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Paediatrics > Neonates > Flashcards

Neonates Flashcards

1
Q

What is the definition of prematurity?

A

Less than 37 weeks gestation

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2
Q

What is very preterm?

A

28-32 weeks

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3
Q

What is extremely preterm?

A

< 28 weeks

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4
Q

What is the typical birth weight of a baby at 24 weeks?

A

620g females

700g males

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5
Q

What does a preterm infants skin look like and what does this make them prone to?

A

Red, thin, gelatinous

Prone to evaporative heat loss and easily damaged -> high infection risk

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6
Q

What might you see if you examined a preterm infant?

A

Adopts extended posture with uncoordinated movements
Eyelids may be fused or partially open - infrequent eye movements in contrast to term infant
Unlikely to breathe w/o resp support
Uncoordinated suckling - most required NG feeding +/- TPN

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7
Q

When does the suckling reflex develop?

A

34-35 weeks

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8
Q

At what birth weight are babies most at risk of complications?

A

< 1.5kg

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9
Q

What preterm complications can you get?

A 
Respiratory distress syndrome
Infection
PDA
Necrotising enterocolitis
Periventricular-intraventricular haemorrhage
Periventricular leukomalacia
Retinopathy of prematurity
Osteopenia of prematurity
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10
Q

Why do preterm babies develop respiratory distress syndrome?

A

Lack of pulmonary surfactant production resulting in high surface tension at alveolar surface
Less functional alveoli
Lacking sufficient cartilage to keep airways patent

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11
Q

Which cell produces surfactant in the lungs?

A

Type II pneumocyte

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12
Q

What antenatal intervention can reduce to rate of RDS?

A

Steroids

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13
Q

How does RDS present?

A 
Poor APGAR scores at birth
Nasal flaring
Grunting
Recessions
Tracheal tug
Tachypnoea
Poor sats
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14
Q

What might the CXR of a preterm baby with RDS look like?

A

Diffuse granular opacities (ground glass) bilaterally, low lung volumes, bell-shaped thorax

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15
Q

How do you prevent a baby getting RDS?

A

Antenatal steroids to induce surfactant production

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16
Q

How can you treat RDS in a newborn?

A

Surfactant replacement - LISA less invasive surfactant administration
Respiratory support - CPAP, IPPV (mechanical ventilation)

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17
Q

What is the APGAR score?

A 
Appearance
Pulse
Grimace (reflex irritability)
Activity (muscle tone)
Respiration
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18
Q

What is a common complication of intubation and ventilation?

A

Pneumothorax

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19
Q

At 36 weeks corrected gestational age, the baby is still having low sats of 80-90% in room air with some brief apnoeas. What complication has developed?

A

Bronchopulmonary dysplasia of chronic lung disease AKA chronic lung disease

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20
Q

What is chronic lung disease of the newborn?

A

Dependence on O2 therapy either at 28 days or 36 weeks gestation - babies undergo oxygen challenge test

  • No BPD sats > 90% for 60 mins in room air
  • BPD sats < 90% during obs period. Any apnoeas, bradys, or increased O2 requirement means BPD occurred
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21
Q

What is the pathogenesis of chronic lung disease (BPD) of newborn?

A

Underdeveloped lungs due to prematurity
Initial injury to lungs due to primary disease process eg RDS
Ventilator induced lung injury due to barotrauma (high pressure)
Volutrauma (inappropriately high or low tidal volume delivery when ventilated)
Oxygen toxicity
Inflammatory cascade
Inadequate nutrition

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22
Q

How is chronic lung disease treated?

A

Supportive

May require O2 treatment at home

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23
Q

What is the prognosis of BPD?

A

Majority will achieve normal lung function and thrive
Higher risk of death in first year of life
Increased risk of viral infections esp RSV, growth failure, and neurodevelopmental abnormalities

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24
Q

What is the pathology of a PDA?

A

Left-to-right shunting

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25
Q

What can PDA lead to?

A 
Pulmonary oedema
Congestive cardiac failure
Haemodynamic instability - hypotension
Pulmonary haemorrhage
Increased risk of BPD
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26
Q

What does the murmur in PDA sound like?

A

Continuous, machinery murmur

Left infraclavicular area

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27
Q

What is the prognosis of a PDA?

A

In infants > 1kg birthweight 2/3 close spontaneously

In infants < 1kg birthweight 1/3 will close spontaneously

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28
Q

What keeps the PDA patent?

A

Prostaglandin E2

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29
Q

What is the first-line options to close PDA if intervention is needed?

A

Ibuprofen

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30
Q

What is a duct dependent lesion?

A

Lesion dependent on blood flow through the PDA for adequate circulation

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31
Q

How do duct dependent lesions present?

A

Severe cyanosis

Shock or collapse as PDA constricts within hours/days after birth

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32
Q

How do you treat duct-dependent lesions?

A

Prostaglandin infusion to maintain PDA patency (E1/2)

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33
Q

Name 2 duct dependent systemic circulation conditions

A

Coarctation of aorta
Critical aortic stenosis
Hypoplastic left heart syndrome

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34
Q

Name 2 duct dependent pulmonary circulation conditions

A

Pulmonary atresia
Critical pulmonary stenosis
Tricuspid atresia
Tetralogy of Fallot

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35
Q

Name a duct dependent systemic and pulmonary circulation condition

A

Transposition of great vessels with restrictive circulation

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36
Q

What are the features of hypoplastic left heart syndrome?

A

Small left ventricle
Mitral valve closed or atretic
Aorta reduced in diameter
Oxygenated blood goes through ASD, mixes with deoxygenated blood
Mixed blood goes to both lungs, through PDA into systemic circulation
Blue baby

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37
Q

What is a periventricular-intraventricular haemorrhage?

A

Most common neurological complication of preterm infants
Rupture of fragile network in subependymal matrix
Impaired cerebral autoregulation (unable to maintain normal cerebral blood flow within normal limits with blood pressure fluctuation)
Abnormal coagulation
Different gradings and classification

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38
Q

How is periventricular-intraventricular haemorrhage diagnosed?

A

Serial cranial ultrasounds to detect haemorrhage

Also looking for porencephalic cysts, ventricular dilatation, hydrocephalus ect

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39
Q

What is periventricular leukomalacia?

A

Periventricular white matter injury resulting from ischaemia due to hypoperfusion of the area and inflammation

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40
Q

How common is periventricular leukomalacia?

A

3% incidence in very low birth weight infants

High incidence of diplegic cerebral palsy, poor visuo-spatial skills, low IQ scores

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41
Q

What might you see on USS for periventricular leukomalacia?

A

Focal areas of necrosis in the PV white matter from 2 weeks of birth

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42
Q

Why might newborns get osteopenia of prematurity?

A

Phosphate deficiency
Increased PTH
Reduced bone mineralisation, resorption

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43
Q

What are the S&S of osteopenia of prematurity?

A

Widening and cupping of wrists, knees, and ribs on XR (looks like rickets)
Failure in linear growth
Fractures esp of ribs and long bones
Skull deformities, bone softening/widening

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44
Q

What might the bloods of a child with osteopenia of prematurity look like?

A

Low phosphate
Calcium normal/raised
High ALP

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45
Q

How is osteopenia of prematurity treated?

A

Oral phosphate and vit D supplements +/- calcium

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46
Q

Why might newborns get retinopathy of prematurity?

A

Major cause of visual impairment and blindness in preterm
Retinal vessels only complete development towards end of pregnancy and require a relatively hypoxic environment to grow properly
Abnormal retinal vessels form which can lead to bleeding, scarring, and retinal detachment

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47
Q

What can be related to an increased risk of retinopathy of prematurity?

A

Oxygen therapy

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48
Q

How is retinopathy of prematurity treated?

A

Maintain sats 91-95%, avoid wide fluctuations in O2 sats
Laser coagulation of vessels if significant ROP has developed
Injection of anti-vascular endothelial growth factor

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49
Q

A baby born at 28 weeks gestation develops the following after two weeks on the NICU - abdominal distension and tenderness, bilious aspirates, and bloody stools. What complication is most likely to have developed?

A

Necrotising enterocolitis

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50
Q

What is necrotising enterocolitis?

A

Most serious abdominal complication of preterm infants
Inflammation of bowel wall which may progress to necrosis and perforation
May be localised to a section of bowel or generalised

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51
Q

How common is necrotising enterocolitis?

A

2-12% of very low birth weight infants
Incidence decreases with gestational age, onset usually at 1-4 weeks of age (peak incidence at 29-31 weeks corrected)
Occasionally occurs in term infants, usually days after a hypoxic-ischaemic insult

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52
Q

What is the prognosis of NEC?

A

15-25% mortality rate

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53
Q

What can increase a baby’s risk of getting NEC?

A 
Prematurity
IUGR and perinatal asphyxia
PDA
Severe anaemia
Blood transfusion
Postnatal asphyxia
Formula feeds
Hyperosmolar feeds
Rapid increase of enteral feeds > 30mls/kg/day
Antibiotics
Other infection
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54
Q

What does the AXR of NEC look like?

A 
Dilated bowel loops
Thickened intestinal wall
Intramural air (pneumotosis intestinalis)
Air in portal venous system
Pneumoperitoneum
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55
Q

How is NEC managed?

A

Stop feeds
NG//OG to decompress
Broad spectrum abx - amoxicillin, gentamicin, metronidazole
Supportive care
Surgical intervention if perforation/deterioration despite conservative treatment

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56
Q

What are the survival rates for preterm babies?

A 
< 22 weeks close to 0
22 weeks 10% change survival
24 weeks 60%
27 weeks 89%
31 weeks 95%
34 weeks equivalent to baby born at term
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57
Q

What are the long-term health outcomes for preterm babies?

A

1 in 10 will have permanent disability such as lung disease, cerebral palsy, blindness, or deafness
1 in 2 born before 26 weeks will have some sort of disability including mild disability like wearing glasses
Higher incidence of behavioural and psychomotor difficulties eg ADHD, motor and coordination impairment
More hospital admissions - the lower the birthweight the more

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58
Q

What 3 bloods would you do to check for haemolysis or risk of haemolysis?

A

FBC + blood film - checks for haemolysis
Direct Coomb’s test/direct antiglobulin test - checks for antibodies against RBCs
Neonatal split bilirubin - guides treatment

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59
Q

What enzyme conjugates bilirubin in the liver?

A

Uridine 5-diphospho-glycoyronyl transferase

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60
Q

What type of jaundice is most common in babies?

A

Unconjugates

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61
Q

How common is jaundice?

A

60% term babies in 1st week
80% preterm babies in 1st week
10% breast-fed babies at 1 month

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62
Q

Why do babies get jaundice?

A 
Polycythaemia
Shorter life span of HbF
Immaturation of UDPGT
Low intrahepatic binding proteins
High beta-glycuronidase in small bowel brush border (reverses conjugation)
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63
Q

When do we worry about jaundice?

A

Too early < 24 hrs
Too high levels
Prolonged > 14 days

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64
Q

What is the major complication we are trying to prevent by treating bilirubin levels that are too high?

A

Kernicterus

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65
Q

What are the S&S of kernicterus?

A

Poor feeding, absent reflexes, seizures, learning disability, movement disorders, hearing loss, opisthotonus

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66
Q

What happens in kernicterus?

A

Deposition especially in brain stem and basal ganglia
Bilirubin exceeds albumin binding capacity
Lipid-soluble, crossed BBB
Irreversible

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67
Q

What can cause early (<24 hours) jaundice?

A

Haemolysis
- ABO incompatibility
- Rhesus disease
- Red cell enzyme deficiency eg G6PD deficiency
- Red cell membrane defect eg spherocytosis
Sepsis
Bruising

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68
Q

What can cause mid-term jaundice?

A 
Breast milk jaundice
Enclosed bleeding - cephalohaematoma
Haemolysis
Sepsis
Hypothyroidism
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69
Q

What can cause prolonged jaundice?

A

Hepatic enzyme defects
- Gilbert syndrome (reduced UDPGT activity)
- Crigler-Najjar syndrome (no/partial UDPGT enzyme)
Inborn errors of metabolism eg galactosaemia
Hypothyroidism

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70
Q

How is unconjugated jaundice treated?

A

Phototherapy
Exchange transfusion
IV immunoglobulin as adjunct in rhesus or ABO incompatibility disease if prolonged haemolysis and significant rise in bilirubin levels

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71
Q

How does phototherapy work?

A

Photo-oxidation adds O2 to unconjugated bilirubin so it dissolves easily in water

72
Q

What S&S would you get in conjugated bilirubinaemia?

A

Pale stools

Dark urine

73
Q

What significant condition should you rule out with conjugated bilirubinaemia?

A

Biliary atresia

74
Q

What is conjugated jaundice?

A

Conjugated fraction > 25umol/L

75
Q

What can cause conjugated jaundice?

A 
Biliary tract obstruction
Sepsis
TPN
TORCH infections
Galactosaemia (initially unconjugated)
CF
76
Q

What are the TORCH infections?

A

Toxoplasmosis
Rubella
CMV
HSV

77
Q

What is early onset sepsis?

A

< 72 hours after birth

78
Q

What is late onset sepsis?

A

> 72 hours after birth

79
Q

What organism is the most common cause of early onset sepsis?

A

GBS

80
Q

What other organisms can cause early onset sepsis?

A 
MRSA
Listeria
E coli
H influenzae
Candida
Chlamydia
HSV
81
Q

Why do babies get early onset sepsis?

A

Infant exposed to bacteria from maternal ascending infection or during passage through birth canal

82
Q

What increases the risk of early onset sepsis?

A

Prolonged rupture or membranes (> 24 hrs in term, > 18 hrs in preterm)
Maternal GBS colonisation (high vaginal swab or in urine)
Maternal sepsis or chorioamnionitis (temp > 38, leucocytosis, tender uterus, offensive liquor)
Previous infant with GBS sepsis
Suspected or confirmed sepsis in co-twin/triplet
Spontaneous preterm labour < 37 weeks

83
Q

Name a GBS

A

Streptococcus agalactiae

84
Q

How common is GBS sepsis?

A

Fatality rate 6% in term infants, up to 20% in pre-term
Colonisation rate 21% pregnant women
< 1% colonised women will have babies with GBS sepsis
0.5 per 1000 live births
Universal screening of all pregnant women
If +ve prophylactic antibiotics between 35 and 37 weeks

85
Q

How is sepsis treated?

A

Benzylpenicillin + gentamicin IV
If suspect listeria + amoxicillin/ampicillin
If meningitis cefotaxime + amoxicillin/ampicillin (for listeria)

86
Q

How is sepsis screened for?

A

FBC, CRP, blood cultures

  • 2x CRP < 20 and blood cultures negative at 36 hrs stop abx
  • If CRP > 40 min 5 days abx + LP
  • CRP 20-40 depends on cultures and judgement
87
Q

Why do babies get late onset sepsis?

A

Tends to be acquired from environment or caregivers
GBS still commonest cause - more associated with meningitis, causes recurrent infections in 1%
Coagulase negative staphylococcus commonest cause in very low birth weight infants - produces biofilm that facilitates adherence to lines and catheters
Treatment with antibiotics according to protocol and cultures
Typically vanc if CONS

88
Q

How common is HSV infection?

A

2-3 per 100,000 live births but most serious infection
25-60% risk if mum had primary infection at delivery
Risk low in recurrent HSV infection or if primary infection happened well before delivery

89
Q

What are the 3 types of HSV infection presentation?

A

Localised - usually skin vesicular rash, or mouth lesions or conjuntivitis
Encephalitis - 10-15% mortality
Systemic - presents at 10-12 days with resp failure, shock, and deranged clotting, mortality up to 50%, high neurodisability rate amongst survivors

90
Q

How is HSV infection treated?

A

IV acyclovir
CSF and blood PCR to rule out
Treat infants born by vaginal delivery with primary HSV infection at time of delivery
If c-section observe w/o active treatment

91
Q

What is the definition of hypoglycaemia in neonates?

A

< 2.6mmol/L

92
Q

Why do neonates get hypoglycaemia?

A

Physiological phenomena
Foetus doesn’t make glucose from glycogen - dependent on placental glucose
Takes some hours for gluconeogenesis to switch on
Liver stores of glycogen only sufficient for a few hours of fasting
Unlike adults, lactate and ketones are utilised by brain readily and fuel is stored in astrocytes
Healthy term neonates don’t develop symptomatic hypoglycaemia

93
Q

What are the symptoms of hypoglycaemia?

A 
Poor feeding and/or vomiting
Apnoea
Hypothermia
Jitteriness, grunting, irritability
Bluish or pale skin
Lethargy
Tremors or seizures
94
Q

What can increase the risk of neonatal hypoglycaemia?

A 
Maternal DM - transient hyperinsulinaemia due to exposure to high levels of insulin in utero
Preterm
Infection/sick infant
Adrenal insufficiency
Glucagon deficiency
Panhypopituitarism
GH deficiency
Congenital hyperinsulinaemia
Inborn errors of metabolism
95
Q

What are the potential consequences of neonatal hypoglycaemia?

A

Blood glucose < 1.0 mmol/L persistent beyond 1-2 hours associated with acute neurological dysfunction and presents the greatest risk for cerebral injury
Wide spectrum of cerebral injury associated but predominantly posterior pattern

96
Q

How do you manage infants at risk of hypoglycaemia?

A

Early energy provision - early feeding within 1hr after birth
Blood glucose monitoring - pre-feed measurements, discontinue if 2 readings > 2mmol/L
Maintain energy provision - max 3hrly feed interval, initiate IV dextrose if unable to feed
Buccal glucogel if BM between 1.0 and 2.0 + top up feeds/decrease interval ect

97
Q

What to do if BM < 1.0 or the baby has significant clinical signs?

A

Take bloods but don’t wait for results
Bolus IV 10% dextrose 2.5ml/kg repeat if necessary
Commence IV 10% dextrose infusion at appropriate rate for gestation and age
Consider IV/IM glucagon if not responding to treatment
Investigate further for causes if persistently low

98
Q

How much fluids should you give to a term baby from birth to day 1?

A

50-60ml/kg/day

99
Q

How much fluids should you give a term baby by day 7?

A

150ml/kg/day

100
Q

How much fluids should a preterm baby get on day 1?

A

60-70ml/kg/day

101
Q

How much fluids should a preterm baby get by day 7?

A

Up to 180ml/kg/day

102
Q

Why is it important to consider fluid choice in neonates?

A

Immature renal function
Limited ability to handle solute load in fluids
Immature renin-angiotensin mechanism

103
Q

What is the fluid of choice in neonates?

A

10% dextrose with Na, K, Cl as needed

104
Q

How much fluids should a term baby get on day 2?

A

70-80ml/kg/day

105
Q

How much fluids should a term baby get on day 3?

A

80-100ml/kg/day

106
Q

How much fluids should a term baby get on day 4?

A

100-120ml/kg/day

107
Q

How much fluids should a term baby get on day 5?

A

120-150ml/kg/day

108
Q

What is normal in terms of neonatal weight loss?

A

Lose 10% of birth weight in first week of life

109
Q

Why do babies lose weight?

A

Physiological contraction of extracellular water volume and catabolism secondary to low calories intake initially

110
Q

When should a baby have regained the weight lost?

A

2 weeks

111
Q

What happens if baby has lost more than 10%?

A

Hypernatraemic dehydration

112
Q

What is the average weight gain of a baby during the first 6 months of life?

A

30g per day
Doubled by 4-5 months
Trebled by 1 year

113
Q

How much should a 1 year old weigh roughly?

A

10kg

114
Q

How long are you recommended to breast feed for?

A

Exclusively for 6 months

Ongoing + solid food until 2 years

115
Q

Why is breast best?

A

Reduction in infections, particularly gastroenteritis and otitis media and to some extent LRTIs
Reduction in eczema
Reduction in CVD in adulthood
Reduction in obesity
Reduced risk of NEC in preterm babies
Protective against SIDS but could be due to maternal education, socio-economic factors, and birth weight

116
Q

What are the benefits to mum in breast feeding?

A

Lowers risk of breast and ovarian cancer
Lowers risk of osteoporosis
Lowers risk of CVD and obesity
Promotes bonding with baby

117
Q

How common is meconium aspiration syndrome?

A

Meconium-stained amniotic fluid occurs in 13% of all delivery, only small proportion of those will develop MAS

118
Q

What happens in meconium aspiration syndrome?

A

Airways obstruction + air trapping + pulmonary parenchymal injury + inflammatory cascade

119
Q

What is the prognosis of meconium aspiration syndrome?

A

30-60% will require mechanical ventilation
10-25% will develop pneumothorax
2-5% will diet

120
Q

How are babies with thick meconium at birth treated?

A 
Mec obs for 12 hours
If well discharge
Provide resp support
Prevent air leaks using newer styles of ventilation
Treatment of PPHN
121
Q

What is persistent pulmonary hypertension of the newborn?

A

Pulmonary vascular resistance should fall rapidly after birth
If this doesn’t happen get PPHN

122
Q

What happens in PPHN?

A

Right to left shunting of blood through foramen ovale and ductus arteriosus leading to hypoxaemia

123
Q

What are the symptoms of PPHN?

A 
Hypoxia
Hypercarbia
Acidosis 
Due to vasoconstriction and elevated pulmonary pressure
Vicious cycle
124
Q

What can PPHN be secondary to?

A

Asphyxiation
Meconium aspiration
Sepsis/pneumonia
Rarely - primary pulmonary/cardiac abnormalities eg pulmonary hypoplasia, congenital diaphragmatic hernia, congenital pulmonary airway malformations, left ventricular outflow tract obstruction

125
Q

How is PPHN treated?

A

Mechanical ventilation + other supportive measures
Inhaled nitric oxide (vasodilator)
Extracorporeal membrane oxygenation if inadequate response to above measures

126
Q

What can cause neonatal encephalopathy?

A

Hypoxic-ischaemia encephalopathy
Infection - sepsis, meningitis, encephalitis
Trauma and haemorrhage - subgaleal, extradural, subdural haematoma
Metabolic - non-ketotic hyperglycinaemia, mitochondral myopathies, aminoacidaemias
Neuronal migration defects - lissencephaly
Congenital myotonia - myasthenia gravis, peroxismal disorders, Prada-Willi
Neonatal stroke

127
Q

How common is hypoxic-ischaemia encephalopathy?

A

2-5 per 1000 live births

128
Q

How does hypoxic-ischaemic encephalopathy present?

A

Variable presentation - level of consciousness, tone, posture, reflexes, suck, HR, seizures

129
Q

What can cause hypoxic-ischaemic encephalopathy?

A

Decreased umbilical flow eg cord prolapse
Decreased placental gas exchange eg placental abruption
Decreased maternal placental perfusion
Maternal hypoxia
Inadequate postnatal CPR

130
Q

How is hypoxic-ischaemic encephalopathy treated?

A

Resuscitation if needed, supportive treatment
Rule out infections or metabolic disturbances as causes
Start cerebral function analysis monitoring - like EEG
Mild fluid restriction initially - omit milk feeds for 1-2 days if severe, then reintroduce slowly
Therapeutic hypothermia - mainly in moderate or severe, within 6 hours of insult

131
Q

What non-modifiable risk factors can mean a premature baby is more likely to die?

A

Beginning of gestational week
Foetal growth restriction
Male
Multiple pregnancy babies

132
Q

What is the survival rate pre-23 weeks gestation?

A

30% at best

133
Q

How can you reduce risk of death if mothers waters break early?

A

Steroids - 12mg betamethasone 2 doses 24 hours apart up to 24 hours before delivery

134
Q

When might you repeat steroid doses?

A

Several weeks later if baby remains in utero

135
Q

What might you also give with steroids?

A

MgSO4 as neuroprotection 30% risk reduction in 24 hours before birth

136
Q

What is the role a neonatal doctor?

A 
Social issues
Trivial problems
Everything involving babies before they go home
Critically sick babies
Long term survival issues
137
Q

How common is admission for neonatal care?

A

Approx 10% of newborns require admission for neonatal care

Only 3% of newborns require full intensive care

138
Q

How common is prematurity?

A

5-6% born between 32-36 weeks gestation
1% born between 28-31 weeks gestation
0.5% 20-27 weeks gestation

139
Q

What adaptations need to be made to ex-utero life?

A 
Neurological
Cutaneous
Respiratory
CVS
GI
Immunological
Haematological
Endocrine
MSK
Sensory
140
Q

What neurological adaptations need to occur?

A

Control of own movements
Thermoregulation
Feeding

141
Q

What respiratory adaptations need to occur?

A

Lungs filled with air
Surfactant released
Gas exchange

142
Q

What CVS adaptations need to occur?

A 
Closure of foetal shunts
Perfusion of lungs
Fall in pulmonary artery pressure
Increased in systemic BP
Increased in cardiac output
Foetal lung fluid removed
143
Q

What immunological adaptations need to occur?

A

Immunocompetence

144
Q

What haematological adaptations need to occur?

A

Conversion to adult haemoglobin

145
Q

What happens during growth in utero?

A

Implantation - weeks 1-2 following missed period
Embryo - up to 8/9 weeks, by the end of this stage you are fully formed
Foetus
- 12 to 16 weeks movement felt by mother
- All systems present and functioning to varying degrees
- Each system is growing and developing further
- Last 4 to 6 weeks virtually all growth, mainly fat

146
Q

What counts as very low birth weight?

A

< 1500g

147
Q

What counts as extremely low birth weight?

A

< 1000g

148
Q

What counts as incredibly low birth weight?

A

< 750g

149
Q

What are premature babies lacking in the respiratory system?

A

Surfactant - retained in type 2 pneumocytes

Alveoli - absent at 24 weeks then exponential increase towards term

150
Q

What is the most common mode of death in premature babies?

A

Respiratory failure

151
Q

What makes lung damage in premature babies worse?

A

O2
Sepsis
Ventilation

152
Q

What is chronic lung disease of prematurity?

A 
Needing O2 at 36 weeks corrected age
Reduced lung volume
Reduced alveolar surface area
Diffusion defect
Increased mortality
153
Q

What is the prognosis of chronic lung disease of prematurity?

A

40% stage IV
Post discharge 7% especially is discharged on O2
SIDS rate increased x7

154
Q

What is the readmission rate in babies with chronic lung disease of prematurity?

A

50% in first year
20% in second
Average of 5 admission in first 2 years

155
Q

What happens in the brain when you are premature?

A 
Still developing brain cells
Brain cells still migrating
Not made all synapses yet
Brain stem not myelinated until 34/35 weeks - breathing and CVS problems
Changes in cerebral blood flow
Changes in O2 and CO2 levels
156
Q

What is apnoea of prematurity?

A

Brain stem not fully myelinated until 32-34 weeks
Forget to breathe, bradycardia associated
Made worse by sepsis

157
Q

How is apnoea of prematurity treated?

A

Physical - NCPAP, stimulation

Drugs - caffeine (equivalent to 10 espresso)

158
Q

How common are ventricular haemorrhages?

A

80% babies < 32 weeks have normal scan
14% have small bleeds
Worrying as can have not enough blood to perfuse rest of body

159
Q

How common is cystits periventricular leukomalacia?

A

5% < 32 weeks

160
Q

What are the risks of prematurity later in life?

A

More likely to die
More likely to be admitted to neonatal unit
More likely to have moderate/severe handicaps
Lower birth weight = more likely to have increased need for special schooling/learning support

161
Q

What are the infant benefits of breast feeding?

A 
Less infection - diarrhoea, otitis media, RSV, respiratory infection, enhanced vaccine response
Less immune driven/allergic disease - wheezing, childhood cancer, eczema, Hodgkin's disease, MS, Crohn's, DM
Enhanced immunological development
Reduced risk of NEC
Reduced risk of SIDS
Reduced GOR
Lower risk of childhood inguinal hernia
Higher IQ
Better cognitive development
By far the best
162
Q

What are the maternal benefits of breast feeding?

A 
Reduces cancer risk for breast, uterine, ovarian and endormetrial cancers
Improved health with less postpartum haemorrhage, postnatal depression, decreased insulin requirements in diabetics, osteoporosis later in life reduced, less child abuse
Promotes post-partum weight loss
Optimum child spacing
Less food expense
Less medical expense
More ecological
Delays fertility
163
Q

What is the problem with breast feeding and premature infants?

A

Require support with IV fluids/parenteral nutrition
Start small volumes of expressed breast milk
Steadily build to full feeds
Monitor growth
Suck and swallow starts from 32-34 weeks

164
Q

What happens with high levels of unconjugated bilirubin?

A

Kernicterus

165
Q

Why do babies get unconjugated jaundice?

A 
Haemolysis
Prematurity
Sepsis
Dehydration
Hypothyroid
Metabolic disease
166
Q

Are high levels of conjugated jaundice a concern?

A

No

167
Q

What can cause conjugated jaundice?

A 
Prolonged parenteral nutrition
NEC
Sepsis
Metabolic
Anatomical problems
168
Q

When would you investigate jaundice in term babies?

A

> 2 weeks

169
Q

When would you investigate jaundice in preterm babies?

A

> 3 weeks

170
Q

Why are preterm babies more likely to get sepsis?

A

Last 3 month of gestation active IgG transfer
The more premature you are the less of this you get
Cell mediated immunity less active
Multiple invasive procedures
Plastic tubes not patrolled by immune system
Infection with organisms that are not normally pathogenic - GBS, pseudomonas, coagulase negative staph
Bacteria that are pathogenic
Fungal sepsis due to needing lots of antibiotics and poor immune function

171
Q

Why do preterm babies get retinopathy of prematurity?

A 
Hyperoxic insult due to lots of O2
Arrest of normal vascular growth
Fibrous ridge forms
Vascular proliferation
Retinal haemorrhages
Retinal detachment
Blindness
172
Q

How can retinopathy of the newborn be treated?

A

Laser therapy

173
Q

What support can be given to parents of preterm babies?

A 
Antenatal counselling
Post-delivery counselling
Prognostic counselling
Regular updates
Palliative counselling
Bereavement counselling
174
Q

What is important with the law and preterm babies?

A

Duty of care to treat patients
Parents wishes are paramount but cannot force you to administer therapy that you believe is ineffective
Forcing treatment upon someone could be assault
May want to treat when the parents don’t wish the same

175
Q

When is surfactant produced?

A

Between 24 and 28 weeks

176
Q

When else might babies develop respiratory distress syndrome if not premature?

A

Mother has diabetes
Baby underweight
Baby’s lungs not developed properly

Paediatrics (21 decks)

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