Respiratory Distress Syndrome in Newborn and Surfactant Therapy

What is Surfactant?

The alveoli contain many types of cells. Among them Type 2 Pneumocytes produces surfactant. The main function of surfactant is to reduce surface tension, so that decrease the work of breathing. Surfactant forms a thin monomolecular layer at the air fluid interface. Surfactant layer is not static. It is continuously secreting and reabsorbing. Deficiency of surfactant causes Respiratory Distress Syndrome (ARDS) in Newborn. It is also called hyaline membrane disease.

How Surfactant Forms and Reabsorbed?

Type 2 Pneumocytes forms a membrane-bound organelle – lamellar inclusion bodies containing phospholipids. They are secreted into the alveolar lumen by exocytosis. The lamellar bodies are converted to phospholipid film. Lung surfactant has a very short half-life. It is about only 14 hours. The Surfactant is taken up by the alveolar macrophages but more is taken by the endocytosis in type 2 epithelial cells.The major constituents of surfactant are dipalmitoylphosphatidylcholine (lecithin), phosphatidylglycerol, apoproteins, and cholesterol. With advancing gestational age, increasing

The major constituents of surfactant are dipalmitoylphosphatidylcholine (lecithin), phosphatidylglycerol, apoproteins, and cholesterol. With advancing gestational age, increasing a number of phospholipids are synthesized and stored in type-2 alveolar cell These surface active agents are released into the alveoli to maintain alveolar stability by reducing surface tension.

Is Endocrine Hormone influence surfactant level?

Thyroid hormone: Increases the number of inclusions in type 2 cells

Glucocorticoids (cortisol): Accelerates maturation of type 2 cells and therefore production of surfactant. Baby delivered by cesarean section are at greater risk of developing respiratory distress syndrome because the reduction of cortisol produced because the lack of stress that happens during vaginal delivery. Cortisol increases in high stress and helps in the maturation of type 2 cells of the alveoli that cause surfactant.

Insulin: Inhibits SP-A accumulation in cultured human fetal lung tissue.

When is Surfactant level decreased?

1. ARDS of the premature baby
2. Baby born to the diabetic mother.
3. Pneumonia
4. Lung collapse
5. Cigarette smoking.

What Does Surfactant Do?

Surfactant reduces surface tension within alveoli. That means less inspiratory force is needed to inflate the lung. It prevents the collapse of the lung during expiration. Surfactants also increases compliance and stability of lungs.
It is suggested that surfactant has some bactericidal functions.

Deficiency of Surfactant:

Respiratory distress syndrome (RDS) is defined as respiratory difficulty starting shortly after birth, commonly in a preterm newborn, and is due to deficiency of pulmonary surfactant. It occurs in 15-30% of those between 32 and 36 weeks of gestational age, in about 5% beyond 37 weeks and rarely at term.

Deficiency of pulmonary surfactant leads to alveolar atelectasis, edema, and cell injury. Subsequently, serum proteins that inhibit surfactant function leak into the alveoli. The Majority of RDS/HMD is self-limiting. Microscopically there are eosinophilic membranes in collapsed alveoli (so is the name HMD) and sometimes pulmonary hemorrhage and interstitial emphysema.

How to Diagnose Respiratory Distress Syndrome?

The typical presentation is the respiratory difficulty that develops – shortly after birth (usually within minutes of birth), may peak at 12-24 hr. The respiratory distress may improve in 3-5 days or may be rapidly fatal within few hours. Expiratory grunting, tachypnea, intercostal and subcostal recessions, Nasal flaring, Head nodding and cyanosis are the presenting symptoms.

Diagnostic Criteria for RDS:

1. Tachypnea (>60/min)
2. Expiratory grunting
3. Sternal and Intercostal recession
4. Cyanosis in room air

These sign must develop in neonate before 4 hours of age and persist after 24 hours.

At least two of the above signs plus typical chest x-ray usually confirms the diagnosis of RDS.

Chest x-ray alone almost confirms the diagnosis. The typical x-ray findings (develop during, the first 6 hours) are low lung volume, a generalized haziness or reticulogranular “ground glass” appearance in the lung fields, and when severe, obscuring heart borders and an air bronchogram due to air in the major bronchi being highlighted against the white opacified lungs. The typical radiological features of RDS are not evolved from the beginning and progress according to the severity of the disease. Radiological features may improve considerably soon after effective treatment.

Blood: Complete blood count may help to exclude neonatal sepsis.

Read also : High Amniotic Fluid (Polyhydramnios) During Pregnancy- Cause, and Treatment

What are the Tests of fetal lung maturity:

Test for surfactant function: Shake test (bed side test): Serial dilutions of ethanol are added to the amniotic fluid or gastric aspirate to allow for removal of non-surfactant foam. The sample is then shaken for 15 seconds to permit formation of a stable foam layer. The presence of bubbles in presence of adequate surfactant that persists on the surface for 15 minutes is considered a positive test; implying a very low risk for RDS.

Test for surfactant biochemistry and composition: Lecithin/sphingomyelin (L/S) ratio testing is the “gold standard” for fetal lung maturity. An amniotic fluid L/S ratio of >2: 1 is considered equivalent to fetal lung maturity, and a value <2:1 indicates immaturity of fetal lung. Phosphatidylglycerol (PG) is estimated in case of the baby of a diabetic mother.’

How to Prevent Respiratory Distress Syndrome?

Assessment of fetal lungs maturity before delivery by amniotic fluid indices: L/S ratio, PG concentration.
Maternal corticosteroid therapy: If an infant is of <34 weeks’ gestation with the evidence of pulmonary immaturity (L/S < 2:1), The mother should be given betamethasone or dexamethasone over 48 hours. It is appropriate to administer IM to all pregnant women who are likely to deliver in 1 week between 24 and 34 weeks.
Dose:
Inj. betamethasone 12 mg IM every 12 hr, 4 doses;
Or Ini. dexamethasone 6 mg IM (every 12 hr, 4 doses) fist dose of surfactant (cost is high) into the trachea of the symptomatic preterm baby immediately alter birth or during the first 24 hours of life.

Immediate Treatment of Respiratory Distress Syndrome?

Oxygen: Lowest concentration of humidified Oxygen to maintain the SPO2.

Surfactant replacement therapy: Early administration of exogenous surfactant via the endotracheal tube to premature infants significantly reduces the severity of RDS. The surfactant is indicated in all neonates with RDS. The route of administration is intratracheal. It can either be given as rescue treatment in neonates or prophylactically in all neonates <28 weeks of gestation. Even those babies who have been given surfactants will need ventilatory support.
Beractant (Suravanta): 4 ml/kg via endotracheal tube q 6 hours x 4 doses.
Colfosceril palmitate (Exosurf): 5 ml/kg via endotracheal tube q 12 hours x 2-4 doses.Follow blood pressure and cardiac function carefully.

Follow blood pressure and cardiac function carefully. Fluid and electrolyte balance should be maintained, but relative dehydration decreases the incidence and severity of RDS. Metabolic acidosis should be corrected with bicarbonate infusion. Antibiotic is given to prevent secondary infection and sepsis.

Source:

Essence of Pediatrics by Prof MR Khan and Prof Ekhlasur Rahman
Guyton Physiology

For More Information:

Wikipedia

www.nhlbi.nih.go

www.nhs.uk (It’s really good to understand)

Surfactant Replacement Therapy for Preterm and Term Neonates With Respiratory Distress

The Dangers of Respiratory Distress Syndrome in Newborns

by Health Science Channel

Thanks that’s for all now.