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I. Definition. Hyaline membrane disease (HMD) is another name for RDS. This clinical diagnosis is
warranted in a preterm newborn with respiratory difficulty, including tachypnea (>60 breaths/min),
chest retractions, and cyanosis in room air that persists or progresses over the first 48-96 h of life,
and
a characteristic chest x-ray appearance (uniform reticulogranular pattern and peripheral air
bronchograms). The clinical course of the disease varies with the size of the infant, severity of
disease, use of surfactant replacement therapy, presence of infection, degree of shunting of blood
through the patent ductus arteriosus (PDA), and whether or not assisted ventilation was initiated.
Clinical presentation
A. History. The infant is often preterm, either by dates or by gestational examination, or has a
history of asphyxia in the perinatal period. Infants have some respiratory difficulty at birth, which
becomes progressively more severe. The classic worsening of the atelectasis seen on chest x-ray film
and increasing oxygen requirement for these infants have been greatly modified by the availability
of
exogenous surfactant therapy and our increased ability to provide effective mechanical ventilatory
support.
B. Physical examination. The infant with HMD exhibits tachypnea, grunting, nasal flaring, and
retractions of the chest wall. The infant may have cyanosis in room air. Grunting occurs when the
infant partially closes the vocal cords to prolong expiration and develop or maintain some FRC. This
mechanism actually improves alveolar ventilation. The retractions occur and increase as the infant is
Management
A. Prevention.
Conference on the effect of corticosteroids for fetal maturation on perinatal outcomes concluded
that
antenatal corticosteroids reduce the risk of death, HMD, and IVH. Use of antenatal betamethasone
to
enhance fetal pulmonary maturity is now established and generally considered to be standard of
care.
The recommended glucocorticoid regimen consists of the administration to the mother of two 12-
mg
because of increased risk for cystic periventricular leukomalacia among very premature infants
2. Several preventive measures may improve the survival of infants at risk for HMD and
includeantenatal ultrasonography for more accurate assessment of gestational age and fetal well-
being,
continuous fetal monitoring to document fetal well-being during labor or to signal the need for
intervention when fetal distress is discovered, tocolytic agents that prevent and treat preterm labor,
and assessment of fetal lung maturity before delivery (lecithin-sphingomyelin [L-S] ratio and
B. Surfactant replacement (see also Chapter 6) is now considered a standard of care in the
treatment of intubated infants with HMD. Since the late 1980s, more than 30 randomized clinical
trials involving >6000 infants have been conducted. The systematic review of these trials (Soll &
Andruscavage, 1999) demonstrates that surfactant, whether used prophylactically in the delivery
room to prevent HMD or in the treatment of the established disease, leads to a significant decrease
in
the risk of pneumothorax and the risk of death. These benefits were observed in both the trials of
natural surfactant extracts and synthetic surfactants. Surfactant replacement, although proved to be
immediately effective in reducing the severity of HMD, has not clearly been shown to decrease the
long-term oxygen requirements or the development of chronic lung changes. Currently, long-term
follow-up studies have not shown significant differences between surfactant-treated patients and
nontreated control groups with regard to PDA, IVH, ROP, NEC, and BPD. Evidence exists that the
length of stay on mechanical ventilation and total ventilator days have been reduced with the use of
surfactant at all gestational age levels, even with the increase of extremely low birth weight infants.
A
dramatic fall in deaths from HMD began in 1991. This probably reflected the introduction across the
C. Respiratory support
1. Endotracheal intubation and mechanical ventilation are the mainstays of therapy for
infants with HMD in whom apnea or hypoxemia with respiratory acidosis develops. Mechanical
ventilation usually begins with rates of 30-60 breaths/min and inspiratory-expiratory ratios of 1:2. An
initial PIP of 18-30 cm H2O is used, depending on the size of the infant and the severity of the
disease. A PEEP of 4-5 cm H2O results in improved oxygenation, presumably because it assists in the
maintenance of an effective FRC. The lowest possible pressures and inspired oxygen concentrations
are maintained in an attempt to minimize damage to parenchymal tissue. Ventilators with the
capacity
to synchronize respiratory effort may generate less inadvertent airway pressure and lessen
barotrauma. The early use of HFOV has become an increasingly popular and frequently used
ventilator mode for low birth weight infants (Gerstmann et al, 1996; Plavka et al, 1999).
2. CPAP and nasal synchronized intermittent mandatory ventilation (SIMV). Nasal CPAP
(NCPAP) or nasopharyngeal CPAP (NPCPAP) may be used early to delay or prevent the need for
endotracheal intubation. To minimize lung injury associated with intubation and mechanical
ventilation, there has been a recent interest in using CPAP as an initial treatment strategy to treat
HMD even in very low and extremely low birth weight infants. In some centers, this practice has
been used successfully and resulted in decreased incidence of BPD (Aly, 2001; De Klerk & De
Klerk, 2001; Van Marter et al, 2000). In addition, early treatment with surfactant, administered
during a short period of intubation followed by extubation and application of NCPAP is increasingly
being used in Europe. This approach has been used in premature infants <30 weeks' gestation and
significantly reduces the subsequent need for mechanical ventilation (Kamper, 1999; Verder et al,