RDS
Definition
Syndrome in premature infants caused by developmental insufficiency of surfactant production and structural immaturity in the lungs
Risk Factors
Prematurity
Male
Hypothermia
Maternal diabetes
Cesarian
Perinatal asphyxia
Multiple pregnancy
FHx of RDS
Differential diagnosis
Epidemiology
Affects about 1% of newborn infants and is the leading cause of death in preterm infants
Incidence decreases with advancing gestational age
About 50% in babies born at 26–28 weeks
About 25% at 30–31 weeks
> 90% at 28 weeks?
50% at 32 weeks?
More frequent in infants of diabetic mothers and in the second born of premature twins
Aetiology
Surfactant deficiency
=> full lung closure on expiration
Clinical features
chest wall retractions (recession)
expiratory grunting
breath against a partially closed glottis
flaring of the nostrils
Progression over 2-3 days
More O2 required
Either => death or recovery by 72 h
Pathophysiology
Deficit in surfactant
Complex system of lipids, proteins and glycoproteins
Produced in specialized lung cells called Type II cells or Type II pneumocytes
Packaged by the cell in structures called lamellar bodies, and extruded into the air-spaces
Unfold into a complex lining of the air-space
Reduces the surface tension of the fluid that lines the air-space
Surface tension is responsible for approximately 2/3 of the elastic recoil forces
Prevents the air-spaces from completely collapsing on exhalation
Allows re-opening of the air-space with a lower amount of force
Without adequate amounts of surfactant, the air-spaces collapse and are very difficult to expand
Lungs are characterized by collapsed air-spaces alternating with hyper-expanded areas, vascular congestion and, in time, hyaline membranes.
Hyaline membranes are composed of fibrin, cellular debris, red blood cells, rare neutrophils and macrophages
Appear as an eosinophilic, amorphous material, lining or filling the air spaces and blocking gas exchange
As a result, blood passing through the lungs is unable to pick up oxygen and unload carbon dioxide
Structural immaturity, as manifest by decreased number of gas-exchange units and thicker walls, also contributes to the disease process
Therapeutic oxygen and positive-pressure ventilation, while potentially life-saving, can also damage the lung
Investigations
Fetal lung maturity may be tested by sampling the amount of surfactant in the amniotic fluid, obtained by inserting a needle through the mother's abdomen and uterus
Several tests are available that correlate with the production of surfactant
Lecithin-sphingomyelin ratio ("L/S ratio")
less than 2:1 => fetal lungs may be surfactant deficient
Presence of phosphatidol glycerol (PG)
presence of PG usually indicates fetal lung maturity
Surfactant/albumin (S/A) ratio
S/A ratio <35 indicates immature lungs, between 35-55 is indeterminate, and >55 indicates mature surfactant production
Blood gases
respiratory and metabolic acidosis along with hypoxia
CXR
Pulmonary mechanics testing (PMT)
Reduced complience
Management
http://eng.mapofmedicine.com/evidence/map/respiratory_distress_syndrome1.html
a) conservative
b) medical
Pre-term glucocorticoids speed the production of surfactant
Ventilation
High frequency oscillatory ventilation
Continuous positive airway pressure (CPAP)
High-speed mechanical ventilation (> 40 breaths per min)
Oxygen
Intravenous fluids to stabilize the blood sugar, blood salts, and blood pressure
Extracorporeal membrane oxygenation (ECMO)
Not appropriate for premature babies
Exogenous surfactant
Pig better than synthetic
c) surgical
Prognosis
Most common single cause of death in the first month of life of the developed world
Complications:
metabolic disorders (acidosis, low blood sugar)
secondary end-organ disorder due to hypoxia
secondary bacterial pneumonia
pneumonia
low blood pressure
chronic lung changes