Respiratory Distress Syndrome (RDS)
RDS or hyaline membrane disease (HMD) is a subset of respiratory distress
due to surfactant deficiency which leads to atelectasis, decreased functional
residual capacity, poor compliance, increased work of breathing, V-Q mismatch
with intrapulmonary R to L shunting, hypoventilation, and hypoxia.
The incidence is 60% in infants less than 30 weeks, 15-20% from in infants
from 32-36 weeks, and 2-5% in infants greater than 37 weeks. It is
more common and severe in infants of diabetic mothers (IDM), males, and
white infants.
Pathophysiology
Alveoli are lined by fluid forming an air-liquid interface; the molecular
attraction forces along the surface of the interface (surface tension)
tend to collapse the alveolus. The tendency to collapse was described
by LaPlace:
Surfactant interrupts the molecular attractions and decreases surface
tension allowing less pressure or work to open the alveoli. Note
that the radius is related to the volume of the alveolus and that small
alveoli are harder to keep open that larger ones. However, surfactant lowers
surface tension more effectively when the alveolus is small, somewhat counterbalancing
the effect of the size (radius) of the alveolus. The counterbalancing
of the two factors allows alveoli of different sizes to co-exist.
Surfactant release starts in the later stages of pregnancy. At less
than 28 weeks, the predominant problem is the absolute lack of alveolar
surface area.
RDS is classicially associated with PDA in infants less than 1 to 1.2
kilograms in weight. Over the first 24 to 72 hours, the PDA gradually
allows left to right shunting causing pulmonary edema and systemic hypotension
with decreased uring output and increased risk of IVH and NEC. If
the PDA does not close, the typical time course of RDS (early onset, progression
x 12-24 hours, resolution after 3-5 days) is prolonged and worsened.
Increased support with ventilator and oxygen leads to increased risk of
bronchopulmonary dysplasia. Surfactant may lead to earlier onset
of the left to right shunt.
Signs of RDS:
Tachypnea, grunting, flaring, retracting, cyanosis.
Investigations
Monitor blood gas. The chest x-ray will demonstrate ground-glass
pattern to white out, and air bronchograms. It is not possible to
differentiate this appearance from pneumonia or other pathology.
Treatment
Exogenous surfactant has been shown to improve survival and decrease pneumothorax
and BPD. PEEP or CPAP helps to maintain the expiratory volume (the
radius). Sometimes a "sigh" breath is helpful in recruiting alveoli
and avoiding encroaching atelectasis. Because ventilators and oxygen
contribute to the pathogenesis of BPD, they should be used judiciously.
Chest percussion, suction, attention to hydration and infection status,
and judicious use of bronchodilators and diuretics with documentation of
pulmonary mechanics (PFTs) may be helpful in keeping ventilator and oxygen
support to a minimum. The "textbook" blood gases which may be achieved
with the ventilator are often not necessary. Early use of steroids
may shorten/reduce the need for oxygen and ventilation.
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Last modification: July 8, 1997