pediatric respiratory distress
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8/7/2019 Pediatric Respiratory Distress
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RDS is the most common cause of respiratory distressin premature infants and by definition develops duringthe first few hours after birth and lasts longer than 24hrs.
It occurs most commonly in infants born at less than 28weeks of gestation, effects about one third of infantsborn at 28 to 34 weeks and less than 5% of those bornafter 34 weeks.
The severity of symptoms is inversely related to bothgestational age and birth weight; infants born before 26weeks of gestational age may present with apnea atbirth.
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RDS remains the primary cause of morbidityand mortality in preterm infants, with malesmore likely to both develop and die from RDS
than females. Factors that predispose an infant to the
development of RDS include prematurity,cesarean section, asphyxia and maternaldiabetes.
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The lungs of infants with respiratory distress syndrome aredevelopmentally deficient in a material called surfactant,which helps prevent collapse of the terminal air-spaces (thefuture site of alveolar development) throughout the normal
cycle of inhalation and exhalation. Surfactant is a complex system of lipids, proteins and
glycoproteins which are produced in specialized lung cellscalled Type II cells or Type II pneumocytes.
The surfactant is packaged by the cell in structures calledlamellar bodies, and extruded into the air-spaces.
The lamellar bodies then unfold into a complex lining of theair-space. This layer reduces the surface tension of the fluidthat lines the air-space.
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Surface tension is responsible for approximately 2/3 of the
elastic recoil forces. In the same way that a bubble will
contract to give the smallest surface area for a given volume,so the air/water interface means that the liquid surface will
tend towards being as small as possible, thereby causing the
air-space to contract.
By reducing surface tension, surfactant prevents the air-spaces
from completely collapsing on exhalation. In addition, thedecreased surface tension allows re-opening of the air-space
with a lower amount of force.
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Therefore, without adequate amounts of surfactant, the air-spaces collapse and are very difficult to expand.
Microscopically, a surfactant deficient lung is characterized
by collapsed air-spaces alternating with hyper-expanded
areas, vascular congestion and, in time, hyaline membranes.
Hyaline membranes are composed of fibrin
, cellular debris,red blood cells, rare neutrophils and macrophages.
Blood oxygen levels fall and carbon dioxide rises, resulting
in rising blood acid levels and hypoxia. Structural
immaturity, as manifest by decreased number of gas-exchange units and thicker walls, also contributes to the
disease process.
Therapeutic oxygen and positive-pressure ventilation, while
potentially life-saving, can also damage the lung.
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Prenatal corticosteroids (betamethasone) to the mother before
delivery to boost the production of surfactant in the fetus.
Exogenous surfactant therapy
Supportive careSupplemental nutrition, hyperalimentation
Fluid and electrolyte replacement
Supplemental oxygen
Nasal prong continues positive airway pressure (N PAP),
convential mechanical ventilation with pressure support or high-frequency oscillating ventilation (HF V)
Airway clearance technique for secretion management