Hospitalized patients are often assessed for nutritional status prior to or at the time of admission. This may include a history, an interview by a dietician, and laboratory tests. Of particular concern for patients undergoing surgery are the risks of postoperative infection and poor wound healing. If the results of these tests indicate possible nutritional deficits, patients may be provided nutritional supplementation prior to a surgery or procedure and be monitored regularly during recovery.
Three different plasma proteins are measured to assess protein status. Each of them has a different circulating half-life. They reflect severity of illness and are used in conjunction with other clinical data to determine therapy.
Serum albumin is synthesized in the liver and has the longest half-life at 18 to 20 days. It is an indicator of dietary intake during the preceding three weeks. Low serum albumin (<2.2 g/dL) is a marker of a negative catabolic state, and a predictor of poor outcome. Many other conditions affect serum albumin levels. Serum albumin is not a good nutritional marker in the setting of disorders causing large protein losses from the circulation, such as ascites, protein losing enteropathy, proteinuria, liver disease, or extensive burns and inflammation. Serum albumin concentration gradually returns to normal after initiation of nutritional therapy, but this may take up to three weeks.
Serum transferrin has an intermediate half-life of eight to nine days, reflecting protein status over the past two to four weeks. Transferrin also reflects iron status, and low transferrin should be considered an indicator of protein status only in the setting of normal serum iron.
Prealbumin (also called transthyretin) is a plasma protein that is synthesized in the liver. Prealbumin is turned over rapidly with a half-life of two to three days. Serum prealbumin concentrations fall rapidly in patients with poor dietary intake and rise to low-normal values within 10 days of initiation of nutritional therapy and adequate refeeding. Thus, prealbumin is a good predictor of protein and energy adequacy of the diet in the days prior to testing, and can serve as a marker of an acute reduction in food consumption. However, it is a negative acute-phase reactant, meaning that concentrations fall in the presence of inflammation. Inflammatory cytokines decrease prealbumin synthesis by the liver. Prealbumin can also be decreased in patients with renal and hepatic diseases. Therefore, prealbumin levels do not accurately reflect nutrition status in patients with these conditions.
In addition to assessing protein status, a few other laboratory studies may be helpful. Electrolytes, glucose, BUN and creatinine help assess overall clinical and fluid volume status and need to be obtained if parenteral (intravenous) nutrition is a possibility. Plasma calcium, magnesium, and phosphorous concentrations should also be assessed periodically, particularly in the setting of poor oral intake or diarrhea. They are monitored regularly in patients receiving parenteral nutrition.
A complete blood cell count (CBC) can be used to identify patients with nutritional deficiencies of iron, folate, or vitamin B12. A macrocytic anemia suggests folic acid and/or vitamin B12 deficiency. Iron deficiency anemia, associated with hypochromic, microcytic red cell morphology, is the most common nutritional deficiency. Plasma ferritin is the most sensitive measure of the adequacy of body iron status, but it is an acute-phase reactant and may be elevated during infectious or inflammatory diseases. Additional tests that are useful in the evaluation of microcytic anemia include serum iron, total iron-binding capacity, and transferrin.
Testing for specific vitamin deficiencies may be necessary in patients who have gastrointestinal malabsorption. Serum concentrations of vitamins A, E, and 25-hydroxyvitamin D can be measured directly. Prothrombin time can be used to assess vitamin K adequacy.
Vitamin A is a lipid soluble vitamin that is also called retinoic acid. Vitamin A plays an essential role in light detection by the retina and cellular differentiation of epithelial tissues. Together with carotenoids, vitamin A enhances immune function.
Vitamin A deficiency is rare in the United States, but is a common nutritional deficiency in underdeveloped countries. In the United States, vitamin A deficiency may be seen with disorders causing fat malabsorption such as biliary cholangitis, Crohn disease, and bariatric surgery. Night blindness is an early symptom that may be followed by xerophthalmia, corneal ulcers, scarring, and blindness.
Vitamin D is the hormone that enhances intestinal absorption of calcium and insures healthy bone formation. Vitamin D metabolism is dependent on sunlight exposure, intestinal absorption, and liver and kidney function. Vitamin D malabsorption may be associated with several GI disorders including Crohn disease, celiac disease, and pancreatic insufficiency. Severe vitamin D deficiency causes increased secretion of parathyroid hormone (PTH), which promotes calcium absorption from bone. Vitamin D deficiency is a major risk factor for bone loss, weakness and fracture.
Vitamin E is a tocopherol that functions as an antioxidant, protecting the integrity of lipid membranes and preventing oxidative damage to retinol.Vitamin E deficiency can be caused by conditions that cause fat malabsorption such as cholestatic liver disease, pancreatic insufficiency and small intestinal resection or disease. Deficiency of Vitamin E in adults and children causes reversible neuropathy and hemolysis.
Deficiency of water-soluble vitamins is less common, and levels should be measured only when clinically indicated. Water soluble vitamins (in addition to folate and vitamin B12) include vitamins C, B1 (thiamin), B2 (riboflavin), B3 (niacin) and B6 (pyridoxine).
Vitamin C deficiency results in scurvy. Generalized symptoms of scurvy include fatigue, myalgias, arthralgias, weakness, anorexia, weight loss, and irritability. Although a low plasma vitamin C level is specific for the diagnosis of scurvy, plasma vitamin C levels quickly normalize with enteral intake of ascorbic acid and do not reflect tissue levels.
Thiamine (Vitamin B1) deficiency causes Wernicke's encephalopathy, which is characterized by the classic triad of mental confusion, oculomotor dysfunction, and gait ataxia. Thiamine diphosphate is the active form of thiamine. It is present predominantly in erythrocytes, with very little occurring in plasma. Measurement of thiamine diphosphate in whole blood by liquid chromatography and mass spectrometry is the preferred method for determining nutritional status. Riboflavin is quantitated in plasma using high performance liquid chromatography and tandem mass spectrometry.
Riboflavin is also called Vitamin B2. Deficiency is called ariboflavinosis and is usually caused by reduced dietary intake. Symptoms include sore throat, cheilosis, angular stomatitis, glossitis, corneal vascularization, dermatitis, and normocytic, normochromic anemia.
Vitamin B3 (niacin) deficiency predisposes to pellagra. Pellagra is extremely uncommon in the western world except as a complication of alcoholism, anorexia nervosa, or malabsorption. The most characteristic finding is a symmetric hyperpigmented rash on sun exposed areas of skin. Other clinical findings include red tongue, diarrhea and vomiting. Neurologic symptoms include insomnia, anxiety, disorientation, delusions, dementia, and encephalopathy.
The primary reason for ordering vitamin B6 is to diagnose pyridoxine deficiency, which has been associated with microcytic hypochromic anemia, dermatitis, neuritis, stomatitis and cheliosis. Pyridoxal-5- phosphate is the active form of vitamin B6 in the body. It is the vitamer that is measured in serum or plasma to determine vitamin B6 levels.