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Respiratory distress syndrome


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Respiratory distress syndrome

  1. 1. P H O N G T H O R N T U N T I V A R A R U T P R E S E N T E R U R A R O M P A N T U M A P O L A D V I S O R Respiratory Distress Syndrome
  2. 2. Respiratory Distress Syndrome (RDS)  Also known as Hyaline Membrane Disease (HMD)  RDS occurs primarily in premature infants; its incidence is inversely related to gestational age and birthweight Gestational age Percentages Less than 28 wks 60-80% 32-36 wks 15-30% 37-39 wk 5% Term Rare Nelson Textbook of Pediatrics, 18th Ed.
  3. 3. Incidence of RDS  The risk of developing RDS increases with :  Maternal diabetes, multiple births, cesarean section delivery, perinatal asphyxia, cold stress, and a history of previously affected infants  The risk of RDS is reduced in pregnancies with :  Chronic or pregnancy-associated hypertension, maternal heroin use, prolonged rupture of membranes, and antenatal corticosteroid prophylaxis
  4. 4. Etiology & Pathophysiology  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  Dipalmitoyl phosphatidylcholine (lecithin) <- Major component  Phosphatidylglycerol  Apoproteins (surfactant proteins SP-A, -B, -C, -D)  Cholesterol
  5. 5. Nelson Textbook of Pediatrics, 18th Ed.
  6. 6. Etiology & Pathophysiology  Surfactant is produced by Type II pneumocytes (Great alveolar cells) and present in high concentrations in fetal lung by 20 wk of gestation, but it does not reach the surface of the lungs  Surfactant appears in amniotic fluid between 28 and 32 wk of gestation  Mature levels of pulmonary surfactant are usually present after 35 wk (L/S ratio = 2:1)
  7. 7. Etiology & Pathophysiology Advancing gestational age Increasing amounts of phospholipids are synthesized and stored in type II alveolar cells Surface-active agents are released into the alveoli (Air-Liquid Interface) Reduce surface tension of the water and help maintain alveolar stability by preventing the collapse of small air spaces at end-expiration
  8. 8. Etiology & Pathophysiology  Genetic disorders may contribute to respiratory distress :  Abnormalities in surfactant protein B and C genes  Abnormalities in gene responsible for transporting surfactant across membranes (ABC transporter 3 [ABCA3])
  9. 9. Fetal rat lung, day 20 (term, day 22) showing developing type II cells, stored glycogen (pale areas), secreted lamellar bodies, and tubular myelin Nelson Textbook of Pediatrics, 18th Ed.
  10. 10. Etiology & Pathophysiology  Synthesis of surfactant depends in part on  Normal pH  Temperature  Perfusion  The epithelial lining of the lungs may also be injured by high oxygen concentrations and the effects of respirator management, thereby resulting in a further reduction in surfactant
  11. 11. Etiology & Pathophysiology  The highly compliant chest wall of preterm infants offers less resistance to the natural tendency of the lungs to collapse  At end-expiration, the volume of the thorax and lungs tends to approach residual volume, and atelectasis may develop
  12. 12. Etiology & Pathophysiology Deficient synthesis or release of surfactant Atelectasis and results in perfused but not ventilated alveoli Hypoxia Small respiratory units and a compliant chest wall
  13. 13. Nelson Textbook of Pediatrics, 18th Ed.
  14. 14. Pathology  The lungs appear deep purplish red and are liver- like in consistency  Extensive atelectasis with engorgement of the interalveolar capillaries and lymphatics
  15. 15. Liver-like consistency of the lungs
  16. 16. Clinical manifestations  Characteristically, tachypnea, prominent (often audible) grunting, intercostal and subcostal retractions, nasal flaring, and duskiness are noted  Signs of RDS usually appear within minutes of birth, although they may not be recognized for several hours in larger premature infants until rapid, shallow respirations have increased to 60/min or greater
  17. 17. Clinical manifestations  Breath sounds may be normal or diminished with a harsh tubular quality  Fine rales may be heard, especially posteriorly over the lung bases  Apnea and irregular respirations occur as infants tire and are ominous signs requiring immediate intervention
  18. 18. Clinical manifestations  In most cases, the symptoms and signs reach a peak within 3 days, after which improvement is gradual  Death is rare on the 1st day of illness, usually occurs between days 2 and 7  associated with alveolar air leaks (interstitial emphysema, pneumothorax), pulmonary hemorrhage, or IVH.  Mortality may be delayed weeks or months if BPD develops in mechanically ventilated infants with severe RDS
  19. 19. Clinical diagnosis  On X-ray, the lungs may have a characteristic, but not pathognomonic appearance  Fine reticular granularity of the parenchyma  Air bronchograms  More prominent early in the left lower lobe because of superimposition of the cardiac shadow  Typical pattern developing at 6–12 hr.  Laboratory findings are initially characterized by hypoxemia and later by progressive hypoxemia, hypercapnia, and variable metabolic acidosis
  20. 20. Infant with respiratory distress syndrome. Note the granular lungs, air bronchogram, and air-filled esophagus. ( A is the endotracheal tube; B is the umbilical venous catheter at the junction of the umbilical vein, ductus venosus, and portal vein; C is the umbilical artery catheter passed up the aorta to T12) Nelson Textbook of Pediatrics, 18th Ed.
  21. 21. Ground glass appearance • Fine reticulogranular • Air bronchogram
  22. 22. Progression of the disease  Acute phase  First 48-72 hr. after birth, newborn begins to have tachypnea, chest tightness  The sign and symptoms are peak on day 1-2  Patients may death if they did not receive adequate treatment  Recovery phase  Started on day 3-5  Type II Pneumocytes are regenerated  Decreased oxygen requirement
  23. 23. Differential diagnosis  Group B streptococcal pneumonia  Transient tachypnea of the newborn (TTNB)  Diaphragmatic hernia  More common in term newborn  Total anomalous pulmonary venous return (TAPVR)
  24. 24. Treatments  Because most cases of RDS are self-limited, the goal of treatment is to minimize abnormal physiologic variations and superimposed iatrogenic problems  There are 4 main treatments for RDS :  Supportive treatments  Oxygen therapy  Mechanical ventilation  Surfactant replacement therapy
  25. 25. Supportive treatment  Body temporature  Scheduled “touch times” to avoid hypothermia and minimize oxygen consumption  Placed in an isolette or radiant warmer to maintaine core temperature between 37 ± 0.5 °C
  26. 26. Supportive treatment  Nutritional support  For the 1st 24 hr, 10%DW should be infused through a peripheral vein at a rate of 65–75 mL/kg/day  For VLBW and ELBW, TPN should be added  Day 2-3, Na 3-4 mEq/kg/day and K 2-3 mEq/kg/day should be added (TV not more than 90 ml/kg/day)  Excessive fluids (>140 cc/kg/day) contribute to the development of PDA and BPD  On day 1, if good clinical, step feed by started at 0.5-1 ml/kg x 8 feeds drip in 1-2 hr with TPN (TV 80-100)
  27. 27. Supportive treatment  Others  Give a blood transfer when Hct is less than 40% (* Protocol)
  28. 28. Hgb RESPIRATORY SUPPORT AND/OR SYMPTOMS TRANSFUSION VOLUME Hct ≤ 35/ Hgb ≤ 11 Infants requiring moderate or significant mechanical ventilation (MAP > 8 cm H2O and Fio2 > 0.4) 15 mL/kg PRBCs[*] over period of 2–4 hr Hct ≤ 30/ Hgb ≤ 10 Infants requiring minimal respiratory support (any mechanical ventilation or endotracheal/nasal CPAP > 6 cm H2O and Fio2 ≤ 0.4) 15 mL/kg PRBCs over period of 2–4 hr Hct ≤ 25/ Hgb ≤ 8 Infants not requiring mechanical ventilation but who are receiving supplemental O2 or CPAP with an Fio2 ≤ 0.4 and in whom 1 or more of the following is present: 20 mL/kg PRBCs over period of 2–4 hr (divide into 2–10 mL/kg volumes if fluid sensitive) • ≤24 hr of tachycardia (HR > 180) or tachypnea (RR > 80) • An increased oxygen requirement from the previous 48 hr, defined as a ≥4-fold increase in nasal canula flow (i.e., 0.25 to 1 L/min) or an increase in nasal CPAP ≥ 20% from the previous 48 hr (i.e., 5 to 6 cm H2O) • Weight gain <10 g/kg/day over the previous 4 days while receiving ≥100 kcal/kg/day • An increase in episodes of apnea and bradycardia (>9 episodes in a 24-hr period or ≥2 episodes in 24 hr requiring bag and mask ventilation) while receiving therapeutic doses of methylxanthines • Undergoing surgery Hct ≤ 20/ Hgb ≤ 7 Asymptomatic and an absolute reticulocyte count <100,000 cells/μL 20 mL/kg PRBCs over period of 2–4 hr (2–10 mL/kg volumes) * RBC should be irradiated prior to transfusion Nelson Textbook of Pediatrics, 18th Ed.
  29. 29. Oxygen therapy  Warm humidified oxygen should be provided at a concentration initially sufficient to keep PaO2 50-80 mmHg, pH 7.25-7.45, PaCO2 40-50 mmHg and SpO2 90–95%  to maintain normal tissue oxygenation while minimizing the risk of oxygen toxicity  O2 box is not recommended for newborn with VLBW and ELBW because of high concentration of O2 may increase risk of ROP
  30. 30. Oxygen therapy  If the PaO2 cannot be maintained above 50 mmHg at inspired oxygen concentrations of 60% or greater, applying CPAP at a pressure of 5–10 cm H2O by nasal prongs  CPAP prevents collapse of surfactant-deficient alveoli, improves FRC, and improves ventilation-perfusion matching  The amount of CPAP required usually decreases abruptly at about 72 hr of age, and infants can be weaned from CPAP shortly thereafter
  31. 31. Mechanical ventilation  Continue positive airway pressure (CPAP) is being use with 4-8 cm·H2O  To make Functional residual capacity (FRC) for the lung to prevent atelectasis  Usually started with 5 cm·H2O and increased by 1 cm·H2O in subsequent with increase oxygen by 10%  Routes of administration  Nasal prongs  Nasopharyngeal tube
  32. 32. Mechanical ventilation  Indication for ventilator  Apnea with no improvement  Cyanosis or PaO2 ≤ 40 mmHg (when using CPAP and high oxygen concentration)  Signs of Respiratory failure  PaCO2 > 60 mmHg  Metabolic acidosis
  33. 33. Surfactant replacement therapy  Surfactant replacement therapy can reduce mortality and incidence of Chronic pulmonary disease  There are 2 types of surfactant : 1. Natural surfactant extract  Bovine(Survanta), Porcine(Curosurf), Surfacten, Alveofact and Calf (Infasurf) 2. Synthetic surfactant  Exosurf and ALEC (Artificial Lung Expanding Compound)
  34. 34. Surfactant replacement therapy  Natural surfactants appear to be superior, perhaps because of their surfactant-associated protein content  Natural surfactants have a more rapid onset and are associated with a lower risk of pneumothorax and improved survival
  35. 35. Surfactant replacement therapy  The 2 main indications :  Prophylactic treatment  Being use for infant delivered during 23-29 wk of gestation and birth weight 600-1250 g  Results :  Improve dyspnea in first 48-72 hr of life (Decrease O2 requirement, ventilation improved)  Decreased incidence of pneumothorax and BPD  Not affect the incidence of IVH and PDA  Decrease mortality
  36. 36. Surfactant replacement therapy  The 2 main indications :  Therapeutic or Rescue treatment  Initiated as soon as possible in the 1st 24 hr of life  Repeated dosing is given via the endotracheal tube every 6–12 hr for a total of 2 to 4 doses, depending on the preparation  Results :  Clinical improved (Decrease O2 requirement)  Decreased incidence of pneumothorax  Not affect the incidence of BPD, IVH and PDA  Decrease mortality There is no significantly difference between single dose and multiple dose of surfactant replacement therapy (Dunn et al. and Speer et al.)
  37. 37. Complication  Bronchopulmonary dyaplasia (BPD)  Result of lung injury in infants requiring mechanical ventilation and supplemental oxygen  disease of more mature preterm infants with RDS treated with positive pressure ventilation and oxygen  BPD is usually defined as a need for supplemental oxygen at 36 wk after conception  Another definition of BPD is based on the severity of disease  Neonates on positive pressure support or receiving >30% supplemental oxygen are diagnosed with BPD
  38. 38. GA <32 WK ≥32 WK Time point of assessment 36 wk PMA or discharge home Treatment with >21% oxygen for at least 28 days plus > 28 days but < 56 days postnatal age or discharge home Treatment with 21% oxygen for at least 28 days plus Mild BPD Breathing room air at 36 wk PMA or discharge Breathing room air by 56 days postnatal age or discharge Moderate BPD Need[*] for < 30% oxygen at 36 wk PMA or discharge Need[*] for < 30% oxygen at 56 days postnatal age or discharge Severe BPD Need[*] for ≥ 30% oxygen and/or positive pressure (PPV or NCPAP) at 36 wk PMA or discharge Need[*] for ≥ 30% oxygen and/or positive pressure (PPV or NCPAP) at 56 days' postnatal age or discharge * A physiologic test confirming that the oxygen requirement at the assessment time point remains to be defined. Nelson Textbook of Pediatrics, 18th Ed.
  39. 39. Complication  Physiologic test  Those receiving 30% oxygen or less undergo a stepwise 2% reduction in supplemental oxygen to room air while under continuous observation and oxygen saturation monitoring.  Outcomes are “no BPD” (saturations 88% or greater for 60 min) or “BPD” (saturation <88%)  This test is highly reliable and correlated with discharge home in oxygen, length of hospital stay, and hospital readmissions in the 1st yr of life
  40. 40. Complication  Patent ductus arteriosus (PDA)  Delayed closure of the PDA is associated with hypoxia, acidosis, increased pulmonary pressure secondary to vasoconstriction, systemic hypotension, immaturity, and local release of prostaglandins, which dilate the ductus  As RDS resolves, pulmonary vascular resistance decreases, and left-to-right shunting may occur and lead to left ventricular volume overload and pulmonary edema
  41. 41. Complication  Patent ductus arteriosus (PDA)  Manifestations of PDA may include :  Apnea for unexplained reasons in an infant recovering from RDS  Hyperdynamic precordium, bounding peripheral pulses, wide pulse pressure, and a continuous or systolic murmur with or without extension into diastole or an apical diastolic murmur, multiple clicks resembling the shaking of dice  Carbon dioxide retention  Increasing oxygen dependence  X-ray evidence of cardiomegaly and increased pulmonary vascular markings  Hepatomegaly
  42. 42. Complication  Intraventricular hemorrhage (IVH)  Commonly occurs on day 3-4 in preterm newborn with low birth weight and severe RDS  Can be detected by Brain ultrasonography
  43. 43. Complication  Intraventricular hemorrhage (IVH)  Grading of IVH  Grade 1 - bleeding occurs just in a small area of the ventricles  Grade 2 - bleeding also occurs inside the ventricles  Grade 3 - ventricles are enlarged by the blood  Grade 4 - bleeding into the brain tissues around the ventricles
  44. 44. Prevention  Avoidance of preterm labor  Avoidance of unnecessary cesarean section  Evaluation of L/S ratio for lung maturity  L/S ratio = 2:1 in mature lung  Foam test (Shake test)  Administration of corticosteroid before labor
  45. 45. Prevention  Corticosteroid administration is recommended for all women in preterm labor (24–34 wk gestation) who are likely to deliver a fetus within 1 wk Betamethasone 12 mg IM q 24 hr for 2 doses  Repeated weekly doses of betamethasone until 32 wk Dexamethasone 6 mg IM q 12 hr for 4 doses
  46. 46. Prevention  Prenatal dexamethasone may be associated with a higher incidence of periventricular leukomalacia than betamethasone  The relative risk of RDS, IVH and death is higher with antenatal dexamethasone treatment when compared with betamethasone
  47. 47. Prevention Administration of a 1st dose of surfactant into the trachea of symptomatic premature infants immediately after birth (prophylactic) or during the 1st few hours of life (early rescue) reduces air leak and mortality from RDS
  48. 48. References  Robert M. Kliegman, Richard E. Behrman, Hal B. Jenson, Bonita M.D. Stanton. Nelson Textbook of Pediatrics. Saunders; 18th edition, 2007:  พิมลรัตน์ ไทยธรรมยานนท์. การดูแลทารกแรกเกิด. ชัยเจริญ, 2554: 149-157
  49. 49. …Thank you…