Respiratory distress in newborn Flashcards

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1
Q

What is RDS in the Newborn?

A

Deficiency of alveolar surfactant, commonest in premature infants (mature cause of preterm infant death)
Insufficient surfactant causes atelectasis; reinflation with each breath exhausts baby and respiratory failure follows

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2
Q

What complications are associated with RDS?

A

Hypoxia leads to :

  • Decreased CO
  • HNT
  • Acidosis
  • Renal failure
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3
Q

What factors increase the risk of RDS?

A
91% risk if 23-25w; 52% risk if 30-35w
Maternal diabetes
Males
Second twin
Caesareans
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4
Q

What signs are associated with RDS?

A

Tachypnoea >60 breath/min
Laboured breathing, chest wall recession (sternal/subcostal indrawing)/nasal flaring
Expiratory grunting
Cyanosis (if severe)

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5
Q

What should be performed in infants with suspected RDS?

A

HR/RR monitoring on NICU
CXR (cause identification)
Non invasive respiratory support (adjuvant 02, CPAP)

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6
Q

What are the causes of RDS?

A
Common
-Transient tachypnoea of the newborn
Less common 
-Meconium aspiration
-Congenital pneumonia (GBS)
-RDS
-Pneumothorax (air leak)
-Persistent pulmonary HNT of the newborn
-Milk aspiration
Rare
-Diaphragmatic hernias
-TOF
-Pulmonary hypoplasia
-Airway obstruction (e.g. choanal atresia)
Non-respiratory problems
-Congenital heart disease
-Hypoxic ischaemic injury/neonatal encephalopathy
-Severe anaemia
-Metabolic acidosis
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7
Q

What can be given to prevent respiratory distress?

A

Betamethasone or dexamethasone for all women at risk of preterm birth 23-35w
High risk mothers should be managed at specialist centres

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8
Q

What is TTN?

A

Transient tachypnoea of the newborn
Most common cause respiratory distress in term infants with mature lungs
Caused by delay in resorption of lung liquid (delayed clearance of lung fluid)
More common after CS birth

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9
Q

When does TTN classically onset?

A

1-3hrs after birth (may take several days to resolve completely)

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10
Q

How is TTN diagnosed?

A

Inc working of breathing in term infant

On CXR - coarse streaking and fluid in interlobar fissures (wet lung)

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11
Q

How is TTN managed?

A
Suspect and treat infection
Respiratory support
-stop feeds
-02
-nasal CPAP
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12
Q

What is meconium aspiration syndrome?

A

MAS is aspiration of meconium, often in response to foetal hypoxia or distress. This is accompanied by gasping and aspiration of meconium into lungs.
Meconium acts as a pleural irritant, causing:
-mechanical airway obstruction
-chemical pneumonitis
-surfactant inactivation/dysfunction
-predisposition to infection

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13
Q

How is MAS diagnosed?

A

Presence of meconium in liquor
CXR
-hyperinflation of lungs with coarse streaking/patchy consolidation
-pneumothorax, pneumomediastinum and pneumonia commonly follow due to high chance of air leak

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14
Q

How is MAS managed?

A

Mechanical ventilation often required
Intrapartum suction makes no difference to outcomes, neither does cricoid/chest compression at birth
Surfactant, inhaled NO2, abx may be helpful

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15
Q

What can MAS progress to?

A

Persistent pulmonary HNT of newborn (difficult to achieve adequate oxygenation despite high pressure ventilation)
Severe MAS associated with significant morbidity and mortality

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16
Q

What is congenital pneumonia associated with?

A
PROM (>18-24hrs)
Septicaemia, esp GBS
Chorioamnionitis
Low birthweight
Can occur at any gestation
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17
Q

How is congenital pneumonia diagnosed?

A

Can mimic RDS (similar clinical presentation/identical CXR appearance)
Delayed onset (24-48hrs)
May be associated with shock sepsis
Always suspect infection

18
Q

How is congenital pneumonia managed?

A
Intrapartum abx (prevention of GBS transmission)
Broad spectrum abx (penicillin and aminoglycosides)
19
Q

What is an air leak?

A
Alveolar rupture (can be spontaneous or complication of respiratory illness e.g. RDS, MAS, congenital pneumonia etc)
Can also be complication of treatment e.g. positive pressure ventilation, CPAP
Pneumothorax may occur spontaneously in 2% deliveries
20
Q

How can an air leak be diagnosed?

A

CXR

Transillumination of thorax

21
Q

How is an air leak managed?

A

Decompression (chest drain) if tensioning

Low level ventilation for prevention

22
Q

When does milk aspiration occur?

A

Preterm infants and those with RDS or neurological damage
Bronchopulmonary dysplasia (as babies have GORD, predisposing aspiration)
Cleft palate babies prone to aspiration

23
Q

What is persistent pulmonary HNT of newborn?

A

PPHN occurs due to right-to-left shunting within lungs and at atrial and ductal levels, due to high pulmonary vascular resistance

24
Q

What is PPHN associated with?

A
Birth asphyxia
MAS 
RDS 
Septicaemia
May be primary disorder
25
Q

How is PPHN diagnosed?

A

Infants cyanotic soon after birth
CXR - heart normal, pulmonary oligaemia (Westermark sign, dilation of pulmonary vessels)
Echocardiogram - exclude congenital heart disease, look for signs of pulmonary HNT

26
Q

How is PPHN managed?

A

Mechanical ventilation and circulatory support
Inhaled NO2 (vasodilation)
Sildenafil may be used
Extracorporeal membrane oxygenation (ECMO), but only performed in specialist centres

27
Q

How common is diaphragmatic hernia?

A

1 in 4000 births

28
Q

How does diaphragmatic hernia present?

A

Failure to respond to resuscitation
RDS
Mainly diagnosed on antenatal USS (left sided herniation through posterolateral foramen of diaphragm)

29
Q

How is diaphragmatic hernia diagnosed?

A

Apex beat and HS often displaced to right side of chest
Poor air entry on left side
CXR and AXR confirm diagnosis

30
Q

How is diaphragmatic hernia managed?

A

Vigorous resuscitation may cause pneumothorax in normal lung
Large NG tube passed and suction applied (stops distension of intrathoracic bowel)
Can be repaired surgically once stabilised

31
Q

What is the main complication with diaphragmatic hernia?

A

Pulmonary hypoplasia secondary to compression by herniated viscera
If the lungs are hypoplastic, mortality is high

32
Q

What other upper airway problems can cause respiratory distress?

A
Laryngomalacia
Mechanical obstruction
-Haemangioma
-Granuloma from trauma (e.g. ET suction)
-Sub-glottic stenosis (ETT)
Vocal cord palsy
33
Q

How can RDS be managed?

A

Establish lung volume
-ventilation
-nasal CPAP
Surfactant therapy

34
Q

How can respiratory distress be managed broadly?

A

Delay cord clamping (promote placenta-foetal transfusion)
Give 02 (but consult senior if HR not improving)
Attach oximeter (85% normal in first 5-10mins life, but if remain low increase 02 by 10% each minute until sats increase)
If spontaneously breathing, attach CPAP
If <26w, give endotracheal prophylactic surfactant (and intubate) +/- 2 doses 02
Aim for sats 85-93% to reduce risk of bronchodysplasia and retinopathy of prematurity
Give fluids and inositol (essential for promoting maturity of surfactant and in early neonatal development) - also helps prevent IVH and bronchopulmonary dysplasia

35
Q

What should be checked if baby with RDS continues to decline?

A
DOPE
Displaced ETT
Obstructions (secretion, blood)
Pneumothorax
Equipment failure (ventilator, tubing)
36
Q

What are the markers of poor prognosis in RDS?

A

Deterioration despite full management implemented

Parental counselling advised

37
Q

What is bronchopulmonary dysplasia?

A

BPD is a complication for ventilating babies with RDS who are <1kg
Persistent hypoxia +/- difficult ventilatory weaning

38
Q

What causes BPD?

A

Mainly from barotrauma (damage from high pressures) and oxygen toxicity
Surfactant-related BPD is multifactorial, with airway infection causing inflammatory cascades
May be oxidative causes (but role of anti-oxidants unproven)

39
Q

What Ix are used for BPD?

A

CXR - hyperinflation, rounded radiolucent areas with thin denser lines
Histology - necrotising bronchiolitis with alveolar fibrosis

40
Q

What are the sequelae of BPD?

A

Early
-Feeding problems (02 desaturation during feeds, severe RSV bronchiolitis, GORD)
Late
-Decreased IQ
-CP
-By adolescence/early adulthood, main challenges are asthma and exercise limitation

41
Q

How can BPD be prevented?

A

Steroids (antenatal and postnatal)
Surfactant
‘Suitably high’ calorific feeding

42
Q

When might pulmonary hypoplasia be suspected?

A

Persisting neonatal tachypnoea +/- feeding difficulties, prenatal oligohydramnios e.g. Potter’s syndrome or PROM
Very rare
May be consequence of diaphragmatic hernia and cystic adenomatoid malformations
Normally detected on foetal anomaly scan