Respiratory distress syndrome
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RDS report during internship
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Respiratory distress syndrome
- 1. Respiratory Distress Syndrome Max Angelo G. Terrenal Veterans Memorial Medical Center Post-Graduate Intern
- 2. Respiratory Distress Syndrome or Hyaline Membrane Disease
- 3. acute lung disease new bo r n Pulmonar y Sur factant Deficiency
- 4. Incidence ā¢ Premature Infants ā¢ Inversely related to gestational age and birth weight ā¢ 60-80% of <28 weeks ā¢ 15-30% of 32-36 weeks ā¢ Rarely >37 weeks
- 5. Who are at risk? ā¢ Maternal diabetes ā¢ Multiple births ā¢ Cesarean delivery ā¢ Precipitous delivery ā¢ Asphyxia ā¢ Cold stress ā¢ Maternal history of previously affected infants ā¢ Highest in preterm male or white infants
- 6. Who are less likely to have RDS? ā¢ Chronic or pregnancy-associated hypertension ā¢ Maternal heroin use ā¢ Prolonged rupture of membranes ā¢ Antenatal corticosteroid prophylaxis
- 7. Etiology ā¢ Surfactant deficiency ā¢ (decreased production and secretion)
- 8. Surfactant
- 10. Assessment of Fetal Lung Maturity ā¢ Lecithin:sphingomyelin ratio in amniotic fluid: ā¢ >2 means mature lungs ā¢ <1.5 means HMD
- 14. Clinical Manifestation ā¢ Early onset ā¢ Rapid and shallow respirations ā¢ Tachypnea > 60 breaths/min ā¢ Prominent grunting ā¢ Intercostal and subcostal retractions ā¢ Nasal flaring ā¢ Cyanosis ā¢ Breath sounds may be normal or diminished ā¢ With harsh tubular quality on deep insipiration ā¢ Fine rales may be heard
- 15. Natural Course ā¢ Severity peaks at 24-48 hours, resolution by 72-96 hours (without surfactant therapy) ā¢ If not treated, BP may fall ā¢ Fatigue, cyanosis, and pallor increase, and grunting disappears as the condition worsens ā¢ Apnea and irregular respirations : immediate intervention ā¢ Mixed respiratory-metabolic acidosis ā¢ Respiratory failure
- 16. Outcome ā¢ Improvement ā¢ Spontaneous Diuresis ā¢ Improved Blood Gas at lower inspired oxygen ā¢ Death ā¢ Severe impairment of gas exchange ā¢ Alveolar air leaks ā¢ Pulmonary hemorrhage ā¢ IVH
- 17. Diagnosis
- 18. Differential Diagnosis ā¢ Early-onset sepsis ā Maternal Group B Streptococcus ā¢ Pneumonia ā¢ Cyanotic heart disease ā TAPVR ā¢ Persistent Pulmonary Hypertension ā¢ Transient tachypnea of newborn ā¢ Spontaneous pneumothorax ā¢ Pleural effusion ā¢ Diaphragmatic hernia ā¢ Lobar emphysema
- 19. Prevention ā¢ Avoidance of unnecessary or poorly timed cesarean section, ā¢ appropriate management of high-risk pregnancy and labor, and ā¢ prediction of pulmonary immaturity with possible in utero acceleration of maturation
- 20. Treatment ā¢ Avoid hypothermia ā¢ IV Calories and fluids ā¢ Warm humidified oxygen ā¢ CPAP : prevents collapse of surfactant-deficient alveoli ā¢ Assisted ventilation ā¢ High-frequency ventilation (HFV )
- 21. ā¢ Surfactant replacement therapy ā¢ is initiated as soon as possible in the hours after birth. Repeated dosing is given via the endotracheal tube every 6-12 hr for a total of 2 to 4 doses, depending on the preparation.
Editor's Notes
- RDS or HMD is an acute lung disease of the newborn caused by Pulmonary Surfactant Deficiency Most common cause of respiratory distress in premature infants, correlating with structural & functional lung immaturity.
- RDS or HMD is an acute lung disease of the newborn caused by Pulmonary Surfactant Deficiency Most common cause of respiratory distress in premature infants, correlating with structural & functional lung immaturity.
- Premature Infants Inversely related to gestational age and birth weight XXXXXXXXXXXXXXXXXX 60-80% of <28 weeks XXXXXXXXXXXXXXXXXX 15-30% of 32-36 weeks XXXXXXXXXXXXXXXXXX Rarely >37 weeks
- Risk increases with maternal diabetes, multiple births, cesarean delivery, precipitous delivery, asphyxia, cold stress and a maternal history of previously affected infants Highest in preterm male or white infants
- Risk is reduced in pregnancies with chronic or pregnancy-associated hypertension, maternal heroin use, prolonged rupture of membranes, and antenatal corticosteroid prophylaxis
- Surfactant deficiency (decreased production and secretion) is the primary cause of RDS The 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.
- The major constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin), phosphatidylglycerol, apoproteins (surfactant proteins SP-A, SP-B, SP-C, and SP-D), and cholesterol XXXXXXXXXXXXXXXXXX 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
- With advancing gestational age, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells. XXXXXXXXXXXXXXXXXX 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. XXXXXXXXXXXXXXXXXX Because of immaturity, the amounts produced or released may be insufficient to meet postnatal demands. XXXXXXXXXXXXXXXXXX Synthesis of surfactant depends in part on normal pH, temperature, and perfusion.
- Amniotic fluid L/S ratio increases progressively with gestational age. L/S ratio greater than two signifies maturity of surfactant system of lung
- Surfactant is present in high concentrations in fetal lung homogenates by 20Ā wk of gestation, but it does not reach the surface of the lungs until later. It appears in amniotic fluid between 28 and 32Ā wk. Mature levels of pulmonary surfactant are present usually after 35Ā wk.
- Deficient synthesis or release of surfactant, together with small respiratory units and a compliant chest wall, produces atelectasis and results in perfused but not ventilated alveoli, causing hypoxia. XXXXXXXXXXXXXXXXXX Decreased lung compliance, small tidal volumes, increased physiologic dead space, and insufficient alveolar ventilation eventually result in hypercapnia. XXXXXXXXXXXXXXXXXX The combination of hypercapnia, 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. XXXXXXXXXXXXXXXXXX leak of plasma (proteinaceous material) into the alveolar spaces ācombine with fibrin & necrotic alveolar pneumocytes & form hyaline membrane Hyaline membranes: coagulum of sloughed cells and exudate, plastered against epithelial basement membrane XXXXXXXXXXXXXXXXXX Pulmonary blood flow is reduced and ischemic injury both to the cells producing surfactant and to the vascular bed results in an effusion of proteinaceous material into the alveolar spaces
- leak of plasma (proteinaceous material) into the alveolar spaces ācombine with fibrin & necrotic alveolar pneumocytes & form hyaline membrane XXXXXXXXXXXXXXXXXX Hyaline membranes: coagulum of sloughed cells and exudate, plastered against epithelial basement membrane
- Early onset Rapid and shallow respirations Tachypnea > 60 breaths/min Prominent grunting Intercostal and subcostal retractions Nasal flaring Cyanosis Breath sounds may be normal or diminished With harsh tubular quality on deep insipiration Fine rales may be heard
- The natural course of untreated RDS is characterized by progressive worsening of cyanosis and dyspnea. XXXXXXXXXXXXXXXXXX If the condition is inadequately treated, blood pressure may fall; cyanosis and pallor increase, and grunting decreases or disappears, as the condition worsens. XXXXXXXXXXXXXXXXXX Apnea and irregular respirations are ominous signs requiring immediate intervention. XXXXXXXXXXXXXXXXXX Patients may also have a mixed respiratory-metabolic acidosis, edema, ileus, and oliguria. Respiratory failure may occur in infants with rapid progression of the disease.
- Improvement 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.
- The clinical course, chest radiographic findings, and blood gas and acid-base values help establish the clinical diagnosis. XXXXXXXXXXXXXXXXXX On radiographs, the lungs may have a characteristic but not pathognomonic appearance that includes a fine reticular granularity of the parenchyma and air bronchograms XXXXXXXXXXXXXXXXXX
- early-onset sepsis may be indistinguishable from RDS. XXXXXXXXXXXXXXXXXX In pneumonia manifested at birth, the chest roentgenogram may be identical to that for RDS. XXXXXXXXXXXXXXXXXX Cyanotic 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). XXXXXXXXXXXXXXXXXX Persistent pulmonary hypertension, aspiration (meconium, amniotic fluid) syndromes, spontaneous pneumothorax, pleural effusions can generally be differentiated from RDS through radiographic evaluation. XXXXXXXXXXXXXXXXXX Transient 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.
- Administration of antenatal corticosteroids to women between 24 and 34Ā wk of gestation significantly reduces the incidence and mortality of RDS as well as overall neonatal mortality. XXXXXXXXXXXXXXXXXX Antenatal 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.
- 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?C XXXXXXXXXXXXXXXXXX Calories and fluids should initially be provided intravenously. For the 1st 24Ā hr, 10% glucose and water should be infused through a peripheral vein at a rate of 65-75Ā mL/kg/24Ā hr. 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. XXXXXXXXXXXXXXXXXX Warm humidified oxygen should be provided at a concentration initially sufficient to keep arterial oxygen pressure between 40 and 70Ā mmĀ Hg (85-95% saturation) in order to maintain normal tissue oxygenation while minimizing the risk of oxygen toxicity. XXXXXXXXXXXXXXXXXX If oxygen saturation cannot be kept > 85% at inspired oxygen concentrations of 40-70% or greater, applying CPAP at a pressure of 5-10Ā cm H2O via nasal prongs is indicated and usually produces a sharp improvement in oxygenation. XXXXXXXXXXXXXXXXXX Infants 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. XXXXXXXXXXXXXXXXXX HFV 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.
- Immediate effects of surfactant replacement therapy include improved alveolar-arterial oxygen gradients, reduced ventilatory support, increased pulmonary compliance, and improved chest radiograph appearance . XXXXXXXXXXXXXXXXXX Treatment is initiated as soon as possible in the hours after birth. Repeated dosing is given via the endotracheal tube every 6-12Ā hr 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.