Respiratory distress syndrome

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<p>Respiratory Distress Syndrome</p> <p>Respiratory Distress SyndromeMax Angelo G. TerrenalVeterans Memorial Medical Center Post-Graduate Intern1Respiratory Distress Syndromeor Hyaline Membrane DiseaseRDS or HMD is an acute lung disease of the newborn caused by Pulmonary Surfactant Deficiency</p> <p>Most common cause of respiratory distress in premature infants, correlating with structural &amp; functional lung immaturity. </p> <p>2acute lung diseasenewborn Pulmonary Surfactant DeficiencyRDS or HMD is an acute lung disease of the newborn caused by Pulmonary Surfactant Deficiency</p> <p>Most common cause of respiratory distress in premature infants, correlating with structural &amp; functional lung immaturity. </p> <p>3IncidencePremature InfantsInversely related to gestational age and birth weight60-80% of 37 weeksPremature InfantsInversely related to gestational age and birth weightXXXXXXXXXXXXXXXXXX60-80% of 37 weeks4Who are at risk?Maternal diabetesMultiple birthsCesarean deliveryPrecipitous deliveryAsphyxiaCold stressMaternal history of previously affected infantsHighest in preterm male or white infants</p> <p>Risk increases with maternal diabetes, multiple births, cesarean delivery, precipitous delivery, asphyxia, cold stress and a maternal history of previously affected infantsHighest in preterm male or white infants</p> <p>5Who are less likely to have RDS?Chronic or pregnancy-associated hypertensionMaternal heroin useProlonged rupture of membranesAntenatal corticosteroid prophylaxis</p> <p>Risk is reduced in pregnancies with chronic or pregnancy-associated hypertension, maternal heroin use, prolonged rupture of membranes, and antenatal corticosteroid prophylaxis</p> <p>6EtiologySurfactant deficiency(decreased production and secretion)Surfactant deficiency (decreased production and secretion) is the primary cause of RDSThe failure to attain an adequate FRC and the tendency of affected lungs to become atelectatic correlate with high surface tension and the absence of pulmonary surfactant.7</p> <p>SurfactantThe major constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin), phosphatidylglycerol, apoproteins (surfactant proteins SP-A, SP-B, SP-C, and SP-D), and cholesterol XXXXXXXXXXXXXXXXXX</p> <p>With advancing gestational age, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells (Fig. 95-3). These surface-active agents are released into the alveoli, where they reduce surface tension and help maintain alveolar stability by preventing the collapse of small air spaces at end-expiration</p> <p>8Pathophysiology</p> <p>With advancing gestational age, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells. XXXXXXXXXXXXXXXXXXThese surface-active agents are released into the alveoli, where they reduce surface tension and help maintain alveolar stability by preventing the collapse of small air spaces at end-expiration. XXXXXXXXXXXXXXXXXXBecause of immaturity, the amounts produced or released may be insufficient to meet postnatal demands. XXXXXXXXXXXXXXXXXXSynthesis of surfactant depends in part on normal pH, temperature, and perfusion.</p> <p>9Assessment of Fetal Lung MaturityLecithin:sphingomyelin ratio in amniotic fluid: &gt;2 means mature lungs 60 breaths/minProminent gruntingIntercostal and subcostal retractionsNasal flaringCyanosisBreath sounds may be normal or diminishedWith harsh tubular quality on deep insipirationFine rales may be heardEarly onsetRapid and shallow respirationsTachypnea &gt; 60 breaths/minProminent gruntingIntercostal and subcostal retractionsNasal flaringCyanosisBreath sounds may be normal or diminishedWith harsh tubular quality on deep insipirationFine rales may be heard</p> <p>14Natural CourseSeverity peaks at 24-48 hours, resolution by 72-96 hours (without surfactant therapy)If not treated, BP may fallFatigue, cyanosis, and pallor increase, and grunting disappears as the condition worsens Apnea and irregular respirations : immediate interventionMixed respiratory-metabolic acidosis Respiratory failure </p> <p>The natural course of untreated RDS is characterized by progressive worsening of cyanosis and dyspnea. XXXXXXXXXXXXXXXXXXIf the condition is inadequately treated, blood pressure may fall; cyanosis and pallor increase, and grunting decreases or disappears, as the condition worsens.XXXXXXXXXXXXXXXXXXApnea and irregular respirations are ominous signs requiring immediate intervention. XXXXXXXXXXXXXXXXXXPatients may also have a mixed respiratory-metabolic acidosis, edema, ileus, and oliguria. Respiratory failure may occur in infants with rapid progression of the disease.</p> <p>15OutcomeImprovementSpontaneous DiuresisImproved Blood Gas at lower inspired oxygenDeathSevere impairment of gas exchangeAlveolar air leaksPulmonary hemorrhageIVHImprovement is often heralded by spontaneous diuresis and improved blood gas values at lower inspired oxygen levels and/or lower ventilator support. Death can be due to severe impairment of gas exchange, alveolar air leaks (interstitial emphysema, pneumothorax), pulmonary hemorrhage, or IVH. Death may be delayed by weeks or months if BPD develops in infants with severe RDS.16Diagnosis</p> <p>The clinical course, chest radiographic findings, and blood gas and acid-base values help establish the clinical diagnosis.XXXXXXXXXXXXXXXXXXOn radiographs, the lungs may have a characteristic but not pathognomonic appearance that includes a fine reticular granularity of the parenchyma and air bronchogramsXXXXXXXXXXXXXXXXXX17Differential DiagnosisEarly-onset sepsis Maternal Group B StreptococcusPneumoniaCyanotic heart disease TAPVRPersistent Pulmonary HypertensionTransient tachypnea of newbornSpontaneous pneumothoraxPleural effusionDiaphragmatic hernia Lobar emphysema </p> <p>early-onset sepsis may be indistinguishable from RDS. XXXXXXXXXXXXXXXXXXIn pneumonia manifested at birth, the chest roentgenogram may be identical to that for RDS. XXXXXXXXXXXXXXXXXXCyanotic heart disease (total anomalous pulmonary venous return) can also mimic RDS both clinically and radiographically. Echocardiography with color-flow imaging should be performed in infants who show no response to surfactant replacement, to rule out cyanotic congenital heart disease as well as ascertain patency of the ductus arteriosus and assess pulmonary vascular resistance (PVR). XXXXXXXXXXXXXXXXXXPersistent pulmonary hypertension, aspiration (meconium, amniotic fluid) syndromes, spontaneous pneumothorax, pleural effusions can generally be differentiated from RDS through radiographic evaluation. XXXXXXXXXXXXXXXXXXTransient tachypnea may be distinguished by its short and mild clinical course and is characterized by low or no need for oxygen supplementation. Congenital alveolar proteinosis (congenital surfactant protein B deficiency) is a rare familial disease that manifests as severe and lethal RDS in predominantly term and near-term infants.18PreventionAvoidance of unnecessary or poorly timed cesarean section, appropriate management of high-risk pregnancy and labor, and prediction of pulmonary immaturity with possible in utero acceleration of maturationAdministration of antenatal corticosteroids to women between 24 and 34wk of gestation significantly reduces the incidence and mortality of RDS as well as overall neonatal mortality.XXXXXXXXXXXXXXXXXXAntenatal steroids also reduce (1) the need for and duration of ventilatory support and admission to a neonatal intensive care unit (NICU) and (2) the incidence of severe IVH, necrotizing enterocolitis, early-onset sepsis, and developmental delay.</p> <p>19TreatmentAvoid hypothermia IV Calories and fluids Warm humidified oxygen CPAP : prevents collapse of surfactant-deficient alveoli Assisted ventilation High-frequency ventilation (HFV )To avoid hypothermia and minimize oxygen consumption, the infant should be placed in an incubator or radiant warmer, and core temperature maintained between 36.5 and 37?CXXXXXXXXXXXXXXXXXXCalories and fluids should initially be provided intravenously. For the 1st 24hr, 10% glucose and water should be infused through a peripheral vein at a rate of 65-75mL/kg/24hr. Electrolytes should be added on day 2 in the most mature infants and on days 3 to 7 in the more immature ones. Fluid volume is increased gradually over the 1st week. XXXXXXXXXXXXXXXXXXWarm humidified oxygen should be provided at a concentration initially sufficient to keep arterial oxygen pressure between 40 and 70mmHg (85-95% saturation) in order to maintain normal tissue oxygenation while minimizing the risk of oxygen toxicity. XXXXXXXXXXXXXXXXXXIf oxygen saturation cannot be kept &gt; 85% at inspired oxygen concentrations of 40-70% or greater, applying CPAP at a pressure of 5-10cm H2O via nasal prongs is indicated and usually produces a sharp improvement in oxygenation.XXXXXXXXXXXXXXXXXXInfants with respiratory failure or persistent apnea require assisted mechanical ventilation. The goal of mechanical ventilation is to improve oxygenation and elimination of carbon dioxide without causing pulmonary injury or oxygen toxicity.XXXXXXXXXXXXXXXXXXHFV may improve the elimination of carbon dioxide and improve oxygenation in patients who show no response to conventional ventilators and who have severe RDS, interstitial emphysema, recurrent pneumothoraces, or meconium aspiration pneumonia. 20Surfactant replacement therapyis initiated as soon as possible in the hours after birth. Repeated dosing is given via the endotracheal tube every 6-12hr for a total of 2 to 4 doses, depending on the preparation. Immediate effects of surfactant replacement therapy include improved alveolar-arterial oxygen gradients, reduced ventilatory support, increased pulmonary compliance, and improved chest radiograph appearance .XXXXXXXXXXXXXXXXXXTreatment is initiated as soon as possible in the hours after birth. Repeated dosing is given via the endotracheal tube every 6-12hr for a total of 2 to 4 doses, depending on the preparation. Exogenous surfactant should be given by a physician who is qualified in neonatal resuscitation and respiratory management and who is able to care for the infant beyond the 1st hr of stabilization.</p> <p>21</p>