Chapter 073. Enteral and Parenteral Nutrition (Part 5) Disease-Specific Nutritional Support SNS is basically a support therapy and is primary therapy only for the treatment or prevention of malnutrition. Certain conditions require modification of nutritional support because of organ or system impairment. For instance, in nitrogen accumulation disorders, protein intake may need to be reduced. However, in renal disease, except for brief periods of several days, protein intakes should approach requirement levels of at least 0.8 g/kg or higher up to 1.2 g/kg as long as the blood urea nitrogen does not exceed 100 mg/dL. If this is not possible, then dialysis or hemofiltration should be considered to allow better feeding. In hepatic failure, intakes of 1.2–1.4 g/kg up to the optimal 1.5 g/kg should be attempted, as long as encephalopathy due to protein intolerance is not encountered. In the presence of protein intolerance, formulas containing 33–50% branched-chain amino acids are available at the 1.2–1.4-g/kg level. Cardiac patients, and many severely stressed patients, often benefit from fluid and sodium restriction to levels of 1000 mL of total parenteral nutrition (TPN) formula and 5–20 meq of sodium per day. In patients with severe chronic PCM characterized by severe weight loss and tissue wasting, TPN must be instituted gradually because of the profound antinatriuresis, antidiuresis, and intracellular accumulation of potassium, magnesium, and phosphorus. This is usually accomplished by limiting fluid intakes initially to about 1000 mL containing modest carbohydrate content of 10– 20% dextrose, low sodium, and ample potassium, magnesium, and phosphorus, with careful assessment of fluid and electrolyte status. Protein need not be restricted.[newpage] The Design of Individual Regimens Fluid Requirements The normal daily requirement for fluid is 30 mL/kg of body weight from all sources (IV infusions, per tube, or oral intake), plus any replacement of abnormal losses such as an osmotic diuresis, nasogastric drainage, wound output, or diarrheal/ostomy losses. Electrolyte and mineral losses can be estimated or measured and also need to be replaced (Table 73-3). Fluid restriction may be necessary in patients with fluid overload, and fluid inputs can be limited to 1200 mL/d if urine is the only significant fluid output. When severe fluid overload occurs, the optimal PN solution for central venous administration is a concentrated 1-L solution of 7% crystalline amino acids (70 g) and 21% dextrose (210 g), which provides an amount of nitrogen and glucose that is effective at protein- sparing. Table 73-3 Enteric Fluid Volumes and Their Electrolyte Content a L/ d Na K Cl HCO 3 H Oral intake 2– 3 Enteric secretions Saliva 1– 2 15 30 15 50 — Gastric juic e 1.5 –2 50– 70 5– 15 90 –120 0 70 –100 Bile 0.5 –1.5 120 –150 5– 15 80 –120 30– 50 — Pancreati c 0.5 –1 100 –140 10 70 –100 60– 110 — Small intestine 1– 2 80– 140 10 –20 80 –120 20– 40 — a All in mEq/L. Source: Adapted from previous chapter by Lyn Howard, MD, in Harrison's Principles of Internal Medicine Patients requiring PN or EN in the acute care setting generally have some element of associated hormonal adaptations (e.g., increased secretion of antidiuretic hormone, aldosterone, insulin, glucagon, or cortisol) that cause fluid retention and hyperglycemia. Weight gain in the critically ill, whether receiving SNS or not, is invariably the consequence of fluid retention, since lean tissue accretion is minimal in the acute phase of illness. Because excess fluid removal can be difficult, limiting fluid intake to allow for balanced intake and output is more effective. . Chapter 073. Enteral and Parenteral Nutrition (Part 5) Disease-Specific Nutritional Support SNS is basically a support therapy and is primary therapy only for. level. Cardiac patients, and many severely stressed patients, often benefit from fluid and sodium restriction to levels of 1000 mL of total parenteral nutrition (TPN) formula and 5–20 meq of sodium. weight loss and tissue wasting, TPN must be instituted gradually because of the profound antinatriuresis, antidiuresis, and intracellular accumulation of potassium, magnesium, and phosphorus.