1.1 Effect of intrauterine & perinatal events Flashcards
What is the definition of prematurity?
Prematurity is defined as being born < 37 weeks gestation (with < 28 weeks being extreme)
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
germinal matrix ;
supported by more connective tissue;
post-haemorrhagic ventricular dilatation;
cranial ultrasound (CRUSS)
What is Grade I intraventricular haemorrhage?
Grade I (bleeding only in germinal matrix)
What is Grade II intraventricular haemorrhage?
Grade II (bleeding into ventricles itself)
What is Grade III intraventricular haemorrhage?
Grade III (IVH with ventricular dilatation)
What is Grade IV intraventricular haemorrhage?
Grade IV (involves parenchyma)
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
exposure to high levels of oxygen;
optic disc;
middle ridge;
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 _________________
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
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)
thermoregulation, fluid regulation & transepidermal fluid loss as well as an ineffective barrier to infection
transplacental immunoglobulins (IgG)
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 _______________
12 – 24 hours after birth;
left-to-right shunt (from aorta into pulmonary artery as aortic pressure is higher)
what factors keep the ductus arteriosus open in utero?
- 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
what factors keep the ductus arteriosus closed at birth ?
- 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
what is the classic murmur heard in PDA?
“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
What are signs of clinically significant PDAs?
difficulty weaning ventilator support, wide pulse pressure, easily felt (full) peripheral pulses (due to dynamic circulation), tachypnoea, tachycardia
what are complications of untreated PDAs?
heart failure, pulmonary haemorrhage, increased risk of NEC (shunting of blood away from gut), respiratory infections, poor growth
How does one close a PDA?
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)
How does one open a PDA?
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)
how does respiratory distresss syndrome present?
• 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
what is the cxr shown for respiratory distress syndrome?
“ground glass” appearance, air bronchogram
what does lung surfactant help with?
reduce surface tension, increase lung compliance, stabilise alveoli and prevent atelectasis, and prevent transudation of fluid (across the alveolar wall)
what are the risk factors of developping respiratory distress syndrome?
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
What is the indications of giving surfactant down the endotracheal tube (straight into the lungs)
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
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
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
what are the risk factors for developping chronic lung disease?
Prematurity, high initial oxygen requirements, long periods on ventilation (with high pressures and tidal volumes), sepsis in utero (including NEC), chorioamnionitis, pulmonary haemorrhage
what is the prognosis of chronic lung disease?
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
what is low birthweight?
< 2.5kg at birth
what is very low birthweight?
< 1.5kg at birth
what is extremely low birthweight?
< 1 kg at birth
what is small for gestational age (SGA)?
Birthweight < 10th centile for gestational age
what is large for gestational age (LGA)?
Birthweight > 90th centile for gestational age
what is IUGR?
Intrauterine growth restriction (IUGR) is defined as pathological slowing of foetal growth velocity → may be symmetric or asymmetric:
what are the causes of low birth weight?
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
what are the complications of IUGR?
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)
