1. Hyaline Membrane Disease
Li wei-zhong

2. Introduction
HMD, frequently referred to as neonatal respiratory distress syndrome (NRDS), occurs primarily in premature infant.
There is rapid or labored breathing, beginning at or immediately after birth.
Surfactant deficiency is the primary cause of HMD.

3. Epidemiology HMD occurs primarily in Premature infant
Infants less than 28 wk of GA: 60-80%
Infants between 28 and 32 wk: 60%
Infants between 32 and 36wk of GA: 15-30%
Infants beyond 37 wk of GA: 5%

4. Epidemiology
The incidence of HMD is highest among premature male or white infants.
The incidence is higher for cesarean section without labor than vaginal delivery.
HMD is more common in gestational diabetes and in insulin-dependent mother.
Second-born twin is at greater risk.

5. Etiology Surfactant Deficiency Prematurity predisposes
Cesarean section
Male > female
White > nonwhite
Second- born twin

6. Etiology Maternal diabetes Maternal hemorrhage Maternal stress
Intrauterine growth retardation
Prolonged rupture of membranes (>16 hr)
Asphyxia

7. Etiology Hypoxemia Pulmonary Ischemia Hypovolemia and Hypotension
Cold Stress
High Oxygen concentration

8. Pathophysiology
Surfactant deficiency increases surface tension in Alveolus
Surfactant decreases surface tension in the alveolus during expiration, allowing the alveolus to remain partly expanded and in that way maintaining a functional residual capacity.

9. Pathophysiology
The surface tension in the alveolus results in poor lung compliance and atelectasis.
decreased tidal volumes
increased physiologic dead space
Poor lung distensibility
Poor alveolar stability

10. Pathophysiology increased work of breathing
perfused but not ventilated alveoli
Ventilated but not perfused alveoli
Respiratory failure

11. Pathophysiology
The combination of hypercarbia, hypoxia and acidosis produces pulmonary arterial vasoconstriction with increased right-to-left shunting through the foramen ovale and ductus arteriosus and
within the lung itself.
Reduced effective pulmonary blood flow

12. Pathology Lung extensive atelectasis Injury to epithelial calls
Lung congestion and edema
Lung hemorrhage
Hyaline membranes contains fibrin and cellular products

13. Clinical Findings
Onset near the time of birth or within 4-6 hr after birth
Rapid, shallow respirations ≥ 60/ min
Intercostal and subcostal retractions and progressive respiratory distress
Expiratory grunt
Cyanosis or pallor

14. Clinical Findings Hypothermia hypotension Fine inspiratory rales
Pulmonary or intraventricular hemorrhage
Course to death or improvement 3-5d

15. Clinical Findings Laboratory diagnosis Arterial blood gases Hypoxemia
Hypercapnia
Mixed respiratory-metabolic Acidemia

16. Clinical Findings Lecithin/sphingomyelin ratio (L/S)<2:1
Low phosphatidylglycerol(PG)
Low saturated phosphatidylcholine (PC)
Low surfactant protein A/saturated PC (SP-A/SPC) ratio

17. Clinical Findings Chest x-ray Typical pattern at 24 hr after birth
Ground-glass appearance
Air bronchograms
Doming of diaphragm and underexpansion (white out)

18. Diagnosis Tachypnea, cyanosios, and expiratory grunting
Poor air movement despite increased work of breathing
Blood gases, pH values, and other laboratory finding
Chest x-ray showing hypoexpansion and air bronchograms

19. Differential Diagnosis
Wet lung of the newborn (Transient dyspnea)
Amniotic fluid and meconium aspiration syndrome
Group B streptococcal pneumonia
Diaphragmatic hernia

20. Treatment
The basic defect requiring treatment is inadequate pulmonary exchange of oxygen and carbon dioxide.
Metabolic acidosis and circulatory insufficiency are secondary manifes-tations.

21. Treatment Supportive care of LBW infant Surfactant replacement therapy
Oxygen therapy
Continuous positive airway pressure (CPAP)
Assisted mechanical ventilation
Blood pressure support
Alkali therapy

22. Prevention Prenatal glucocorticoids for >24 hr
Prophylactic administration of exogenous surfactant at birth