1.1 Effect of intrauterine & perinatal events Flashcards

1
Q

What is the definition of prematurity?

A

Prematurity is defined as being born < 37 weeks gestation (with < 28 weeks being extreme)

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2
Q

Intraventricular haemorrhage is the most common neurological problem in preterm babies:
• Commonly occur in the __________ (highly vascular area of the developing brain which regresses as babies approach term)
• High risk of blood vessel rupture and bleeding into the ventricles in premature babies (mostly occur in the first 1 – 3 days → uncommon in the 1st week)
o Vessels become ___________________ with maturity
• Handling the baby or having to transport them increases risk of rupture

Bleeds are classified based on their severity and complications which result from it:
• Grades III and IV are more likely to cause long-term issues → risk of _________________ due to clots forming in the ventricular system
o Impedes circulation and reabsorption of CSF
o Precedes development of hydrocephalus

• Tested and examined using _____________ → used in NICU to monitor for IVH → 5 images in coronal plane and move left and right in sagittal plane
o Look for asymmetry and areas of brightness around the ventricles

A

germinal matrix ;

supported by more connective tissue;

post-haemorrhagic ventricular dilatation;

cranial ultrasound (CRUSS)

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3
Q

What is Grade I intraventricular haemorrhage?

A

Grade I (bleeding only in germinal matrix)

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4
Q

What is Grade II intraventricular haemorrhage?

A

Grade II (bleeding into ventricles itself)

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5
Q

What is Grade III intraventricular haemorrhage?

A

Grade III (IVH with ventricular dilatation)

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6
Q

What is Grade IV intraventricular haemorrhage?

A

Grade IV (involves parenchyma)

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7
Q

Retinopathy of prematurity (ROP) is a condition which may lead to visual impairment:
• Occurs due to ________________ (premature babies often need high
oxygen levels due to respiratory problems → increased risk)
• Pathogenesis: retina is vascularised centrally from ___________ and progresses peripherally → exposure to high oxygen before completion of vascularisation → relative ischaemia between vascularised and non-vascularised areas → rapid growth of poorly formed fragile vessels in ____________ (prone to bleeding → retinal damage → blindness)
• Risk factors: prematurity, low birth weight, exposure to high levels of oxygen (chronic lung disease), IVH, necrotising enterocolitis

A

exposure to high levels of oxygen;

optic disc;

middle ridge;

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8
Q

Necrotising enterocolitis is a life-threatening condition where the bowel becomes necrotic and may perforate:
• Exact aetiology is not fully understood → loss of ___________
• Timing of onset is inversely proportional to gestational age → more common in premature babies, but presents later than those less premature and presenting early
• Increased risk in those with _____________________
• Reduced risk by _________________

A

mucosal integrity + bacteria;

low gestational age, low birth weight, growth restriction and reduced gut perfusion (e.g. abruption, twin-to-twin transfusion syndrome, sepsis, large PDA ex utero which diverts blood away from the gut);

breastfeeding, early slow feeds (with controlled increase), vigilance

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9
Q

Babies have a very largesurface area to volume ratio, which is compounded by the fact that it is thin, fragile, poorly keratinised and lacks subcutaneous fat:
• Causes problems in __________________

Premature babies have a higher risk of infection as the premature skin provides a poor barrier, they have multiple invasive procedures, and have a less developed immune system:
• Baby’s immune system is supplemented by _____________ → passage of IgG increases as gestation increases → less in premature babies
• Cord IgG levels are ~0.04 g/L at 28 weeks → 1.8 g/L by term (45-fold increase)

A

thermoregulation, fluid regulation & transepidermal fluid loss as well as an ineffective barrier to infection

transplacental immunoglobulins (IgG)

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10
Q

Patent ductus arteriosus (PDA) is a remnant of the foetal circulation which connects the pulmonary artery to the aortic arch:
• Diverts blood away from lungs (high resistance in utero) into systemic circulation
• Normally closes _______________ in term babies (90% close by 60 hours)
• If the DA does not close, it results in a _______________

A

12 – 24 hours after birth;

left-to-right shunt (from aorta into pulmonary artery as aortic pressure is higher)

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11
Q

what factors keep the ductus arteriosus open in utero?

A
  • Prostaglandin E2 and prostacyclin I2 produced by the placenta have direct effects on ductal muscle to keep it open
  • High pulmonary vascular resistance and low oxygen tension in utero makes it easier for blood to pass through duct than lungs
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12
Q

what factors keep the ductus arteriosus closed at birth ?

A
  • Prostaglandin production falls (due to placental delivery) + increased prostaglandin metabolism in the active lungs
  • Oxygen tension greatly increases → direct effects on ductal muscle
  • Pulmonary vascular resistance falls → blood diverted away from duct
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13
Q

what is the classic murmur heard in PDA?

A

“continuous” murmur heard over the upper left sternum:

• Not always heard in premature babies due to high pulmonary pulse pressure → sometimes systolic murmur or no murmur

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14
Q

What are signs of clinically significant PDAs?

A

difficulty weaning ventilator support, wide pulse pressure, easily felt (full) peripheral pulses (due to dynamic circulation), tachypnoea, tachycardia

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15
Q

what are complications of untreated PDAs?

A

heart failure, pulmonary haemorrhage, increased risk of NEC (shunting of blood away from gut), respiratory infections, poor growth

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16
Q

How does one close a PDA?

A

baby is struggling with the presence of PDA → should tray and close it:
• Prostaglandin antagonists (commonly NSAIDs) given first
• Surgical ligation (at a later date)

17
Q

How does one open a PDA?

A

If blood flow to lungs is restricted (e.g. in duct-dependent congenital lesions like pulmonary atresia):
• Prostaglandin infusions (keep blood flowing to the lungs while waiting for surgery at a later date) → alprostadil (prostaglandin E1), dinoprostone (prostaglandin E2)

18
Q

how does respiratory distresss syndrome present?

A

• Present within 4 hours of birth with tachypnoea and signs of increased work of breathing (intercostal and subcostal recession, flaring of nostrils, grunting)
• Worsens over the next 24 – 36 hours without
treatment as small quantities of surfactant disappear and with inhibitory effect of plasma proteins (leak into alveoli)
• Improves after 36 hours as endogenous surfactant production increases

19
Q

what is the cxr shown for respiratory distress syndrome?

A

“ground glass” appearance, air bronchogram

20
Q

what does lung surfactant help with?

A

reduce surface tension, increase lung compliance, stabilise alveoli and prevent atelectasis, and prevent transudation of fluid (across the alveolar wall)

21
Q

what are the risk factors of developping respiratory distress syndrome?

A

Prematurity (< 28 weeks give all babies surfactant), maternal diabetes, abruption, hypothermia, birth asphyxia, elective C-section (< 38 weeks)
• Things which increase in utero production of steroids (and thus surfactant) will decrease the risk of RDS (e.g. stress in utero from IUGR, threatened preterm labour)
• Giving the mother steroids in anticipation of early delivery also increases surfactant and reduces risk of RDS

22
Q

What is the indications of giving surfactant down the endotracheal tube (straight into the lungs)

A

Surfactant (Curosurf®) given down endotracheal tube (straight into lungs):
• For all babies < 28 weeks gestation (insufficient time in utero to produce enough surfactant themselves)
• For babies requiring a lot of oxygen or showing clinical signs of respiratory distress
• For both preterm and term babies in various other neonatal scenarios to improve respiratory function

23
Q

Chronic lung disease (bronchopulmonary dysplasia/BPD) is defined as _______________:
• Preterm lungs are fragile and underdeveloped → become scarred and inflamed easily → less effective → require oxygen to maintain saturation
• Scarring occurs due to ___________________ → try to use minimum pressure needed to ventilate effectively, extubate quickly and use surfactant early to increase lung compliance

A

oxygen dependency after 28 days of life or after 36 weeks corrected gestational age/post-menstrual agel

ventilation with high pressures and high tidal volumes

24
Q

what are the risk factors for developping chronic lung disease?

A

Prematurity, high initial oxygen requirements, long periods on ventilation (with high pressures and tidal volumes), sepsis in utero (including NEC), chorioamnionitis, pulmonary haemorrhage

25
Q

what is the prognosis of chronic lung disease?

A

Children continue to develop new terminal air sacs until 2 years of age → potential for lungs to subsequently continue to grow and develop:
• Often wheezy for first few years of life and more susceptible to respiratory illnesses (e.g. RSV bronchiolitis) → offer immunisation with Palivizumab
• Mild cases gradually wean from oxygen; severe cases may become ventilator-dependent

26
Q

what is low birthweight?

A

< 2.5kg at birth

27
Q

what is very low birthweight?

A

< 1.5kg at birth

28
Q

what is extremely low birthweight?

A

< 1 kg at birth

29
Q

what is small for gestational age (SGA)?

A

Birthweight < 10th centile for gestational age

30
Q

what is large for gestational age (LGA)?

A

Birthweight > 90th centile for gestational age

31
Q

what is IUGR?

A

Intrauterine growth restriction (IUGR) is defined as pathological slowing of foetal growth velocity → may be symmetric or asymmetric:

32
Q

what are the causes of low birth weight?

A

Maternal: Extremes of age (very young or old mothers), poor SES, illnesses in mother (hypertension, renal disease), small mother (suggesting small baby), alcohol/drugs, multiple pregnancy

Foetal: Constitutionally small, chromosomal anomalies, metabolic disorders, infection

33
Q

what are the complications of IUGR?

A

Babies with IUGR have a higher mortality (in utero death/stillbirth) with higher risk of:
• Blood disorders (polycythaemia, neutropenia, thrombocytopenia)
• Higher risk of infection and NEC
• Impaired glucose control (hypoglycaemia)
• Impaired temperature regulation (hypothermia)