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MBCHB3: Reproduction, Development and Ageing > Lecture 16: Preterm Labour > Flashcards

Lecture 16: Preterm Labour Flashcards

1
Q

What is preterm?

A

<37 weeks

VPTB <32 weeks
EPTB <28 weeks

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2
Q

What is spontaneous vs indicated preterm birth?

A

Indicated is dr initiated because of threat to either mum or babe.

Spontaneous prematurity is a pathology of uterine quiescence

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3
Q

What are the possible pathological processess of premature baby?

A

Endocrine - fetal/maternal stress
Inflammation / infection
Decidual haemorrhage
Uterine distension

Leads to abnormal stimulation and thus labour

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4
Q

What possibly triggers the cascade leading to stimulation and labour?

A 
Infammation
Mechanical
Hormonal
Fetal (genomic/HPA)
melatonin and circadian rhythms
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5
Q

What causes pre-term activation of HPA, and what are two examples?

A

Increased fetal or maternal stress -> Prem. activation of fetal HPA

i. e Uteroplacental vascular insufficiency (FGR or PET) and thus spon. PTB
i. e Maternal major psychological stress can activate HPA axis

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6
Q

What sort of infections can cause PTB?

A
  • Ascending infection into membranes i.e STI

Degrades barrier of cervix and infiltrates around membranes -> Inflammation (i.e because of phospholipase A2 or endotoxins) (this inflam interferes with normal pathway, enhancing the processes)

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7
Q

How does decidual heamorrhage (Pathology) come about?

A

Damaged decidual blood vessels -> Retroplacental hematoma

Thrombin activation as part of the normal coagulation cascade.

  • > Directly increases myometrial contractions
  • > upregulates MMPs -> pprom
  • > Inhibits expression of progesterone receptors i.e activates as progesterone withdrawal.
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8
Q

What are some causes of distension and what physiological changes do they cause that possible lead to labour?

A
  • Multiple pregnancy
  • Polyhydramnios
  • Enhanced stretching
  • Increased CAP
  • Increased connexin 43
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9
Q

What is cervical insufficiency?

A
  • Dilation or effacement without contractions (i.e conditions for labour)
  • Usually previable loss
  • Clercage may be helpful
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10
Q

Is there strictly one pathophysiology?

A

No they all interrelate i.e slide 14

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11
Q

What are the short term costs of preterm?

A

Many different impacts as it can cause probelms in all systems

Psychosocial and financial impact on parents and families.

Often forced speration due to treatments, hard to bond. Also might be maternal complications

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12
Q

What are the long term costs of preterm?

A
  • Recurrent hospitalisations
  • Neurodevelopmental disabilities i.e cognition, motor dificits, sensory impairment, behaviour or psychology
  • Chronic health issues
  • Adulthood might be insulin resistance, diabetes etc
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13
Q

What is viability?

A

GA where a baby can be resus’d at delivery and survive without significant morbidity ~23 weeks

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14
Q

What determiens perivaibility?

A
  • GA
  • Use of corticosteroids
  • Sex
  • Infection / rupture of membranes

Essentially though its lung development and being in a tertiary care centre

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15
Q

What are two pathologies of periviabiltiy babes:

A
  • Bronchopulmonary dysplasia

- Resp. distress syndrome

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16
Q

Why are anenatal corticosteroids needed?

A
  • Induce surfactant production to overcome the tension of water in lungs to breathe
  • Other effects:
  • > Reduce fetal lung fluid
  • > Alter responsive to oxidative stress
17
Q

What are the risk factors for preterm birth?

A
  • Previous PTB
  • Short interval between preg.
  • INFECTION
  • SMOKING AND SUBSTANCE ABUSE
  • Cervical age
  • Poor antenatal care
  • Conditions where there is increased uterine stretch
18
Q

What are the modifiable risk factors prior to pregnancy that might alter preterm risk?

A
  • Decreased need for cervical surgery
  • Optimise interpreg interval
  • Optimise maternal health
19
Q

What are modifiable risk factors in pregnancy that might alter preterm risk?

A
  • Stop smoking/substances
  • Screen and treat for STI / UTI
  • Encourage prenatal care
  • Decrease risk of PET (aspirin / Ca)
20
Q

What are some biomarkers for preterm birth?

A

Many studies, non great in asymptomatic patients but:

FFN (Fetal fibronectic, fuses membranes)
- (present in cervico vaginal fluids in first trimester)

In combination with CL and history factors to improve sensitivity but still isnt great (CL - cervical length)

21
Q

Whats a screening test for PTB?

A

Cervical length

CL at 16-24 weeks is proportionate to gestation at birth

BUT need to screen 1000 women to prevent six cases (treated with progesterone)

22
Q

How else can we prevent PTB?

A

Modifiable social determinants of health i.e advocate

Otherwise:

  • Progesterone
  • Cervical clercage
  • Preterm birth clinics for those at high risl
23
Q

Do we know how cervical clercage works?

A

No

24
Q

What does not work for PTB prevention?

A
  • Maintainence tocolytics
  • Untargeted antibiotics
  • Relaxation therapy
  • Bedrest
  • Probiotics
25
Q

If labour is predicted and you are preterm what can you do?

A

Use tocolysis to buy time in order to:

  • Transfer to tertiary unit
  • Antenatal corticosteroids
  • MgSO4 for neuroprotection (against CP)
26
Q

What drugs are for tocolysis?

A

Ca channel blockers
Oxytonin receptor blockers
B2 agonists
PG synthase inhibitors

27
Q

If fetal fibronectin comes back positive…. what does in indicate?

A

30% deliver in 7-10 days

  • ive 99.5% dont deliver
    i. e should not be positive between 22-25 weeks)
28
Q

How often do membranes rupture in preterm birth and what are the indications?

A

30% rupture in sPTB

  • Membranes weakened
  • Exposure of decidual tissue may increase PGS = labour
  • Loss of barrier increases risk of infection
29
Q

How do you treat premature membrane rupture and PTB?

A
  • Erythromycin prolongs latency, reduces Resp. distress syndrome, major cerebral abnormalities
  • Optimise fetal condition steroids, MgSO4, transfer to tertiary center and monitor for infection
  • Aim to deliver at term

MBCHB3: Reproduction, Development and Ageing (24 decks)

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