RDS Flashcards

1
Q

What causes RDS?

A

Deficiency of alveolar surfactant
This leads to atelectasis, re-inflation with each breath exhausts the baby and respiratory failure follows
Hypoxia leads to reduced cardiac output, hypotension, acidosis and renal failure

Blood gases show hypoxaemia and acidosis

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2
Q

What are signs of RDS?

A
Increased work of breathing shortly after birth (1st 4h)
Tachypnoea (>60/min RR)
Grunting
Nasal flaring
Intercostal recession
Subclavicular recessions
Tracheal tug
Cyanosis
Tachycardia >160 bpm
Hypotension
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3
Q

What is seen on CXR in RDS?

A

Diffuse granular patterns (ground glass appearance)

Air bronchograms

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4
Q

How is RDS prevented?

A

Betamethasone or dexamethasone should be offered to all women at risk of preterm delivery from 23-35 weeks
Maternal steroids help maturation of fetal lungs

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5
Q

What is management for RDS?

A

Delay clamping of cord to promote placento-fetal transfusion
Give oxygen via oxygen-air bledner
Sats of 85% are normal in first 5-10 minutes of life
IF spontaneously breathing stabilise with CPAP
If <26wks gestation, intubate and give prophylactic surfactant via ET tube
Aim SaO2 85-93% to avoid retinopathy of prematurity and bronchopulmonary dysplasia

Wrap up warmly and take to NICU incubator
If blood gases worsen, intubate and support ventilation
If deterioration, check DOPE - displaced ET tube, obstructed, pneumothorax, equipment failure

Fluids - 10% glucose IV
Nutrition - inositol is an essential nutrient promoting surfactant maturation

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6
Q

What is bronchopulmonary dysplasia? Tests?

A

Persistent hypoxia ± difficult ventilatory weaning
Mainly from barotrauma and oxygen toxicity whereas surfactant related BPD is multifactorial with airway infections triggering inflammatory cascades

CXR:
Hyperinflation, rounded, radiolucent areas alternating with thin, denser lines

Histology:
Necrotising bronchiolitis with alveolar fibrosis

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7
Q

What is transient tachypnoea of the newborn? When is it more common? Investigation? Management?

A

Commonest cause of respiratory distress in the newborn period caused by delayed resorption of fluid in the lungs.
More common following Caesarean sections possibly due to lung fluid not being squeezed out during passage through the birth canal
No hypoxia or cyanosis usually seen

CXR: hyperinflation and fluid in the horizontal fissure, may show some perihilar markings
Blood gas normal

Settles within 1-2 days without intervention

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8
Q

What is meconium aspiration syndrome? Features?

A

Respiratory distress in the newborn as a result of meconium in the trachea. It occurs in the immediate neonatal period.
This follows the aspiration of meconium stained amniotic fluid.

Partial/total airway obstruction - thick sticky consistency - may lead to atelectasis
Foetal hypoxia - VQ mismatch, mechanical obstruction, airways oedema, surfactant inactivation
Pulmonary inflammation
Infection - due to inflammation
Surfactant inactivation - loss of surface tension in alveoli - reducing gas exchange
Remodelling of pulmonary vascular bed in response to hypoxia - persistent pulmonary hypertension

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9
Q

What is meconium?

A

Meconium is the dark green, sticky and lumpy faecal material produced during pregnancy. It is usually released from the bowels after birth.

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10
Q

What are risk factors for MAS?

A
Gestational age > 42 weeks
Foetal distress 
Intrapartum hypoxia due to placental insufficiency
Thick meconium paritcles
Chorioamnionitis
Apgar > 7
Oligohydramnios
IUGR
Maternal HTN, DM, pre-eclampsia, smoking
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11
Q

What investigations for MAS?

A

Bedside:
Dual Pulse Oximetry SaO2 - RUL and on either lower limb to determine hypoxia and assess potential right to left shunts
BP

Bloods:
FBC, CRP, Blood culture for infection
ABG - pH, PaO2, PaCO2, metabolic acidosis

Imaging: 
CXR:
Increased lung volumes
Asymmetrical patchy pulmonary opacities
Pleural effusions
Pneumothorax
Multifocal consolidation due to chemical pneumonitis

Echocardiography for congenital heart abnormalities causing pulmonary hypertension - PDA, PFT, Tricuspid valve regurgitation

Cranial US - hypoxic brain injury

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12
Q

What is management for MAS?

A

Observation:
SaO2

Routine care:
Placed under infant warmer
SaO2 monitoring
BM, U&amp;E, FBC, CRP assessment
Nutritional support - IV fluids - switch to NG and oral feed when permitting

Nasal cannula oxygen therapy
CPAP via nasal prongs (Can cause air trapping - regular CXRs)
Aim for SaOI2 of 92-97%
Wean if no respiratory distress
If ineffective, intubation and mechanical ventilation in NICU

Antibiotics if suspicion of infection - ampicillin IV, gentamicin IV

Surfactant bolus in newborns with moderate MAS or if a pneumothorax is present.

Inhaled nitric oxide to reduce pulmonary HTN (vasodilator)

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13
Q

What are complications of MAS?

A

Air leak - alveolar hyperdistension leading to penumothorax or pneumoperitoneum
- Needle aspiration

Persistent pulmonary hypertension of newborn
- ECHO for investigation of right to left shunt and iNO for treatment

Cerebral palsy - from cerebral hypoxia

Chronic lung disease

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