Infant respiratory distress syndrome

Infant respiratory distress syndrome (IRDS), also called hyaline membrane disease, is the most common cause of neonatal mortality. In the United States alone, it kills 40,000 neonates every year. IRDS occurs in premature neonates and, if untreated, is fatal within 72 hours of birth in up to 14% of neonates weighing less than 5½ lb (2.5 kg). Aggressive management using mechanical ventilation can improve the prognosis, but some surviving neonates may develop some degree of bronchopulmonary dysplasia.

Causes and incidence

Although airways and alveoli of a neonate’s respiratory system are present by 27 weeks’ gestation, the intercostal muscles are weak and the alveolar capillary system is immature. The premature neonate with IRDS develops widespread alveolar collapse due to a lack of surfactant, a lipoprotein pres-ent in alveoli and respiratory bronchioles. Surfactant lowers surface tension and helps prevent alveolar collapse. This surfactant deficiency results in widespread atelectasis, which leads to inadequate alveolar ventilation with shunting of blood through collapsed areas of lung, causing hypoxemia and acidosis.

IRDS occurs almost exclusively in neonates born before 37 weeks’ gestation (in 60% of those born before the 28th week). The incidence is greatest in the 1,000 to 1,500 g birthweight group. Infants of diabetic mothers, those born by cesarean delivery, second-born twins, infants with perinatal asphyxia, and those delivered suddenly after antepartum hemorrhage are more commonly afflicted.

Signs and symptoms

Although a neonate with IRDS 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.

Severe disease is marked by apnea, bradycardia, and cyanosis (from hypoxemia, left-to-right shunting through the foramen ovale, or right-to-left intrapulmonary shunting through atelectatic regions of the lung). Other clinical features include pallor, frothy sputum, and low body temperature as a result of an immature nervous system and the absence of subcutaneous fat.

Diagnosis

CONFIRMING DIAGNOSIS Although signs of respiratory distress in a premature neonate during the first few hours of life strongly suggest IRDS, a chest X-ray and arterial blood gas (ABG) analysis are necessary to confirm the diagnosis.

❑ Chest X-ray may be normal for the first 6 to 12 hours (in 50% of neonates with IRDS), but 24 hours after birth it will show the characteristic ground-glass appearance and air bronchograms.

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

❑ Chest auscultation reveals normal or diminished air entry and crackles (rare in early stages).

When a cesarean delivery is necessary before 36 weeks’ gestation, amniocentesis enables the determination of the lecithin/sphingomyelin (L/S) ratio and the presence of phosphatidylglycerol. An L/S ratio of more than 2:1 and the presence of phosphatidylglycerol decrease the likelihood of IRDS.

Treatment

Treatment of an infant with IRDS 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 PEEPor continuous positive airway pressure (CPAP), administered by nasal prongs or, when necessary, endotracheal (ET) intubation. Special ventilation techniques are now used on the patients refractory to conventional mechanical ventilation. These include high-frequency jet ventilation and high-frequency oscillatory ventilation. Extracorporeal membrane oxygenation is the last choice for ventilation and is only available in certain specialized facilities. Treatment of IRDS also includes:

❑ a radiant 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 (Studies show that this treatment can prevent or improve the course of IRDS as well as reduce mortality.)

Special considerations

Neonates with IRDS require continual assessment and monitoring in an intensive care nursery.

❑ Closely monitor blood gases 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 complications, such as infection, thrombosis, or decreased circulation to the legs. If the neonate has a transcutaneous oxygen monitor, change the site of the lead placement every 2 to 4 hours.

❑ 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 fraction of inspired oxygen and PEEP or CPAP by monitoring arterial oxygen saturation or ABG levels. Adjust the PEEP or CPAP as indicated, based on findings.

❑ Mechanical ventilation in neonates is usually done in a pressure-limited mode rather than the volume-limited mode used in adults.

❑ When the neonate is on mechanical ventilation, watch carefully for signs of barotrauma (an increase in respiratory distress and subcutaneous emphysema) and accidental disconnection from the ventilator. Check ventilator settings frequently. 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 the premature neonate, so preventive measures are essential.

❑ As needed, arrange for follow-up care with a neonatal ophthalmologist to check for retinal damage. Premature neonates in an oxygen-rich environment are at increased risk for developing retinopathy of prematurity.

❑ Teach the parents about their neonate’s condition and, if possible, let them participate in his care (using sterile 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 the neonate with IRDS by detecting respiratory distress early. Recognize intercostal retractions and grunting, especially in a premature neonate, as signs of IRDS; make sure the neonate receives immediate treatment.

Book Source Details

• Book Title: Professional Guide to Diseases (Eighth Edition)
• Author(s): Springhouse
• Year of Publication: 2005
• Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.

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