8.Infant Respiratory Distress Syndrome Flashcards

1
Q

what is Infant Respiratory Distress Syndrome

A

hypoxia and hypercapnea d/2 inadequate lung surfactant in infants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

IRDS pathogenesis

A
  • Inadequate surfactant production causes
  • air sacs to collapse on expiration and leads to
  • drastically reducing lung compliance and difficulty breathing
  • development of interstitial oedema worsens the condition and causes

.-hypoxia and

  • hypercapnea and
  • CYANOSIS- d/2/ RIGHT TO LEFT SHUNT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the 2 possible types of R-L shunts in IRDS

A

occurs
through collapsed lung (intrapulmonary)

if pulmonary hypertension is severe, across the ductus arteriosus and
foramen ovale (extrapulmonary).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

surfactant

A

produced after 30 weeks of gestation.

by type II pneumocytes

to lower surface tension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what determines the incidence/severity of IRDS

A

inverse relationship w/ gestational age

affects 50% of infants at 28-32wks gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

RF for IRDS

A
Premature delivery.
Male infants.
Caeserean 
Hypothermia.
Perinatal asphyxia. Maternal diabetes. Multiple pregnancy.
Family history of IRDS.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

prophylactic factors against IRDS

A

use of antenatal steroids.

Pregnancy-induced/ chronic maternal hypertension.

Prolonged rupture of membranes.

Maternal narcotic addiction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what can cause secondary surfactant deficiency in infants

  • parenchymal damage,
  • atypical growth
  • oxygen excess/insuff
A

Intrapartum (birth) asphyxia.

Pulmonary haemorrhage.

Pulmonary infection
(group B beta-haemolytic streptococci)

pulmonary hypoplasia.

Meconium aspiration pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

classic presentation

A

Usually preterm delivery.

swift postbirth presentation of
respiratory distress: tachypnoea, expiratory grunting, subcostal and intercostal
retractions, diminished breath sounds, cyanosis and nasal flaring.

rapidly progress to fatigue, apnoea and hypoxia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

sx of respiratory distres in infants

A

tachypnoea,
expiratory grunting,

subcostal and intercostal
retractions,

diminished breath sounds,

cyanosis

nasal flaring.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

dx of IRDS are other causes of respiratory distress in infants other than inadequate surfactant

A

Pulmonary air leaks
(eg, pneumothorax , pneumomediastinum, pneumopericardium).

puilmonary infection

Congenital lung anomalies
-diaphragmatic hernia, -chylothorax,
-

Congenital heart anomalies.

Primary persistentpulmonary hypertensionof
-dg of exclusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

investigation in IRDS

A

Blood gases: respiratory and metabolic acidosis along with hypoxia.
- Metabolic acidosis results from poor tissue
perfusion.

 Pulse oximetry: non-invasive tool to monitor oxygen saturation, which should be maintained at 85-93%.

 CXR.

 Monitor FBC (anemia) electrolytes, glucose, renal and liver function.

 Echocardiogram:

  • diagnose PDA
  • determine the direction and degree of shunting,
  • diagnose of pulmonary hypertension
  • excluding structural heart disease.

 Cultures to rule out sepsis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

management of IRDS

A

Surfactant replacement therapy via endotracheal tube:

Oxygen:

Supportive therapy:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Supportive therapy:

A

Temperature regulation: .

Fluids, metabolism and nutrition:

 Circulation and anaemia: monitor heart rate, peripheral perfusion and blood pressure

 Antibiotics:
cultures. Discontinue antibiotics after three to five days if blood cultures are negative.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

acute complications of IRDS

A

Alveolar rupture: pneumothorax, pneumomediastinum, pneumopericardium, interstitial emphysema.

Intracranial haemorrhage: the risk is increased in those who require mechanical ventilation.

pulmonary haemorrhage after surfactant therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Chronic complications

A

Retinopathy of prematurity

Neurological impairment d/2/ hypoxia and infection

bronchopulmonary dysplasia d/2/ trauma during mech vent

17
Q

prognosis pf IRDS

A

baby’s over 1500g have increased prognosis

18
Q

how to prevent IRDS

A

Antenatal corticosteroids (dexamethasone) - 40% irds reduct d/2 accelerate fetal surfactant production and lung maturation.

delaying premature births

  • use of tocolytics
    e. g. atosiban, nifedipine allows time for corticosteroids to be given

avoid hypothermia

19
Q

what is retinopathy of the newborn

A

normally, the retinal vessels grow in an environment of relative hypoxia.

In phase I, after premature birth, the retina is relatively hyperoxic (exposed to increased oxygen), resulting in reduced levels of vascular endothelial growth factor (VEGF)

reduced VEGF stops vascular growth from the optic disc but the eye carries on growinng causing preipheral ischemia and hypoxia in the reitna

peripheral hypoxia increases VEGF in phase 2

effects of increased vegf in phase 2

  • tortuous vessels
  • growth of fibrous vessels and retinal detatchment