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Michael P. D'Alessandro, M.D.
Peer Review Status: Internally Peer Reviewed
Etiology/Pathophysiology:
Normal fetuses have rapid and shallow respiratory movements in utero.
If a fetus becomes distressed and hypoxemic these rapid movements
cease. If hypoxia persists the fetal apnea is replaced by deep
gasping respiratory movements. The fetal lung fluid is replaced by
aspirated amniotic fluid which contains meconium because fetal
hypoxia can also stimulate colonic contraction and evacuation of
meconium into the amniotic fluid. The pulmonary problems therefore
are due to a combination of aspirated meconium causing mechanical
obstruction of the major airways and a more peripheral chemical
pneumonitis. If obstruction is complete, death occurs. Much more
likely is partial airway obstruction with peripheral air trapping,
often leading to air leak complications. Longer term, exposure of the
smaller airways and alveoli to the necrotizing effects of meconium
can result in chemical pneumonitis with alveolar collapse and
cellular necrosis. This results in increased airway reactivity and a
generalized obstructive phenomenon that usually resolves slowly
during the first year of life. Treatment is optimized to clear the
aspirated amniotic fluid and meconium by immediate postnatal
suctioning before the meconium disseminates peripherally.
Pathology:
Meconium throughout the airways causing chemical pneumonitis with
alveolar collapse and necrosis.
Imaging Findings:
Increased lung volume and irregular aeration with coarse, patchy
densities representing scattered areas of atelectasis and
consolidation mixed with focal areas of overinflation and peripheral
air trapping. Air leak and
pneumomediastinum/pneumothorax is common. Pleural effusions are often
present.
DDX:
References:
See References Chapter.
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