Respiratory distress syndrome affects 10% of all premature infants and only rarely affects those born at full-term. The disease is caused by a lack of pulmonary surfactant, a chemical that normally appears in mature lungs.

This substance reduces the surface tension within the air sacs, keeping them from collapsing and allowing them to inflate with air more easily.

In respiratory distress syndrome, the air sacs collapse (electasis) and prevent the child from breathing properly. Symptoms usually appear shortly after birth and become progressively more severe.

Risk factors are prematurity, diabetes mellitus in the mother, and stress during delivery that produces acidosis in the newborn at birth.

• rapid breathing (tachypnea)
• unusual breathing movement -- drawing back of the chest muscles with breathing (see intercostal retractions)
• shortness of breath and grunting sounds while breathing
• nasal flaring
• cessation of breathing (apneic episode)
• bluish coloration of the skin and mucus membranes (cyanosis)
• extremities puffy or swollen (edematous)

• A blood gas analysis shows low oxygen and acidosis.
• A chest X-ray shows findings consistent with respiratory distress (the lungs develop a characteristic "ground glass" appearance).
• Pulmonary function studies may be necessary.
• Blood cultures and a sepsis work-up are usually done to rule out infection and sepsis as a cause of the respiratory distress.

The treatment is prompt resuscitation of all high-risk and premature infants by a pediatric resuscitation team. High oxygen and humidity concentrations are given initially.

Infants with mild symptoms are given supplemental oxygen, while those with severe symptoms are managed on a ventilator to deliver both oxygen and pressure to keep the lungs inflated.

Oxygen and pressure will be decreased as soon as possible to prevent side effects associated with too much oxygen or pressure.

Artificial surfactant is sometimes instilled through an endotracheal tube into the lungs of an infant at high risk for respiratory distress syndrome immediately after birth (see lung surfactant).

Studies find that this treatment can prevent or improve the course of respiratory distress syndrome and enough research has now been done on surfactants to show that they reduce mortality from IRDS.

The condition may persist or worsen for two to four days after birth with improvement thereafter. Some infants with severe respiratory distress syndrome will die.

Long-term complications may develop as a result of oxygen toxicity, high pressures delivered to the lungs, the severity of the condition itself, or periods when the brain or other organs did not receive enough oxygen.

• pneumothorax
• pneumomediastinum
• pneumopericardium
• bronchopulmonary dysplasia
• hemorrhage into the brain (intraventricular bleed)
• hemorrhage into the lung (sometimes associated with surfactant use)
• thrombotic events associated with an umbilical arterial catheter
• retrolental fibroplasia and blindness
• delayed mental development and mental retardation associated with anoxic brain damage or hemorrhage

Since IRDS usually occurs as a result of prematurity, every effort is usually made to help the mother carry the baby to term. This begins with the first prenatal visit, which should be scheduled as soon as a mother discovers that she is pregnant. Statistics clearly show that good prenatal care results in larger, healthier babies and fewer premature births.

If a mother does goes into labor prematurely, every effort is made to stop the labor and allow the pregnancy to continue to full term. A lab test called the L/S ratio (a measurement of the fetus' lung maturity) is made and labor is usually halted until the L/S ratio shows that the lungs have matured. The infant's chances of not developing IRDS, if not 100% , are at least improved.

When it appears that premature delivery is unavoidable, administration of corticosteroids to the mother two to three days prior to delivery may help the fetal lung tissue mature in certain cases.