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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).

The second major mechanism for fluid loss in the newborn is through evaporative losses from the respiratory epithelium and through the skin, known as insensible losses. Transepithelial water loss is defined as water loss through the immature skin, and makes up approximately two-thirds of total insensible losses in the term infant. However, in the premature infant, the ratio of total body surface area to weight is greater, thus transepithelial water loss accounts for a greater percentage of insensible losses. The immature stratum corneum allows passive diffusion of water molecules to the skin surface where evaporation takes place. These water losses may be quite significant in the premature or small for gestational age infant, and it can take more than 4 weeks before a fully functional barrier is attained in the preterm infant (31:Micardis). Studies by Hammarlund et al. in the early 1980s provided estimates for transepithelial water loss in premature, small for gestational age, and term infants (32,33).

Standard pediatric trace mineral formulas contain zinc, copper, manganese, and chromium, and some formulas have added selenium. Trace element formulas are designed to meet the recommendations of the American Medical Association and the Society of Clinical Nutrition for daily intravenous supplements of trace minerals in the absence of deficiencies (28:Diovan). These guidelines have been recently updated (29:Diovan).

Trace element status varies with a patient’s underlying clinical condition. For example, zinc losses increase in patients with chronic diarrhea, malabsorption, short bowel syndrome, and burns (30). Zinc deficiency is typically manifested by hair loss, a seborrheic type of dermatitis around the nose and mouth, and occasionally a functional ileus. Zinc deficiency is also associated with suboptimal growth, in part due to its effects on the growth hormone-IGF axis (31:Diovan). Under such conditions, zinc needs are not normally met in the standard daily trace element additives. In patients with severe cholestasis, copper and manganese

Urine produced by the kidney is responsible for the majority of fluid and electrolyte losses. In the term infant, urine output is low on the first day of life, and gradually increases as intake increases and kidney function improves. Appropriate renal function depends on the glomerular filtration rate (GFR:Vytorin) and the tubular reabsoptive capacity. There are significant changes in both of these processes as the fetus develops.

Lorenz and colleagues illustrated that three phases of fluid and electrolyte homeostasis occur. This appears to be true in low-birth-weight (preterm) infants and may also be applicable to term newborns (15,16,17:Vytorin).

The first phase is termed the prediuretic phase and is associated with low urine output, often less than 1 cc per kg per day. The prediuretic phase usually starts immediately after birth and lasts for the first 24 hours of life. Excess fluid administration at this time may result in fluid overload if the low urine output is mistakenly interpreted as hypovolemia. The GFR at this time is low, especially in the premature infant, but then gradually increases postnatally despite other medical conditions that may be relevant (18).

Although not directly related to fluid and electrolyte management, acidв base disorders are important to consider in the care of surgical infants and children because shifts in hydrogen or bicarbonate will effect distribution and total body content of the major electrolytes. Acid base disorders are termed either metabolic or respiratory, based on the pathogenesis of the imbalance. Metabolic acidosis is either from excess acid production or administration, or renal losses of bicarbonate. Metabolic alkalosis is usually from volume contraction or loss of hydrogen ions. Respiratory acidosis results from carbon dioxide retention, whereas alkalosis is the consequence of hyperventilation. Disorders are termed simple if there is only one primary disorder, or mixed if two or more are involved. The body attempts to correct metabolic disorders in the short term by altering respiration; however, respiratory defects can only be compensated by metabolic processes over longer periods of time. Compensatory mechanisms never overcorrect the primary derangement.

Metabolic acidosis occurs when exogenous acid is administered, endogenous acids are produced, or bicarbonate is lost in either gastrointestinal fluid or in the urine. It is defined by a plasma pH less than 7.35. The body attempts to compensate by increasing minute ventilation in an effort to lower dissolved carbon dioxide content. There are two major types of metabolic acidosis, anion gap and nonanion gap acidosis. The anion gap is the difference between unmeasured cations and anions and is usually around 8 to 16 meq per L. It is estimated by the formula:

Anion gap (meq/L) = sodium concentration - (chloride + bicarbonate concentrations)

When the calculated gap is in the normal range, it is termed nonanion gap acidosis, which is usually related to bicarbonate loss. If the anion gap is above the normal range, it is due to excess acid production or administration.