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3a > Paediatrics: Neonatology > Flashcards

Paediatrics: Neonatology Flashcards

1
Q

What cells produce surfactant?

A

Type II pneumocytes (alveolar cells)

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2
Q

What is the action of lung surfactant?

A
  • Reduces the surface tension of the fluid in the lungs => keep alveoli inflated + maximise alveolar SA
  • Promotes equal expansion of all alveoli (because this out as alveolus expands)
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3
Q

what is the impact of surfactant on lung compliance? explain this

A

Increases lung compliance (reduces force needed to expand alveoli)

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4
Q

At how many weeks gestation does surfactant start to be produced?

A

starts being produced between 24-34 weeks gestation

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5
Q

After birth: what helps expand previously collapsed alveoli? (first breath)

A

stress of labour => Ad + cortisol release => stimulate resp effort

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6
Q

explain how the first breath leads to foramen ovale. what does this eventually become?

A

Alveoli expand => reduced pulmonary resistance => LA>RA pressure => squash atrial septum => foramen ovale (functional closure) => fossa ovalis (structural closure)

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7
Q

Describe how early neonatal cardio-respiratory changes lead to ligamentum arteriosus formation

A

increased blood oxygenation => decreased relative prostaglandins => ductus arteriosus closure => ligamentum arteriosus

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8
Q

When does the ductus arteriosus stop functioning

A

within 1-3 days of birth
(due to relative decrease in prostaglandins)

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9
Q

Describe how early neonatal cardio-respiratory changes lead to ligamentum venosum formation

A

umbilical cord clamping => no umbilical vein blood flow => ductus venosus closure => ligamentum venosum

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9
Q

Explain what can cause common hypoxia in neonates

A

during labour, contractions mean placenta is unable to carry out normal gaseous exchange => hypoxia

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9
Q

What do you do immediately after the baby has been born? (7)

A
  • Skin to skin
  • Delayed cord clamping
  • Dry the baby
  • warm the baby with hat and blankets
  • Vitamin K
  • Label baby
  • Measure weight and length
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9
Q

What can extended hypoxia in neonates lead to? plus the in between bits

A

extended hypoxia => anaerobic respiration + bradycardia => decreased consciousness + decreased resp effort => hypoxic-ischaemic encephalopathy

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10
Q

What score is an indicator of progress over the fist few minutes of life

A

APGAR

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11
Q

what does APGAR stand for? is high or low bad?

A

Appearance
Pulse
Grimace
Activity
Respiration
(lower => bad)

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12
Q

Why is delayed cord clamping good?

A

allows for placental transfusion
- Fetal blood from placenta => fetal circulation

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13
Q

What examination can estimate gestational age when it is unknown/unclear?

A

Dubowitz/ballard examination

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14
Q

Describe the categories for:
- Extreme preterm
- Very preterm
- Moderate to late preterm
- Term

A

<28 weeks (extreme preterm)
28-32 weeks (very preterm)
32-37 weeks (moderate to late preterm)
37-42 (term)

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15
Q

If fetus is going to preterm, how can you try to delay birth? (not in labour yet)

A
  • prophylactic vaginal progesterone (progesterone helps to reduce contractions)
  • prophylactic cervical cerclage
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16
Q

When labour is suspected in a preterm fetus, what can you do?

A
  • Tocolysis (nifedipine - CCB, progesterone (maintenance)
  • Maternal corticosteroids
  • IV Mg Sulphate
  • delayed cord clamping
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17
Q

what can be given antenatally to aid lung development in a preterm fetus?

A

corticosteroids - dexamethasone

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18
Q

Why might IV Mg Sulphate be given antenatally?

A

in a suspected preterm fetus
- Protect fetal brain (neuroprotective)

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19
Q

What can be used in neonatal prematurity for treatment of apnoea ? in how many weeks of life is this used

A

caffeine
(<34 weeks CGA)

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20
Q

What Resp complications might a preterm neonate have? (3)

A
  • RDS
  • Surfactant deficient lung disease (insufficient surfactant => increased alveolar surface tension => lung collapse => poor gas exchange => hypoxia)
  • CLD
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21
Q

What cardiovascular complications might a preterm neonate have? (2)

A
  • Hypotension
  • PDA
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22
Q

What neuro complications might a preterm neonate have? (3)

A
  • Intraventricular haemorrhage
  • Developmental delay
  • CP
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23
Q

What GI complications might a preterm neonate have? (1)

A

NEC

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24
Q

What eye complications might a preterm neonate have? what do you have to do to manage?

A

retinopathy of prematurity
- avoid excessive oxygen exposure

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25
Q

how many weeks gestation is retinal blood vessel dev completed? stimulated by what?

A

finished by 37-40 weeks gestation stimulated by hypoxia

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26
Q

What might you not what a neonates oxy sats at 100%

A

risk of retinopathy of prematurity
- High oxy sats => abnormal retinal dev =>scarring + retinal detachment + blindness

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27
Q

What vitamin is given to babies at birth? how is it given?

A

babies are usually born with a deficiency in vit K (important in normal blood clotting)
- usually given IM

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28
Q

benefits of skin-to-skin contact? (4)

A
  • Warms baby
  • Improve mother + baby interaction
  • Calms baby
  • Improves breast feeding
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29
Q

Normal care after birth: what is done once out of the delivery room?

A
  • Initiate breast or bottle feeding a soon as baby is alert enough
  • NIPE (<72 hrs)
  • Blood spot test
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30
Q

When blood spot test done? what does it test for? how long for results?

A

days 5
- screens for 9 congenital conditions
- results take 6-8 weeks

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31
Q

what reflexes should a baby have?

A
  • Moro
  • Suckling
  • Rooting
  • Grasping
  • Stepping
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32
Q

What is caput saccedaneum?

A

birth injury
- fluid (oedema) collecting in scalp outside periosteum

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33
Q

Where can fluid in caput go to?

A

fluid collecting outside the periosteum so is able to cross suture line

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34
Q

Caput saccedaneum management?

A

does not require treatment + will usually resolve within a few days

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35
Q

What is cephalohaematoma? where can blood go?

A

birth injury
- collection of blood between skull + periosteum => the lump does not cross suture lines of scalp

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36
Q

Cephalohaematoma managment?

A

usually does not require intervention but risk of anaemia and jaundice due to blood clot + breakdown

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37
Q

What is erbs palsy? which nerves?

A

result of damage to C5/C6 nerves in brachial plexus during birth

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38
Q

symptoms of an erbs palsy?

A

weakness of shoulder abduction + external rotation, arm flexion, finger extension

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39
Q

erbs palsy management?

A

function to arm usually returns in a few moths
- if not the requires surgical input

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40
Q

What physiology causes hypoxic ischaemic encephalopathy ? can lead to what?

A

HIE occurs in neonates as a results of hypoxia during birth
- can lead to permanent damage of the brain => cerebral palsy

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41
Q

what can cause HIE?

A
  • maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord
42
Q

Management of HIE?

A
  • supportive care
  • therapeutic hypothermia
43
Q

what is the time frame of early onset neonatal sepsis (EONS)

A

sepsis occuring with the first 72 hrs of life

44
Q

Common organisms of EONS? most common

A
  • Group B Strep (GBS) [most common]
  • e.coli
  • listeria
  • s.aureus
45
Q

why is GBS the most common cause of EONS?

A

common bacteria found in vagina => infection by direct contact

46
Q

Mum is found to have GBS in vagina, what is done?

A

prophylactic Abx used during labour

47
Q

EONS RF?

A
  • maternal vaginal GBS colonisation
  • GBS sepsis in prev baby
  • Maternal sepsis
  • Prematurity
  • Early ROM
  • Prolonged ROM
48
Q

EONS clinical features?

A
  • Fever, decreased tone + activity, poor feeding, resp distress or apnoea, vomiting, tachy/bradycardia, hypoxia, seizures
49
Q

EONS red flags?

A
  • Confirmed or suspected maternal sepsis
  • signs of shock
  • seizures
  • Resp distress starting more than 4 hrs after birth
  • need for mechanical ventilation in a term baby
  • suspected or confirmed infection in co-twin
50
Q

EONS managment? which Abx?

A
  • Start Abx within 1 hr: IV benzylpenecillin + gentamycin
  • Blood cultures, baseline FBC + CRP, lactate
  • Consider LP if meningitis suspected
  • Monitor urine output
51
Q

EONS differential?

A

surfactant deficient lung disease, meconium aspiration, haemolytic disease of the new-born

52
Q

what is the mortality of EONS due to GBS infection in term babies?

A

2-3%

53
Q

what is jaundice? generally

A

abnormally high levels of bilirubin in the blood

54
Q

where is bilirubin conjugated?

A

in the liver

55
Q

where can conjugated bilirubin go to? (3)

A
  • excreted in the urine
  • released in the bile and excreted in stool
  • released in bile and reabsorbed in small intestine back into blood
56
Q

How does phototherapy work to reduce jaundice?

A

converts unconjugated bilirubin to isomers of bilirubin that can then be excreted in urine and stool
(bypasses the liver function)

57
Q

Why is physiological jaundice common?

A
  • high conc of RBC in fetus + neonates + liver function less developed
  • fetal RBC breakdown more rapidly than normal RBC and normally excreted by placenta
58
Q

RF for pathological jaundice?

A
  • Premature
  • SGA
  • Prev sibling requiring phototherapy
  • exclusive breast feeding
    (- jaundice <24 hrs)
59
Q

is breast feeding or bottle feeding a RF for pathological jaundice ?

A

breast feeding only is a RF for pathological jaundice

60
Q

What 2 categories can pathological jaundice be split into? give examples

A
  • increased production: haemolytic disease of newborn, ABo incompatibility, haemorrhage, sepsis + DIC, G6PD deficiency
  • decreased clearance of bilirubin: prematurity, breast milk jaundice
61
Q

baby presents with jaundice in <24 hrs of life. what differential do you need to consider?

A

sepsis! need to consider

62
Q

what is haemolytic disease of newborn? caused by?

A

caused by incompatibility of RBC surface rhesus antigen between mother and fetus (after prev pregnancy with sensitisation)

63
Q

what is the management of neonatal jaundice?

A
  • Measure and plot serum bilirubin (SBR) levels on treatment threshold chart (specific for GA of abby at birth)
  • if above threshold level for phototherapy: commence
  • increase no. of phototherapy lights as SBR approaches transfusion line
64
Q

When do you stop phototherapy in jaundiced neonate

A

continue till >50 um below threshold line

65
Q

What is the main concerning complication of neonatal jaundice? explain

A

kernicterus: brain damage caused by excessive bilirubin levels
- bilirubin crosses BBB => damage to CNS =>. CP, LD + deafness

66
Q

Which structure/s in the brain does excessive bilirubin affect?

A

basal ganglia

67
Q

What is necrotising entercollitis?

A

serious + sometimes fatal GI infection of typically formula fed preterm infants => bowel perforation => peritonitis + shock

68
Q

What is the cause of NEC

A

unclear, not really understood
may be infective - E.Coli ?

69
Q

NEC RF?

A
  • v low birth weight or v preterm
  • Formula fed
  • sepsis
  • PDA
70
Q

NEC presentation?

A

premature neonate wo becomes intolerant to feeds, starts vomiting, generally unwell, adobo distention/tenderness, absent bowel sounds, blood in stool

71
Q

what would the vomit in NEC be like?

A

bilious or blood stained

72
Q

What investigation would you do for suspected NEC?

A
  • FBC, CRP, blood cultures (if sepsis suspected)
  • abdo XR (diagnostic)
73
Q

what would be seen on abdo XR of neonate with NEC?

A
  • dilated loops of bowel
  • Bowel wall oedema (thickened bowel walls)
  • Gas in bowel wall or peritoneal cavity (bad sign)
74
Q

what is the management of NEC?

A
  • Bill by mouth with IV fluids + TPN + IV Abx
  • AXR
  • Surgical emergency
75
Q

complications of NEC surgery?

A
  • Intestinal stricture
  • Short bowel syndrome
76
Q

What is meconium aspiration syndrome? when?

A

respiratory distress in newborn infant following aspiration of meconium stained amniotic fluid (antenatally or at birth)

77
Q

describe pathophysiology of MAS?

A

meconium aspirated => inflam response + inhibit surfactant action
- Causes partial/total airway obstruction: thick meconium => ball valve effect => pulmonary pressure => V/Q mismatch => R ro L shunt => hypoxia

78
Q

MAS RF?

A

things that causes fetal hypoxia or fetal gasping
- >42 weeks gestation
- fetal distress
- maternal smoking

79
Q

Clinical features of MAS?

A
  • signs of RDS (high RR + HR, cyanosis, grunting, nasal flaring, recessions, hypotension)
  • mecpmium stained liquor
  • preterm ( I think )
80
Q

what investigations would you do for MAS? what would they show? diagnostic test?

A

(clinical diagnosis)
CXR: increased lung vol, asymmetrical patch pulmonary opacities

81
Q

management of MAS?

A

depends on severity of RDS
- Observation, ventilation, Abx (if infection indicated), surfactant

82
Q

More than 90% of SIDS deaths occur before babies reach how many months?

A

6 months

83
Q

What percentage of pregnant women carry Group B Streptococcus in their genital tract?

A

25%

84
Q

What percentage of breast fed babies have jaundice at 1 month?

A

10%
(Higher risk than bottle fed)

85
Q

A 3 day old neonate is though to have Hirschsprung’s disease. What is the gold standard for investigation?

A

Rectal biopsy

86
Q

What septal defect is most common in those with downs syndrome?

A

atrioventricular septal defect

87
Q

what is neonatal hypoglycaemia ? under what value ?

A

neonatal hypoglycaemia but a figure of < 2.6 mmol/L
(I think consider management when <1)

88
Q

What could cause neonatal hypoglycaemia ?

A
  • preterm birth (<37 weeks)
  • GDM
  • IUGR
  • hypothermia
  • neonatal sepsis
89
Q

Feautres of neonatal hypoglycaemia ?

A
  • asymptomattic
  • jitteriness
  • irritable
  • tachypnoea
  • reduced/poor feeding
  • pallor
  • weak cry
  • Siezures
90
Q

managment of asymptomatic hypoglycaemia ?

A
  • encourage normal feeding (breast or bottle)
  • monitor blood glucose
91
Q

When would you treat neonatal hypoglycaemia ? (2) how would you treat ?

A

symptomatic or very low blood glucose (<1mmol/L)
- admit to the neonatal unit
- intravenous infusion of 10% dextrose

92
Q

what is neonatal TORCH infection? what does it stand for ?

A

group of congenital conditions, infection of developing fetus inter or newborn
- Toxoplasma gondii
- Other agents
- Rubella
- CMV
- HSV

93
Q

how are TORCH infections transmitted ? (3)

A

in utero (though placenta)
during labour
breast feeding

94
Q

complications of TORCH infection ?

A
  • miscarriage
  • stillbirth
  • IUGR
95
Q

neonatal TORCH infection sx ? generally

A
  • microcephaly
  • lethargy
  • cataracts
  • hearing loss
  • CHD
96
Q

neonatal TORCH infection Dx ?

A
  • prenatal: history, fetal abnormaliels
  • pre/postnatal: PCR testing, viral cultures, antibody testing
97
Q

TORCH Mx ?

A

Abx or antivirals
- supportive care

98
Q

What is oesophageal atresia ? often associated with ?

A

rare condition wehre oesophagus no formed properly so not connected to stomach
- trachea-oeophgeal fistula ends to occur alongside OA: oesophagus is joined to trachea

99
Q

how is oesophageal atresia diagnosed ?

A
  • sometimes seen antenatally
  • ty to pass NG tube but does not work
100
Q

oesophageal atresia Mx ? complication of this ?

A

surgical
- post surgery: increased risk of tracheomalacia (due to floppy wind pipe)

101
Q

what does atresia mean ?

A

a complete blockade (obstruction or lack of continuity

102
Q

what is the most common location for small bowel atresia ?

A

jejunoileal atresia: most common type of neonatal intestinal obstruction

103
Q

how is small bowel atresia Dx ? describe the findings

A

prenatal US
- dilated bowel
- double bubble (duodenal atresia)

104
Q

small bowel atresia Px antenatally ? explain

A

polyhydramnios (usually baby continuous swallow amniotic fluid by can’t due to blockage)
- this => increase risk of preterm birth

105
Q

small bowel atresia Mx ?

A

surgical repair

3a (43 decks)

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