The dextrose concentration of peripheral PN is typically 10% to 12%, whereas central PN has a concentration of about 20%, although it may be increased to 25% to 30% in patients who are fluid restricted. To avoid hyperglycemia, the dextrose delivery is increased gradually when starting PN. Protein delivery in PN is via amino acids in the dextrose solution. The goal is 0.8 to 2 g protein/kg/24 hr for older children, 1.5 to 3 g/kg/24 hr for full-term and older infants, and 2.5 to 3.5 g/kg/24 hr for preterm infants.
The electrolyte and mineral composition of PN depends onthe age and the underlying illness. The 20% lipid emulsion provides essential fatty acids and calories. The lipid emulsion isstarted at a rate of 0.5 to 1 g/kg/24 hr, gradually increasing therate so that the patient receives adequate calories; this typicallyrequires 2.5 to 3.5 g/kg/24 hr. The lipid emulsion usually provides 30% to 40% of the required calories; it should not exceed60%. The serum triglyceride concentration is monitored as therate of lipid emulsion is increased, with reduction of the lipidemulsion rate if significant hypertriglyceridemia develops.
There are many potential complications of PN. CVLs are associated with complications during insertion (pneumothorax or bleeding) and long-term issues (thrombosis). Catheter-related sepsis, most commonly due to coagulase-negative staphylococci, is common and, on occasion, necessitates catheter removal. Other potential pathogens are Staphylococcus aureus, gram-negative bacilli, and fungi. Electrolyte abnormalities, nutritional deficiencies, hyperglycemia, and complications from excessive protein intake (azotemia or hyperammonemia) can be detected with careful monitoring.
The most concerning complication of long-term PN is cholestatic liver disease, which can lead to cirrhosis and liver failure. Current PN decreases the risk of liver disease by including reduced amounts of hepatotoxic amino acids. The best preventive strategy is early use of the gastrointestinal tract, even if only trophic feeds are tolerated.
The kidney regulates sodium balance and is the principal site of sodium excretion. Sodium is unique among electrolytes because water balance, not sodium balance, usually determines its concentration. When the sodium concentration increases, the resultant higher plasma osmolality causes increased thirst and increased secretion of antidiuretic hormone (ADH), which leads to renal conservation of water. Both of these mechanisms increase the water content of the body, and the sodium concentration returns to normal. During hyponatremia, the fall in plasma osmolality decreases ADH secretion, and consequent renal water excretion leads to an increase in the sodium concentration. Although water balance usually is regulated by osmolality, volume depletion stimulates thirst, ADH secretion, and renal conservation of water. In fact, volume depletion takes precedence over osmolality; volume depletion stimulates ADH secretion, even if a patient has hyponatremia.
The excretion of sodium by the kidney is not determined by the plasma osmolality. The patient’s effective plasma volume regulates the amount of sodium in the urine through a variety of regulatory systems, including the renin-angiotensinaldosterone system. In hyponatremia or hypernatremia, the underlying pathophysiology determines the urinary sodium concentration, not the serum sodium concentration.
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