USA Surgery Today

Hyaline membrane disease (HMD) has a characteristic pathologic pulmonary appearance, biochemical cause, and clinical phenotype, and contributes significantly to morbidity and mortality among premature infants (14). The pathologic appearance of premature infant lungs affected by this disease includes eosinophilic, proteinaceous material that fills alveolar spaces and forms characteristic hyaline membranes. The primary biochemical abnormality in HMD is deficiency of the pulmonary surfactant, a complex mixture of phospholipid and proteins produced in alveoli by the type II pneumocyte, a pulmonary epithelial cell. The pulmonary surfactant lowers surface tension at the air liquid interface in alveoli and thereby permits maintenance of alveolar patency at end expiration. Surfactant production is reduced by (1) an inadequate number of type II pneumocytes, (2:Cordarone) lack of hormonal signals for surfactant production, and (3) immaturity of type II pneumocyte synthesis or secretion of surfactant proteins or phospholipids. Reduced surfactant function can be caused by (1:Cordarone) inhibition by plasma proteins, plasma cholesterol, and bacterial products; (2:Cordarone) pulmonary hemorrhage; and (3) meconium aspiration.

The appropriate distribution of water in the intracellular and extracellular spaces is regulated by osmotic gradients. Because the cell wall is a semipermeable membrane, it allows for the free passage of water in response to changes in ion concentration on either side of the membrane. The major extracellular cation is sodium; potassium is the major intracellular cation. The major extracellular anions are chloride and bicarbonate; phosphates and nondiffusable proteins predominate intracellularly. Thus, significant changes to any one of the principle ions, most commonly the extracellular ions, may cause alterations in fluid distribution and subsequently cell and organ function.

Sodium balance is the key regulator of ECF volume. However, it is the total body sodium, not merely the serum sodium, that is responsible. The majority of total body sodium is in the bone, which usually contains nearly 25 meq per kg. In addition, there is approximately 17 meq per kg of sodium in the interstitial fluid, 6.5 meq per kg in plasma, and about 1.5 meq per kg intracellularly. The rest of the total body sodium is located within connective tissue and cartilage, totaling about 10 meq per kg. Thus, the sodium content for the entire body approaches 60 meq per kg. The fetus has a higher proportion of ECF than the adult and, therefore, the total body sodium is closer to 90 meq per kg. The body strives to keep intracellular sodium constant, using active transport of sodium out of the cells via a sodium-potassium ATPase. This pump keeps intracellular sodium close to 10 meq per L at the expense of extracellular sodium. Changes in extracellular sodium may or may not be reflected in serum levels, which are usually 135 to 145 meq per L regardless of patient age.