MALNUTRITION

Malnutrition may be defined as a state of relative nutrient deprivation and metabolic perturbation that compromises host defenses and increases the risk of complications and death. For years, protein-calorie malnutrition has been characterized by weight loss, hypoalbuminemia, decreased skeletal muscle mass, reduced fat stores, and decreased total lymphocyte counts. In 1936, Hiram O. Studley first identified preoperative malnutrition as a specific operative risk factor in patients with peptic ulcer disease. He noted a ten-fold increase in mortality in patients who had lost over 20% of their body weight, and wondered if this might be reversible with a preoperative method for overcoming this deficit. Multiple studies performed since his time have confirmed that malnutrition results in poor wound healing, increased infection rates, and prolonged postoperative ileus with resultant lengthened hospital stays and increased mortality.

METABOLIC STRESS

Patients who are injured or submitted to extensive and complicated surgery manifest a pronounced acute phase reaction in response to tissue injury, reperfusion, and hemodynamic disturbances. A metabolic environment of increased catecholamines and cortisol orchestrates an increase in energy expenditure and protein turnover. The resultant insulin resistance is responsible for the decreased peripheral use of glucose and an increase in the rates of lipolysis and proteolysis for the provision of amino acids and fatty acid subunits as fuel. The conversion of peripherally mobilized amino acids (primarily alanine) to glucose by gluconeogenesis is not suppressed by hyperglycemia or the infusion of glucose solutions in this environment. The amino acid pool rapidly becomes depleted of essential amino acids as the high-branched chain amino acids are used as fuel in skeletal muscle while large amounts of the conditionally-essential amino acid glutamine are required for metabolic processes in the intestinal mucosa. Decreased protein synthesis in skeletal muscle and eventually in the intestine, is accompanied by increased breakdown, with the shuttling of amino acids to lung, cardiac, liver, and splenic tissue, where protein synthesis is maintained. As this catabolic process is perpetuated by cytokine activation, the critically ill and injured patient remains catabolic and consumes muscle and fat reserves rapidly. The previous disturbances can deplete important trace elements and vitamins, whose deficiencies may be associated with end-organ dysfunction.

In the stress state, malnutrition may be manifest as a functional deterioration in organ system function along with poor wound healing or wound breakdown. Respiratory muscle weakness can predispose to atelectasis, pneumonia and prolonged ventilator dependence. In addition, all aspects of the immune response may be impaired by malnutrition. Host barrier function may be compromised along with cell-mediated and humoral immunity as cell growth and turnover are diminished.

PREOPERATIVE NUTRITION

There are two circumstances in which preoperative nutritional support should be considered. One is for patients who will require major operative intervention, but cannot undergo immediate surgery and will have a prolonged fast for more than 5 days. The other circumstance is when operative intervention is delayed to treat patients with significant nutritional deficits that could increase postoperative morbidity (Figure 1).

Figure 1 Algorithm for preoperative nutritional support.

In the preoperative patient, the response to starvation is associated with a redistribution of substrate flow from peripheral tissues to meet metabolic demands. The falling level of insulin promotes the release of fatty acids and amino acids from adipose tissue and skeletal muscle. Although most peripheral tissues can utilize fatty acids as fuel, proteolysis continues to fuel gluconeogenesis in order to support the fuel requirements of the glucose dependent tissues (Figure 2). Over time, there is adaptation to starvation as the brain becomes able to use ketones for 50% of its fuel needs. As fat-derived fuel sources are utilized more, the dependence on protein catabolism decreases from 85% to 35% (Figure 3).

Figure 2 Fasting state: the Cori cycle. The falling level of insulin promotes the release of fatty acids and amino acids from adipose tissue and skeletal muscle. Although most peripheral tissues can utilize fatty acids as fuel, proteolysis continues to fuel gluconeogenesis in order to support the fuel requirements of the glucose-dependent tissues.

Figure 3 Fasting state: fatty acids. Over time, there is adaptation to starvation as the brain becomes able to use ketones for 50% of its fuel needs. As the use of fat-derived fuel sources increases, dependence on protein catabolism decreases from 85% to 35%. FFA, Free fatty acids; TGA, triglycerides.

Patients with upper gastrointestinal tract malignancies have the highest incidence of protein-calorie malnutrition, with over 30% of patients demonstrating significant nutritional deficits. Preoperative chemotherapy and radiation, combined with cancer cachexia, obstruction, increased nutrient losses, and abnormal substrate metabolism, increase nutritional risk.¹

Prospective studies have shown a decrease in major complications such as anastomotic leak and wound disruption when surgery is delayed and preoperative parenteral nutrition is administered to severely malnourished patients. However, there is an increase in infectious complications without clinical benefit when preoperative parenteral nutrition is administered to patients who are well nourished or onlymildly malnourished. It is important, therefore, to precisely define malnutrition to appropriately select patients for this treatment modality.²

Severe malnutrition can be diagnosed using a clinical nutritional evaluation tool, such as the Subjective Global Assessment.³ In 1982, Baker demonstrated the validity of a clinical assessment relative to one made on the basis of more objective laboratory values. The clinician uses historical information about recent food intake or unintentional weight loss and examines the patient for signs of nutritional depletion. Patients with multiple or severe stigmata of malnutrition or more than 15% weight loss within six months would be considered as seriously depleted. However, in patients with biopsy proven carcinoma, a weight loss of more than 10% in six months would indicate a high-risk group that would benefit from a course of preoperative nutritional support.

After selection of a patient for preoperative nutrition, it is necessary to decide on a formulation and treatment course. Although the optimal duration of therapy has yet to be determined, preoperative therapy from 7–15 days is standard. Total nonprotein calories should be calculated at 150% of basal energy expenditure as measured using indirect calorimetry or derived from the Harris-Benedict equations (Table 1). It is prudent to start patients with severe malnutrition and starvation at a basal energy rate for several days to prevent refeeding syndrome before increasing support to goal rates. After 3 days, support may be increased to 125% of basal requirements and then increased to goal as tolerated.

Table 1 Harris-Benedict Equations

Data from Van Way CW 3rd: Variability of the Harris-Benedict equation in recently published textbooks. J Parenter Enteral Nutr 16:566–568, 1992.