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71 Cards in this Set
- Front
- Back
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How many infants with RDS each year?
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50,000
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What is clinical syndrome of RDS?
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respiratory failure with atelectasis, hypoxemia, decreased lung compliance, small airway epithelial damage, pulmonary edema
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What is the principle cause of RDS?
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pulmonary surfactant deficiency
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What does pulmonary sufactant do
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decreases the surface tension at the air/fluid interface in the alveoli and prevents alveolar collapse, facilitates clearance of pulmonary fluid, prevents pulmonary edema, and stabilizes alveoli during aeration
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What stimulates the synthesis and secretion of pulmonary surfactant?
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endogenous cortisol
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How long before sufficient pulmonary surfactant?
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34 weeks gestation
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What is result of lack of surfactant?
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surface tension in the alveoli is so great that alveoli collapse resulting in poor gas exchange
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What does aeration of the surfactant deficient lung result in?
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cyclic collapse and distention of bronchioles with bronchiolar epithelial injury and necrosis
epithelial damage causes pulmonary edema |
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What is hyaline membrane disease?
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necrotic epithelial debris and proteins form a fibrous hyaline membranes, not specific to surfactant deficiency
aka, RDS |
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What are risk factors for RDS?
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prematurity, mal, gestational DM, cesarean section with no labor, second born twins, perinatal asphyxia and maternofetal hemorrhage
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What s/s of RDS?
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tachypnea (RR 65 breaths/minute), cyanosis, retracting respirations, grunting, nasal flaring hypoxemia, hypercapnia, mixed respiratory and metabolic acidosis
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When do clinical manifestations classically present?
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within the first 6hrs of life
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What is the first sign of RDS?
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tachypnea
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What is tachypnea compensating for?
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inadequate ventilation, hypercapnia, and acidosis
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How can RDS be prevented?
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prolong pregnancy long enough for fetal lungs to mature, accelerate production of pulmonary surfactant
suppress premature labor with tocolytic |
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What is used to accelerate fetal lung maturation and decrease the incidence and severity of RDS?
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maternal administration of gluccorticoids
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What are the only 2 recommended regimens to accelerate lung maturation?
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betamethasone 12mg IM Q24 for 2 doses or dexamethasone 6mg IM Q12h for 4 doses
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What does a ratio of lecithin to sphingomyelin greater than 2 indicate?
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functionally mature fetal lungs and a decreased risk of RDS
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What tx reduces neonatal mortality and risk for periventricular leukomalacia
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betamethasone only
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How do glucocorticoids work?
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increase production of fibroblast pneumocyte factor, which stimulates the biosynthesis of surfactant in type II pneumocytes
mimics the physiological response of fetal lungs to theincreased cortisol production that normally begins at 30-32 weeks gestation |
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Low RDS with what conditions in mother?
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HTN, infection, CV disease, hemoglobinopathis, heroin addiction, premature rupture of membranes greater than 48hrs, decreased placental function
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Why should all pts with severe RDS receive AB?
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it is difficult to distinguish between RDS and infection
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RDS a consequence of?
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surfactant deficiency
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What secretes human surfactant?
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type II alveolar epithelial cells of the lung
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What does human surfactant contain?
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80% phospholipids, 8% neutral lipids, 12% proteins
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What is the major surface active component in human surfactant?
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dipalmitoylphosphatidylcholine (DPPC), aka colfosceril or lecithin
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What enhances spreadability and surface adsorption of human surfactant?
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other phospholipids and 4 surfactant apoproteins (SP-A, SP-B, SP-C, SP-D)
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What apoproteins play a role in immune regulation and providing host defense?
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SP-A, SP-D
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What else does SP-A do?
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regulate alveolar surfactant reuptake and metabolism
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What are the 2 most important apoproteins responsible for promoting adsorption and surface spreading of the surfactant in the alveoli to form phospholipid monolayer?
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SP-B SP-C
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Where are natural sufactants from?
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bovine or porcine lung lipid or lavage extracts, or human amniotic fluid
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What are modified natural surfactants?
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lung lipid extracts supplemented with phospholipids or other components
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Survanta
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beractant, modified natural surfactant
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Infasurf
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calfactant, natural surfactant
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Curosurf
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poractant alfa, natural surfactant
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Exosurf
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colfosceril palmitate, synthetic surfactant without a protein analog, not available
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Surfaxin
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lucinactant, synthetic surfactant that contains a protein analogue, new awaiting approval for tx and prevention RDS
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What surfactants FDA approved for prevention of RDS?
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beractant (Survanta) and calfactant (Infasurf)
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What surfactants approved for tx of RDS?
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beractant (Survanta), poractant alfa (Curosurf), colfosceril palmitate (Exosurf)
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How is beractant (Survanta) produced?
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mincing bovine lung, cholesterol is removed and synthetic DPPC is added to improve surface activity, SP-B is removed with cholesterol, only trace amounts of SP-B, 99% is SP-C
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How is calfactant (Infasurf) produced?
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washings of newborn calves lungs, fewer contaminating lung cell components, 40% SP-B, 60% SP-C
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How is poractant alfa produced?
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extracted from washings of pigs lungs and is purified by liquid gel chromatography to remove neutralized lipids (cholesterol), 99% lipids, 1% apoproteins (SP-B 30% and SP-C 70%)
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Do any of the surfactants contain SP-A?
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no
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What are the effects of exogenously administered surfactant in RDS?
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oxygenation and lung compliance improve, supplemental oxygen and mechanical ventilation reduced, decrease in incidence of pneumothorax and PIE, decrease in complications
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How much does survival increase with the use of surfactant in RDS?
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40%
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How much is mortality decreased in RDS?
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to 20%
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What route are surfactants given?
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intratracheally
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Is more than 1 dose of surfactant needed?
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usually
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What causes nonresponse to surfactant?
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surfactant inhibition by proteins that leaked into alveolar space, inactivation of surfactant by inflammatory mediators, presence of conditions that can decrease surfactant effectiveness (pulmonary edema), poor delivery to alveoli
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How does age affect response to surfactant?
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response decreases with increase in age
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What is major clinical indicator for retreatment of surfactant?
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persistence of respiratory failure
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What a/A ratio for retreatment with surfactant?
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less than 0.2
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What is average number of doses of surfactant?
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2
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Does prophylactic tx always prevent RDS?
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no
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When is prophylactic given?
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within 30 min after birth, theoretically before 1st breath to avoid early lung injury in RDS that interferes with surfactant distribution, bioavailability, and effectiveness
as soon as clinical signs of RDS appear |
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table 94-6
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94-6
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What AE from surfactants?
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bradycardia and oxygen desaturation secondary to vagal stimulation and airway obstruction during administration
others: mucous plugging with obstruction, BP changes, altered EEG tracings increased risk of pulmonary hemorrhage, apnea |
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What is tx for apnea?
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methylxanthine
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How do natural sufactants (calfactant and poractant alfa) compare to modified natural surfactant (Survanta(beractant))?
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natural have longer duration, require less supplemental oxygen and mean airway pressures
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What is approved for prevention of RDS?
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new synthetic surfactant: lucinactant
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What is lucinactant?
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phospholipids and high concentration of recombinant proteins designed to mimic human SP-B
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Which surfactants must the pt be disconnected from the ventilator?
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beractant (Survanta) and poractant alfa (Curosurf)
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How can calfactant be given?
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disconnect ventilator or via a side port adapter into the ETT without disconnecting the vent
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What potential AE for all surfactants from natural sources (beractant, calfactant, and poractant alfa)?
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potentially antigenic, may cause immunologic response (no reports)
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How is diuresis in the first 48-72 hrs of life?
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urine output greater than 80% of fluid intake
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What is result of diuresis?
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improvement in pulmonary function from decrease of alveolar or interstitial pulmonary fluid
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What is result if pt doesn't have this diuresis or has it after 72 hrs?
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more likely to develop bronchopulmonary dysplasia
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What is benefit of using early prophylactic furosemide?
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greater increase in urine output, decrease in ventilator mean airway pressures and improvement in oxygenation
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What AE from using furosemide?
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hemodynamic instability and greater postnatal wt loss, hypercalciuria, renal calcifications, hyponatremia, hypochloremia and hypokalemia
patency of the ductus arteriosus and worsen pulmonary edema |
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Is routine administration of diuretics in RDS indicated?
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no
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When might furosemide be used?
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signs of pulmonary edema with compromised pulmonary function (hypoxemia and hypercapnia)
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