Respiratory Distress Syndromeor Hyaline Membrane Disease

Question 1

Incidence and severity depend on

Answer 1

inversely proportional to gestational age and birth wt

Question 2

Respiratory Distress Syndrome Contributing factors

Answer 2

Neonates younger than 37 weeks
Weight less than 2500g
Maternal diabetes (will lead to sever RDS cause of congenital heart disease / the insulin inhibit surfactant production)
Cesarean delivery without preceding labour ( no steroid less surfactant)
Fetal asphyxia (cause neurological manifestation and acidosis which affect the function of surfactant)
Second part of twins
White infants

Question 3

Secondary surfactant deficiency may occur in infants with the following

Answer 3

Pulmonary infections e.g. group B Strep (same clinical pic. And x-ray  بنمشي ال premature على antibiotic )
Pulmonary hemorrhage  PDA , sepsis
Meconium aspiration pneumonia  inhibit surfactant function  pulmonary hypertension
Oxygen toxicity; barotrauma or volutrauma
to the lungs
Congenital diaphragmatic hernia (cyanosis / respiratory distress/ scaphoid abdomen) space occuping lesion pulmonary hypertension

Question 4

Factors decrease the risk of RDS

Answer 4

Use of antenatal steroids
Pregnancy-induced or chronic maternal hypertension ( stress condition  inc. steroids)
Prolonged rupture of membranes ( before delivary 18-72 h بحمي من RDS & sepsis بس اذا كان chronic rupture  oligohydration  lung hypoplasia)
Maternal narcotic addiction (stress condition )

Question 5

surfactant production begins at

Answer 5

surfactant production begins at 24-28 weeks of gestation, and gradually increases until full gestation

Question 6

Surfactant composition

Answer 6

Surfactant is a complex lipoprotein composed of 6 phospholipids and 4 apoproteins.
Lipids 90% of lung surfactant

Dipalmitoylphosphatidylcholine DPPC  (Lecithin) (  during pregnancy ) is functionally the principle  phospholipid
Protein 10% of lung surfactant
Consists of small proteins
Hydrophobic protein 
SP-B and SP-C
Hydrophilic proteins
SP-A and SP-D

Question 7

SP-B

Answer 7

Protein of Pulmonary Surfactant
SP-B (most important )
Required for normal pulmonary function
Mutation result in deficiency SP-B Can cause severe lung disease that is lethal in perinatal period

Question 8

SP-C

Answer 8

Promotes formation of phospholipid film lining of alveoli

Human with SP-C deficiency develop interstitial pulmonary fibrosis in early childhood
SP-C deficiency do not cause respiratory distress at birth

Question 9

SP-A and SP-D

Answer 9

They are host defense of the lung
Kill bacteria
Kill viruses
They have carbohydrate recognition domain allows coating, and phagocytosis of virus and bacteria

Question 10

difference between RDs and TTN

Answer 10

TTN (disease of full term & post term baby with mature lung )المشكلة fluid in the lung )benign disease
Usually improve while RDS deteriorate within 48h with good prognosis
Oxygen requirement is less in TTN
X-RAY
Prominent perihilar streaking
Fluid in the fissures
Small pleural effusions may be seen
Patchy infiltrates have also been described

Question 11

Progressive signs of respiratory distress include the following

Answer 11

Tachypnea
 Hypoxia
 Cyanosis
 Expiratory grunting (from partial closure of glottis)
 Subcostal and intercostal retractions ?
 Nasal flaring ?
 Extremely immature neonates may develop apnea and    
    hypothermia

Question 12

Treatment of RDS

Answer 12

Oxygen - Maintain Pao2 50-80mmHg
Spo2 88-92%

Surfactant
Infection control

Question 13

Curosurf Warnings

Answer 13

Curosurf: if transient episodes of bradycardia and decreased oxygen saturation occur
Discontinue the dosing procedure and initiate
measures to alleviate the condition

Curosurf: produces rapid improvements in lung oxygenation and compliance that may require immediate reductions in ventilator settings and Fio2 (may lead to pneumothorax

Question 14

Side effects of Animal-DerivedSurfactant

Answer 14

Transient hypoxia
Bradycardia
Acute airway obstruction
Transient full in blood pressure and cerebral blood flow (لازم نسيطر عالضغط لأنو ممكن يصير rupture of vesseles )
Slight increase in risk of pulmonary hemorrhage
No long-term effect on babies
Fewer pneumothorces with slightly reduced mortality
rate compared to infant treated with synthetic surfactant
Potential sensitization to animal proteins

Question 15

Prevention of RDS

Answer 15

Intubation of infant born at or before 30 weeks gestation in the delivery

Prophylactic natural surfactant therapy is administrated through the ET as soon as the infant is stable after intubation

Do not delay surfactant for CXR
No CXR is necessary to confirm proper tube placement
Antenatal Steroids should be given to any pregnant women at 24 to 34 weeks of gestation with intact membranes at high risk for preterm delivery.

After administration of surfactant and if the infant is active and exhibit spontaneous respiratory effort :
extubation and stabilization on CPAP rather than continued intubation and M.V

Question 16

Acute complications

Answer 16

Alveolar rupture
Infection
Intracranial hemorrhage and periventricular leukomalacia
Patent ductus arteriosus (PDA)
Pulmonary hemorrhage
Necrotizing enterocolitis (NEC) and/or GI perforation
Apnea of prematurity

Question 17

Chronic complications

Answer 17

Bronchopulmonary dysplasia (BPD)
Retinopathy of prematurity (ROP):
Neurologic impairment