Neonatal Respiratory Distress

Front 1

Clinical signs of respiratory distress in a newborn infant

Back 1

Tachypnoea > 60bpm
Grunting (due to expiration against a partially closed glottis)
Intercostal, subcostal recession due to the use of accessory mm
Cyanosis
Nasal flaring

Front 2

Common causes of neonatal respiratory distress

Back 2

Hylaine membrane disease
Transient tachypnoea of the newborn
Meconium aspiration
Pneumonia
Pneumothorax
Pulmonary haemorrhage

Front 3

What is a tracheo-oeophageal fistula

Back 3

congenital malformation of oesophagus and trachea

Front 4

Clinical features of a TOF

Back 4

Polyhydramnios
Excess mucosy secretions from mouth following birth
Cyanosis with feeds, respiratory distress, recurrent pneumonia, (reflux of gastric contents into lungs)
May present after 3 months (if no oesophageal atresia) with coughing, gagging, vomiting
Associtaed with VACTERL syndrome

Front 5

What changes are seen on CXR of TOF

Back 5

blind upper oesophageal pouch
If there is a fistula - gas in intestines

Front 6

Management of TOF

Back 6

Multiple end-hole catheter into upper oesophageal pouch with continuous or intermittent suction of secretions
Nurse in semi-upright position
Avoid mechanical ventilation if possible (potential gastric rupture)
surgery -

Front 7

Complications with TOF

Back 7

Pneumonia, sepsis, reactive airways disease
Following repair: oesophageal stenosis and strictures at repair site, GORD, poor swallowing (dysphagia and regurgitation)

Front 8

How common is TTN

Back 8

1-2% of newborns

Front 9

Pathophysiology of TTN

Back 9

Delayed resorption of fetal lung fluid --> accumulation of fluid in peribronchial lymphatics and vascular spaces --> tachypnoea

Front 10

Risk Factors of TTN

Back 10

CS (lungs are not compressed during passage through pelvic floor)
absence of labour/short labour
mild prematurity
diabetic mother

Front 11

Clinical features of transient tachypnoea of the newborn

Back 11

Tachypnoea from birth
Mild retractions, grunting, nasal flaring, without signs of severe resp distress
Resolution within 48 hours

Front 12

Appearance on CXR of TTN

Back 12

Pulmonary venous congestion (peri-hilar structures)
Fluid in plural fissures
May have blunting of costophrenic angles

Front 13

How common is hylaine membrane disease

Back 13

1% of all newborns
80% 30 weeks
20% 34 weeks
Occasionally seen 36-38 weeks

Front 14

Pathogenesis HMD

Back 14

Deficiency of surfactant
Normally produced by type II cells
No surfactant --> high surface tension and inward pulling pressure --> alveoli collapse (atelectasis) and overexpansion of other alveoli (due to high pressure to open alveoli) --> decreased surface area for gas exchange --> hypoxia and acidosis --> respiratory distress

Front 15

Predisposing factors of HMD

Back 15

Prematurity
poor steroid administration
low birth weight
hypoxia and acidosis --> may give secondary surfactant deficiency
maternal diabetes
More common following CS

Front 16

Clinical features of HMD

Back 16

Respiratory distress within 6 hours worsens over 24-72 hours
Grunt as infant breathes out against a closed glottis to keep alveoli distended (ie tries to produce own CPAP)
Fluid retention
Resolution as baby produces its own surfactant

Front 17

CXR features of HMD

Back 17

diffuse fine granular homogenous (ground glass)
+ air bronchograms
Due to fine atelectasis (alveolar)

Front 18

Treatment of HMD

Back 18

Supportive O2, assisted ventilation (CPAP, intubation and mechanical ventilation)
administer fluids cautiously to avoid pulmonary oedema
Endotracheal surfactant administration

Front 19

Complications of HMD

Back 19

Pneumothorax
IVH
Chronic lung disease (Bronchopulmonary dysplasia)

Front 20

How common is meconium aspiration syndrome

Back 20

10% of infants at birth have meconium stained liquor
only a small % will develop meconium aspiration

Front 21

Pathogenesis of MAS

Back 21

Often pre-existing physiological stress (e.g., poor placental blood flow) and more common in postterm neonates (increased physiological passage of meconium and perinatal stress)
Fetal distress or asphyxia --> meconium
fetal distress --> "breathing" movements antenatally or during delivery - inhalation of meconium --> plugging of airways (atelectasis) with over distension of other airways -> generalised over distension and chemical inflamamtion
Secondary surfactant deficiency
May be associated with persistent pulmonary hypertension
May develop secondary infection

Front 22

Risk factors for MAS

Back 22

Fetal distress in utero
Pre-existing physiological stress - poor placental blood flow, IUGR
post term infant (increased physiological passage of meconium and increased risk of perinatal stress)
Associated with persistent pulmonary hypertension

Front 23

Clinical features of MAS

Back 23

respiratory distress within hours of birth - perinatal asphyxia is common
meconium at birth
chest hyperinflated
severe hypoxaemia with persistent pulmonary hypertension

Front 24

CXR of MAS

Back 24

Coarse, fluffy, irregular
major areas of bronchi atelectasis (meconium plugs)
excessive over inflation

Front 25

Prevention of MAS

Back 25

Delivery babies at < 40+10
Identify babies at risk (IUGR, fetal distress, meconium stained liquor) and provide suction and resusctation after delivery

Front 26

Management of MAS

Back 26

Supportive care
Assisted ventilation
+/- NO for PPHN
+/- Antibiotics for infection
Surfactant replacement (surfactant function is inhibited by presence of meconium)

Front 27

What are the most common organisms in neonatal pneumonia?

Back 27

Group B beta haemolytic strep
E. Coli
HIB
Listeria monocytogenes
May be acquired as an ascending infection from the genital tract or in utero via transplacental passage from mother with bacteraemia

Front 28

Predisposing factors to neonatal pneumonia

Back 28

ruptured membranes
chorioamniotis
GBS colonisation
gram negative organisms

Front 29

Clinical features of neonatal pneumonia

Back 29

Nonspecific: lethargy, apnoea, bradycardia, temperature instability, feed intolerance

Front 30

CXR appearance of neonatal pneumonia

Back 30

May show consolidation or may have generalised changes and look like HMD

Front 31

Prevention of neonatal pneumonia

Back 31

Identify mothers with GBS
Give antibiotics during delivery

Front 32

Management of neonatal pneumonia

Back 32

GBS - penicillin or ampicillin
gram -ve - gentamicin
Give both penicillin and gent if symptomatic
O2, assisted ventilation, volume expansion, inotropic drugs

Front 33

How common is pneumothorax in neonates

Back 33

1%

Front 34

Pathogenesis of pneumothorax in neonates

Back 34

Direct alveolar rupture due to barotrauma
May be spontaneous

Front 35

RF for pneumothorax in neonates

Back 35

Hypoplastic lungs - oligohydramnios
Stiff lungs or collapsed lungs - HMD
Positive pressure ventilation
hyperinflated lungs - MAS

Front 36

Clinical features of pneumothorax

Back 36

Acute deterioration in a baby with respiratory distress or acute onset of respiratory distress in a baby who is otherwise well
OR sudden deterioration (inc. hypotension) in a ventilated baby
Cyanosis, bradycardia, poor peripheral perfusion

Front 37

Treatment of neonatal pneumothorax

Back 37

Insertion of tube or catheter into pleural space

Front 38

Pathophysiology of persistent pulmonary hypertension of newborn

Back 38

Due to persistence of fetal circulation as a result of persistent elevation of pulmonary vascular resistance
R - L shunt through PDA, foramen ovale, intrapulmonary channels --. decreased pulmonary blood flow and hypoxaemia --> further pulmonary vasoconstriction

Front 39

RF for PPHN
secondary - RF
primary - absence of RF

Back 39

asphyxia
MAS
RDS
sepsis
Structural abnormalities (diaphgramgatic hernia, pulmonary hypoplasia)

Front 40

Clinical features of PPHN

Back 40

Usually a term or near term infant
poor oxygenation despite high ox/ventilator settings
post-ductal O2 lower than pre-ductal O2

Front 41

Investigations in PPHN

Back 41

pre and post ductal O2
ECHO - increased pulmonary artery pressure and a R-L shunt

Front 42

Management of PPHN

Back 42

HIgh inspired O2
Mechanical ventilation (hyperventilation)
Mm relaxation
maintain alkalotic or high normal pH
NO (pulmonary vasodilator)
extracorporeal membrane oxygenation (ECMO) used in some centres

Front 43

Pathogenesis of pulmonary haemorrhage

Back 43

Usually haemorrhagic pulmonary oedema
May be secondary to coagulopathy, persist PDA, surfactant therapy, severe Rhesus isoimmunisation, asphyxia, cold injury

Front 44

Clinical features of pulmonary haemorrhage

Back 44

acute deterioration with pallor, shock, cyanosis, bradycardia,
Pink or red frothy fluid from mouth or ETT

Front 45

Appearance of CXR in pulmonary haemorrhage

Back 45

Widespread opacification of lungs

Front 46

Management of Pulmonary haemorrhage

Back 46

O2
Increased assisted ventilation with PEEP
Correct coagulopathy with FFP, vit K
correct loss of volume with blood transfusion

Front 47

How does a diagphragmatic hernia present

Back 47

respiratory distress, cyanosis
scaphoid abdomen and barrel shaped chest
affected side dull to percussion and breath sounds absent, may hear bowel sounds instead
HS shifted to contralateral side

Front 48

Describe how to cacluate an APGAR score

Back 48

1 and 5 mins post delivery
HR - > 100bpm - 2; < 100 bpm - 1; no HR - 0
RR - Regular breathing = 2; irregular = 1; none = 0
MM tone; active = 2; moderate = 1; limp = 0
Reflex irritability; cry = 2; whipmering = 1; silence = 0
Colour; pink = 2; blue = 1, totally blue = 0
Score < 3 = critical
7-10 = normal

Front 49

Describe the changes that occur in circulation on birth

Back 49

Cord is tied - blood flow through low resistance placenta is lost - systemic resistance increases
Fetal lungs inflate and reduce lung resistance
Foramen ovale closes
Ductus arteriosus - reverses direction and eventually closes (indomethacin can be given to make it close)
Ductus venosus closes - not sure why

Front 50

What is the difference between primary and secondary apnoea

Back 50

Primary apnoea - baby is cyanosed but HR > 100bpm, some respiratory effort
Will usually start breathing spontaneously
Secondary apnoea - baby cyanosed HR < 60bpm, no respiratory effort, baby is floppy and unresponsive

Front 51

What triggers closure of the PDA after birth

Back 51

Increase in PaO2
Changes in prostaglandin metabolism
Closes permanently within 2-3 weeks by combination of thrombosis, intimal proliferation and fibrosis

Front 52

At what age has the PDA closed

Back 52

Closes functionally 10-15 hours after birth
Closes permamentnly within 2-3 weeks

Front 53

At what age does complete closure of the ductus venosus occur

Back 53

3-7 days