Parturition: Preterm Birth Flashcards
Is a ‘post-term’ baby (>42 weeks) a thing?
Not very often, and there’s two types
- Baby who biologically just wants to be 42 weeks
- Babies who are too old for their placenta: can die
Hard to distinguish which one!
What is ‘pre-term labour’
Preterm: Labour before 37 weeks gestation (9%)
Very Preterm: <32(~2%)
More then just dates, preterm is an abnormality: a failure of the uterine quiscence (a failure of the uterus to keep the baby in until the right time)
What’s the ‘cost’ of neonatal preterm birth?
- Complications
- Personal cost: loss of mother-child bonding
- Long term health problems
- Individual and family costs
- Societal costs ($26.5 bill US annualy)
- It costs $1500 NZ/day in NICU, can be upto > 100,000 by discharge; huge stress on couples!
- ONE baby with Neonatal encephelopathy $30-50 mill
Is babies survival rates gettoing better or worse?
Over the last 50 years have increased, but we are now reaching a plateau!
Plateau of survival is currently
- >29 weeks; less then this survival rates decline.
- >1250g; less then this survival rates decline
Gestation and birthweight determine survival rates!
But we can not just look at preterm survival rates! What else should we be focussing on?
Lowering the major-moderate handicap % in preterm neonates.
<10% at 28-29 weeks
BUT it is still present even up till around 36 weeks (not always due to uterine quiescence, but mum/baby are unwell)
WHat do we think the ‘causes’ of preterm labour could be
- Stress of severe life event → disruption of quiescence
- 4-5% women in pregancy bleed: this increases preterm risk
- Infection increases risk
- Increased stretch (due to more then 1 baby in the uterus)
These are trigger events for the labour activation pathway. BUT causes a disordered cascade that can intertwin pathways!
Why is there a failure of quiescence?
We don’t know why! What we do know is that inflammation or infection acts as a potent stimulus.
1 or more of these abnormal/removed can interfere
Preterm Activation
- Uterine stretch: Excess fluid (eg twins)
- Upregulation of myometrium: abnormally is membranes rupture early or are infected
- Cervical change/damage
Noones proven that the uterus is abnormal in it’s timing, still born in early hours of the morning.
The earlier the baby is born, the more likely it is to have has an __________ or _________ eitiology.
And because of this, it is likely to open _________.
The earlier the baby is born, the more likely it is to have has an inflammatory or infectious eitiology.
And because of this, it is likely to open up the cervix prematurely, which exposes fetal membrane to vagina (and therefore infection → rupture)
Is measurement of cervical length by trans vaginal US an effective way to predict preterm birth?
Why/why not?
No.
- We would have t screen a huge amount of mothers; not viable cost wise
- Individual variability between cervix
Cervical ripening:
Active, inflammatory like process.
Infiltration of leukocytes, increase in cytokines and MMPs occur.
Independent of uterine activity, so can be symptom free!
What are the abnormal triggers** to upset the peace
((Quiescense))
- Membrane Disruption: INFECTION causes rupture of chorio-placental membranes → release of PGs
- Myometrial Distention: twins, excess fluid (Can also cause membrane disrup.)
- Tissue damage (esp cervix)
- Placentation
- Low Growth of fetus (poorly plugged in placenta)
- Hormone P4
- PG release
- Placental bleeding (bad attachment)
How does infection affect preterm labour?
Normally in pregnancy the cervix is long and plugged (creating a bacteriostatic barrier)
But is you’ve chopped some off some cervix due to an abnormal smear, or born with congenital defect; the barrier is weakend.
These women are more likely to deliver preterm; also bacteria gets into the choriodecidual space (rupture), and may even cross into the placenta (if gets into fetus its fatal)
Health problems of preterm birth?
- Immature fetus so often unwell
- Malpresentation: breech (butt 1st)
- Maternal co-morbidities
- complicated caesarean sections
- Risk of recurrence
- Poor health outcomes
Lung development determines _________
Limit of viability, determined by the fetal organ of gas exchange, the placenta.
If the type II cells in our lungs can’t effectively produce surfactant, which coats alveoli and reduces surface tension, and babies would require huge amount of energy to overcome this and expand lungs
How do you fix preterm lung issues?
Artificial surfactant ( SIr Graham Liggins)
How many preterm births are Iatrogenic (docotr initiated), and why?
~50%
Maternal Disease (preeclampsia: placental disease)
Fetal Health (IUGR) (placental vascular disease, baby getting malnourished
What should you consider in a previous risk assessment for preterm birth?
Take a history
- Previous PTB (highest indicator, but most women having first baby!)
- Smoking*
- multiple pregnancy
- cervical surgery
- uterine anomaly
- maternal disease
- antepartum bleeding
- Polyhydramnios (too much AF)
Consider modifiable vs non-modifiable risks
Cervical length as a screening for PTB
The shorter the cervix, the higher the risk, BUT the screening PositivePredictiveValue is less then 50%, is this worth it?
People are looking at a combination of _________ to screen for PTB, but what remains the issu
Serum biomarkers, Cervico-vaginal fluids and cervical length are tested in a combination, but there is still little supportive evidence of this working!
What is fetal fibronectin
Biological glue: high MW glycoproteins
Between the decidua and chorion membranes
Present in cervico-vaginal fluids in 1st trimester and end of 3rd trimester: Not meant to be present pre 25weeks
Seen in CV fluids of 20-30% women with preterm labour (shows membrane has ruptured etc)
How do we measure Fetal fibronectin in threatened PTL
- If positive: 30% deliver in 7-10 days
- Negative: 99.5% don’t deliver in 7-10days (what you want)
Used to decide who to transfer and who to treat with steroids
Checks if decidual lining is intact!
Intervention to suppress PTL: Tocolysis
Drugs: various modes of action, but the main ones are
- antagonists of Ca2+ channel blockers** (Nifedipine)
- Oxytocin receptor blocker (atosiban $$$)
Used to be B2 agonist salbutammol, PG antagonists
Intervention to suppress PTL: Steriods
For pulmonary maturation to avoid Resp. distress SYndrome
Also less InterVentricular Haemorrhage and NecrotisingEncophelitis (inflam/infec of neonatal gut)
Betamethasone, always give babies
Intervention to suppress PTL: Magnesium Sulphate
Give MgSO4 6 hours before birth for neuroprotection
(Loading Dose:4g Maintenence Dose: 1g/hr up to 24hr)
4 hour infusion optimal
NNT to prevent cerebral palsy in 1:63 women
What can we as clinicians do in terms of prevention strategies and risk assessment?
- stop Smoking
- Cervical cerclage next time (to strengthen)
- Drug therapies: P4 for quiescence (unsure on evidence)
- Supportive social care?
- Maori are higher!
Who do you give P4 to prevent sPTB
Women with a short Cervix: highest risk factor
Cervix length 10-20mm: 19-23 weeks use a P4 gel
45% reductionin PTB
#NeededToTreat 12-14
**not effective if Cx too short.
THoguht CX xerclage + P4 better?
injection not safe
useless once contractions start
Some treatments don’t work/do harm
Maintenance: nonsteroidal, ABs and MgSO4- may do harm
Prophylaxis: injected P4 may do harm
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