Respiratory Distress Syndrome (Hyaline Membrane Disease)

Question 1

Definition

Answer 1

Respiratory distress syndrome occurs primarily in premature infants; its incidence is inversely related to gestational age and birth weight. It occurs in 60-80% of infants <28 wk of gestational age.

Question 2

Surfactant definition

Answer 2

35 wk. A lipoprotein produced by alveolar cells type II starting after 20 th week of gestation and mature after 35 th weeks (near term).

Question 3

Causes of RDS

Answer 3

1. Prematurity o The leading cause of RDS o Incidence & severity of RDS are related inversely to the gestational age of the newborn infant e.g. about 60% of prematures < 28 weeks develop RDS
2. Infant of diabetic mother
   - Fetal cortisone is essential for surfactant production
   - Maternal hyperglycemia p fetal hyperinsulinemiap ļļ fetal cortisone
3. Cesarean section(CS) and precipitate labor:
   - Due to lack of stressful delivery p reduced fetal cortisone.
4. Intrapartum asphyxia
   - Due to hypoxemia of alveolar cells type II.
5. Others : Second twin, male Sex, RDS in Siblings

Question 4

Patho-physiology OF RDS

Answer 4

1. ⬇️ Surfactant ➡️⬆️ alveolar surface tension ➡️ diffuse alveolar collapse during expiration
2. Low lung compliance (higher pressure is required to initiate lung inflation)pincreased work of breathing ➡️ respiratory distress
   . 3. Impaired gas exchange with ➡️Hypoxemia Hypercapnia Respiratory acidosis
3. Hypoxemia➡️ alveolar cells type II dysfunction➡️ more surfactant deficiency ➡️ Progressive atelectasis

Question 5

Clinical picture of of RDS

Answer 5

o Progressive signs of respiratory distress are noted soon after birth and include the following:

y Tachypnea y Nasal flaring y Expiratory grunting (from partial closure of glottis) y Subcostal and intercostal retractions y Cyanosis y Extremely immature in neonates may develop apnea and/or irregular respirations y Patients may also have edema, ileus, and oliguria

o Course

Endogenous surfactant production usually become sufficient by 48-72 hoursp Clinical improvement is often heralded by spontaneous diuresis and improved blood gas values at lower inspired oxygen levels and/or lower ventilator support y Severe cases may end in death or complications

Question 6

Diagnosis

Answer 6

1. Clinical
   RDS is suspected clinically in cases with early respiratory distress in presence of risk factors particularly prematurity
2. Chest radiographs

A. Mild to moderate RDS o Bilateral, diffuse, reticulo- granular infiltrates (ground-glass appearances) o Air bronchograms represent aerated airways superimposed on a background of collapsed alveoli o Poor lung expansion (small lungs volumes)

B. Severe RDS Opacification of both lungs (White airless lungs)

3. Blood gases analysis
   o In Milder RDS: Hypoxemia o In Severe RDS: Hypoxemia +
   Hypercapnia + Respiratory acidosis
4. Sepsis workup: blood cultures, a complete blood count with differential, and C-reactive protein
   5-Fetal lung maturity tests

Question 7

Differential diagnosis:

Answer 7

1. Early-onset sepsis
2. Pneumonia
3. Cyanotic heart disease
4. Persistent pulmonary hypertension,
5. Aspiration (meconium, amniotic fluid) syndromes,
6. Spontaneous pneumothorax,
7. Pleural effusions,
8. Congenital anomalies such as cystic adenomatoid malformation,
9. Pulmonary lymphangiectasia,
10. Diaphragmatic hernia
11. Lobar emphysema

Question 8

Prevention

Answer 8

 Antenatal corticosteroid therapy (betamethasone 12 mg/dose IM for 2 doses, 24 hrs apart, for pregnant women 24-34 wks’ gestation at high risk of preterm delivery within the next 7 days.

 Prophylactic surfactant therapy in preterm infants <27 wks’ gestation.

 Early CPAP administration in the delivery room.

Question 9

Treatment

Answer 9

 Administer oxygen (depending on the severity of illness).

 Provide appropriate intravenous fluids  Correct metabolic abnormalities (acidosis, hypoglycemia).

 Provide an adequate nutrition. Infants with sustained RR >60 breaths/min

should not be fed orally & should be maintained on gastric tube or total

parentral nutrition.

 Obtain a blood culture & begin an antibiotic coverage (ampicillin +

gentamicin) while awaiting the results of the culture.

 Initiate continuous positive airway pressure (CPAP) as early as possible.

 Start MV (mechanical ventilation) if respiratory acidosis (PaCO2 >60 mmHg,

PaO2 <50 mmHg or SaO2 <90%), or severe frequent apnea.

 Administer surfactant therapy: early rescue therapy within 2 hrs after birth by

ETT (endotracheal tube).

Question 10

Complications:due to prematurity or management

Answer 10

Patent Ductus Arteriosus Pulmonary Air Leaks: pneumomediastinum, Pneumothorax Pulmonary hemorrhage Intraventricular hemorrhage Bronchopulmonary Dysplasia (Chronic Lung Disease) Retinopathy of Prematurity (Retrolental Fibroplasia)

Question 11

Retinopathy of prematurity (Retro-lental fibroplasia) definition + risk factors

Answer 11

Definition o Retinal vascular proliferation which may progress to retinal detachment, fibrosis and even blindness
Risk factors o All babies < 1500 g birth weight or < 32 weeks’ gestational age o Exposed to uncontrolled high concentrations of oxygen (controversial)