新生儿呼吸窘迫综合症(Neonatal-Respiratory-Distress-Syndrome)课件

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Neonatal Respiratory Distress Syndrome(NRDS)Neonatal Respiratory Distress 1Hyaline membrane disease(HMD)Hyaline membrane disease(HMD)Most Most common common cause cause of of respiratory respiratory failure failure in in the the first days in the premature infantsfirst days in the premature infantsReason Reason is is surfactant surfactant insufficient insufficient in in lungs lungs which which lead lead to to breathing breathing failure failure and and need need the the assistant assistant ventilation ventilation Occurring Occurring in in 12%12%of of newborn newborn infants,infants,increases increases by by smaller smaller GA:GA:50%50%of of GA GA 28w,28w,less less than than 30%30%of of 3236w)3236w)Hyaline membrane disease(HMD)2SurfactantKeep the lung alveoli openStart synthesis in GA 2428w by lung type II alveolar cellsIncrease in 2835w,but produce adequate amounts after 35wdouble in alveolar within 24h after birth,to adult level after 37d of birthhalf-life 1224hSurfactantKeep the lung alveol3Surfactant CompositionPhospholipid(PL)90%(neutral 5%)90%(neutral 5%)Phosphatidyl cholin(PC,Lecithin)40 Phosphatidyl cholin(PC,Lecithin)40 Phosphatidyl glycerol(PG)5 Phosphatidyl glycerol(PG)5 Sphingonyeline(S)2%Sphingonyeline(S)2%others others ProteinProtein 10 10 A,3035kDa,18 oligomer,A,3035kDa,18 oligomer,D,43kDa,12 oligomer D,43kDa,12 oligomer B,8kDa,dimer,B,8kDa,dimer,C,4kDa,dimer C,4kDa,dimer Surfactant CompositionPhosphol4Function of Pulmonary Surfactantlower alveolar surface tension,reduces respiratory workMaintain alveoli Maintain alveoli inflation and and functional residual capacity Accelerate lung fluid absorption,Accelerate lung fluid absorption,reduce alveolar effusion reduce alveolar effusionPathogen Opsonization,alveolar macrophage activationPathogen Opsonization,alveolar macrophage activation Effects:Effects:increase oxygenation,increase oxygenation,ameliorate ventilation/perfusion ameliorate ventilation/perfusion anti-inflammation anti-inflammation Function of Pulmonary Surfacta5EtiologyF Risk factors:Caucasian or male babies Previous birth of baby with RDS Cesarean delivery(more water in lung)Perinatal asphyxia Multiple births(multiple birth babies are often premature)Infants of diabetic mothers(too much insulin in a babys system may delay surfactant production)Perinatal infection Babies with patent ductus arteriosus(PDA)Etiology Risk factors:6PathophysiologyFLack of surfactant in the lungs of infants Avery and Mead,Am J Dis Child 1959 progressive atelectasis loss of functional residual capacity(FRC)alteration of ventilation-perfusion ratioFWeak respiratory muscles and compliancy of chest wall impair alveolar ventilationFDiminished oxygenation,cyanosis and acidosisincreased pulmonary vascular resistance(PVR)right-to-left shunting through ductus arteriovenous intrapulmanary ventilation-perfusion mismatchPathophysiology7Etiology and PathophysiologyF Pulmonary immaturity results in surfactant deficiencyF Alveoli collapse at the end of expiration leads to respiratory failureF Surfactant deficiency may arise after asphyxia /shock and acidosisalveolar surface tension is higherDiminished PSPulmonary atelectasisImpaired gas exchange(hypoxia and acidosis)Pulmonary artery hypertensionRightto-left heart shuntPulmonary capillary permeability increaseForming pulmonary hyaline membraneEtiology and Pathophysiologyal8Pathologyatelectasis,pulmonary edema,vascular congestion,hemorrhage,generalized capillary leak and mucosal necrosis leads to the smaller air filled terminal airways;the respiratory bronchioles and alveolar ducts are surrounded by collapsed alveoli filled with debris in a near uniform distribution(hyaline membranes)Pathologyatelectasis,pulmonar9Clinical PresentationFPresent at birth or first 2 to 6 h of birth:respiratory difficulty that gets progressively worse tachypnea(rapid breathing)cyanosis(blue coloring)with increasing oxygen requirementschest retractions nasal flaring grunting sounds with breathingFCharacterized by progressive worsening of cyanosis and dyspneaFsymptoms usually peak on 2 to 3 day,and will recovery after 3 d Clinical PresentationPresent a10DiagnosisDiagnosis can be decided by a combination of assessments,including GA,a history of risk factors,the signs,chest X-ray and blood gases.DiagnosisDiagnosis can be deci11Radiographic Changes of RDS a bell shaped thorax with diffuse and symmetrical“ground glass”called reticulogranular pattern with“air bronchogram”,or severe bilateral opacity and obliterate the cardiac border,“white-out lung”Radiographic Changes of RDS a12Laboratory FindingsFMixed acidosisFLecithin(L)/Sphingomyelin(S)0.6,PaO250mmHg or TcSO285%Pressure:410cm H2O,flow 5L/min,32C,humidity 100%FConventional Mechanical Ventilation(CMV)Indication:PaO250mmHg or TcSO270mmHg;or frequent apnea Complication:PAL(pulmonary air leak)BPD(bronchopulmonary dysplasia;or CLD)Retinopathy of prematurity(ROP)VAP(ventilator-associated pneumonia)Respiratory ManagementContinuo18Application of Pulmonary SurfactantIntratracheal instillation:50200mg/kg,612h intervalFNeonatal Respiratory Distress Syndrome(NRDS)Fmeconium aspiration syndrome(MAS)FPneumonic Respiratory failureFAcute lung injury,ARDSFRespiratory failure after open-chest surgery or lung transplantationApplication of Pulmonary Surfa19PreventionFAvoidance of preterm birth:most importantFCareful maternal care and fetal monitoringFAccelerate fetal lung maturation Maternal glucocorticoids(betamethasone,examethasone,)24h before birthAdministration of a first dose of PS into the trachea of symptomatic premature infants immediately after birth or during the first 24hr of life The most effective way to prevent RDS is to prevent preterm delivery.If preterm delivery is inevitable,attempts to“mature the fetus”are reasonable.PreventionAvoidance of preterm20Question:What is NRDS/HMD?Which infants do not have adequate surfactant?What are risk factors of NRDS?What is the clinical course of NRDS?How do you diagnose NRDS?What are other causes of respiratory distress?How do you manage or prevent NRDS?Question:21Thank you!22
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