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- hyaline membrane disease
- affects premature infant < 36 weeks
- deficiency of lipoprotein pulmonary surfactant and structural immaturity of lungs
pathophysiology
- lipoproteins produced by type II pneumocytes
- concentrated in cell lamellar bodies
- then transported to cell surface and expressed on alveolar luminal surface
- lipoproteins combine with surface surfactant proteins A, B, C and D to form tubular myelin
- tubular myelin lowers alveolar surface tension, prevents acing collapse on expiration
- if alveoli collapse, poor gas exchange, hypoxia, hypercarbia and acidosis
- alveolar ducts, terminal bronchioles distended lined by hyaline membranes containing fibrin, cellular debris and fluid. Occurs due to ischemia, barotrauma, increased oxygen concentration in assisted ventilation
clinical features
- symptomatic within minutes of birth
- grunting, retractions, cyanosis, tachypnea
- chest Xray findings may pop up immediately after birth, but usually seen maximum 6-24 hours after birth
Pre therapeutic imaging findings
- under-aeration of the lungs
- fine granular opacification, diffuse, symmetrical with air bronchograms (collapsed alveoli with distended bronchioles and alveolar ducts)
- lesser the dissension of lungs, more the opacification
- white lungs – atelectasis, edema, hemorrhage and sometimes superimposed infection are the causes
Post treatment imaging findings
- corticosteroid administration 2 days prior to delivery cause significant reduction in HMD
- liquid bolus administered via endotracheal tube
- uneven distribution of steroid leads to areas of atelectasis interspersed with good aeration
- radiographic findings similar to interstitial emphysema or neonatal pneumonia
- infants > 27 weeks best respond to steroid
- infants < 27 weeks, lungs clear up but alveoli poorly developed, hence needs prolonged ventilation, hazy lung and occasionally picture of bronchopulmonary dysplasia
patent ductus arteriosus
- common in premature infants
- rigid lungs of HMD, associated hypoxia and hypercarbia causes right to left shunting
- with surfactant therapy, decrease in pulmonary resistance results in left to right shunting
- initial treatment with ibuprofen. if ineffective, surgical or endovascular occlusion needed
- sudden cardiac enlargement, left atrial enlargement, elevation of left main bronchus, varying degrees of pulmonary edema
Ventilation
- continuous positive airway pressure ventilation used in infants to reduce complications
- high frequency oscillatory ventilation reduced barotrauma
- mean airway pressure optimally adjusted if diaphragm at 8th to 10th ribs
- side effects: pneumothorax, pneumomediastinum, pulmonary interstitial emphysema, pneumopericardium
bronchopulmonary dysplasia or chronic lung disease of prematurity
- long term complication of IRDS
- higher incidence in infants with previous Ureaplasma urealyticum pneumonitis
- diffuse interstitial shadowing, mild to moderate hyperinflation
- pulmonary vein stenosis is an association, can cause pulmonary hypertension
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