Anemia of Prematurity - Portal Neonatal

Picture 5. A schematic diagram of the surfactant metabolism. A single alveolus is shown with the
location and movement of surfactant components depicted. Surfactant components are synthesized
from precursors (1) in the endoplasmic reticulum (2) and transported through the Golgi apparatus (3)
via multivesicular bodies. The components are ultimately packaged in lamellar bodies (4), which are
intracellular storage granules for surfactant before secretion. After secretion (exocytosis) into the
liquid lining of the alveolus, the surfactant phospholipids are organized into a complex lattice called
tubular myelin (5). The tubular myelin is believed to generate the phospholipid that provides material
for a monolayer (6) at the air-liquid interface in the alveolus, which lowers surface tension.
Subsequently, surfactant phospholipids and proteins are taken back into type II cells, possibly in the
form of small vesicles (7), apparently by a specific pathway that involves endosomes (8), and
probably transported for storage into lamellar bodies (9) for recycling. Some surfactant in the liquid
layer is also taken up by alveolar macrophages (10). A single transit of the phospholipid components
of surfactant through the alveolar lumen normally requires a few hours. The phospholipid in the
lumen is taken back into type II cell and is reused 10 times before being degraded. Surfactant
proteins are synthesized in polyribosomes and extensively modified in endoplasmic reticulum, Golgi
apparatus, and multivesicular bodies. Surfactant proteins are detected within lamellar bodies or in
secretory vesicles closely associated with lamellar bodies before secretion into the alveolus.
Picture 6. Chest radiograph of a premature infant with respiratory distress syndrome before and
after surfactant treatment. Initially, radiograph exhibits poor lung expansion, air bronchogram, and
reticular granular appearance. The chest radiograph repeated when the neonate is aged 3 hours
following surfactant therapy demonstrates marked improvement.
BIBLIOGRAPHY Section 11 of 11
• Ablow RC, Driscoll SG, Effmann EL, et al: A comparison of early-onset group B steptococcal
neonatal infection and the respiratory-distress syndrome of the newborn. N Engl J Med 1976
Jan 8; 294(2): 65-70[Medline].
• Adamkin DH: Issues in the nutritional support of the ventilated baby. Clin Perinatol 1998 Mar;
25(1): 79-96[Medline].
• Avery ME, Mead J: Surfactant properties in relation to atelectasis and hyaline membrane
disease. Am J Dis Child 1959; 97: 517.
• Clark RH, Gerstmann DR: Controversies in high-frequency ventilation. Clin Perinatol 1998
Mar; 25(1): 113-22[Medline].
• Clyman RI, Jobe A, Heymann M, et al: Increased shunt through the patent ductus arteriosus
after surfactant replacement therapy. J Pediatr 1982 Jan; 100(1): 101-7[Medline].
• Donn SM, Sinha SK: Controversies in patient-triggered ventilation. Clin Perinatol 1998 Mar;
25(1): 49-61[Medline].
• Fletcher MA, MacDonald MG, eds: Atlas of Procedures in Neonatology. 2nd ed. Philadelphia:
JB Lippincot Co; 1993.