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Hyaline Membrane Disease

Hyaline Membrane Disease. Li wei-zhong. 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.

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Hyaline Membrane Disease

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  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

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