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CH > Preterm Babies > Flashcards

Preterm Babies Flashcards

1
Q

What are some of the respiratory complications of prematurity?

A

RDS
Apnoea of Prematurity
Bronchopulmonary dysplasia

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2
Q

What is the primary and secondary pathology in RDS?

A

Primary: surfactant deficiency and structural immaturity

Secondary: alveolar damage, formation of exudate from leaky capillaries, inflammation, repair

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3
Q

How common is RDS?

A

75% of infants before 29wks

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4
Q

How does RDS present?

A

Shortly after birth with:

Tachypnoea 
Grunting
Intercostal recessions
Nasal flaring
Cyanosis

Worsens over mins-hrs

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5
Q

What is the clinical course of RDS?

A
  • As disease progresses, baby may develop ventilatory failure (rising CO2) and aponea
  • Clinical course 2-3days whether tx or not
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6
Q

What is the tx of RDS?

A

Maternal steroid
Surfactant
Ventilation (CPAP)

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7
Q

What does RDS look like on CXR?

A

“ground glass” appearance

Air bronchograms

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8
Q

What are the complications of RDS?

A

Pneumothorax
Lung collapse
Mediastinal shift

Chronic lung disease (O2 requirement at 28days of life)

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9
Q

What is the definition of aponea of prematurity?

A

Cessation of breathing by a premature infant that lasts >20s for is accompanied by hypoxia or bradycardia

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10
Q

What are the underlying causes of apnea of immaturity?

A

Obstructive (baby’s neck flexed)
Central (lack of resp effort)
Mixed

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11
Q

What is the pathophysiology of apnea of immaturity?

A
  • Ventilatory drive is dependent on response to increasing CO2 levels and acid in the blood.
  • Hypoxia is a secondary stimulus.
  • Responses to these stimuli are impaired in premature infants due to immaturity of specialised regions in brain that sense these changes
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12
Q

What is the tx of apnea of prematurity?

A

Caffeine

CPAP

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13
Q

How does pneumothorax in the premature infant arise and what is the tx?

A
  • In RDS air from over distended alveoli track into interstitial, results in pulmonary interstitial emphysema
  • In up to 10% infants ventilated for RDS: pneumothorax
  • Tx: chest drain for tension pneumothorax
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14
Q

What is bronchopulmonary dysplasia?

A

“chronic lung disease”

Babies still require oxygen >36wks

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15
Q

How does bronchopulmonary dysplasia arise?

A

Lung damage comes from pressure and volume trauma from artificial ventilation, oxygen toxicity and infection

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16
Q

What does a CXR show in bronchopulmonary dysplasia?

A
  • Widespread areas of opacification, sometimes with cystic changes
  • Fibrosis and lung collapse
  • Overdistension of lungs
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17
Q

What does hypothermia lead to in a premature baby?

A

Increased energy consumption
Hypoxia and hypoglycaemia
Failure to gain weight
Increased mortality

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18
Q

Why are preterm infants at an increased risk of hypothermia?

A
  1. Large S.A to vol ratio, therefore greater heat loss.
  2. Skin is thin and heat permeable so transepidermal water loss in first week of life.
  3. Little subcut fat for insulation
  4. Nursed naked and cannot conserve heat by shivering
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19
Q

How can heat loss be prevented in newborns

A
  1. CONVECTION
    - clothing, incubator
  2. RADIATION
    - cover baby, double walls for incubators
  3. EVAPORATION
    - dry and wrap at birth, place in plastic bag
  4. CONDUCTION
    - nurse on heated matress
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20
Q

What happens to the ductus arteriosus during development and at birth?

A

Development: DA kept open by vasodilator prostaglandin E2 made by placenta & DA itself.

At birth:

  • O2 levels increase, lungs become source of oxygenated blood, E2 levels fall and DA closes.
  • Lungs produce bradykinin to help close off DA (day 1)
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21
Q

What are the CV complications of prematurity?

A

PDA

Systemic hypotension

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22
Q

What is the pathophysiology of PDA?

A
  • Classed as acyanotic, however when atrial pressure increases, can result in a R–>L shunt and cyanosis in lower extremities.
  • Connection between pulmonary trunk and descending aorta.
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23
Q

What is the association with PDA?

A
  • More common in premature infants

- Associated with PDA in first trimester

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24
Q

What are the clinical signs/symptoms in PDA?

A 
Left subclavian thrill
Continuous 'machinery' murmur 
Large vol, bounding, collapsing pulse
Wide pulse pressure
Heaving apex beat
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25
Q

What does PDA lead to?

A

Symptoms of congestive heart failure

Exacerbates RDS

26
Q

What is the fluid balance in premature infants?

A

First day of life: about 60-90ml/kg needed.

Subsequent fluid vol increased by 20-30ml/kg/day to 150-180ml/kg/day

27
Q

How much does premature babies’ weight increase by?

A

At 28wks: double their weight in 6wks, treble in 12wks

28
Q

How does term babies’ weight increase?

A

Double in 4.5months, treble in one year

29
Q

What are some neurology complications of prematurity?

A

IVH

HIE

30
Q

How does IVH arise?

A

Typically bleeds occurs in the germinal matrix above the caudate nucleus which contains a fragile network of blood vessels

31
Q

What is the presentation of IVH?

A
  • Most occur within 72hrs of life

- More common following severe perinatal asphyxia and RDS.

32
Q

What is a significant risk factor for IVH?

A

Pneumothorax

33
Q

How is IVH graded?

A

Cranial US grades this according to whether it is periventricular or spreads into the ventricles/parenchyma

34
Q

What is the most severe IVH?

A

Unilateral haemorrhagic infarction involving the brain parenchyma, usually resulting in hemiplegia

35
Q

What is a major risk with IVH?

A
  • A large IVH can impair drainage and reabsorption of CSF, build up.
  • This can resolve spontaneously or progress to hydrocephalus
36
Q

What is the tx of hydrocephalus in the neonate?

A

Initially LP then shunt

37
Q

What are the greatest risks associated with IVH?

A

Hydrocephalus and cerebral palsy

38
Q

What is the clinical presentation of IVH?

A
  • Inverse relationship between gestational age and birth
  • 2 major risk factors: prematurity and RDS
  • Up to 90% occur in first 72hrs
  • 25-50% clinically silent
39
Q

What are some of the preventative measures in IVH?

A

Antenatal steroids
Prompt and appropriate resuscitation
Avoid haemodynamic instability
Avoid: hypoxia, hypercarbia, swings in BP

40
Q

What is the grading for IVH?

A

Grade 1+2:

  • Neurodevelopment delay in up to 20%
  • Mortality 10%

Grade 3+4:

  • Neurodevelopment delay in up to 80%
  • Mortality 50%
41
Q

How does HIE arise?

A
  • Due to compromise of placental or pulmonary gas exchange resulting in cardiopulmonary depression.
  • Placenta, baby (IUGR, anaemia), failure of adaptation
42
Q

What is the sequelae of HIE?

A
  • Hypoxia, hypercarbia and metabolic acidosis follow.

- Compromised cardiac output diminishes tissue perfusion casing HIE to brain and other organs

43
Q

When do symptoms of HIE arise?

A

Immediately or up to 48hrs after asphyxia

44
Q

What constitutes mild, moderate and severe HIE?

A

Mild: irritable and responds to stimulation.
Moderate: abnormalities of tone and movement, can’t feed.
Severe: no spontaneous movements or response to pain

45
Q

What is the primary and secondary cause of neuronal damage in HIE?

A

Primary: immediate from neuronal death

Secondary: delayed from reperfusion injury

46
Q

What is the tx of HIE?

A

Resp support, ionotropes, electrolytes

47
Q

What is the prognosis for HIE: mild/moderate/severe?

A

Mild: complete recovery

Moderate: if feeding well and normal neuro= good prognosis. If abnormalities, full recovery unlikely.

Severe: mortality 40%, CP 80%

48
Q

What are the complications of HIE?

A

CP, LD, epilepsy, hearing and visual impairment

49
Q

What is NEC?

A
  • One of the leading causes of death among premature infants.
  • During first few weeks of life, a portion of the bowel dies.
50
Q

NEC is more likely to develop if on cow’s milk compared to breast-feeding T/F?

A

True

51
Q

What are some of the initial symptoms of NEC?

A
  • Feeding intolerance
  • Abdominal pain
  • Distension of abdomen
  • Vomiting
  • Bloody stools
52
Q

How can NEC progress?

A
  • Can progress quickly to abdominal distension, perforation and peritonitis.
  • May require ventilation
53
Q

How does vomiting arise in NEC?

A

Baby stops tolerating feeds, milk is aspirated from the stomach and there may be vomiting which is bile stained.

54
Q

What might an AXR show in NEC?

A
  • Dilated bowel loops (asymmetrical in distribution)
  • Bowel wall oedema
  • Pneumonalis intestinalis (intramural gas)
  • Pneumoperitoneum
  • Air inside and outside bowel wall (Rigler’s sign)
  • Air outlining falciform ligament (football sign)
55
Q

What is the tx for NEC?

A
  • Stop oral feeding–>TPN
  • Broad spectrum Abx
  • Artificial and circulatory support may be needed
  • Surgery for bowel perforation
56
Q

What are some of the complications of NEC?

A
  • Significant morbidity and mortality
  • Development of strictures
  • Malabsorption if extensive bowel resection necessary
57
Q

How does Retinopathy of prematurity arise?

A
  • In utero, blood vessels grow from central retina outwards and is complete a few weeks before birth.
  • Incomplete in premature babies.
  • Blood vessels may grow and branch abnormally and bleed.
  • Band membranes formed pull up retina, causing detachment and blindness <6months.
58
Q

What is the sequelae of ROP?

A

Vascular proliferation–> retinal detachment, fibrosis and blindness

59
Q

What are the risk factors for ROP?

A
  • Prematurity
  • High exposure to O2
  • Low birth weight
  • Infections
  • Cardiac defects
60
Q

What is the tx for ROP?

A
  • At risk babies (<1.5kg or <32wks) require ophthalmology screening every week.
  • Laser tx for severe disease
61
Q

Who is at risk of severe bilateral visual impairment in ROP?

A

In 1% of v.low birthweight babies <28wks

CH (7 decks)

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