Chapter 072. Malnutrition and Nutritional Assessment (Part 4)

Protein CatabolismThe rate of endogenous protein breakdown (catabolism) to supply energy needs normally falls during uncomplicated energy deprivation. After about 10 days of total starvation, the unstressed individual loses about 12–18 g/d protein (equivalent to approximately 2 oz of muscle tissue or 2–3 g of nitrogen). By contrast, in injury and sepsis, protein breakdown accelerates in proportion to the degree of stress, to 30–60 g/d after elective surgery, 60–90 g/d with infection, 100–130 g/d with severe sepsis or skeletal trauma, and 175 g/d with major burns or head injuries. These losses are reflected by proportional increases in the excretion...
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Chapter 072. Malnutrition and Nutritional Assessment (Part 4) Chapter 072. Malnutrition and Nutritional Assessment (Part 4) Protein Catabolism The rate of endogenous protein breakdown (catabolism) to supply energyneeds normally falls during uncomplicated energy deprivation. After about 10days of total starvation, the unstressed individual loses about 12–18 g/d protein(equivalent to approximately 2 oz of muscle tissue or 2–3 g of nitrogen). Bycontrast, in injury and sepsis, protein breakdown accelerates in proportion to thedegree of stress, to 30–60 g/d after elective surgery, 60–90 g/d with infection,100–130 g/d with severe sepsis or skeletal trauma, and >175 g/d with major burnsor head injuries. These losses are reflected by proportional increases in theexcretion of urea nitrogen, the major byproduct of protein breakdown. Gluconeogenesis The major aim of protein catabolism during a state of starvation is toprovide the glucogenic amino acids (especially alanine and glutamine) that serveas substrates for endogenous glucose production (gluconeogenesis) in the liver. Inthe hypometabolic/starved state, protein breakdown for gluconeogenesis isminimized, especially as ketones derived from fatty acids become the substratepreferred by certain tissues. In the hypermetabolic/stress state, gluconeogenesisincreases dramatically and in proportion to the degree of the insult, to increase thesupply of glucose (the major fuel of reparation). Glucose is the only fuel that canbe utilized by hypoxic tissues (anaerobic glycolysis), white blood cells, and newlygenerated fibroblasts. Infusions of glucose partially offset a negative energybalance but do not significantly suppress the high rates of gluconeogenesis in thecatabolic patient. Hence, adequate supplies of protein are needed to replace theamino acids utilized for this metabolic response. In summary, the hypometabolic patient is adapted to starvation andconserves body mass by reducing the metabolic rate and using fat as the primaryfuel (rather than glucose and its precursor amino acids). The hypermetabolicpatient also uses fat as a fuel but rapidly breaks down body protein to produceglucose, causing loss of muscle and organ tissue and endangering vital bodyfunctions. Micronutrient Malnutrition The same illnesses and reductions in nutrient intake that lead to PEM oftenproduce deficiencies of vitamins and minerals as well (Chap. 71). Deficiencies ofnutrients that are stored in small amounts (such as the water-soluble vitamins) arelost through external secretions, such as zinc in diarrhea fluid or burn exudate, andare probably more common than generally recognized. Deficiencies of vitamin C, folic acid, and zinc are reasonably common insick patients. Signs of scurvy such as corkscrew hairs on the lower extremities arefrequently found in chronically ill and/or alcoholic patients. The diagnosis can beconfirmed with plasma vitamin C levels. Folic acid intakes and blood levels areoften less than optimal, even among healthy persons; when illness, alcoholism,poverty, or poor dentition is present, deficiencies are common. Low blood zinclevels are prevalent in patients with malabsorption syndromes such asinflammatory bowel disease. Patients with zinc deficiency often exhibit poorwound healing, pressure ulcer formation, and impaired immunity. Thiaminedeficiency is a common complication of alcoholism, but its manifestations areoften prevented by therapeutic doses of thiamine in patients treated for alcoholabuse. Patients with low plasma vitamin C levels usually respond to the dosesfound in multivitamin preparations, but patients with deficiencies should besupplemented with 250–500 mg/d. Folic acid is absent from some oralmultivitamin preparations; patients with deficiencies should be supplemented withabout 1 mg/d. Patients with zinc deficiencies resulting from large external lossessometimes require oral daily supplementation with 220 mg of zinc sulfate one tothree times daily. For these reasons, laboratory assessments of the micronutrientstatus of patients at high risk are desirable. Hypophosphatemia develops in hospitalized patients with remarkablefrequency and generally results from rapid intracellular shifts of phosphate incachectic or alcoholic patients receiving intravenous glucose (Chap. 46). Theadverse clinical sequelae are numerous; some, such as acute cardiopulmonaryfailure, can be life-threatening. Nutritional Assessment Because interactions between illness and nutrition are complex, manyphysical and laboratory findings reflect both underlying disease and nutritionalstatus. Therefore, the nutritional evaluation of a patient requires an integration ofthe hist ...