Hyaline Membrane Disease,站,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.,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%,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.,站,Etiology,Surfactant Deficiency Prematurity predisposes Cesarean section Male female White nonwhite Second- born twin,Etiology,Maternal diabetes Maternal hemorrhage Maternal stress Intrauterine growth retardation Prolonged rupture of membranes (16 hr) Asphyxia,Etiology,Hypoxemia Pulmonary Ischemia Hypovolemia and Hypotension Cold Stress High Oxygen concentration,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.,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,Pathophysiology,increased work of breathing perfused but not ventilated alveoli Ventilated but not perfused alveoli Respiratory failure,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,Pathology,Lung extensive atelectasis Injury to epithelial calls Lung congestion and edema Lung hemorrhage Hyaline membranes contains fibrin and cellular products,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,Clinical Findings,Hypothermia hypotension Fine inspiratory rales Pulmonary or intraventricular hemorrhage Course to death or improvement 3-5d,Clinical Findings,Laboratory diagnosis Arterial blood gases Hypoxemia Hypercapnia Mixed respiratory-metabolic Acidemia,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,Clinical Findings,Chest x-ray Typical pattern at 24 hr after birth Ground-glass appearance Air bronchograms Doming of diaphragm and underexpansion (white out),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,Differential Diagnosis,Wet lung of the newborn (Transient dyspnea) Amniotic fluid and meconium aspiration syndrome Group B streptococcal pneumonia Diaphragmatic hernia,Treatment,The basic defect requiring treatment is inadequate pulmonary exchange of oxygen and carbon dioxide. Metabolic acidosis and circulatory insufficiency are secondary manifes-tations.,Treatment,Supportive care of LBW infant Surfactant replacement therapy Oxygen therapy Continuous positive airway pressure (CPAP) Assisted mechanical ventilation Blood pressure support Alkali therapy,Prevention,Prenatal glucocorticoids for 24 hr Prophylactic administration of exogenous surfactant at birth,站,