Neonatology Flashcards

1
Q

Antenatal steroids are protective against (5)

A
NEC
IVH
RDS
Systemic infection in the first 48 hours of life
Neonatal mortality
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2
Q

Ventilation: PaO2 is influenced by… (3)

A
  • FiO2
  • MAP
  • Gas exchange surface area and diffusion
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3
Q

Ventilation: PaCO2 is influenced by… (3)

A
  • Tidal volume
  • RR
  • Gas exchange surface area and diffusion
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4
Q

Risk factors for cerebral palsy

A

Low birth weight
Chorioamnionitis
Elevated cytokines: IL-1, IL-6, IL-8, TNF-alpha
Maternal thyroid disease
Multiple births - twins x6 risk, triplets x15 risk
Maternal thrombophilia
Other congenital abnormalities

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5
Q

HHHFNC vs CPAP

A
  1. Post-extubation support: HHHFNC equivalent to CPAP
    - Significantly less nasal trauma seen with HF
  2. Primary respiratory support: CPAP superior to HHHFNC
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6
Q

Advantage and disadvantage of HHHFNC

A
  • Mechanism: generation of pharyngeal pressure, supports inspiration, washes out deadspace, heating and humidification
  • Advantage: less nasal trauma, can continue to breastfeed, parental/nursing preference
  • Disadvantage: possibly remain on respiratory support for longer, no clear weaning regimen established
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7
Q

NIPPV

A
  • CPAP with superimposed inflations set to peak pressure
  • Mechanism:
  • -> Pressure delivery: increased MAP, increases recruitment and FRC
  • -> Decreased WOB
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8
Q

Advantages of NIPPV

A
  • Reduced extubation failure –> more effectively than CPAP
  • May benefit severe apnoea
  • No increased GI side effects
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9
Q

Disadvantages for NIPPV

A
  • No evidence for:
  • -> Increased TV
  • -> Reducing inflammation
  • No effect on CNLD or mortality
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10
Q

Surfactant administration

A
  • InSurE technique: intubate, surfactant, extubate

- Reduces need for ventilation and BPD

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11
Q

Synchronised ventilation vs IMV

A
  • Significantly reduced risk of PTX and duration of ventilation
  • No significant longer term effects on death or BPD
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12
Q

Volutrauma

A
  • Causes significant lung injury (most significant)
  • Mechanism in preterm:
  • -> Very compliant chest walls - accepts high tidal volume
  • -> Synergistic effects with biotrauma and oxytrauma
  • -> Likely to receive resuscitation with manual ventilation
  • In preterm lambs, lung injury due to:
  • -> Oedema and air leak, inflammatory response, decreases lung compliance
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13
Q

Volume guarantee ventilation

A
Good for:
- Rapidly changing compliance
- Weaning
- Post-surgery, relaxed muscle
Bad for:
- Large air leaks (>60%)
- BPD - different areas of lung fill differently
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14
Q

Long-term benefits of VG ventilation vs pressure-limited ventilation

A
  • Decreased death or BPD at 36wk CGA
  • Decreased PTX
  • Decreased duration of ventilation
  • Decreased hypocarbia
  • Decreased PVL w/ or w/o grade III-IV IVH
  • Not associated with any increased adverse outcomes
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15
Q

Other complications of maternal gestational diabetes

A
  • Temperature instability
  • Hypocalcaemia
  • Hypomagnesemia
  • Cardiomegaly/HOCM
  • Lumbosacral dysgenesis, caudal regression
  • Small left colon syndrome
  • Renal anomalies
  • Renal vein thrombosis
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16
Q

Risk factors for prematurity

A
  • Maternal age: extremes of age
  • Maternal drug use
  • Uterine malformation
  • Cervical weakness e.g. previous midtrim pregnancy loss, cone Bx etc
  • Multiple pregnancies
  • Infection e.g. chorioamnionitis
  • PIH/PET/Eclampsia: delivered early to maintain maternal health
  • APH/placenta praevia
  • Amniotic fluid volume: oligo and polyhydramnios
  • Foetal anomalies
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17
Q

Magnesium sulphate

A
  • Neuroprotective role for antenatal MgSO has been proven
  • NNT to benefit 1 baby avoiding CP is 63
  • Beneficial effect on gross motor development in EARLY childhood
  • Administer before 30 weeks
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18
Q

Survival rates and gestational age

- Excluding babies who die before NICU admission/not resuscitated

A
  • <24 wks: 43%
  • 24 wks: 66%
  • 25 wks: 84%
  • 26 wks: 88%
  • 27 wks: 94%
  • 28-32 wks: 97%
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19
Q

Long-term outcomes of extreme prems

A
  • Neurodisability can occur in <26 weekers, even in absence of obvious CNS damage/hamorrhage
  • Higher than expected ADHD, autistic features, learning difficulties
  • Final stature, IQ and visual function can all be impaired
  • -> Still able to carry out activities of daily living
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20
Q

Preterm complications: pulmonary immaturity

A
  • Apnoea
  • RDS
  • CLD
  • PTX/air leak/pneumonia can occur
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21
Q

Preterm complications: fragile capillary network in subependymal area

A
  • High risk of IVH –> esp in swings of cerebral perfusion pressure and CO2 levels
  • Large IVH can cause venous infarction or hydrocephalus
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22
Q

Preterm complications: White matter injury

A
  • PV white matter are susceptible to ischaemic damage esp if sensitised to foetal inflammation
  • Preterms less able to tolerate asphyxia
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23
Q

Preterm complications: thermal instability

A
  • Hypothermia exacerbates RDS and inc mortality

- If environmental temp low, baby will expend energy to generate heat at the expense of GROWTH

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24
Q

Preterm complications: feed intolerance

A
  • Immature, absent suck-swallow and gag reflex
  • Requires NG feeding
  • Poor gut motility
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25
Q

Preterm complications: PDA

A
  • Increases risk of heart failure
  • RF for IVH, NEC and CNLD
  • Increases shunting from aorta to pulmonary arteries –> pulm congestion and reduced systemic blood flow during diastole
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26
Q

Preterm complications: ROP

A
  • Hyperoxia delays vascularisation of retina, VEGF release –> abN angiogenesis
  • Peripheral retina becomes hypoxic
  • Zones: periphery –> central
  • Stages 1-5
  • Plus dz: dilatation and tortuosity of posterior pole retinal vessels, assoc. w/ worse outcomes
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27
Q

Preterm complications: jaundice

A
  • High RBC mass and poor liver conjugation –> hyperbili inevitable
  • Poor BBB and acidosis –> higher risk of kernicterus
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28
Q

Preterm complications: renal immaturity

A
  • Inability to concentrate urine or excrete an acid load, low HCO3 threshold
  • Can result in late metabolic acidosis –> failure to gain wt
  • Tx: NaHCO3 and breast feed/preterm formula feeds
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29
Q

Preterm complications: Metabolic disturbance

A
  • Hypoglycemia, hypoCa, hypoMg, hypoNa, hypernat

- Rickets of prematurity due to low Phos > hypoCa

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30
Q

Preterm complications: infection

A
  • Relative immunodeficiency, central and umbilical lines

- Maternal and nosocomial infections

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31
Q

Preterm complications: haematological

A
  • DIC
  • Vit K def
  • Iatrogenic or Fe def anaemia
  • Aim for haematocrit >0.35
  • Physiological nadir ~5-7 wks where Hb can fall to 70 and Hct 0.25
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32
Q

Preterm complications: surgical

A
  • UDT

- Inguinal and umbi hernias

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33
Q

Breast milk fortifier

A

Commenced for preterms <32 weeks

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34
Q

Ferrous sulphate (Fe) supplements

A
  • Prevention of Fe deficiency anaemia

- Infants <2kg or <34 wks should be commenced on Fe supps from day 14 unless on formula feeds

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35
Q

Growth: target weight gain for preterms <2000g

A

15g/day

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36
Q

Growth: target weight gain for neonates >2000g

A

Wt: 20g/day
Lth: 0.7-1cm/wk
HC: 0.7-1cm/wk

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37
Q

Indications to start TPN (5)

A
  1. Preterms <30 wks and/or <1000g
  2. Preterms >30wks who are unlikely to establish full enteral feeds by 7 days
  3. Severe IUGR with abnormal doppler flow studies
  4. NEC
  5. GIT abnormalities
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38
Q

Predictors of outcome in HIE: APGAR scores

A
  • <2 at 10min is assoc. w/ death or moderate disability at 18-22mths
  • 0 at 10min is assoc. w/ death or severe disability at 18-22mths
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39
Q

Predictors of outcome in HIE: umbi cord arterial/venous pH

A

Lower arterial pH within 60min after birth associated with death and injury in 2nd wk after birth

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40
Q

Predictors of outcome in HIE: base deficit

A

Meh

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41
Q

Predictors of outcome in HIE: lactate

A
  • Lactate >4.4 predictive of severity of encephalopathy when COMBINED with uric acid, LDH and CK
  • On its own, poor predictor of good outcome
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42
Q

Predictors of outcome in HIE: Sarnat scores

A
  • Stage II and III at 24hrs after birth associated with death and disability at 18-22mths
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43
Q

Predictors of outcome in HIE: aEEG

A

Abnormal aEEG by 48 hours after
birth can predict death or disability at
18–22 months

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44
Q

Predictors of outcome in HIE: MRI

A

Major neonatal MRI abnormalities
predict death or severe disability at
18 months

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45
Q

MOA of caffeine

A
  • Increase central resp drive by lowering threshold of response to hypercapnia (increase chemoreceptor responsiveness)
  • Enhancing contractility of diaphragm and reducing diaphragmatic fatigue
  • Generalised excitation of CNS
46
Q

Caffeine: short term benefits

A
  • Reduced CLD
  • Reduced PDA requiring medication and surgery
  • Reduce assisted ventilator time
  • Reduced severe ROP
47
Q

Caffeine: long term benefits

A
  • Decreased composite outcome of death or disability, CP and cognitive delay
  • Increased disability free survival at 20mths
  • At 5yr f/u: no statistically significant difference
  • At 11yr f/u: reduced functional impairment and reduced risk of motor impairment
48
Q

Caffeine: disadvantages

A
  • Reduces weight gain in neonatal period

- No effect on NEC

49
Q

Antenatal corticosteroids: benefits

A

Significantly reduces the risk and mortality of RDS
Significantly reduces overall neonatal mortality
Reduce need and duration of ventilatory support and admission to NICU
Reduce incidence of severe IVH, NEC, neurodevelop. impairment
Does not impair postnatal growth
Repeated doses of AC after 7 days are assoc. w/ improved short term outcomes (>48hrs and <7days)

50
Q

Antenatal corticosteroids: no effect on…

A
  • Risk of developing CLD
  • Chorioamnionitis
  • Maternal death
51
Q

Indications for I&V and surfactact for RDS

A
  • pH <7.2
  • PCO2 >60
  • O2 sats <90% at FiO2 40-70 and PEEP 5-10cmH2O
  • Persistent apnoeas
52
Q

Surfactant: benefits

A
  • Reduces air leak
  • Improves survival
  • Reduces need for mechanical ventilation
  • Reduces incidence of PTX
  • Prophylactic surfactant is effective, multiple doses are more effective than single dose
53
Q

Surfactant: no effect on…

A
  • IVH
  • NEC
  • CLD
  • ROP
  • PDA
  • But, increases rates of pulmonary haemorrhage
54
Q

Mechanical ventilation: improve oxygenation by…

A
  • Increase FiO2 or mean airway pressure

- Increase MAP: increasing PIP, PEEP, I:E ratio

55
Q

Mechanical ventilation: improve CO2 elimination by…

A
  • Increasing PIP (increases tidal vol)
  • Increase tidal volume
  • Increase RR
56
Q

In preterms: targetting saturations between 91-95% showed (SUPPORT trial)…

A
  • Reduction in mortaility
  • Higher risk of ROP, but no increased risk of blindness
  • Less risk of NEC
  • Higher risk of CNLD (having supplemental oxygen)
57
Q

Major findings from SUPPORT trial (target for SaO2 in extreme preterms)

A
  • Target of 85-89% vs 91-95% had no significant difference in primary composite outcome of death or major disability at corrected age of 18-24mths
  • Lower O2 targets: increased death and NEC, reduced ROP treatment
58
Q

Postnatal corticosteroids

A

Early (<8 days) corticosteroids: decreased CLD
Late (>7 days) corticosteroids: decreased CLD, no effect on CP, increase in ROP, but no blindness, reduces neonatal mortality before 28 days, but no significant difference after hospital discharge

59
Q

Postnatal corticosteroids: adverse effects

A
  • Short term adverse effects – hyperglycaemia, hypertension, GI bleed, GI perf, HOCM, poor weight gain, poor head growth
  • Long term: adverse neurodevelopmental outcomes, increased risk of CP
60
Q

Mechanical ventilation for congenital diaphragmatic hernia showed…

A
  • Decreased duration of ventilation
  • Less chance of requiring ECMO
  • Less need for iNO or sildenafil
  • Shorter duration of vasoactive medications
  • No difference in primary outcome: death or CNLD
61
Q

Complications and ongoing issues of congenital diaphragmatic hernia

A
  • Develop BPD and pulmonary issues later in life
  • FTT
  • Neurocognitive defects in 67% of those requiring ECMO, 27% w/o ECMO
  • Recurrent hernia 5-20%
  • Intestinal obstruction 20%
  • GORD 50%
  • Pectus excavatum and scoliosis
62
Q

NEC can occur in term babies with risk factors for gut ischaemia which include… (4)

A
  • Perinatal asphyxia
  • Congenital heart disease
  • Hirschprung disease
  • Exchange transfusion
    These babies can present with NEC within days
63
Q

Classic triad for NEC

A

Abdo distension
Bloody stools
Bile-stained aspirates

64
Q

Pathognomonic sign for NEC on XR

A

Pneumatosis intestinalis - gas in submucosal and subserosal surfaces of bowel wall

65
Q

Bell’s stage 1A: suspect NEC

A
  • Presentation: apnoea, temperature instability, lethargy, bradycardia
  • O/E: abdominal distension, aspirates, positive FOBT
  • AXR: normal, mild distension or ileus
66
Q

Bell’s stage 1B: suspect NEC

A
  • Presentation: apnoea, temperature instability, lethargy, bradycardia, feed intolerance
  • O/E: Fresh PR blood
  • AXR: normal, mild distension or ileus
67
Q

Bell’s stage 2A: proven NEC - mildly ill

A
  • Presentation: apnoea, temperature instability, lethargy, bradycardia, feed intolerance
  • O/E: abdominal distension, biliary aspirates, tenderness, absent bowel sounds
  • AXR: distension, pneumatosis intestinalis, ileus
68
Q

Bell’s stage 2B: proven NEC - moderately ill

A
  • Presentation: mild metabolic acidosis, thrombocytopenia
  • O/E: tenderness, absent bowel sounds, abdominal cellulitis, RLQ mass
  • AXR: distension, pneumatosis intestinalis, ileus, portal vein gas +/- ascites
69
Q

Bell’s stage 3A: severely ill NEC - bowel intact

A
  • Presentation: hypotension, bradycardia, apnoea
  • O/E: peritonitis, marked distension and tenderness
  • AXR: distension, pneumatosis intestinalis, ileus, portal vein gas, ascites
70
Q

Bell’s stage 3B: severely ill NEC - perf

A
  • Presentation: hypotension, bradycardia, apnoea
  • O/E: peritonitis, marked distension and tenderness
  • AXR: pneumoperitoneum, distension, pneumatosis intestinalis, ileus, portal vein gas, ascites
71
Q

Pathogenesis of NEC

A
  • Immaturity of barrier, ischaemia, toxins, milk feeds, bacterial overgrowth/alteration in gut flora, viruses and bacteria all contribute to the disruption of the mucosal layer of bowel
  • Bacterial penetrates bowel wall (translocation) –> mucosal damage and inflammation –> NEC
72
Q

Causes/RF for NEC

A
  1. IUGR foetuses with absent or reversed end diastolic flow on Dopplers
  2. PDA
    - Indomethacin had no effect on incidence of NEC
  3. Gut pH - use of any H2 blocker associated with incr risk of NEC
    - i.e. changing acidity of gut environment
  4. ?Blood transfusions (contentious)
  5. Bacterial colonisation of bowel
    - Major determinant of necrosis - esp gram neg
  6. IV antibiotic use (contentious)
73
Q

ADEPT study outcomes: feeding preterm growth-restricted infants

A
  • <35wks, <10th centile with abnormal antenatal dopplers
  • Early (day 2) vs late (day 6) commencement of enteral feeds
  • NO difference in incidence of NEC in both groups
  • Earlier fed infants: reduced time to establish feeds, shorter time on TPN, less jaundice, greater wt at D/C
74
Q

SIFT trial outcomes: slow and fast advancement of enteral feeds

A
  • In VLBW infants, higher rates of enteral feeding (30ml/kg/day) did not increase the incidence of NEC
  • Even for babies who are ELBW, growth restricted, SGA or with absent/reverse end diastolic flow
75
Q

Breast milk and NEC

A
  • Breast milk is better at reducing risk of NEC (trials included donor milk or AF)
  • No increased incidence of NEC in infants on fortifier
76
Q

Bacterial colonisation: Term vs preterm, breast-fed vs AF

A
  • Term breastfed: during birth process + thereafter, microbes from mother and surrounding environment colonise GIT of baby –> lactobacilli, bifidobacteria
  • Term formula fed: coliforms, enterococci and bacteroides predominate in gut
  • Preterm: acquire colonising bacteria from nursery environment rather than mother’s vaginal canal/milk etc
  • -> Gut flora diversity also greatly reduced as multiple antibiotic therapy
  • -> Gram negatives: E. coli, Klebsiella
  • -> C. diff
77
Q

Probiotics and NEC

A

Reduces:

  • Incidence of severe NEC
  • Incidence of late onset sepsis
  • All cause neonatal mortality
78
Q

Probiotics: single or multiple strain?

A
  • Infloran contains lactobacillus acidophilus and bifidobacterium bifidum
  • More protective effect if using more than 1 bacteria
79
Q

Predictors of outcome in Short Bowel Syndrome (resection after NEC) i.e. able to come off TPN

A
  • Amount of residual bowel left
  • Presence of ileocaecal valve
  • % calories tolerated via enteral route at 12 weeks
80
Q

Indications for surgical management of NEC

A
  • Abdominal mass
  • Perforation (pneumoperitoneum)
  • Not responding to medical therapy
  • -> Persistent acidosis, worsening pulmonary status, unremitting neutropenia/thrombocytopenia
81
Q

DDx for NEC

A
  • Malrotation
  • Volvulus
  • Milk bolus
  • First 2 require early surgery as there is high risk of ischaemia
82
Q

DDx for conjugated jaundice

- Note: most cause both early-onset and/or persistent jaundice

A
Sepsis
TORCH infections 
Neonatal hepatitis
Giant cell hepatitis
Galactosemia
A1AT
Hyperalimentation/TPN-related cholestasis 
Cystic fibrosis 
Paucity of bile ducts
Biliary atresia
Disorders of bile acid metabolism
Choledochal cysts
Tyrosinemia
Severe haemolytic anaemia
83
Q

DDx for prolonged unconjugated jaundice

A
Breast MILK jaundice (Dx of exclusion)
- B-glucuronidase activity 
Sepsis
Hypothyroidism
Crigler-Najar Syndrome
Gilbert Syndrome 
Down Syndrome
84
Q

DDx for unconjugated jaundice (normal reticulocyte count)

A
  • Increased enterhepatic circulation: dehydration and decreased caloric intake (breastFEEDING jaundice), delayed/infrequent stooling
  • Enclosed haemorrhage (e.g. cephalhaematoma)
  • Neonatal asphyxia
  • Prematurity
85
Q

DDx for unconjugated jaundice (high reticulocyte count)

A
  1. Haemolytic disease
    - Rhesus disease
    - ABO incompatibility
    - G6PD
    - Pyruvate kinase deficiency
    - DIC
    - Hereditary spherocytosis
  2. Polycythemia:
    - Twin-twin transfusion
    - GDM mother
    - SGA baby
    - Delayed cord clamping
86
Q

Treatment with oral glucose gel in babies with hypoglycemia showed…

A
  • Reduced treatment failure
  • Reduced NICU admission rates for hypoG
  • Reduced maternal-infant separation
  • Increased breast feeding at 2wks of age
87
Q

CHYLD Study outcomes: babies at risk of hypoglycemia, long-term effects

A
  1. At 2yo:
    - No impact of hypoglycemia on executive function or neurosensory development
    - Rather, increased risk of neurosensory development if hyperglycemic or if BSLs went high after a period of hypoglycemia (first 12hrs of life)
  2. At 5yo:
    - No impact of hypoglycemia on neurosensory development
    - Severe hypoglycemia: more likely to have executive function problems, visuomotor problems
88
Q

Air vs oxygen therapy in resuscitation

A
  • Reduces severe HIE

- Reduces mortality

89
Q

Late preterm babies (34-36wk) are at risk of…

A
  • Increased neonatal morbidity and mortality
  • Increased behavioural problems and worse 24mth neurodevelopmental outcomes c.f. term babies
  • > 3x more likely to be Dx with cerebral palsy
90
Q

Risk factors for nosocomial sepsis (6)

A
  • Indwelling cathethers/lines
  • Prematurity/LBW
  • SGA
  • TPN
  • Neutropenia
  • Surgery
91
Q

Group B Streptococcus infection: early vs late

A
  • Early: within 24hrs
  • -> More likely to present with septicaemia, respiratory distress (pneumonia)
  • Late onset: 2-4wks
  • -> More likely to present with septicaemia, meningitis
92
Q

Intrapartum IVAB prophylaxis for GBS

A
  • Effective at decreasing early onset GBS disease

- No effect on late onset sepsis, still birth or GBS-related prematurity

93
Q

GBS sepsis consequences

A

Adverse neurological outcomes

  • PVL associated with infection/chorioamnionitis
  • Sepsis (x2)
  • Meningitis (x4)
94
Q

Worse outcome for ROP

A

Presence of “plus” disease - dilated and tortuous posterior pole vessels

95
Q

PDA closure

A

90% of closure by 60hrs of age

Same for term and preterm unless RDS present

96
Q

Sequalae of PDA due to ductal steal leads to…

A
  • CNLD
  • Pulmonary haemorrhage
  • NEC
  • Renal hypoperfusion
  • IVH

Ductal steal = oxygenated blood being pushed through pulmonary circulation instead of entering other organs via systemic circulation –> pulmonary engorgement

97
Q

Indomethicin vs ibuprofen

A
  • Indomethacin: COX 1&2 inhibitor
  • -> limits production of PG –> significant reduction in blood flow velocities, decrease platelet function, decreased GFR and urine output
  • -> Short = long course in terms of closure rates
  • Ibuprofen: COX2 inhibitor
  • -> Decreased platelet fxn, decrease in GFR and UO
  • -> Less adverse effects
  • -> Same closure rates c.f. indo
98
Q

Indomethacin advantages and disadvantages

A
  • Reduces incidence of severe IVH, symptomatic PDA and need for surgical ligation
  • No effect on neurodevelopmental outcomes
99
Q

Ibuprofen advantages

A
  • Reduces incidence of PDA with need for surgical ligation
100
Q

Surgical ligation advantages and disadvantages

A
  • Reduces incidence of stage II and III NEC

- No effect on mortality or CNLD

101
Q

Spontaneous closure rates PDA

A

30-65%

102
Q

Mechanical vent: aims of PaO2, PCO2, pH

A

PaO2 - 45-70
PaCO2 - 45-60
pH >7.25

103
Q

Mean airway pressure if affected by… (4)

= average P to which lungs are exposed to during respiratory cycle

A

PIP
PEEP
Inspiratory flow
Inspiratory to expiratory ratio

104
Q

Excessive tidal volume causes volutrauma by…

A
  • Epithelial injury/shear stress with increased flow
  • -> Volume = flow x time
  • Protein leak and surfactant inhibition
  • Increased macrovascular permeability/pulmonary oedema
  • Air leak
  • Limit by hypercapnea
105
Q

SIMV

A

Synchronised Intermittent Mandatory Ventilation

  • Set rate with inspiratory and expiratory controls - ventilator inflates at this set rate
  • Synchronises inflations with baby’s breath at SET rate
  • If baby doesn’t breath, ventilator inflates as per SET rate
  • If baby breathes faster –> unsupported breaths, breathing with ETT CPAP
  • Rate is set, inspiratory time is set
106
Q

SIPPV

A

Synchronised Intermittent Positive Pressure Ventilation

  • If baby’s breath is above the trigger threshold (0.2mL), then it will trigger an inflatinon from ventilator. Supports baby’s EVERY BREATH
  • If baby breathes at 100bpm –> it will support 100 breaths
  • Set a back-up rate to deliver breath if baby does not breath
  • Venilation weaned by reduced PIP
  • Set IT, RR, PIP, PEEP
  • Note: watch IT –> if tachypnoeic and IT is long, the baby will start expiring during ventilator inflation, decreases ET –> air trapping and air leak syndrome
107
Q

PSV

A

Pressure support ventilation

  • Safer than SIPPV, still supports every breath taken by baby
  • Set back up rate like SIPPV, PIP and PEEP
  • Baby determines INSPIRATORY TIME, as the ventilator inflation is stopped once the flow down ETT is <15% of max
  • IT and ET can be controlled by baby according to own lung mechanics
108
Q

HFOV Indications

A

Rescue ventilation for recruitable lung disease
Primary treatment of RDS
Rescue ventilation for CDH

109
Q

HFOV treatment outcomes for RDS

A
  • No reduction in death
  • TREND towards reduction in BPD (heterogeneity of data)
  • Increased PTX or PIE risk
  • Decreased ROP
  • No difference in IVH or PVL
  • No clear difference long-term
110
Q

Settings of HFOV to increase oxygenation or CO2 removal

A
  1. To increase O2:
    - Increase MAP or FiO2
  2. To increase CO2 removal:
    - Increase amplitude (of oscillation) –> increases VT
    - Increase frequency
111
Q

What is the main determinant of neonatal cardiac output?

A

Heart rate

- Neonates have limited capacity to increase stroke volume

112
Q

Adverse effects of iNO

A
  • Methaemoglobinemia - Nitrous oxide binds heme ion on Hb –> Methb
  • Pulmonary oedema - NO can react with O2 to form NO2 which is toxic to the lungs –> cellular damage to airway and alveolar epithelium
  • Rebound pulmonary vasospasm - sudden cessation from concentrations above 10ppm can cause rebound and significant deoxygenation
  • Prolonged bleeding time - NO effects on platelets