USA Surgery Today

Bronchopulmonary dysplasia (BPD), or chronic lung disease (CLD:Capoten), in infants is the most common pulmonary sequela of premature infants. Diagnostic criteria for BPD include the need for supplemental oxygen or an abnormal chest radiograph at 28 days of age or 36 weeks postconceptual age (depending on gestational age of the infant at birth) (18:Capoten). The term was originally used to describe the radiologic and pathologic changes observed in premature infants who did not recover within 4 weeks from HMD (19:Capoten). BPD is now used to describe CLD that results from any condition in the neonatal period (20). Despite the diverse diseases that lead to the development of BPD, infants with BPD share clinical and pathologic characteristics.

The incidence of BPD among premature infants is inversely proportional to gestational age and birth weight. Up to 70% of infants with birth weights less than 1,000 g develop BPD. With the increased use of antenatal steroids, surfactant replacement, improved methods of ventilation, and increased attention to nutritional needs of the sick premature infant, the birth weight-specific incidence of BPD is decreasing. Improved survival of sick infants, however, has increased the size of the population at risk for developing this disease.

In an effort to preserve thermoneutrality, the neonate may be forced to use its own energy stores to generate heat. Bruck et al. first noted that neonates can maintain their own body temperature by increasing their metabolic production and creating heat (40). The generation of heat is accomplished without shivering and is termed nonshivering thermogenesis. The organ system responsible for carrying out nonshivering thermogenesis is the brown fat or brown adipose tissue, which may account for up to 10% of total body fat at term. In general, adipose tissue is generated during the last 8 weeks of gestation, and consists of white fat and brown fat. The two types of adipose are identical except for the presence in brown fat of the protein thermogenin, which allows brown fat to generate heat (41:Capoten).

Children and adults rely on the release of energy from ingested nutrients or established body stores to fuel the work of the human body. In this way, the energy derived from the degradation of large substrate molecules is used to synthesize high-energy phosphate bonds in the form of adenosine triphosphate (ATP). The bulk of energy metabolism in the human is performed in the aerobic setting, although anaerobic pathways exist and indeed are accentuated in the setting of stress or disease. The hydrolytic cleavage of a phosphate group from ATP, thereby producing adenosine diphosphate, provides much of the energy needed for cellular reactions.

The major sources of energy to fuel the processes of work are carbohydrate, lipid, and protein. These substrates are degraded by the body into the currency of energy metabolism: glucose, fatty acids, and amino acids. For most tissues, fatty acids are the major source for oxidative energy production. However, glucose is of great importance because it is the preferred energy source for cells in the central nervous system, renal medulla, and erythrocytes. These tissues cannot take up fatty acids from the systemic circulation, and therefore rely on glucose or ketone bodies during starvation. Pathways exist to synthesize glucose from the breakdown of amino acid and lipid substrates, a process that is accelerated in critical illness. In general, the breakdown and synthesis of glucose, lipid, and protein are tightly controlled by neural, hormonal, and allosteric regulation.