Respiratory Distress Syndrome (RDS) PDF

RESPIRATORY DISTRESS SYNDROME ( RDS) HYALINE MEMBRANE DISEASE (HMD)  RESPIRATORY DISTRESS SYNDROME  RDS refers to a condition of surfactant deficiency and physiologic immaturity of the thorax.  The terms respiratory distress syndrome and hyaline membrane disease are most often...

RESPIRATORY DISTRESS SYNDROME ( RDS) HYALINE MEMBRANE DISEASE (HMD)  RESPIRATORY DISTRESS SYNDROME  RDS refers to a condition of surfactant deficiency and physiologic immaturity of the thorax.  The terms respiratory distress syndrome and hyaline membrane disease are most often applied to this severe lung disorder.  RISK GROUPS: 1. It is seen almost exclusively in preterm infants but may also be associated with 2. multifetal pregnancies, 3. infants of diabetic mothers, 4. cesarean section delivery, 5. cold stress, asphyxia, and 6. a family history of RDS. 7. Male gender  The disorder is rarely observed in drug exposed infants or infants who have been subjected to chronic intrauterine stress (e.g., maternal preeclampsia or hypertension  Respiratory distress of a nonpulmonary origin in neonates  Sepsis  cardiac defects (structural or functional)  exposure to cold  airway obstruction (atresia)  IVH  hypoglycemia, metabolic acidosis  acute blood loss, and drugs.  Pneumonia in the neonatal period is respiratory distress caused by bacterial or viral agents and may occur alone or as a complication of RDS  Pathophysiology  RDS results from a combination of structural and functional immaturity of the lungs.  structral :- 1. the final unfolding of the alveolar septa, which increases the surface area of the lungs, occurs during the last trimester of pregnancy, preterm infants are born with numerous underdeveloped and many uninflatable alveoli. 2. In addition, the fetal chest wall is highly compliant because of the predominance of cartilage rather than bone, and 3. the diaphragm, the dominant respiratory muscle, is prone to fatigue.  ………..  Functionally, the fetal lungs are deficient in surfactant, a surface-active phospholipid secreted by type II cells in the alveolar epithelium.  Surfactant is first produced at about 24 weeks of gestational age, but the type II cells in the lung do not fully mature until about 36 weeks of gestation (.  Acting much like a detergent, this substance reduces the surface tension of fluids that line the alveoli and respiratory passages, resulting in uniform expansion and maintenance of lung expansion at low intraalveolar pressure.  Deficient surfactant production causes unequal inflation of alveoli on inspiration and the collapse of alveoli on end expiration.  Without surfactant, infants are unable to keep their lungs inflated and therefore exert a great deal of effort to reexpand the alveoli with each breath.  With increasing exhaustion they are able to open fewer and fewer alveoli.  This inability to maintain lung expansion produces widespread a telectasis  A hyaline membrane  A hyaline membrane is formed as hypoxemia and the increased PVR cause transudation of fluid into the alveoli.  Necrotic cells from damaged alveoli plus the fibrin in the transudate form a membranous layer that lines the alveoli and inhibits gas exchange.  The hyaline membrane contributes to respiratory problems by greatly reducing lung distensibility, or compliance, the elastic quality of lung tissue that permits expansion in response to a given amount of applied pressure during inspiration.  Affected lungs are stiffer and require far more pressure than do normal lungs to achieve an equal amount of expansion.  Clinical Manifestations  Infants with RDS can develop respiratory distress either acutely or over a period of hours, depending on the acuity of pulmonary immaturity, associated illness factors, and gestational maturity.  The observable signs produced by the pulmonary changes usually begin to appear in infants who apparently achieve normal breathing and color soon after birth. 1. In a matter of a few hours, breathing gradually becomes more rapid (>60 breaths/min). EARLIEST SIGN 2. Infants may display retractions—suprasternal or substernal, and supracostal, subcostal, or intercostal—which result from a compliant chest wall. Weak chest wall muscles and the highly cartilaginous rib structure produce an abnormally elastic rib cage, resulting in indrawing, or retraction, of the skin between the ribs.  Silverman Scoring System 10 0 1 2 Neonatal Care 051104  ………..  Within a few hours, respiratory distress becomes more obvious. The respiratory rate continues to increase (to 80 to 120 breaths/min), and breathing becomes more labored.  Infants increase the rate rather than the depth of respiration when in distress.  Substernal retractions become more pronounced as the diaphragm works hard in an attempt to fill collapsed air sacs.  Fine inspiratory crackles can be heard over both lungs  there is an audible expiratory grunt. This grunting, a useful mechanism observed in the earlier stages of RDS, serves to increase end-expiratory pressure in the lungs, thus maintaining alveolar expansion and allowing gas exchange for an additional brief period.  Flaring of the nares is also a sign that accompanies tachypnea, grunting, and retractions in respiratory distress.  Central cyanosis (i.e., a bluish discoloration of oral mucous membranes and generalized body cyanosis) is a late and serious sign of respiratory distress. Initially supplemental oxygen may eliminate cyanosis.  ……………  The use of pulse oximetry and arterial blood gas sampling prevents dependence on color to determine oxygen requirements.  Severe RDS is often associated with a shock like state, with diminished cardiac inflow and low arterial blood pressure.  As a result of extreme pulmonary immaturity, decreased glycogen stores, and lack of accessory muscles, the ELBW and VLBW infant may have severe RDS at birth,  Infants with RDS who are treated with exogenous surfactant have a good chance for recovery. Complications of RDS  Complications include those described as complications of positive pressure ventilation. Associated complications (of prematurity and RDS) include:  PDA  congestive heart failure,  retinopathy of prematurity,  IVH,  BPD,  NEC, and  neurologic sequelae  Diagnostic Evaluation  Laboratory data are nonspecific, and the abnormalities observed are identical to those observed in numerous biochemical abnormalities of the newborn (i.e., the findings of hypoxemia, hypercapnia, and acidosis).  Specific tests are used to determine complicating factors, such as blood glucose (to test for hypoglycemia), blood gas measurements for serum pH (to test for acidosis), and PaO2 (to test for hypoxia).  Pulse oximetry is an important component for determining hypoxia.  Radiographic findings characteristic of RDS include (1) a diffuse granular pattern over both lung fields that resembles ground glass and represents alveolar atelectasis (2) dark streaks, or air bronchograms, within the ground glass areas that represent dilated, air-filled bronchioles ** It is important to distinguish between RDS and pneumonia in infants with respiratory distress.  RDS 16 Prenatal Diagnosis  Fetal lung maturity depends on gestational age and maternal illnesses.  Problems such as maternal diabetes delay fetal lung maturation, whereas fetuses exposed to chronic stress ( IUGR, drug exposure) often have more mature lungs.  Antenatal administration of glucocorticoids enhances fetal lung maturity, especially when combined with postnatal surfactant administration  ………….  Functional maturity of the fetal lung is indicated by surfactant phospholipids in amniotic fluid.  The most commonly tested is the lecithin/sphingomyelin (L/S) ratio, which represents the relationship between these two lipids during gestation.  at approximately 35 weeks. An L/S ratio of 2 : 1 in nondiabetic mothers indicates virtually no risk of RDS  This test measures the amount of 2 substances that are found in the amniotic fluid during pregnancy  What is the function of lecithin in the alveoli?  When air laden with moisture comes in contact with wall of the alveoli, high surface tension can result in the collapse of the wall. Lecithin coating on the wall acts as a surfactant and reduces the surface tension, reducing the possibility of a collapse ……….  Other key surfactant compounds (also phospholipids) that are needed to stabilize surfactant are phosphatidylcholine (PC) and phosphatidylglycerol (PG). Without these compounds, lecithin is not functional as a surfactant.  Concentrations of PC parallel those of lecithin, peaking at 35 weeks and then gradually decreasing.  At 36 weeks PG appears in amniotic fluid and increases until term.  By measuring these phospholipids—L/S ratio, PC, and PG—the clinician can estimate the maturity of the lungs with a high degree of accuracy.  Therapeutic Management  The treatment of RDS includes all the general measures required for any preterm infant, as well as those instituted to correct imbalances. The supportive measures most crucial to a favorable outcome are (1) maintain adequate ventilation and oxygenation with CPAP, high-flow nasal cannula, or mechanical ventilation (2) maintain acid-base balance (3) maintain a neutral thermal environment (4) maintain adequate tissue perfusion and oxygenation (5) prevent hypotension (6) maintain adequate hydration and electrolyte status.   Nipple and gavage feedings are avoided in any situation that creates a marked increase in respiratory rate because of the greater hazards of aspiration. QUALITY PATIENT OUTCOMES Neonatal RDS  Room air or oxygen saturation ≥88%  Respiratory rate