general Flashcards
what is not part of the heelprick?
GSDs
galactossaemia
*CAH just added
give examples of what the following findings on antenatal USS might mean:
- dilated cerebral ventricles
- choroid plexus cysts
- nuchal pad thickening
- dilated renal pelvis
- echogenic bowel
- dilated cerebral ventricles: hydrocephalus, corpus callosum agenesis
- choroid plexus cysts: abnormal karyotype
- nuchal pad thickening: cystic hygroma e.g. T13, T18, Turners
- dilated renal pelvis: PUV, VUR
- echogenic bowel: CF, T21, mec
example causes of oligohydramnios vs polyhydramnios
polyhydramnios: mutiple gestation, T2DM, GIT obstruction, polyuria causes e.g. Barrters, reduced swallowing e.g. neuromuscular, TTTS
oligohydramnios: DRIPPPC - demise, renal abnormalities, IUGR, PROM, post-dates, placental insufficiency, chromosomal abnormalities
genetic tendency for dizygotic vs monozygotic
monozygosity is NOT inherited
4x risk if mum was dizygotic
monochorionic must be what zygotic?
dizygotic must be what chorionic?
monochorionic must be monozygotic
dizygotic must be dichorionic
DCDA
MCDA
MCMA
biggest causes of late deaths?
DCDA = FGR
MCDA = TTTS
MCMA = cord entanglement
TTTS - issues in recipient vs donor
artery-vein shunt
recipient: larger, polyhydramnios, polycythaemia, CV decompensation, hydrops, cardiac hypertrophy
donor: smaller, oligohydramnios, anaemia, hypovolaemia, ‘stuck twin’, microcardia
TRAP syndrome in MC twins
artery-artery shunt
pump twin vs acardiac-acephalic twin (lethal for recipient)
premmie kidneys vs term kidneys
premmie kidneys:
o ↓ GFR
o ↓ tubular reabsorption of sodium and bicarbonate
o ↓ secretion of potassium and hydrogen
o ↓ capacity to concentrate/dilute urine
urine output D1 vs D2 of life
UO D1 1ml/kg/hr, D2 2ml/kg/hr
insensible losses - where are they lost? biggest determinant?
2/3 skin, 1/3 respiratory
ELBW (BW <1000 g) infants - thin skin and higher SA:V ratio
what gestation lacks the ability to coordinate for breastfeeding?
<34 weeks
early PN in VLBW prevents what?
catabolism, and has better neurodevelopmental outcomes
what is the only component in breastmilk not present in cow’s milk?
DHA - incorportated into brain and retinal phospholipid membrane
DDx for neonatal respiratory distress
PSA CHART
Pneumonia
Surgical - diagphragmatic hernia
Aspiration (mec)
Cardiac
HTN (pul)
Airway e.g. bronchogenic cyst, ENT
RDS
TTN
central vs obstructive apnoea
Obstructive apnoea = absence of airflow but persistent chest wall movement; inspiratory efforts persist
Central apnoeas = decreased CNS stimuli to respiratory muscles; inspiratory efforts absent
Pharmacotherapy for apnoeas
methylxanthines
1. Caffeine = fewer side effects (less tachycardia + feed intolerance), longer half-life, enteral absorption more reliable, no monitoring required unless signs of toxicity
2. Theophylline = shorter half-life, narrow therapeutic window, requires monitoring, needs to be given more frequently
complications of severe neonatal apnoeas
BPD
IVH
ROP
apnoea of prematurity - what age does it start?
Attributable to the immaturity of the respiratory centre in the brain. Onset is from days 2-7 of life. Apnoea beginning immediately after birth suggests another cause.
premature breathing vs apnoea
Periodic breathing: Three or more periods with no respiratory effort lasting 3 seconds or more in a 20 second period. This is a normal neonatal breathing pattern and does not involve changes in heart rate or colour
pathogenesis of RDS/HMD
preterm - reduced surfactant and worse quality (less protein and phosphatidylglycerol)
high surface tension
low lung volume and compliance
hypoxaemia from VQ mismatch, atelectasis and oedema
what gestation is mature surfactant present
35 weeks
CXR of RDS
ground glass
hyperinflation, bell thorax
+/- bronchograms
some risks of surfactant therapy
ETT block
PTX due to sudden change in compliance
pulmonary haemorrhage
CPAP vs surfactant for preterm neonate at delivery at risk of RDS
CPAP started at birth is as effective as prophylactic or early surfactant and is the approach of choice for the delivery room management of a preterm neonate at risk for RDS
main risk factor for BPD
<1250g - 97% cases
main pathology of BPD (now, not pre-surfactant)
disruption of lung development with arrest prior to alveolar phase of development (results in larger lungs with fewer alveoli)
when to consider antenatal steroids?
23 to 34 weeks gestation at high risk for pre-term delivery within the next seven days OR
for women having LUSCS 34+0 to 36+6
main risk factors for TTN
- diabetic mother
- maternal asthma
- prem
- caesarean
what is TTN caused by?
pulmonary oedema from delayed resorption and clearance of alveolar fluid
suctioning in MAS - thoughts?
no evidence to suction a vigorous infant
triad for PPHN diagnosis
i. Severe hypoxia in FiO2 100%
ii. Evidence of R to L shunt
iii. TTE confirmation structurally normal heart
3 pathophysiology for PPHN, and which is worst
- pul VC, vessels normal: pneumonia, hypoglycaemia, polycythaemia
- pul vessel hypertrophy: maternal PG inhib use, asphyxia
- reduced pul vascular bed SA: CDH, PPH - almost impossible to reverse
biggest risk factor for PPHN
MAS
explain the finding of pre-post ductal sats in PPHN
often large diff >10% - R to L shunting
PPHN - what Rx? how does it work?
inhaled NO
vasodilates, selectively targets pulmonary vessels
Subcutaneous emphysema in neonate pathognomonic of what?
pneumomediastinum
risk factors for extra-pulmonary air leak
- underlying lung disease
- prem
- assisted ventilation
- oligohydramnios
what is the only severe complication in the neonatal period which is worsened by surfactant treatment?
pulmonary haemorrhage
most common cause of diaphragmatic paralysis in the neonatal period
birth injury - extreme lateral traction on shoulder > phrenic +/- brachial plexus injury
adverse effects and contraindications of inhaled nitric oxide
AE:
- Methaemaglobinaemia
- Nitrogen dioxide -> pulmonary oedema
CI:
- theoretical: IVH - toxic compound ?increases bleeding risk
- coagulopathies
three key features of neonatal encephalopathy
i. Reduced level of consciousness
ii. Difficulty with initiating + maintaining respiration
iii. Depression of tone and reflexes
strongest risk factor of neonatal encephalopathy
IUGR
pathophysiology of HIE
primary neuronal death - cellular hypoxia
secondary phase - latent phase of neuronal death caused by oedema, toxin accumulation
what is the only neuroprotective therapy for HIE
therapeutic hypothermia
- must be >35weeks, <6h old
- 33-35deg, 72h cooling
first line anticonvulsant for HIE
phenobarbitone
areas of brain injury with HIE and their clinical correlates
periventricular = motor esp lower = spastic diplegia
focal white matter / vascular = unilateral findings, seizures
parasagittal injuries = more prox limb weakness, spastic quad
clinical presentation of IVH
50% silent
stuttering most common = over hours/days
catastrophic is least common, mins/hours
when does PVL present
usually asymptomatic until the neurological sequelae of white matter damage become apparent in later infancy as spastic motor deficits
complications of IVH
post-haemorrhagic hydrocephalus (40% will stop by themselves)
PVD
PVHI from venous compression in grade IV
PVL
PVL vs IVH
IVH:
venous injury - bleed into ventricles
asymmetrical
unilateral therefore hemiparesis
90% present within 3rd day of life
PVL:
arterial - watershed infarct
symm
legs > arms
later
what kind of PVL more associated with cognitive deficits
Cystic – most powerful predictor of CP and cognitive defects
what causes most hemiparetic CPs
perinatal stroke
most arterial perinatal strokes occur in which artery distribution
MCA
MCA distribution for humunculus
arm and face > leg (as MCA distribution)
PPHN what direction shunt
R>L through PDA/PFO
