Respiratory Distress Syndrome in Newborn

N. Kononenko

Definition. RDS is an acute pulmonary disorder of premature infants, first described by pathologists who noted widespread atelectasis and eosinophilic material lining the overdistended terminal bronchioles

The condition is a surfactant deficiency syndrome resulting from immaturity. The incidence of this disorder depends of gestational age and increases from 1% in full-term newborn to 5% at 35-36 weeks, 20% at 30-32weeks, to 65% at 29-30 weeks of gestation.

Aetiology of RDS is deficiency of surfactant synthesis, release, destroying, inhibition and immaturity of lung tissue and chest. The main perinatal risk factors for RDS ar 1)factors that affect state of lung development at birth include prematurity, maternal diabetes and genetics factors; 2)factors that may acutely impair surfactant production, release, or function include perynatal hypoxia and asphyxia (hypoxemia, acidosis), congenital infection, cesarean section, multiply pregnancy, hypovolemia, cold stress in newborn.

The source of surfactant

Surfactant is produced by Type II alveolar cells since 20-24 weeks of gestation, but completely present after 35 weeks of gestation.

Components of surfactant
Surfactant. Lipids 90% Phospholipids 80% Phosphatidylglycerol 5% Proteins 10% Neutral lipids 20% Phosphatidylcholine (Lecithin) 70% Other lipids 5%

Saturated Phosphatidylcholine 45%

Desaturated Phosphatidylcholine (dipalmitoyl lecithin). 25%

Surfactant is a surface-active material comprised of a mixture rich in phospholipids, and lesser amounts of proteins and other lipids. Surfactant proteins have big role in the function of surfactant (A, B, D). The most important B.

Function of surfactant
Surfactant acts as an antiatelectasis factor in the alveolar lining by lowering surface tension at diminished lung volumes. This allows for maintenance of functional residual capacity, which acts as a reservoir to prevent wide fluctuation in arterial PO2 and PC02 during respiration.

Function of surfactant

Prevent collapse of alveoli during expiration Protect alveolar epithelium from damage and promote mucociliar clearance Provide antibacterial activity against Gram positive microorganisms Stimulate macrofages Participate in regulation of microcirculation and permeability of alveolar wall, that allows to prevent lung edema

Pathogenesis of RDS
Prematurity > decreased surfactant synthesis and release >deficiency in pulmonary surfactant >increased alveolar surfase tension > atelectasis > pulmonary hypoventilation > hypoxemia, hypercarbia > acidosis > increased pulmonary vascular resistance and vasoconstriction > pulmonary hypoperfusion > increased vascular permeability and pulmonary capillary leak > deposition of serum protein, fibrin > hyaline membranes formation>diffusion block.

Symptoms of RDS
Tachypnoe >60 per min Chest retractions Expiratory grunting Cyanosis

Silverman Retraction Score Silverman Retraction Score

Results of Silverman Retraction Score assessment: <4 beginning RDS, 4-5 mild RDS,

6-8 moderate RDS, 9-10 severe RDS.

The chest x-ray film

reticulogranular pattern of lung at the

beginning of RDS, the progressing RDS

air bronchograms at

"ground-glass" appearance due to

diffuse bilateral atelectasis.

Tests for estimating surfactant maturity

Foam stability or shake test.

These tests depend on the ability of surfactant-rich fluid to form stable bubbles when mixed and shaken with ethanol. Stable bubbles all the way around the test tube are suggestive of mature lungs. No bubbles or single, vary small bubbles in meniscus - high risk of RDS.

Tests for estimating surfactant maturity

Lecithin/sphingomyelin ratio: Since lecithin is a major

component of surfactant, and sphingomyelin concentration is relatively constant during gestation, the L/S ratio can be used as a measure of lung maturity. An L/S of > 2.0 carries a low risk of RDS and is generally attained at 34-35 weeks' gestation. Ratios of 1.5-2.0 carry a 40% risk of RDS, values of <1.5 carry a risk of 75%. The L/S ratio is not reliable in Rh disease or maternal diabetes, on fluid contaminated with blood or meconium.

Phosphatidylglycerol: This surface-acting, stabilizing factor

is present at > 35 weeks' gestation. Thus, its presence is indicative of lung maturity, but its absence offers no definitive help in management. The measurement can be performed on blood- or meconium-contaminated fluid.

Laboratory studies.

Monitoring of heart rate, respiratory rate, blood pressure, pulsoxymetria. Complete blood count - diagnose anemia, polycythemia, infection. Arterial blood gas measure PaO2 , PaCO 2, acid-base status. Blood glucose, blood culture, coagulation test.

Causes of respiratory distress in the newborn.

There are many pulmonary and nonpulmonary causes of RD in the neonatal period. Pulmonary: RDS, meconium aspiration syndrome, neonatal pneumonia, persistent pulmonary hypertension, transient tachypnea of the newborn, congenital pulmonary malformation; non-pulmonary: congenital heart disease, anemia, CNS injury, asphyxia, hypoglycemia, metabolic disease

To distinguish neonatal cardiac disease from pulmonary disease

to place the infant in 100% oxygen (less than 5 minutes), so called hyperoxia test. In general, the child with cyanotic congenital heart disease will not be able to generate a PaO2 greater than 100 mm Hg because of fixed intracardiac shunting that bypasses the pulmonary circulation. The child with severe lung disease, however, will be able to improve oxygenation substantially greater than 100 mm Hg, especially if given positive pressure ventilation (PPV).

Management of RDS.

The keys to management of infants with RDS: to prevent hypoxia and acidosis (this allows normal tissue metabolism, optimises surfactant production, and prevents right-to-left shunting), to optimise fluid management (avoiding hypovolemia and shock on the one hand and edema, particularly pulmonary edema, on the other), to reduce metabolic demands, to prevent worsening atelectasis, to minimise barotrauma and hyperoxic lung damage. General supportive care includes: optimal thermal environment to keep the skin temperature of infant at 36.50C, fluids, electrolytes and nutritional support, protection from infection.

Respiratory therapy.

The goal is the provision of adequate supplemental oxygen to maintain arterial oxygen tension (PaO2) of 60-80 mm Hg and an arterial saturation of 9295%. PaO2 levels less than 50 mm Hg are associated with pulmonary vascular vasoconstriction, and those greater than 100 mm Hg may increase the risk of retinopathy of prematurity and pulmonary oxygen toxicity. Warmed (32- 340C), humidified oxygen may be delivered via a clear, plastic hood or via nasal prongs, or a respirator.

Surfactant Replacement Therapy

In patients with RDS, surfactants have been shown to decrease the need for supplemental oxygen therapy, lower mortality rates, and decrease the incidence of air-leak syndromes. The incidence of BPD has also been reduced in some studies. Two general classes of surfactant are available for replacement therapy: natural surfactants prepared from mammalian lungs Survanta, Curosurf, Alveofact synthetic surfactants Exosurf, Pneumactant Although natural surfactant extracts seem to have a better immediate effect (less supplemental oxygen required, fewer pneumothoraces), long-term clinical outcomes (e.g., chronic lung disease, death) with synthetic surfactants are comparable.

Surfactant therapy: prophylaxis for infants at high risk for RDS (infants less than 30 weeks' gestation, less than 1250 g) "rescue" treatment

Continuous Positive Airway Pressure (CPAP)

is applied when FiO2 greater than 0.40-0.60 is required to maintain PaO2 at 5080 mm Hg, or when there is significant clinical worsening during the first day of life. Method using CPAP (4-8 cm H2O) - a face mask, nasal prongs, nasopharyngeal tube, or endotracheal tube. The application of CPAP opens atelectatic alveoli, conserves the functional properties of surfactant.

Incication for mechanical ventilation in RDS

Mechanical ventilation is initiated when the diagnosis of respiratory failure is made.

Laboratory criteria for respiratory failure

Respiratory acidosis with pH < 7.20 and PCO2 > 60 mm Hg

Severe hypoxemia with PaO2 < 50-60 mm Hg despite an FiO2 of 0.7-1.0 and an adequate trial of continuous positive airway pressure
1. Severe retractions 2. Cyanosis 3. Intractable apnea

Clinical criteria for respiratory failure

Complications of RDS
acute air leak syndrome (pneumothorax, pneumopericardium, pneumomediastinum, pulmonary interstitial emphysema), patent ductus arteriosus, intracranial hemorrhage, infections (pneumonia, sepsis), pulmonary hemorrhage; chronic bronchopulmonary dysplasia, retinopathy of prematurity, neurologic sequel.

Preventive Strategies

The prenatal and perinatal management of women to prevent premature labor is still the most critical issue. The use of maternal glucocorticoid therapy to pharmacologically induce surfactant maturation, production, and secretion in the fetus. Antenatal steroids (ANS) strongly recommended in all pregnancies between 24 and 34 weeks' gestation at risk for preterm delivery. ANS should not be used in infants greater than 34 weeks' gestation unless there is evidence of pulmonary immaturity. In addition, mothers less than 30 to 32 weeks' gestation with premature rupture of membranes in the absence of amnionitis also should be treated. ANS preparations used are either dexamethasone 6 mg intramuscularly every 12 hours for four doses or betamethasone 12 mg intramuscularly every 24 hours for two doses. The optimal effect for ANS is 24 hours to 7 days after treatment.

Thank your for attention!