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Neonates Flashcards

1
Q

ADEPT trial

A

No difference in NEC in early vs late oral feeds in <35 weeks IUGR abnormal dopplers

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2
Q

What things increase the risk of NEC (6)

A

PDA (indomethacin makes no difference)
Blood transfusions
H2 blockers
Antenatal augmentin
IVABs for >4 days (also increase death from NEC)
Targeting O2 sats 85-89% in extreme prems

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3
Q

What things do not increase the risk of NEC (5)

A 
Indomethacin for PDA
Trophic feeds
Early vs late feeds
Increasing feeds by 30mL/kg/day
Fortifier
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4
Q

What things decrease the risk of NEC (3)

A

Antenatal steroids
Donor breast milk compared to formula
Probiotics (reduce incidence of severe NEC)

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5
Q

Things that are protective against IVH (3)

A

Antenatal steroids
Indomethacin
Surfactant

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6
Q

Reduce the risk of RDS (2)

A

Antenatal steroids

Caffeine (decrease assisted ventilation time)

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7
Q

Reduce the risk of CNLD (1)

A

Caffeine (also decreased assisted ventilation time)

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8
Q

Reduces the need for PDA ligation (1)

A

Caffeine

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9
Q

Benefits of caffeine (CAP trial) (8) + 1 other finding of CAP

A 
Decreased assisted ventilation time
Decreased CNLD
Decreased need for PDA ligation
Increased disability free survival
Decreased risk CP
Decreased cognitive delay
Reduced functional impairment and motor impairment at 11 years
Decreased severe ROP

No significant different in mortality or developmental indices at 5 years

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10
Q

Benefits of antenatal steroids (5)

A

Protective against NEC
Protective against IVH- decreased mortality, decreased grade 3 & 4, decreased PVL
Reduced RDS
Reduced mortality
Reduced risk systemic infections in the first 48 hours

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11
Q

Things that reduce the risk of mortality (4)

A

Probiotics
Antenatal steroids
Resus in air vs O2
Targeting 90-95% in extreme prems (vs 85-89%

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12
Q

Resus in air vs O2 (2)

A

Reduced severity HIE

Reduced mortality

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13
Q

Worse developmental outcomes (4)

A

Hypoglycaemia- slightly worse
Hyperglycaemia- risk neurosensory issues
Low O2 85-89%- increased CP prems
Late preterm compared to term- worse dev 24 months, 3x incidence CP compared to term

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14
Q

Indomethacin (3)

A

No difference in neurodevelopmental outcomes
Protective against IVH
No difference to NEC risk

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15
Q

Sepsis (2)

A

Probiotics = reduced risk late onset sepsis

Antenatal steroids = reduced risk systemic infections in the first 48 hours

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16
Q

ROP (2)

A 
Caffeine = decreased severe ROP
Oxygen = increased
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17
Q

Probiotics

A

Reduced risk late onset sepsis
Reduced risk overall mortality
Reduced incidence severe NEC

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18
Q

Components of breast milk not found in formula (7)

A

Secretory IgA
Lactoferrin- immunomodulation, iron chelation, antimicrobial action, trophic for intestinal growth
K-Casein
Oligosacccarides- prevention of bacterial attachment
Cytokines
Growth factors
Enzymes

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19
Q

Conditions for which human milk has been suggested to have a protective effect (5)

A

Infections- diarrhoea, OM, UIT, NEC, sepsis
GI- coeliac disease, Crohns
Malignancy- all childhood cancer, lymphoma, leukaemia
Allergy
Obesity
Hospitalisations

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20
Q

Complications of TPN (9)

A 
Line complications eg. infection, thrombosis
Hypoglycaemia
Azotemia
Nephrocalcinosis
Hypoglycaemia if feeds suddenly stopped
Hyperlipidaemia and hypoxia from lipid infusion
Hyperammonaemia
Metabolic bone disease (long term)
Cholestatic jaundice/liver disease
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21
Q

Cephalohaematoma

A

1-2%
Reabsorbed within 2/52-3/12
Can remain as a bony prominence of cyst-like defect
Assoc with underlying skull fracture 10-25%

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22
Q

Subgaleal haemorrhage

A

Rupture of the emissary veins connecting the dural sinus to the superficial veins of the scalp
Resolves in 2-3 weeks
Risk of consumptive coagulopathy

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23
Q

Predisposing factors to IVH (7)

A

Prem (unable to regulate cerebral blood flow), RDS, HIE, pneumothorax, hypovolaemia, hypertension, bleeding disorders (DIC, alloimmune thrombocytopenia, vit K deficiency eg. maternal phenytoin/phenobarbitone)

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24
Q

Incidence IVH <1.5kg

Incidence PVL<1kg

A

30% <1.5kg

3% <1kg

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25
Q

Germinal matrix

A

o Gelatinous supependymal germinal matrix- site of origin for embryonal neurons and fetal glial cells, which migrate outwardly to cortex
This region prone to bleeding due to being highly vascular + poor tissue support
Involutes as infant approaches term gestation

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26
Q

PVL

A

Focal necrotic lesions in the periventricular white matter- causing cerebral white matter injury resulting in motor abnormalities

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27
Q

Timing of IVH

A

75% dx within first 3 days
Small percentate late(day 14-30)
Rare after day 30

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28
Q

Clinical features IVH

A

Mostly asymptomatic
Severe- acute deterioration on day 2-3 of life- hypotension, pallor, apnoea, cyanosis, neurological signs, metabolic acidosis, anaemia

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29
Q

IVH grading

A

 Grade 1: bleeding isolated to the GM
 Grade 2: bleeding within the ventricle, no ventricle dilatation
 Grade 3: IVH with ventricular dilatation
 Grade 4: IVH and parenchymal haemorrhage
 Ventriculomegaly: mild = 0.5cm-1cm, moderate = 1-1.5cm, severe >1.5cm

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30
Q

US features PVL

Clinical features PVL

A 
Usually present day 3-10 as early echodense phase, followed by echolucent (cystic) phase day 14-20
Spastic diplegia (lower motor extremity tracts)
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31
Q

Incidence post-haemorrhagic hydrocephalus

A

3-5% all VLBW

10-15% all LBW with IVH

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32
Q

Clinical signs hydrocephalus, prognosis

A

Enlarging head circ, bulging fontanelle, widely split sutures, lethargy, apnoea, bradys
Signs may be delayed by 2-4 weeks
3-5% require VP shunt, may have spontaneous regression

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33
Q

IVH prognosis- percent with Bayley Scales <70 in mental development, psychomotor development CP, blindness or deafness

A 
Grade 1: no sig different
Grade 2: 50%
Grade 3: 55%
Grade 4: 70%
Prognosis worse in PVL, cystic PVL and hydrocephalus
Worse again with VP shunt insertion
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34
Q

Risks of high dose corticosteroids in VLBW (postnatal)

A

Week 1: metabolic derangements, poor growth, sepsis, bowel perf
After week 1: CP and neurodevelopmental delay, impaired growth
Risk worse with >6 weeks course

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35
Q

Pathophysiology of HIE

A

Neuronal necrosis of the cortex = cortical atrophy = cognitive delay, CP, dystonia, epilepsy, ataxia, bulbar and pseudobulbar palsy
Parasagittal injury = Spastic quadriparesis, cognitive delay, visual and auditory processing difficulty
More likely to have focal or multifocal cortical infarcts leading to focal seizures and hemiplegia

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36
Q

HIE stage 1

A

Hyperalert, normal tone/posture, hyperreflexia, myoclonus, strong moro reflex, mydriasis
No seizures and normal EEG

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37
Q

HIE stage 2

A

Lethargic, hypotonic
Flexion posture, hyperreflexia, mycoclonus, weak moro, myosis
Seizures common (~24 hrs due to cerebral oedema), low voltage EEG + seizure activity
Lasts 1-14 days
Variable outcome

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38
Q

HIE stage 3

A

Coma, flaccid tone, decerebrate posturing
Absent reflexes, no myoclonus, absent moro
Pupils unequal with poor light reflex
Decerebrate posturing rather than seizures
EEG- burst supression to isoelectric
Lasts days - weeks, results in death or severe deficits

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39
Q

Ix in HIE

A

Gold standard is diffusion-weighed MRI- increased sensitivity and specificity early
CT can be used to identify focal haemorrhagic lesions, diffusion cortical injury and damage to basal ganglia
US prefered in pre-term infants
Ampliture-intergrated EEG (aEEG)- PPV 85%, NPV 91-96% for adverse neurological outcomes

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40
Q

Therapeutic cooling in HIE

A

Reduces mortality and major neurodevelopmental impairment in term and near-term infants
Decreased apoptpsis, supresses production of neurotoxic mediators (glutamate, free radicals, NO, lactate)
Keep rectal temp 33.5
Start within 6 hours of birth, continue for 72 hours

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41
Q

Complications of therapeutic cooling

A

Thrombocytopenia
Bradycardia
Subcutaneous fat necrosis with hypercalcaemia
Cold injury syndrome

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42
Q

Prognosis of HIE

A

20-30% die in the neonatal period

33-50% of survivors have permanent neurodevelopmental abnormalities

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43
Q

Risk factors for death/severe impairment in HIE (10)

A

pH <6.7 on initial gas (90% death/impairment)
BE >25 (72% mortality)
Apgar 0-3 at 5 mins
Decerebrate posturing
Severe basal ganglia-thalamic lesions
Persistent of signs of severe HIE at 72 hours
Lack of spontaneous activity
Low apgar at 20 mins
Absence of spontaneous resps at 20 mins
Persistent of abnormal neurology at 2 weeks

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44
Q

Erb palsy

A

C5, C6
Waiter-tip arm
Good prognostic sign if retains hand power
Can have associated phrenic nerve injury (C345)

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45
Q

Klumpe paralysis

A

C7, C8, T1

Paralysed hand and ipsilateral horner syndrome

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46
Q

Physiology of transition to pulmonary respiration

A

Increased maternal catecholamine, vasopression, prolactin, glucocorticoids = change lung epithelia from a chloride secretory mode to Na reabsorptive mode = liquid from the lungs is driven into the interstitum
With first breath, surfactant decreased surface tension of the alveoli
With first breath decreased hydrostatic pressure in the pulmonary vasculature increases pulmonary blood flow = better removal of pulmonary fluid
Rising pCO2, declining pH and PO2 = trigger for first breath

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47
Q

Treatment apnoea of prematurity

A

Caffeine or theophylline
- Increase central resp drive by lowering threshold of response to hypercapnia, enhancing contractility of the diaphragm and reducing diaphragmatic fatigue
SIde effects of caffeine- tachycardia, feed intolerance
Doxapram as a second line
HFNP/CPAP if mixed or obstructive picture

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48
Q

Idiopathic apnoea of prematurity- onset, pathophysiology, prognosis

A

Onset first 1-2 weeks of life (may be later with RDS)- needs Ix if onset later than this, or term infant
Usually mixed apnoea- obstructive apnoea leads to paradoxical response- hypoxia results in central apnoea
Usually resolve by 37/40, longer if <28/40
Not an independent risk factor for SUDI

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49
Q

Incidence RDS

A

<28/40 60-80%

32-36 15-30%

50
Q

Risk factors RDS (7)

A 
Maternal DM
Multiple births
LSCS
Precipitous labour
Asphyxia
Cold stress
Affected sibling

Asphyxia, hypocoa, pulmonary ischaemia, cold stress - suppress surfactant production

51
Q

Protective factors RDS

A

Maternal hypertension, maternal heroin use, PROM, antenatal corticosteroids

52
Q

Constituents of surfactant (4)

A

Lecithin
Phosphhatidylglycerol
Apoproteins (surfactant proteins A, B, C, D)
Cholesterol

53
Q

Pathophysiology of RDS

A

Surfactant deficiency –> failure to obtain FRC –> lungs become atelectatic
Prem lungs more compliant - more prone to atelectasis
Atelectasis = VQ mismatch = hypercapnia
Hypercapnia + hypoxia + acidosis = pulmonary arterial vasoconstriction = R to L shunt

54
Q

Surfactant comes from

A

Type II alveolar cels

55
Q

Natural course of RDS

A

Worsening for 3 days, then improvement

56
Q

CXR RDS

A

Fine reticular granularity of the parenchyma and air bronchograms
Typical pattern develops during the first day

57
Q

Indications for surfactant (4)

A

pH <7.2
pCO2 >60
O2 satd <90% at FiO2 40-70% on CPAP
Persistent apnoea

58
Q

Pharmacological treatment for RDS

A

Systemic corticosteroids- mortality and CNLD at 36 weeks sig reduced, but side effects significant
Inhaled corticosteroids- reduced death/CNLD at 36 weeks, no increase in adverse events
Caffeine reduced extubation failure

59
Q

Adverse effects UAC (7)

A

Serious complications 2-5%
Thrombosis- clots on tip 95%, signs of thrombosis include narrowing of the pulse pressure, disappearance of the dicrotic notch
Spasm- treat with topical GTN, remove line
Vascular perforation
Ischaemic/chemical necrosis of abdominal organs
Impairment of circulation to the leg
Infection
Renovascular HTN weeks later

60
Q

Adverse effects UVC (5)

A 
Thrombosis
Vascular perforation
Infection
Cardiac perforation
Portal vein thrombosis --> portal hypertension
61
Q

Pathophysiology CNLD

A

Volutrauma
Free radicals from O2 (immature lungs cannot metabolise free radicals)
Worsened with infection, chorio, PDA, malnutrition
?FHx asthma or atopy

62
Q

Histology CNLD (3)

A

Alveolar hypoplasia
Variable saccular wall fibrosis
Minimal airway disease

63
Q

4 stages of CNLD

A

Acute lung injury
Exudative bronchiolitis
Proliferative bronchiolitis
Obliterative fibroproliferative bronchiolitis

64
Q

Classification of CNLD

A

For infants <32 weeks who had O2 >=28 days, assess at 36 weeks/discharge home (whichever earliest)
For infants >32 weeks who had O2 at least 28 days, assess at 28-56 days postnatal or DC home (earliest)

Mild: now on RA
Moderate: FiO2 <30%
Severe: >30% FiO2 or PPV

65
Q

Prevention of CNLD (2)

Makes no difference (1)

A

Early CPAP and rapid extubation
Vitamin A supplementation in first 4 weeks

Surfactant makes no difference

66
Q

Prognosis CNLD

A

Mortality 10-25% (cor pulmonale or infection esp RSV)
Asthma later in life
Frequent readmissions with pulmonary infections (improve with age)

67
Q

MAS incidence

A

5% of infants with med liquor
30% require mechanical ventilation
3-5% mortality

68
Q

MAS pathophysiology

A

Complete peripheral airway obstruction leads to atelectasis and VQ mismatch
Partial airway obstruction leads to ball-valve effects and therefore air trapping = air leak
Proximal airway obstruction
Inflammation and chemical pneumonitis

69
Q

MAS natural Hx

A

Usually improves within 72 hours

Tachypnoea may persist for days-weeks

70
Q

MAS CXR

A

patchy infiltrates, coarse streaking of both lung fields, increased AP diameter, flattening of the diaphragm

71
Q

Predisposing factors for PPHN

A 
Any respiratory pathology (eg. MAS, TTN)
Being generally unwell
Polycythaemia
Maternal NSAID use (in utero constriction of DA)
Maternal late trimester SSRI use
Amniotic leak/oligohydramnios
72
Q

Clinical features PPHN

A

Presents in the first 12 hours of life
Severe cyanosis with tachypnoea, minimal resp distress
Hypoxia is labile and out of proportion to CXR findings
Hypoxia intermittently unresponsive to O2

73
Q

Treatment PPHN

A

Oxygenation
Ensure adequate BP- ionotropes if required
NO- relaxes vascular smooth muscle (side effects methaemoglobinaemia, nitrous dioxide acting as a pulmonary irritant, rapid wean leading to rebound pulmonary HTN)
ECMO in 5-10%

74
Q

Morgagni diaphragmatic hernia

A

Retrosternal hernation- failure of the sternal and crural portion of the diaphragm to fuse
2-6% of CDH
Often diagnosed incidentally as mass behind heart on CXR
Can have recurrent resp infections, cough, vomiting, GORD, strangulation

75
Q

Bockdaleck diaphragmatic hernia- epidemiology, associations

A

Females 2x more common
90% of CHD
85% L sided, <5% bilateral
Associated abnormalities in 30%- CNS lesions, oesophageal atresia, omphalocele, cardiovascular lesions, T21, T13, T18, Cornelia de Lange, Turner

76
Q

Bockdaleck diaphragmatic hernia diagnosis

A

Antenatal US >50%- polyhydramnios, chest mass, mediastinal shift, gastric bubble/liver in thoracic cavity, fetal hydrops
Best prognostic factor fetal lung:head size on 24-26week US: lung:head < 1 = no survival

77
Q

Bockdaleck diaphragmatic hernia clinical presentation

A

Can have a “honeymoon” period of up to 48 hours
Scaphoid abdo
Resp distress
BS in chest

78
Q

Bockdaleck diaphragmatic hernia prognosis and ongoing issues:

A

67% survival (limited by pulmonary hypoplasia)
Often develop BPD and have ongoing pulmonary issues later in life
GORD 50% - more common in hiatal hernia
Intestinal obstruction 20%
Recurrent hernia 5-20%
FTT in the first few years
Neurocognitive defects – 67% of ECMO, 24% without ECMO
Pectus excavatum and scoliosis

79
Q

Pulmonary haemorrhage and surfactant use

A

Rate increased- 1-5% of patients who receive surfactant

80
Q

Progress of air through the GIT as seen on AXR

A

Air in the jejunum by 15-60 mins
Air in the ileum by 2-3 Air in the colon by 3 hours
No air in rectum at 24 hours is abnormal

81
Q

Things associated with meconium plugs (5)

A 
Small L colon syndrome in infants of diabetic mothers
CF
Rectal agangliosis
Maternal opiate use
Maternal MgSO4 for PET
82
Q

Incidence of NEC

A

1-5% of NICU patients

Incidence and fatality inversely related to gestation and BW

83
Q

Pathogenesis of NEC

A

Mucosal or transmucosal necrosis of the intestine
Most common distal ileum and proximal colon
Triad of intestinal ischaemia, enteral nutrition (metabolic substrate for bacteria) and bacterial
translocation
Clusters of cases suggest an infectious component

84
Q

Modified Bell’s staging for NEC- Stage I

A

Clinical signs: lethargy, temperature instability, apnoea, bradycardia, vomiting, abdominal distension, haematochezia

AXR: intestinal dilatation

Treatment: NBM, TPN, NG suctioning, ABs

85
Q

Modified Bell’s staging for NEC- Stage II

A

Clinical signs: (as per stage I: lethargy, temperature instability, apnoea, bradycardia, vomiting, abdominal distension, haematochezia)
+ metabolic acidosis, thrombocytopenia, abdominal tenderness, absent bowel signs

IIa: mildly ill
IIb: moderately ill

AXR: intestinal dilatation, pneumatosis intestinalis, portal venous gas

Treatment: NBM, TPN, NG suctioning, ABs

86
Q

Modified Bell’s staging for NEC- Stage III

A

IIIa: shock
Can also have ascites
Medical Mx

IIIb: perforation
AXR: pneumoperitoneum
Surgery

87
Q

Indications for surgery for NEC

A 
Perforation
Positive result from abdominal paracentesis culture
Failure of medical Mx
Single fixed bowel loop on XR
Abdominal wall erythema
Palpable mass
88
Q

NEC prognosis

A

Medical Mx fails in 20-40%
Failed medical Mx= 10-30% mortality

Early complications:

  • Dehiscence
  • Infection
  • Complicaions with stoma

Late complications:

  • Strictures 10%
  • Short bowel syndrome
  • Cholestatic jaundice
  • Adverse neurodevelopmental outcomes
89
Q

Cause of 10% weight loss after birth

A

Diuresis driven by ANP release

Increased urinary sodium excretion

90
Q

UVC line placement

A 
Should be at the level of the diaphragm (T8-9)- IVC just outside R atrium
UVC length (cm) = (1.5 x birthweight (kg)) + 5.5
91
Q

UAC line placement

A

High- T6-T9
Low- L3/L4
106% shoulder-to-umbilicus distance (+2cm),
UAC distance (cm) = (birthweight (kg) x4) + 7

92
Q

Ventilation of pre-term infant

A

Rate 60-80
I time 0.5-0.38sec
Volume guarantee- 4mL/kg
PaCO2 45-55mmHg

93
Q

CPAP benefits

A

Reduced need for IPPV
Decreased rate and severity of apnoea
Increased chance of successful extubation
Decreased resp acidosis and O2 requirements post extubation

94
Q

CPAP risks

A

Increased incidence IVH
Nasal trauma
Increased incidence pneumothorax

95
Q

To improve oxygenation

A

Increase FiO2
Increase PIP
Increase PEEP
Increase IT

96
Q

To improve carbon dioxide clearance

A

Decrease PIP
Decrease PEEP
Increase ET
Increase rate

97
Q

Oxygenation index (a measure of how much mean airway pressure is being used to acheive the current arterial oxygen tension- higher = worse lung disease)

A

OI = (MAP/FiO2)/PaO2

98
Q

SIMV

A

Ventilator delivers a mandatory number of breaths at a set PIP and IT, but will attempt to synchronise with the baby’s respirations
If apnoeic- just the back up rate
If breathing- will get the mandatory no of breaths, and baby can take additional breaths
+/- VG

99
Q

SIPPV
AKA Patient triggered ventilation (PTV)
AKA Assist control (A/C)

A

Each spontaneous breath triggers a ventilator breath at a set PIP and IT
If apnoeic/hypopnoeic a backup rate will be delivered
If breathing above the rate, the baby will receive each breath assisted
+/- VG

100
Q

Pressure support ventilation (PSV)

A

Each spontaneous breath delivers a set PIP, but the IT is determined by the baby
+/- VG

101
Q

HFV

A

Background continuous distending pressure = MAP (analagous to PEEP)- determines oxygenation
Oscillation of the airway pressure around the MAP at high frequencies = amplitude - determines CO2 removal (determined by chest wiggle)
Decreased frequency improves CO2 clearance
Frequency = 10-15Hz

102
Q

Criteria for cooling HIE

A

Criteria for acidosis:

  • Apgar =<5 at 10 mins
  • pH <7.00 or BE =10 mins

And either of:

  • Evidence of mod-severe encephalopathy 1-6 hours of age
  • Seizures

And no absolute contraindications:

  • Uncontrolled critical bleeding
  • Uncontrolled hypoxia due to PPHN
  • Imminent withdrawal of life supports planned

And meets all of the following:

  • > =35 weeks
  • BW >= 1800g
  • Able to begin cooling by 6 hours of age
103
Q

Stimulus and timing of PDA closure

A

Functional closure 15-48 hours, anatomical closure by 3 weeks in term babies (longer in prems)
Main stimulus is increased PaO2

104
Q

How much glucose should be given in hypoglycaemia (mg/kg/min)

A

7.5-8 mg/kg/min of glucose

105
Q

Formula for calculating glucose infusion rate (mg/kg/min)

A

(Glucose % x mL/kg/day)/144

106
Q

Threshold for hypoglycaemia screen

A

Requiring >= 10mg/kg/min glucose

Persistent/recurrent after 72 hours

107
Q

How much glucose does the neonatal liver produce

A

6-8mg/kg/min

108
Q

Fractional excretion of Na- calculation, what the results mean

A

FE Na = Urine Na x Serum Cr / Serum Na x Urine CR

FE Na+≥2.5% in term infants suggests renal failure.
FE Na+<2.5% in term infants suggests pre-renal failure
FE Na+ is high in preterm infants because of tubular immaturity.
109
Q

Electrolyte requirements in neonates

A

Na 3 mmol/kg/day
K 2 mmol/kg/day
Ca 1 mmol/kg/day

110
Q

Causes of hyponatremia in prem baby (8)

A

High FE Na due to prematurity (renal tubular immaturity)
Inadequate Na+ intake.
Excessive water intake- Excessive maternal fluid intake during labour/delivery can lead to neonatal hyponatraemia.
Diuretic therapy, especially loop diuretics (e.g. furosemide).
Acute tubular necrosis (tubular Na+ loss) and other causes of renal failure.
Indomethacin- Reduces free water clearance and fractional excretion of sodium, with the lower free water clearance leading to hyponatraemia.
SIADH- ADH has a limited ability to concentrate the urine in the newborn, and acts primarily as a vasopressor.
Excess Na+ loss- Diarrhoea, Gastric, pleural, CSF, 17OH progesterone deficiency.

111
Q

PVL- areas of the brain affected, clinical features

A

Periventricular leucomalacia most commonly involves the optic radiations adjacent to the trigone of the lateral ventricle, and the anterior corticospinal fibres adjacent to the intraventricular foramen
Clinically, it can produce decreased visual acuity, inferior visual field constriction, visual cognitive impairment, ocular motility disturbances, and spastic diplegia.

112
Q

Congenital lobar emphysema

A

Usually becomes apparent in neonatal period
Many diagnosed prenatally
Clinical features: range from mild tachypnoea and wheeze to severe dyspnoea and cyanosis
Affects upper and middle lobes, LUL most common
Affected lobe is nonfunctional due to overdistension which may cause atelectasis of the ipsilateral normal lung
Mediastinal shift due is to overdistension

113
Q

Blood group factors associated with haemolytic disease of the newborn

A

90% D (Rh)

Mostly big C and big E otherwise

114
Q

Amount of Rh positive blood required to enter maternal circulation to mount a response

A

> 1mL

115
Q

Why is ABO incompatibility protective against Rh incompatibility

A

Rh positive cells are rapidly removed from the maternal circulation by pre-existing Anti-A or Anti-B antibodies

116
Q

What metabolic complication is common in babies with haemolytic disease of the newborn

A

Hypoglycaemia- hepatosplenomegaly + large pancreas in utero due to anaemia

117
Q

Kernicterus- pathology

A

Deposition of unconjugated bilirubin in the basal ganglia and brainstem nuclei
At risk babies eg. disease, asphyxia- disruption of the blood-brain barrier leading to earlier kernicterus

118
Q

Kernicterus - clinical features

A

2-5 days after birth
Lethargy, poor feeding, absent moro initially
Opisthotonos
Convulsions and spasms
By 3 years of age: bilateral choreoathetosis, seizures, intellectual impairment, high-frequency hearing loss

119
Q

Impact of Na on growth

Ix to determine if total body Na stores are adequate

A

Sodium is an important growth factor, stimulating cell proliferation and protein synthesis and increasing cell mass
Maintaining urinary Na+ higher than K+ assures that Na+ intake is adequate

120
Q

Changing from CMV to HVF

A

Baseline CXR, ensure large enough ETT with no leaks
Leave FiO2 the same
Set Hz 10-15 (low term, high prem)
MAP ~2-4cmH20 higher than on CMV
Set amplitude required for discernible chest wiggle

121
Q

Outcome ELBW

A

40% mortality
16% no impairment
22% mild impairment
22% mod-severe impairment

Exam (16 decks)

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