Respiratory distress syndrome

Respiratory distress syndrome: Excerpt from Handbook of Diseases

Also called hyaline membrane disease and infant respiratory distress syndrome, respiratory distress syndrome is the most common cause of neonatal mortality.

Respiratory distress syndrome affects 10% of premature infants while rarely affecting infants born at full term. It’s more common in neonates of diabetic mothers and in neonates born with acidosis, such as those delivered under stressful conditions — for example, by cesarean section or suddenly after antepartum hemorrhage.

Aggressive management using mechanical ventilation improves prognosis.

Causes

Although the airways and alveoli of a neonate’s respiratory system are present by the 27th week of gestation, the intercostal muscles are weak and the alveoli and capillary blood supply are immature. In respiratory distress syndrome, the premature neonate develops widespread alveolar collapse because of lack of surfactant, a lipoprotein present in alveoli and respiratory bronchioles.

Surfactant normally lowers surface tension and aids in maintaining alveolar patency, preventing collapse, particularly at end expiration. But a deficiency results in widespread atelectasis, which leads to inadequate alveolar ventilation with shunting of blood through collapsed areas of lung, causing hypoxia and acidosis.

Signs and symptoms

Although a neonate with respiratory distress syndrome may breathe normally at first, he usually develops rapid, shallow respirations within minutes or hours of birth, with intercostal, subcostal, or sternal retractions; nasal flaring; and audible expiratory grunting. This grunting is a natural compensatory mechanism designed to produce positive end-expiratory pressure (PEEP) and prevent further alveolar collapse.

The neonate may also display hypotension, peripheral edema, and oliguria; if he has severe disease, apnea, bradycardia, and cyanosis (from hypoxemia, left-to-right shunting through the foramen ovale, or right-to-left shunting through atelectatic regions of the lung) may be present. Other signs and symptoms include pallor, frothy sputum, and low body temperature as a result of an immature nervous system and the absence of subcutaneous fat.

Diagnosis

Although signs of respiratory distress in a premature neonate during the first few hours of life strongly suggest respiratory distress syndrome, the following tests are necessary to confirm the diagnosis:

❑ Chest X-ray may be normal for the first 6 to 12 hours (in 50% of neonates with respiratory distress syndrome) but later shows a fine reticulonodular pattern.

❑ Arterial blood gas (ABG) analysis shows decreased partial pressure of arterial oxygen (Pao₂); normal, decreased, or increased partial pressure of arterial carbon dioxide; and decreased pH (from respiratory or metabolic acidosis or both).

❑ Pulmonary function studies may be necessary.

When a cesarean section is necessary before the 36th week of gestation, amniocentesis allows determination of the lecithin-sphingomyelin ratio, which helps to assess prenatal lung development and the risk of respiratory distress syndrome.

Treatment

An infant with respiratory distress syndrome requires vigorous respiratory support. Warm, humidified, oxygen-enriched gases are administered by oxygen hood or, if such treatment fails, by mechanical ventilation. Severe cases may require mechanical ventilation with PEEP or continuous positive airway pressure (CPAP), administered by a tightly fitting face mask or, when necessary, endotracheal (ET) intubation.

Treatment also includes:

❑ a radiant infant warmer or Isolette for thermoregulation

❑ I.V. fluids and sodium bicarbonate to control acidosis and maintain fluid and electrolyte balance

❑ tube feedings or total parenteral nutrition if the neonate is too weak to eat

❑ administration of surfactant by an ET tube.

Special considerations

❑ Closely monitor ABG levels as well as fluid intake and output. If the neonate has an umbilical catheter (arterial or venous), check for arterial hypotension or abnormal central venous pressure.

❑ Watch for such complications as infection, thrombosis, or decreased circulation to the legs.

❑ If the neonate has a transcutaneous Pao₂ monitor (an accurate method for determining Pao₂), change the site of the lead placement every 2 to 4 hours to avoid burning the skin.

❑ Weigh the neonate once or twice daily. To evaluate his progress, assess skin color, rate and depth of respirations, severity of retractions, nostril flaring, frequency of expiratory grunting, frothing at the lips, and restlessness. 

❑ Regularly assess the effectiveness of oxygen or ventilator therapy. Evaluate every change in the fraction of inspired oxygen and PEEP or CPAP by monitoring oxygen saturation or ABG levels. Be sure to adjust PEEP or CPAP as indicated, based on findings.

CLINICAL TIP: When the neonate is on mechanical ventilation, watch carefully for signs of barotrauma (increase in respiratory distress or subcutaneous emphysema) and accidental disconnection from the ventilator. Frequently check ventilator settings.

Be alert for signs of complications of PEEP or CPAP therapy, such as decreased cardiac output, pneumothorax, and pneumomediastinum. Mechanical ventilation increases the risk of infection in premature neonates, so preventive measures are essential.

❑ As needed, arrange for follow-up care with a neonatal ophthalmologist to check for retinal damage.

❑ Teach the parents about their neonate’s condition and, if possible, let them participate in his care (using aseptic technique) to encourage normal parent-infant bonding. Advise parents that full recovery may take up to 12 months. When the prognosis is poor, prepare the parents for the neonate’s impending death and offer emotional support.

❑ Help reduce mortality in respiratory distress syndrome by detecting respiratory distress early. Recognize intercostal retractions and grunting, especially in a premature neonate, as signs of respiratory distress syndrome, and make sure the neonate receives immediate treatment.

Book Source Details

• Book Title: Handbook of Diseases
• Author(s): Springhouse
• Year of Publication: 2003
• Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5

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