The syllogism for dietary and nutritional management is to get enough nutrients into the body to restore nutritional adequacy and balance, taking any chronic barriers to uptake and retention into consideration. The blend of nutrients must be tailored to the specific absorptive or utilization problems, e.g., compensatory fat-soluble vitamins in water-miscible forms with severe fat malabsorption, and extra doses of highly available iron with chronic blood loss. These can be delivered within a dietary context with supplements and fortified vehicles in nonacute conditions. Even nondietary routes have been devised as in the treatment of vitamin D deficiency due to Crohn's disease with tanning bed ultraviolet B radiation.
When accumulated undernutrition is dangerously advanced, absorptive barriers are especially severe, or nutrient losses are excessive more concerted nutritional intervention is required. Intensive therapy can be delivered by three routes: orally, with special diets supplemented by liquid formulas; ent-erally, with liquid formulas perfused by intragastric or intraintestinal feeding tubes; and parenterally, with intravenous formulas infused into peripheral or central veins. Up to 50% of patients on dialysis have protein-energy malnutrition, which may continue undetected. For end-stage renal patients, intra-dialytic alimentation (adding nutrients to the dialysis fluids) has been used to reduce nutrient loss. Each approach has its distinct costs, special potential, and limitations and risks, and has been explored and refined in the context of age, physiological status, and specific disease states or surgical indications.
Tailoring of nutrient delivery is required with both enteral and parenteral nutrition, depending upon the pathophysiology of the underlying conditions. Both hypo- and hypermetabolic states can occur; indirect calorimetry with metabolic carts is in vogue for prescribing energy delivery in intensive care. When pulmonary compromise is present, the balance among macronutrients is important to minimize carbon dioxide formation in metabolism.
Maintaining abundant amino acid supply promotes protein-sparing and prevents loss of lean tissue in catabolic states. Enrichment of enteral or parenteral regimens with branched-chain amino acids or keto-analog amino acids has been devised to compensate for the metabolic defects of nitrogen handling in hepatic or renal failure states. The objective of nutritional support in patients with liver failure is to provide adequate macronutrients to ensure the specific substrates for energy and protein synthesis and integrity of normal hepatic tissue function, without inducing or accentuating encephalopathy or otherwise aggravating hepatic insufficiency.
In juvenile cholestasis, large amounts of fat-soluble vitamin supplements and medium-chain triglycerides are usually required for optimum growth. With protracted secretory diarrheal diatheses, fluid and electrolyte balance may be the primary concern, followed by macro- and micronutrient nutriture, invoking the institution of parenteral feeding. Cancer cachexia is a major secondary consequence of disseminated neoplasms. It is tempting to prescribe aggressive nutritional support, but a caveat is that certain nutrients acting with certain neoplasms favor the tumor's growth and dissemination. To the extent that various forms of cachexia are partly driven by catabolic responses mediated by proinflammatory cytokines, antagonists directed at counteracting their action hold promise for retarding the nutrient-wasting in various forms of cachexia.
With intensive nutrition, there are risks and adverse consequences intertwined with the benefits. A variation of the refeeding syndrome, that is hyper-alimentation complications from excessive energy substrate perfusion or infusion, can produce hypo-phosphatemic and hypokalemic episodes. Improper formulation of fluids or liquids with micronutrients can cause deficiency or toxicity states in chronic nutritional support. The hazards of indwelling catheters are multiple, from phlebitis of the veins to sudden dislocation or migration. Fluid overload and sepsis are the most troubling complications of intravenous parenteral nutrition.
For tube-feeding enteral alimentation, tube placement is the crucial element. With nasal placement of the tube, there is a finite risk of respiratory tract inflammation and infection from aspiration of formula and secretions. In hospital, enteral nutrition is a risk factor for nosocomial pneumonia. An alternative site for long-term administration of tube-feeds is percutaneous placement of an intragastric feeding tube under endoscopic control.
Aggressive nutritional support, with its attendant expense and potential morbidity, in critically ill patients remains controversial. In terms of cost-benefit analysis, the use of the intensive formats of enteral artificial nutrition seems to be cost effective to reduce post-hip-fracture hospital stay in underweight women and for preoperative nutritional support, if carried out at home. Preoperative parenteral nutrition has been judged as prohibitively expensive for the small reduction in postoperative morbidity that it produces.
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