NUTRITIONAL SUPPORT OF SURGICAL PATIENTS

Pathophysiology of malnutrition Malnutrition occurs when there is a progressive loss of lean body mass and adipose tissue because of inadequate intake and/or due to an increased protein and calorie demand. An increase in metabolic rate due to insults such as stress, tissue injury and sepsis, in combination with a lack of nutritional intake, leads to rapid lysis of body protein to provide increased glucose production. Protein and caloric malnutrition occurs when the hypermetabolic state becomes chronic or when inadequate calories are provided during the subsequent anabolic phase. Malnutrition in critically ill patients is a different syndrome to simple starvation where a hypometabolic state is secondary to a down-regulation of metabolism. With malnutrition, neuroendocrine responses and local mediators cause a metabolic change from glucose to protein/fat metabolism. Insulin resistance and decreased glucose utilization occur with increased proteolysis and lipolysis. A negative energy balance results in a number of altered physiologic states including: fatigue and skeletal muscle weakness, smooth muscle weakness, depletion of liver glycogen stores, depletion of cardiac and smooth muscle strength and tone, altered cellular replenishment of high energy barriers such as GI mucosa resulting in GI barrier incompetence and a decrease in cells in high turnover pools in the body. A negative protein balance results in a decrease in plasma fibronectin, decreased T lymphocyte function and turnover, decreased cellular immunity, neutrophil dysfunction, a decrease in glutamine and arginine amino acid levels resulting in increases in gut bacterial translocation and decreased cellular immune function, muscle and visceral organ mass loss, a decrease in serum albumin, serum fibrinogen, complement and other small proteins and a decrease in globulin synthesis. Malnutrition therefore has serious detrimental effects to a critically ill patient including alterations in energy metabolism, poor immunocompetence, decreased resistance to infection, inability to withstand shock, surgery and cytotoxic drugs, delayed wound healing, gastrointestinal barrier breakdown, increased intestinal glutaminase activity and glutamine extraction, pneumonia, decreased tolerance to hospital stress, altered intermediary drug metabolism, prolonged hospital stay, organ failure and death. A diagnosis of protein-calorie malnutrition is made if 3 or more of the following criteria are met: - Recent loss of > 10% of usual body weight - Anorexia or hyporexia (suboptimal intake of nutrients) for more than 5 days or an expected decrease in nutrient intake of more than 5 days - Increased nutrient loss (due to vomiting, diarrhoea, burns etc) - Increased nutrient needs (due to trauma, surgery etc) - History of chronic illness - Serum albumin concentration < than or = to 2.5g/dl (only valid for assessing long standing protein malnutrition) Role of nutritional support To avoid the numerous detrimental effects of poor nutrition, aggressive nutritional support is indicated in critically ill patients. Failure to support the higher metabolic rate associated with illness and injury results in energy demands being met by body fat and protein reserves leading to an accelerated catabolic state. Nutritional support has trophic effects on the GI mucosal barrier, thereby decreasing translocation of bacteria. Instances when nutritional support should be considered include any post operative surgical patient in whom 5-7 days of anorexia are anticipated, acute weight loss> 5%, chronic weight loss >10%, generalized muscle wasting and with any diseases known to increase protein loss, induce hypermetabolism, suppress appetite, or interfere with nutrient ingestion, transit or absorption. Nutritional supplementation therefore is indicated to slow catabolism and provide optimum precursors for optimal immune function, tissue synthesis and repair, and to fuel the catabolic state with exogenous sources of protein and fat, thereby sparing endogenous sources. Ideal nutritional therapy predicts malnutrition and supplements nutrients before malnutrition occurs. Techniques of nutritional support

Nutritional support can be provided by both enteral and parenteral routes. If the GI tract functions properly then enteral feeding is preferred as it is more physiologic than parenteral feeding. The presence of luminal nutrients also maintains intestinal mucosal integrity and decreases the translocation of bacteria. The method of enteral nutrition selected depends upon the length of time nutritional support is required, the patients level of consciousness, the functional integrity of the sections of the GI tract, the functional integrity of the GI adnexal organs, the clinician's experience, the facilities, equipment, and tubes available and the concomitant need for anaesthesia and surgery for another reason. Numerous methods of enteral feeding are available including non-invasive nutritional support (food intake encouragement, food intake stimulation- diazepam, cyprohepatadine (serotonin antagonist) and forced feeding), orogastric tubes (especially neonates), nasoesophagostomy tubes, pharyngostomy tubes, esophagostomy tubes, gastrostomy tubes, gastrodenostomy tubes, duodenostomy tubes, gastrojejunostomy tubes, jejunostomy tubes and nasojejunostomy tubes. There are numerous techniques for placing feeding tubes including surgical, laparoscopic assisted and endoscopic assisted placement. Tube sizes are generally 3-5 F for nasooesophageal, gastroduodenostomy and jejunostomy tubes and greater than 8 French for pharyngostomy, esophagostomy and gastrostomy tubes. Smaller sized tubes require a commercial diet such as Clinicare, while blenderized diets can be used for tubes greater than 8F. Gastrostomy, gastroduodenostomy and jejunostomy tubes should remain in place for at least 5 days before being removed to ensure adequate adhesion formation to prevent gastrointestinal leakage. Polymeric diets (Clincare, Osmolite, Jevity) contain nutrients that require digestion before absorption can occur and are generally preferred over monomeric diets (Vivonex HN, Vital HN ), which are composed predominately of simple molecular substrates, including mono- and oligosaccharides and amino acids. The composition of commercial formulas should be relatively isotonic (~300 mOsm/L), have a caloric density of ~ 1.0 kcal/ml, a protein content of at least 4.0g/100kcal or about 16% of total calories, a calorie:nitrogen ration of approximately 125:1 and approximately 30% of calories as fat. If fiber is included, it should be included at 1.0-1.5 g/100kcal. Polymeric diets are less expensive and more physiologic than monomeric diets, however monomeric diets are used when polymeric diets are not tolerated such as short bowel syndromes, pancreatitis, parvovirus, pancreatic abscess, exocrine pancreatic insufficiency and extreme IBD. The volume of food required is based on the animals maintenance energy requirement (MER) (kCal) and the caloric density of the diet. : MER= (30 x body weight {kg} + 70) x a stress factor, usually between 1-1.5). When feeding into the small intestine the volume is gradually increased in daily increments ( calculated daily requirements on first day, increase to calculated daily requirements the second day, increase to calculated daily requirements the third day if no vomiting/diarrhoea and the entire calculated volume during the fourth 24 hours). Complications of tube feeding Complications of tube feeding can be divided into mechanical complications, gastrointestinal complications and metabolic complications. Mechanical complications include improper tube placement, GI perforation by the feeding tube, peritoneal leakage, subcutaneous leakage, leakage through osteotomy site, regurgitation or vomiting the tube, esophageal irritation, infection at tube exit site/focal cellulitis, tube occlusion, tube kinking, premature tube removal by the patient and tube migration. Gastrointestinal complications include vomiting, cramping, abdominal distension, diarrhoea, reflux esophagitis and aspiration pneumonia. Metabolic complications include hyperglycaemia and hypophosphataemia. Tube complications can generally resolved by slowing the feeding rate, replacing the tube, or placing a different type of feeding tube.