L11 Preterm Birth Flashcards
Why might reporting on later cases of preterm birth be limited?
- Lack of data on later cases since they are typically less severe
- As a result, they are lower in priority
Outline the classifications of preterm birth:
- Extreme PTB: <28 weeks
- Very PTB: 28 - 31 weeks
- Moderate PTB: 32 - 33
- Late PTB: 34 - 37
How many live births are preterm in the UK vs worldwide?
- 7.8% in UK
- 1 in 10 globally
- Results in 1 million PTB-related deaths a year
What is the data behind preterm births in twins?
- Over 50% of twin pregnancies deliver preterm
What complications are associated with prematurity?
- KEY: Largest cause of perinatal mortality for a normal fetus, and a major contributor to developmental delay
- Respiratory
- Cardiovascular
- GI
- Metabolic
- Sensory (vision and hearing)
- IVH and white matter injury
- Cerebral palsy, neurodevelopmental delay
- ADHD and behavioural problems
- Failure to thrive
- Insulin resistance, hypertension
Outline some economic pressures for delaying preterm birth:
- Cost of special care/neonatal care stays
- Associated long term costs with conditions of premature babies
- Costs NHS upwards of £2.9 billion a year
What are factors are involved in preterm parturition syndrome?
- Uterine overdistension
- Decidual haemorrhage
- Cervical insufficiency (dilation before term)
- Cervical remodelling
- Infection and inflammation (KEY)
- Other causes, known and unknown
What are the 4 key routes for intrauterine infection?
- Ascending infection (genital tract)
- Haematogenous (via placenta)
- Retrograde (seeding via fallopian tubes)
- Iatrogenic (following invasive procedures)
Evidence for a causal relationship between infection and PTL:
- Present in 25 - 40% of preterm births
- Animal studies: systemic/I-U administration of microbes can provoke PTB
- Extra-uterine infections increase risk of PTB (e.g pyelonephritis, malaria)
- Subclinical intrauterine infection also associated with PTB
- Evolutionary argument (protecting mother and preserving reproductive function)
Outline the broad pathway leading from infection to PTB:
- Microbial invasion of amniotic cavity
- -> Proinflammatory response
- -> Cervical remodelling and myometrial activity
- Preterm delivery
Fetal tissue response to choriodecidual bacterial colonisation:
- Increased CRH by fetus, placenta
- Increased cytokines and chemokines (particularly IL-1B and TNF-a)
- Leading to increased cortisol and increased PGs
- Increase in metalloproteases (degrading structures of chorioamnion and cervix)
- -> Cervical ripening, weakening/rupture of chorioamnion, myometrial contractions
- ->PTB
Maternal response to choriodecidual bacterial colonisation:
- Decidua release cytokines and chemokines
- Neutrophil infiltration and simultaneous PG release
- -> Increase in metalloproteases (degrading structures of chorioamnion and cervix)
- -> Cervical ripening, weakening/rupture of chorioamnion, myometrial contractions
- -> PTB
What 3 cytokines play a key role in infection-driven PTB?
- Proinflammatory: IL-1B and TNF-a
- Antiinflammatory: IL-10
List 4 inherent defenses against infection in the reproductive tract:
- Acid vaginal pH (secondary to lactobacilli)
- Cervical mucus
- Epithelial barriers
- Innate immune system receptors (TLRs)
- Issues with these defences lead to higher risk of infection and PTB
What is ischaemia?
- Ischemia is a less-than-normal amount of blood flow to part of your body
- This lack of blood flow means your tissues aren’t getting the oxygen they need.
Evidence for the link between ischaemia and PTB:
- Obersvational evidence linking placental vascular lesions and PTB (higher rate of vascular lesions in PTB placentas)
- Abruption commoner in PTL/PROM cases than term labour
Mechanism for ischaemia link to PTB:
- Largely unclear
- Keep in mind that under adverse conditions, the body treats the placenta as a terminal organ
When may cervical insufficiency occur?
- More likely in patients with abnormally disrupted cervices
- e.g. Post LLETZ surgery
- e.g. Congenital abnormality
- Also evidence for link between cervical insufficiency and intrauterine infection (50% acute cervical insufficiency cases)
What factors lead to uterine overdistension?
- Multiple gestation
- Polyhydramnios
- Uterine anomalies
Mechanism linking uterine distension and labour induction:
- Increased distension -> increased expression of contraction associated proteins
- This includes gap junction proteins, oxytocin receptors, proteins in PG synthetic pathway
- -> Increased PG release -> Labour induction
- (Also higher levels of collagenase and IL8 in membranes)
Why may an endocrine disorder lead to preterm birth?
- Key role of progesterone in maintaining uterine quiescence during pregnancy, and preventing untimely cervical ripening
- Endocrine control over proinflammatory cytokines and CRH levels
What techniques are currently used to predict preterm birth?
- History-based assessment (most gestational disorders more likely to repeat in mothers who’ve previously had them)
- USS (cervical length)
- Actim partus test
- Infection screening
- Clinical diagnosis
What is the actim partus test?
- Swab for placental proteins
- Particularly interested in pIGFBP1
- Looking for evidence of disruption to placenta (e.g. abruption)
- Indicator for PTB since pIGFBP1 is produced in the fetal decidua and leaks into the cervix when the decidua and chorion detach
- 1 in 6 positive actim partus -> PTB (Good negative predictive value but not very specific so only useful as a screening measure)
Outline the risk factors for PTB:
- History: Previous preterm birth, previous cervical history
- Multiple pregnancy
- Lifestyle: Smoking
- Background: Age, ethnicity
- Clinical: bacterial vaginosis, short cervix, uterine abnormalities