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neonates > general > Flashcards

general Flashcards

1
Q

what is not part of the heelprick?

A

GSDs
galactossaemia
*CAH just added

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2
Q

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

A
  • 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
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3
Q

example causes of oligohydramnios vs polyhydramnios

A

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

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4
Q

genetic tendency for dizygotic vs monozygotic

A

monozygosity is NOT inherited
4x risk if mum was dizygotic

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5
Q

monochorionic must be what zygotic?
dizygotic must be what chorionic?

A

monochorionic must be monozygotic
dizygotic must be dichorionic

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6
Q

DCDA
MCDA
MCMA
biggest causes of late deaths?

A

DCDA = FGR
MCDA = TTTS
MCMA = cord entanglement

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7
Q

TTTS - issues in recipient vs donor

A

artery-vein shunt
recipient: larger, polyhydramnios, polycythaemia, CV decompensation, hydrops, cardiac hypertrophy
donor: smaller, oligohydramnios, anaemia, hypovolaemia, ‘stuck twin’, microcardia

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8
Q

TRAP syndrome in MC twins

A

artery-artery shunt
pump twin vs acardiac-acephalic twin (lethal for recipient)

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9
Q

premmie kidneys vs term kidneys

A

premmie kidneys:
o ↓ GFR
o ↓ tubular reabsorption of sodium and bicarbonate
o ↓ secretion of potassium and hydrogen
o ↓ capacity to concentrate/dilute urine

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10
Q

urine output D1 vs D2 of life

A

UO D1 1ml/kg/hr, D2 2ml/kg/hr

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11
Q

insensible losses - where are they lost? biggest determinant?

A

2/3 skin, 1/3 respiratory
ELBW (BW <1000 g) infants - thin skin and higher SA:V ratio

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12
Q

what gestation lacks the ability to coordinate for breastfeeding?

A

<34 weeks

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13
Q

early PN in VLBW prevents what?

A

catabolism, and has better neurodevelopmental outcomes

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14
Q

what is the only component in breastmilk not present in cow’s milk?

A

DHA - incorportated into brain and retinal phospholipid membrane

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15
Q

DDx for neonatal respiratory distress

A

PSA CHART
Pneumonia
Surgical - diagphragmatic hernia
Aspiration (mec)

Cardiac
HTN (pul)
Airway e.g. bronchogenic cyst, ENT
RDS
TTN

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16
Q

central vs obstructive apnoea

A

Obstructive apnoea = absence of airflow but persistent chest wall movement; inspiratory efforts persist

Central apnoeas = decreased CNS stimuli to respiratory muscles; inspiratory efforts absent

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17
Q

Pharmacotherapy for apnoeas

A

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

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18
Q

complications of severe neonatal apnoeas

A

BPD
IVH
ROP

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19
Q

apnoea of prematurity - what age does it start?

A

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.

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20
Q

premature breathing vs apnoea

A

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

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21
Q

pathogenesis of RDS/HMD

A

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

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22
Q

what gestation is mature surfactant present

A

35 weeks

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23
Q

CXR of RDS

A

ground glass
hyperinflation, bell thorax
+/- bronchograms

24
Q

some risks of surfactant therapy

A

ETT block
PTX due to sudden change in compliance
pulmonary haemorrhage

25
Q

CPAP vs surfactant for preterm neonate at delivery at risk of RDS

A

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

26
Q

main risk factor for BPD

A

<1250g - 97% cases

27
Q

main pathology of BPD (now, not pre-surfactant)

A

disruption of lung development with arrest prior to alveolar phase of development (results in larger lungs with fewer alveoli)

28
Q

when to consider antenatal steroids?

A

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

29
Q

main risk factors for TTN

A
  1. diabetic mother
  2. maternal asthma
  3. prem
  4. caesarean
30
Q

what is TTN caused by?

A

pulmonary oedema from delayed resorption and clearance of alveolar fluid

31
Q

suctioning in MAS - thoughts?

A

no evidence to suction a vigorous infant

32
Q

triad for PPHN diagnosis

A

i. Severe hypoxia in FiO2 100%
ii. Evidence of R to L shunt
iii. TTE confirmation structurally normal heart

33
Q

3 pathophysiology for PPHN, and which is worst

A
  1. pul VC, vessels normal: pneumonia, hypoglycaemia, polycythaemia
  2. pul vessel hypertrophy: maternal PG inhib use, asphyxia
  3. reduced pul vascular bed SA: CDH, PPH - almost impossible to reverse
34
Q

biggest risk factor for PPHN

A

MAS

35
Q

explain the finding of pre-post ductal sats in PPHN

A

often large diff >10% - R to L shunting

36
Q

PPHN - what Rx? how does it work?

A

inhaled NO
vasodilates, selectively targets pulmonary vessels

37
Q

Subcutaneous emphysema in neonate pathognomonic of what?

A

pneumomediastinum

38
Q

risk factors for extra-pulmonary air leak

A
  • underlying lung disease
  • prem
  • assisted ventilation
  • oligohydramnios
39
Q

what is the only severe complication in the neonatal period which is worsened by surfactant treatment?

A

pulmonary haemorrhage

40
Q

most common cause of diaphragmatic paralysis in the neonatal period

A

birth injury - extreme lateral traction on shoulder > phrenic +/- brachial plexus injury

41
Q

adverse effects and contraindications of inhaled nitric oxide

A

AE:
- Methaemaglobinaemia
- Nitrogen dioxide -> pulmonary oedema

CI:
- theoretical: IVH - toxic compound ?increases bleeding risk
- coagulopathies

42
Q

three key features of neonatal encephalopathy

A

i. Reduced level of consciousness
ii. Difficulty with initiating + maintaining respiration
iii. Depression of tone and reflexes

43
Q

strongest risk factor of neonatal encephalopathy

A

IUGR

44
Q

pathophysiology of HIE

A

primary neuronal death - cellular hypoxia
secondary phase - latent phase of neuronal death caused by oedema, toxin accumulation

45
Q

what is the only neuroprotective therapy for HIE

A

therapeutic hypothermia
- must be >35weeks, <6h old
- 33-35deg, 72h cooling

46
Q

first line anticonvulsant for HIE

A

phenobarbitone

47
Q

areas of brain injury with HIE and their clinical correlates

A

periventricular = motor esp lower = spastic diplegia
focal white matter / vascular = unilateral findings, seizures
parasagittal injuries = more prox limb weakness, spastic quad

48
Q

clinical presentation of IVH

A

50% silent
stuttering most common = over hours/days
catastrophic is least common, mins/hours

49
Q

when does PVL present

A

usually asymptomatic until the neurological sequelae of white matter damage become apparent in later infancy as spastic motor deficits

50
Q

complications of IVH

A

post-haemorrhagic hydrocephalus (40% will stop by themselves)
PVD
PVHI from venous compression in grade IV
PVL

51
Q

PVL vs IVH

A

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

52
Q

what kind of PVL more associated with cognitive deficits

A

Cystic – most powerful predictor of CP and cognitive defects

53
Q

what causes most hemiparetic CPs

A

perinatal stroke

54
Q

most arterial perinatal strokes occur in which artery distribution

A

MCA

55
Q

MCA distribution for humunculus

A

arm and face > leg (as MCA distribution)

56
Q

PPHN what direction shunt

A

R>L through PDA/PFO

neonates (4 decks)

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