > 5 cm dilated.
Pharmacological treatments currently in use:
1.
2.
3.
4.
5.
6.
Beta- adrenergic agonists.
Mg sulphate .
NSAIDs.
Ca channel blockers.
Glyceryl trinitrate.
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:
Hypotention, palpitation, arrythmia, ischemia,
pulmonary oedema ,maternal death in patient with
unrecognized cardiac disease , hyperglycaemia.
Pulmonary oedema is the most common serious adverse
effect , 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 osteoporosis
on long term use.
NSAIDs:
As indomethacin ,given orally or rectally ,it can cause fetal
side effect as oligohydramnios ,intraventricular
haemorrhage , 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.
Steroids are recommended between 24-36 weeks
gestation for single or multiple pregnancies, including
those 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.
Management of preterm delivery :
If labour become established certain point are differs
from delivery of term pregnancy:
 Continuous CTG monitoring (more risk of fetal distress ).
 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.
 caesarean section indicated in preterm breech
presentation ,preterm twin or higher order multiple
pregnancy .
 classical C.S. may be indicated in extreme prematurity.
 Assisted delivery to shorten the second stage of labour
by forceps not ventouse to reduce the risk of I.C.trauma.