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Home / FindArticles / Health / Radiologic Technology / March-April, 1996

Hyaline membrane disease

by Karin A. Dawson, Dianne DeVos
Comments Respiratory distress syndrome, also called hyaline membrane disease, is the most common disorder in the intensive-care nursery. First described in 1903, HMD is a lung disease that causes increasing difficulty in breathing and can result in a life-threatening deficiency of oxygen in an infant's blood.[1] Hyaline membrane disease is more frequently encountered in pre-term infants, affecting approximately 0.5% to 2% of all live births and 25% to 30% of babies born early.[1] The disease occurs in infants who are deficient in surfactant, a chemical that holds open the alveoli (air sacs) in the lungs. Surfactant forms a layer between the surface of the alveoli and the air, thus reducing alveolar collapse. The more premature the infant, the smaller the amount of surfactant production and the higher the probability of the incidence of HMD. Immature lungs become progressively atelectatic due to alveolar collapse resulting from the deficiency in surfactant, causing respiratory distress. Diagnosis of HMD Hyaline membrane disease can be diagnosed by clinical presentation, radiographic findings and the progression of the disease. Most neonates with HMD demonstrate clinical findings of respiratory distress in the delivery room or during the first few hours of life. The condition starts with an increase in breathing rate, with respiration then becoming labored and more rapid. In addition to the early onset of respiratory distress, clinical features include tachypnea, intercostal and sternal retractions, expiratory grunt, nasal flaring and decreased lung compliance. Hyaline membrane disease is confirmed by listening to the infant's lungs with a stethoscope, by analyzing blood gases and by examining x-ray images of the chest. The appearance of the chest x-ray varies depending on the severity and progression of the disease, the ventilatory support applied, the use of surfactant replacement therapy and other possible complications of prematurity. Four radiographic features characteristic of HMD are:[2] * Reduced lung volume, with expansion only to the fifth, sixth or seventh thoracic vertebrae rather than to the eighth or ninth, as found in the normally expanded chest. The reduced lung expansion is a

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consequence of atelectasis, which occurs due to a lack of surfactant. Also, the diaphragms will appear unusually high and sometimes domed, and the intercostal spaces will appear narrow. * Air bronchograms, or the outlines of air-filled secondary and tertiary bronchi seen over abnormal lung fields. Because normally expanded lungs and the overlying bronchi are of air density, air bronchograms are not generally seen in the lung fields on a normal chest x-ray. When atelectasis occurs with HMD, the lung density becomes water/tissue density and air is seen outlining the peripheral bronchi over the more opaque lung. With severe atelectasis, air in the lung is greatly reduced, leading to the loss of the air bronchogram signs and more widespread opacity of the lung fields. * A reticulogranular pattern, or ground glass appearance, uniformly distributed throughout both lung fields. This occurs because only a specific portion of the alveoli and terminal airways are expanded against a background of atelectasis in the remainder of the lung. Because of surfactant deficiency, some alveoli in the lung collapse from high surface tension. The alveoli that remain distended have lower surface tension. Air entering the lung goes only to the area of lowest pressure, creating the image of ground glass. * Increased lung opacification. When diffuse lung opacification becomes visible, it usually is the result of nonexpanded alveoli with little or no terminal airway aeration. The heart borders may be visible initially, but the x-ray may progress to a complete loss of visualization of the heart borders, called a "whiteout."[2] Successive chest x-rays gradually grow more opaque, preceded by a granular chest x-ray. In neonates with severe disease, however, the first chest x-ray may display an opaque appearance. Other causes of increasing opacity of lungs on chest x-rays of neonates include pulmonary edema resulting from patent ductus arteriosus or massive bilateral pulmonary hemorrhage.[2] Clinical evaluation for these disorders should be carried out separately as deemed necessary. Expiratory films can give the impression of increasing lung opacity, but recognition of the trachea deviated to the right, domed diaphragms and a stable clinical picture allow for quick, easy discrimination from HMD. The progression and severity of x-ray changes seen in HMD may be broken into four stages. The first, Grade 1, consists of a fine granularity with some air bronchograms visible. Grade 2 is characterized by a more apparent, distinct and coarse granularity to the lung fields, with more extensive air bronchograms. Grade 3 is defined by increasing opacity, with decreasing air bronchograms and granularity. Finally, in Grade 4, diffuse bilateral opacification is present, with lack of apparent heart borders and loss of all air bronchograms -- a "whiteout." Treatment of HMD Surfactant replacement therapy is the primary focus in treating infants with HMD. After studying the chemical and physical properties of the alveolar lining layer, researchers have developed materials that can be instilled into infants' lungs to carry them over the critical first few days until they begin to synthesize their own surfactant.[3] Artificial surfactants are instilled through a endotracheal tube, which is more efficient than aerosol. The material is administered slowly because it can have an immediate effect on the lungs and subsequently on the artificial ventilation requirements of the infant. Questions involved in initiating surfactant replacement therapy include whether to use synthetic or natural surfactant. Products available in the United States include Exosurf, a synthetic product, and Survanta, which is derived from cows' lungs.[3] Additional research is necessary to determine which type of surfactant is best and if either causes any long-term effects. Researchers also are investigating whether it is more advantageous to administer the first dose of surfactant right at birth (preventive-prophylactic) or when the infant begins to exhibit signs of HMD (rescue dose). Trials have indicated that it is advantageous to administer the first dose as a

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prophylactic one.[1] A single dose or up to four doses can be administered. However, some babies do not respond after one dose, and others have an initial response but then relapse. Such observations suggest that some babies need more doses, and now the administration of up to four doses over the first 48 hours of life is widely practiced.[3] Chest x-rays following surfactant administration often show improved lung expansion and clearing lung fields with only a mildly hazy background. In other cases, normal pulmonary radiolucency may be seen after therapy. A small percentage of neonates are nonresponders, and their clinical and x-ray course changes little after surfactant administration. In the recovery phase of HMD, the x-ray appearance of the lungs presents as a mild, diffuse, bilateral haze. In neonates whose course has been typical and who have not received surfactant, the recovery phase occurs between day 4 and day 7 of life and is complete by day 10.[2] The hazy appearance is lost after one or two weeks, and the lung fields return to their normal lucency. X-ray studies contribute to a volume of information gathered during a period of rapid adjustment of the newborn infant to extrauterine life and to this particular disease process. The history, the clinical and diagnostic data gathered and the infant's response to treatment also must be considered in reaching a definitive diagnosis. Preventive health care and increased accessibility to adequate prenatal care are the ideal first steps to the future health of the newborn. Although it is no longer the most common cause of death in premature infants, about 3% of neonates die of hyaline membrane disease. However, the survival rate using modern intensive care procedures and treatments, including surfactant replacement therapy, approaches 90%.[3]

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