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48 Cards in this Set
- Front
- Back
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Definition of a preterm baby
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< 37 weeks
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Definition of a postterm baby
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> 42 weeks
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Definition of low birth weight
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< 2500g - low
< 1500 - very low < 1000g - extremely low |
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Causes for low birth weight?
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premature
intrauterine growth restriction |
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Definition of intrauterine growth restriction?
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Birthweight of less than 10th centile of the weights for babies at that gestational age
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Risk factors for intrauterine growth restriction
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Maternal
- poverty, teenage mothers, single mothers, smoking, ETOH, recreational drugs Uterus/placenta - infection, multiple gestation, uterine abnormalities, placental abruption, placenta praevia, poor placental blood supply resulting in fetal growth restriction or fetal distress Fetal - chromosomal abnormalities, congenital defects, intra-uterine inection |
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Why are tocolytics given?
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to prevent labour by reducing contractions e.g., Ca channel blockers (nifedipine), hydration, beta-mimetics (terbutaline),
They can allow for time to give antibiotics and steroids (reduce complications with prematurity) |
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Why are antenatal corticosteroids given in premature delivery?
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To enhance neonatal lung maturation - reduce RDS
Reduce NEC Reduce IVH Decrease mortality |
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What do you need to look out for with premature birth?
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Asphyxia
thermal instability pulmonary disease metabolic disturbance GIT disturbance renal immaturity cardiac - PDA Haematological - anhaemia, decreased immunity infection neurological - IVH, retinopathy, auditory neuropathy dysynchrony |
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How is excessive heat loss prevented in premature babies?
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Increase temperature on labour ward
Wrap with mother (kangaroon care) polyethylene wrap humidibrib radiant heater |
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What is respiratory distress syndrome (hylaine membrane disease)
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Occurs in preterm infants due to a lack of surfactant (surface tension lowering agent) in the alveloi --> high aleveolar surface tension --> poor long compliance and fine atelectasis --> decreased surface area for gas exchange --> hypoxia and acidosis --> respiratory distress
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At what stage of gestation is there usually sufficient surfactant production?
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36 weeks
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At what stage will onset of hylaine membrane disease be evident?
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within first few hours of life, worsens over next 24-72 hours
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Describe the appearance of the CXR in hyaline membrane disease?
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fine granuar homogenous, ground glass appearance
Air bronchograms NB: due to fine atelactasis |
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Risk factors for respiratory distress syndrome?
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decreasing gestational age
decreasing birth weight male sex advanced maternal age multiple pregnancy elevative and emergency caesarean section |
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Prophylaxis for respiratory distress syndrome
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Steroid therapy for mothers at risk of preterm birth
prophylactic surfactant given to high risk infants (< 28 weeks) at birth monitor lecithin: sphingomuyelin ratio with amniocentesis, L/S > 2:1 indicates lung maturity |
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Management of respiratory distress syndrome
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Supportive
Endotracheal surfactant administration |
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What is bronchopulmonary dysplasia?
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Chronic lung disease associated with very preterm birth
may develop after prolonged intubation/ventilation with high pressures and high O2 concentration (often after ventilation for RDS) |
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Clinical features of bronchopulmonary dyspaslia
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persistent chest infections
crepitations and ronchi on chest auscultation gross hyperinflation of the lungs increased AP chest diameter Most of these infants have a patent PDA and over time may develop RHF (cor pulmonale), pulmonary hypertension, poor growth |
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CXR appearance of chronic lung disease/ bronchopulmonary dysplasia?
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Irregular honeycomb appearance
overinflated lung fields extensive fibrosis multiple cysts of irregular size |
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Management of bronchopulmonary dysplasia?
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No good treatments
gradually wean from ventilator, optimise nutrition Dexamethasone may help decrease inflammation and encourage weaning, (but also associated with increased risk of adverse neurodevelopmental outcome so indications for use are limited) |
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What lasting effects does bronchopulmonary dysplasia have?
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Significant impairment and deterioration in lung function late into adolescence
Some lung abnormalities may persist into adulthood including airway obstruction, airway hyperreactivity, and emphysema Associated with an icnreased risk of a neurodevelopmental outcome |
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What level of glucose indicates hypoglycaemia in the newborn?
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< 2.6 mmol/L (40mg/dL)
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What are some possible causes of hypoglycaemia in a newborn?
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Decreased carbohydrate stores (premature; IUGR)
infant of a diabetic mother: maternal hyperglycaemia --> felta hyperclycaemia and hyperinsulinims --< hypoglycaemia in the newborn infant because of high insulin levels sepsis endocrine: hyperinsulimism due to islet cell hyperpalasia (Beckwigh-Wiedemann syndrome), panhypopituitarism inborn errors of metabolism: fatty acid oxidation defects, galactosemia |
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Clinical findings of hypoglycaemia in the newborn?
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lethargy
poor feeding irritable termors apnoea cyanosis seizures |
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Management of infant hypoglycaemia
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identify and monitor infants at risk (pre-feed blood glucose checks)
oral feeds within first few hours of birth if hypoglycaemia provide glucose IV |
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What is necrotising enterocolitis?
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Intestinal (mainly terminal ileum and colon) inflammation associated with focal or diffuse ulceration and necrosis
Unknown aetiology - perhaps hypoperfusion in an immature gut as a result of perinatal insult |
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Risk factors for necrotising enterocolitis
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prematurity (immature defences)
asphyxia, shock (poor bowel perfusion) - 31-36 weeks hyperosmolar feeds enteral feeding with formula (breast milk can be protective) sepsis absent or reversed umbilical artery flow anteantally and low systemic blood flow in the neonatal period |
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Clinical presentation of necrotising enterocolitis
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distended abdomen
increased amount of gastric aspirate/vomitus with bile staining frank or occult blood in stool feeding intolerance diminished bowel sounds signs of bowel perforation (sepsis, shock, peritonitis, DIC) |
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AXR findings of necrotising enterocolitis?
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dilated and thickened bowe loops +/- air fluid levels
pneumatosis intestinalis (intramural (bowel wall) gas) - hallmark |
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Consequences of necrotising enterocolitis
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Strictures (occur with and w/o surgery)
Short bowel syndrome (if surgery) Bowel obstruction (if surfery Cholestasis (secondary to prolonged TPN) fistula, abscess, malabsorption, reccurent NEC Neurodevelopmental sequale |
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Management of necrotising enterocolitis
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Cessation of enteral feeding
gastric decompression IV fluids Correct electrolyte disturbances TPN with gradual reintroduction to feed IV antibiotics - vanc and gent ? + metronidazole 30-50% require surgery - resection of necrotic bowel, formation of enterostomy and mucosal fistula AND periteoneal drainage Indicated if: failure to respond to optimal medical management |
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Where do intraventricular haemorrhages commonly occur in premature babies?
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Periventricular subependymal germinal matrix (GM)
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How is intraventircular haemorrhage classified?
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Grade
I - isolated germinal matrix haemorrhage II - intraventricular haemorrhage with normal ventricle size III - intraventricular haemorrhage of siffucient severity to dilate the centricles with blood IV - intraparenchymal haemorrhage |
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At what stage after birth do most intraventricular haemorrhages occur?
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Nearly all occur within 72 hours of birth
Most occur within 48 hours |
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Risk factors for intraventricular haemorrhage
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Extreme prematurity
need for vigorous resuscitation at birth Lack of antenatal steroids pneumothorax sudden increase in artieral BP with volume expansion hypotensive event hypertension RDS coagulopathy fluctuating cerebral blood flow |
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Clinical presentation of intraventricular haemorrhage
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Often asymptomatic but sometimes have:
tense anterior fontanelle pallor and drop in haemoatrocrit limp, unresponsive infant tonic fits with decerebrate posturing |
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How is IVH diagnosed?
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Clinical assessment
Ultrasound evaluation - cranial US x 2 given to all infants < 30 weeks gestation 1. day 5-7 2. day 28 |
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Complications with IVH
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May be asymptomatic without long term consequences
can get: death, neurodevelopmental handicap, post haemorrhagic hydrocephalus |
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Prevention of IVH
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Steroids to mothers 48 hours prior to delivery (reduces risk)
Antimicrobial therapy in the expectant management of preterm premature rupture of the membranes (reduces chorioamnionitis, neonatal sepsis, and IVH) |
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Treatment of IVH
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Resuscitation and stabilisation
Avoid hypocapnia Haemodynamic stabilisation Early indomethacin reduces the incidence of IVH |
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What is retinopathy of prematurity
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= a developmental abnormalitiy of the retina which involves interruption in the growth of developing retinal vessels and can result in retinal detachment
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Risk factors for reinopathy of prematurity
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extreme prematurity - most significant
has been thought to be associated with periods of high oxygenation VEGF (normally stimulated by relative hypoxia) downregulated after birth by hyperoxia, --> vaso-obliteration and cessation in the growth of new BV within the retina --> hypoxia of the non-perfused retina |
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Who should be screening for ROP
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Infants born at < 32 weeks (or birthweight < 1500g)
All infants at 4-6 weeks postnatal age and repeated every 2 weeks until vascularisation has progressed into the outer retina |
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Management of ROP
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Stage 1 or 2 will spontaneously resolve
Stage 3 requires intervention Retinal ablation - removes the stimulus for vessel growth |
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What is the lowest age of gestation that is viable?
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23 weeks
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What are the issues for follow-up in premature infants?
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Respiratory problems (increased risk LRTI, increased risk wheeze, overt lung abnormalities resolve over 1-2 years)
Growth and nutrition (catchup growth occurs over 1-3 years, may need increased nutrition during this time, need iron and multivitamin supps till weaned) General health Hearing 2-4% require hearing aids - neurosensory and conductive hearing loss Vision 0.5-1% have sig visual loss, increased risk of myopia, strabismus Motor development (CP increased risk with Low birth weight) Intellectual development |
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When are immunisations given to premature infants?
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at chronological age
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