In surgical practice malnutrition is common, being present before, or occurring after, operations in about 50per cent of patients, possibly more in some parts of the world.
Preoperative malnutrition may be due to starvation or to
a failure of digestion. Starvation is caused by:
• difficulty in obtaining food (poverty);
• difficulty in swallowing food (dysphagia);
• difficulty in retaining swallowed food (vomiting);
• self-neglect, e.g. in the elderly and in alcoholics.
Failure of proper digestion may, for example, be due to pancreatic or biliary disease (carcinoma or jaundice due to stones), and duodenal and jejunal conditions (fistula or blind-loop syndrome).
Postoperative (post-traumatic) malnutrition is, in most cases, of a transient nature consequent upon a short period of starvation and the stress reaction to trauma. Recovery from any nitrogen deficit (Table 5.1) due to protein catabolism will follow on return to normal feeding. Any delay in return to a normal diet, such as may be imposed by the dictates of the operation (oesophagectomy), or a complication (paralytic ileus from peritonitis), means that severe malnourishment is likely to occur.
Hypercatabolic state. Severe sepsis (subphrenic abscess),
severe trauma (burns) and other severe disturbances of major viscera (pancreatitis) are accompanied by an accelerated and profound breakdown of tissue proteins.
In starvation, the metabolic changes are directed to minimising tissue loss and, in some circumstances, humans can survive for about 120 days. Glucose reserves are available only for 24 hours and thereafter are derived principally from muscle, so that catabolism begins almost immediately after food deprivation. In the first 72 hours, there is a rapid weight loss due to loss of sodium and water, then the resting metabolic expenditure falls and daily nitrogen losses over 2 weeks fall from about 10 g to 3—4 g. Progressively fat provides most of the energy requirements yielding 38 kJ/g while carbohydrate derived by gluconeogenesis in the liver from amino acids is utilised by the brain, adrenal glands and red cells — all obligatory glucose users. After about 21 days, the central nervous system adapts to using ketones derived from fat. The gluconeogenesis and ketosis of starvation may be easily inhibited by glucose intake.
Protein in lean tissue is constantly turned over and renewed. Normally the processes of protein synthesis and breakdown act in equal and opposite directions to keep the muscle mass in an adult constant — atabout 40 per cent of total body weight. It seems likely that under normal circumstances the provision of an adequate nutrient supply of amino acids allows protein synthesis to exceed breakdown during and after meals, whereas between meals the opposite pertains, thus maintaining a balance over a 24-hour period. Insulin and amino acids appear to stimulate muscle protein synthesis and insulin inhibits protein breakdown. Lean tissue may be lost by a variety of methods. In starvation, chronic illness and immobilisation, muscle protein synthesis is depressed below the level of protein breakdown. Such a pattern is found in patients suffering from heart failure, carcinoma, emphysema, hypothyroidism and cirrhosis, whereas a patient confined to bed will suffer an exacerbation of the process causing muscle wasting.
In sepsis, inflammation, trauma and burns, the muscle wasting results from a massive loss of amino acids from muscle tissue with depressed muscle protein synthesis and enhanced muscle breakdown. The mechanism is uncertain but injury and sepsis trigger a co-ordinated series of inflammatory and immune responses and the stimulation of macrophages to produce cytokines such as tumour necrosis factor and interleukin-1. These cytokines are associated with proteolysis, particularly the breakdown of myoflbrillar proteins but only in the presence of elevated corticosteroid concentrations.
After injury or surgical operation
There is an increased oxygen and calorie consumption and a negative nitrogen balance (Cuthbertson). The increase in resting metabolic expenditure ranges from minimal after uncomplicated surgery to 30 per cent with multiple fractures, 45 per cent in peritonitis and up to 100 per cent in burns. An increase in metabolic rate and protein catabolism of more than 25 per cent is regarded as a hypercatabolic state.
The endocrine profile, activated by fear, apprehension and nervous stimuli from damaged tissues, is altered after stress with an increase in secretion of most hormones, in turn resulting in changes in substrate handling by the body.
Glycogen breakdown in muscle and liver is accelerated principally by adrenaline and glucagon, leading to increased blood glucose levels, while increased cortisol and glucagon induces gluconeogenesis from amino acids. Lipolysis — fat breakdown — is increased by growth hormone, glucagon and noradrenaline. Thus control of glucose levels is impaired and, together with depressed peripheral clearance, results in ‘the diabetes of injury’.
The stimulated protein breakdown in the postoperative period is associated with a change in synthesis rate in the body cell mass, and this results in a negative nitrogen balance indicating loss of protein derived from muscle and viscera. Larger losses are seen in muscular athletic men and the smallest losses in wasted patients. Epidural anaesthesia inhibits the normal postoperative increases in cortisol, adrenaline, aldosterone and growth hormone, and so may reduce the negative nitrogen balance. Nitrogen balance may be improved during enteral or parenteral feeding if the patient can be mobilised.
Studies following patients for up to 1 year following uncomplicated surgery suggest that the maximum weight loss occurs after 2 weeks and that normal body composition is restored after 6 months.
A particularly unpleasant effect of surgery is the period of mental and physical tiredness that follows it. It is not a particular problem in patients who feel well before surgery, but in those with preoperative tiredness, it is worst postoperatively at the end of the first week; at 4 weeks it is similar to the initial preoperative level, and it usually disappears after 3 months. Voluntary muscle functions deteriorate in a similar pattern to fatigue but postoperative nutrition, which restores muscle mass, does not influence postoperative fatigue, leading to speculation that the symptoms of fatigue have both a physiological and psychological basis.
Uncomplicated, minimally invasive surgery is believed to be associated with minimal postoperative fatigue and a shortened convalescence. Initial studies suggest that the neuroendocrine response is similar to a comparable open operation, and further studies are required to resolve this paradox.
Severe sepsis is characterised by an increased rate of whole body protein catabolism, and when prolonged the depletion of visceral protein results in multiple organ failure. In patients with sepsis, both protein synthesis and catabolism are increased with a much greater increase in catabolism resulting in protein loss. The increase in protein synthesis may be the result of increased hepatic protein synthesis of acute phase proteins. Intermediate metabolism in sepsis is directed at increasing substrate availability by lipolysis, glycogenolysis, protein catabolism and hepatic glucose production. Studies in septic patients have provided evidence that the myoflbrillar proteins, retin and myosin, are particularly catabolised in sepsis. The principal mediators are tumour necrosis factor, interleukin-1 and glucocorticoids.
Fat oxidation increases with sepsis and is the principal source of energy in the patient with sepsis, while hepatic glucose production occurs despite hyperglycaemia and a low respiratory quotient. The increased substrate turnover is accompanied by an increase in resting energy expenditure.
The effects of malnutritioninclude poor wound healing manifesting as wound dehiscence (Chapter 3) and leaking anastomoses of bowel, delayed callus formation, disordered coagulation, reduced enzyme synthesis, impaired oxidative metabolism of drugs by the liver, immunological depression with increasing susceptibility to infection, decreased tolerance to radiotherapy and cytotoxic chemotherapy, all with the severe mental apathy and physical exhaustion of the patient.
Some clinical indications for nutritional support are:
• preoperative nutritional depletion;
• postoperative complications:
— ileus more than 4 days,
— fistula formation;
• intestinal fistula;
• massive bowel resection;
• management of:
— malabsorption syndromes,
— ulcerative colitis,
— radiation enteritis,
— pyloric stenosis;
• anorexia nervosa;
• intractable vomiting;
• maxillofacial trauma;
• traumatic coma;
• multiple trauma;
• malignant disease;
• renal failure;
• liver disease;
• cardiac valve disease.
Asseasment and management
It is essential for the clinician to be aware of the need to assess the state of nutrition of a patient and, if malnutrition is present or threatens, to consider the nutritional requirements, and then to use methods of sustaining normality or rectifying any deficiency. Between I and 2 per cent of elderly patients have serious subnutrition as a consequence of inadequate dietary intake.
A malnourished patient has a characteristic appearance, lean and hungry in most cases of starvation, lean and apathetic in post-traumatic depletion, with a superimposed hectic flush around sunken cheeks and pinched nose in a hypercatabolic state. The clinician, when placing a comforting hand on the patient’s shoulder, discerns the bony scapula bereft of almost all its muscle. However, these clinical observations only detect gross malnutrition and therefore measurement of the nutritional status is essential (Goode). The following parameters are included.
1. Body weight. Careful weighing on a bed weighing machine is the obvious way of detecting the progress or otherwise of the patient. The desirable weight of the patient can be checked by reference to the appropriate tables, or by applying the body mass index (BMI) = weight (kg)/height2 (in). A woman should have an index of 20, 21 or 23, and a man 20.5, 22 or 23.5 according to size of frame (small, medium or large).
2.Upper arm circumference. Feeding is indicated if the circumference is less than 23 cm in females and 25 cm in males.
3.Triceps skin fold thickness. Using a skin fold caliper, the minimum is 13 mm in females and 10 mm in males.
4.Serum albumin should not be less than 35 g/litre.
5. Lymphocyte count. Less than 1500/mm3 indicates an impaired cellular defence mechanism.
6.Candida skin test. A negative reaction also means defective cell-mediated immunity.
7.Nitrogen balance studies. The total nitrogen intake is compared with the loss from all sources, such as urine, fistula drainage and nasogastric aspirate (1 litre = 1 g nitrogen). A greater loss than intake indicates a negative balance and tissue breakdown. A positive balance means anabolism—tissue synthesis.
Other measurements include those determining the rate of muscle breakdown, such as urinary creatinine excretion, or 3-methylhistidine excretion. Body potassium and nitrogen are used to assess the absolute size of the body cell mass. [t4Cj Leucine incorporation is a measure of the synthesis rate, while serum transferrin is used as a measure of visceral protein synthesis (needs to be more than 1.5 g/litre).
These include carbohydrate, fat, protein, vitamins, minerals and trace elements .
Energy is provided by carbohydrate and fat. A healthy adult at rest requires 6300—8400 nonprotein kilojoules per day for energy (1500—2000 calories). Carbohydrate provides 16.8 kJ/g (4.1 kcal/g) and fat 37.8 kJ/g (9.1 kcal/g). The number of nonprotein kilojoules given should bear a definite relationship to the nitrogen intake. A typical regime would feature 8400 kJ (2000 kcal) to 13 g N (about 150 to 1).
Nitrogen requirements. The minimum for dynamic tissue turnover, and so to keep a healthy adult in positive nitrogen balance, is about 35—40 g of protein or 5.5—6.5 g of nitrogen per day. The hypercatabolic patient requiring hyperalimentation may need three or four times this amount of protein. A daily negative nitrogen balance of 10 g is not unusual and is equivalent to a loss of 62.5 g of protein or 300 g of muscle tissue.
Vitamins. Whatever the method of feeding, vitamins are necessary as supplements, as they are essential for the maintenance of normal metabolic function.
The water-soluble vitamins B and C act as coenzymes in collagen formation and wound healing. Postoperatively, the vitamin C requirement increases to 60—80 mg/day. Preoperative depletion is exacerbated by anorexia, smoking, aspirin and barbiturate therapy. Vitamin B12 is given 500 micro gram intramuscularly (i.m.) weekly, particularly to those with initial low levels (coeliac disease, Crohn’s disease, ileal resection or bypass, blind-loop syndrome, tapeworm infestation, reduced pancreatic secretion, tropical sprue, excess alcohol intake, anticonvulsant therapy and after gastric surgery). As the serum folate falls, especially in those on parenteral nutrition, folinic acid is required daily in doses of 3—6 mg i.m.
The fat-soluble vitamins A, D, F and K are reduced in steatorrhoea and the absence of bile. Vitamin A, 5000 units per week, is required after surgery and, when appropriate, it enhances the antitumour effect of cyclophosphamide. Vitamin K 5—10 mg i.m. weekly reduces any bleeding tendency. If commercially available vitamin additives are put into an infusion, the container should be protected from the light.
Minerals and trace elements
Sodium, potassium, iron, calcium and magnesium deficiencies must be identified and made good (Chapter 4). Zinc deficiency is manifest as a rash on the face and perineum which does not respond to antifungal therapy, stomatitis which causes disturbance of taste (dysgeusia) and alopecia. Copper deficiency results in leucopenia and anaemia, while lack of chromium may give rise to glucose intolerance. The 14 trace elements that are considered essential for normal enzyme activities include manganese, cobalt, molybdenum and vanadium. It is to be remembered that long-term parenteral nutrition can result in depletion.
Methods of feeding. These are predominantly enteral and less commonly parenteral.
Obviously, as this is the natural way, it should always be attempted. Only when it is known that this route cannot be used or is ineffective are other methods considered.
Feeding by mouth demands common sense, cleanliness and compassion on the part of the medical attendants. It is common sense to ensure that an adequate, palatable and varied diet, including all the nutritional requirements, is provided at regular intervals, more frequently than regular meal times if necessary. It is common sense to begin with a liquid diet as soon as bowel sounds return after an abdominal operation, and not, for example, to allow a plate of fish and chips to be put in front of a patient the day after a gangrenous appendix has been removed. Promotion to semisolid (light) and then to more solid food (full diet) follows in steps of 3—7 days according to progress.
Cleanliness in the preparation and serving of food and of the utensils used is of paramount importance in avoiding gastrointestinal infection causing vomiting and diarrhoea. A salmonella infection among elderly patients and children may be a mortal blow.
Compassion is needed to ensure that the patient actually receives and ingests the proffered food. Food must be placed within reach of an enfeebled patient. Assistance is often required and should be freely given. Dental care may be necessary to facilitate oral intake and false teeth may need consideration. Table 5.3 shows a representative range of the enteral diets available. Dieticians and pharmacists should be involved in the prescribing of enteral feeding regimes in much the same way as they are involved in parenteral feeding.
By nasogastric tube
A nasogastric tube which has been passed to allow regular gastric aspiration to be performed may also be used for feeding liquidized diets. Fine-bore tubing can be used instead, being favorably received by most patients as less irritating than the larger tube. It is invaluable when passed with the aid of an endoscope through an oesophageal stricture into the stomach, enabling the effects of starvation to be reversed. In some patients, the tube can be sited in the duodenum, especially if there are problems of gastric stasis or oesophagogastric reflux.
Technique of fine-bore tube insertion and usage
The patient may be sitting or lying, preferably the former. The introducer wire is lubricated with water and inserted into the fine-bore tube. Pass the tube through the nose via the nasopharynx and oesophagus into the stomach. Withdraw the wire and tape the tube to the patient. Check the position of the tube by radiography as passage into a bronchus can occur quite easily. Alternatively, a quick check can be made by injecting 5ml of air down the tube and listening through a stethoscope for its bubbling entry into the stomach.
Administration of the feeds is either by gravity or by means of an infusion pump.
Problems of tube feeding
Gastric emptying should he normal. In ill patients ensure that the stomach empties by injecting 60 ml water down a nasogastric tube and aspirate 4-hourly. If after 24 hours fluid is passing through the stomach, commence feeding for the first day and aspirate intermittently to ensure that the stomach empties. Then remove the tube and introduce the fine-bore tube.
Blockage of a 1-mm bore tube is cleared by flushing through with 2 ml water — do not add effervescent potassium to the feed as curdling will follow.
Most fine-bore tubes incorporate a male ‘luer’ lock connector making the nasogastric drip system incompatible with intravenous lines.
Check the drip rate hourly.
All feeds should be stored at 40C until use, not exposed to room temperature for more than 8 hours and discarded if not used after 12 hours. As diet kitchens may be a source of Klebsiellainfection, the bacteriological monitoring of feeds is desirable.
Unwanted effects. Nausea, vomiting and pulmonary aspiration are avoided by regulation of the infusion rate and ensuring initial gastric emptying. Diabetes and hyperosmolar states are related to high carbohydrate intake with particular hazard for the established diabetic. Diarrhoea is common and the pathogenesis is not fully understood, but fluid and electrolytes are secreted into the bowel in response to a high osmotic load. The use of broad-spectrum antibiotics is also associated with diarrhoea. Recent studies suggest that osmolality, electrolyte content and volume of the feed are notimplicated in the onset of diarrhoea. It is now probable that the bypassing of the cephalic phase of feeding when a tube is in situ results in suppression of distal colonic motor activity with the onset of diarrhoea. Commence with half strength feed and increase slowly to standard concentration over days given at a slow, constant rate, avoiding milk because of possible lactose intolerance and a high fat content giving steatorrhoea. Mild disturbances of liver function can be associated with both enteral and parenteral feeding, due to intrahepatic cholestasis. Metronidazole 500 mg twice daily may prevent overgrowth of the anaerobic bacteria responsible.
By tube enterostomy
Tube enterostomy is the operative placement of a tube or catheter into the gastrointestinal tract. It is indicated when the passage of a fine-bore nasogastric tube is not possible or when more than 4 weeks of enteral feeding is anticipated. The common contraindications include complete or partial gastric or intestinal obstruction. The tube is usually placed as a specific surgical procedure or as an adjunct to intraabdominal surgery.
A choice of procedure is to fashion either a gastrostomy or jejunostomy. The contraindications to the former are:
•impaired gastric emptying;
•significant gastro-oesophageal reflux;
•loss of the gag reflex.
Jejunostomy is the procedure of choice for the ease of placement of the tube, the initiation of early postoperative feeding, and the avoidance of the risk of pulmonary aspiration.
There are two long-term types of gastrostomy: Stamm and Janeway. An upper abdominal (midline) incision is optimal for giving the best exposure and the catheter can be placed laterally away from the incision. The Stamm gastrostomy is the simplest to perform and is particularly valuable as a temporary procedure or in the patient who is a poor postoperativerisk. Inadvertent removal of the tube is followed by rapid shrinkage of the cutaneous orifice. To preserve the established gastrostomy a tube must be promptly reinserted. Caution must be exercised to ensure that the new tube is in situ before feeding is recommenced. A Janeway gastrostomy is preferred if there is a need for permanent tube feeding.
When a quick temporary measure is necessary, the ink-well (Kader—Senn) technique is valuable. The tube should be large and, as in all gastrostomies, the end of the tube should be directed towards the fundus.
Complication rates as high as 30 per cent have been associated with gastrostomy procedures, reflecting poor nutritional status, impaired wound healing and pulmonary complications because of immobility. Leakage around the tube can be controlled by inserting a larger catheter with a balloon and taping the tube with gentle traction.
The endoscopic placement of gastrostomy tubes in therapeutic endoscopy is an innovation during the last decade (Fig 5.3 and Fig 5.4). Percutaneous endoscopic gastrostomy has reduced the need for the surgical fashioning of a feeding gastrostomy under general or local anaesthesia. Thus, whenever a surgical gastrostomy is indicated, a percutaneous endoscopic technique may he used. As the gastroscope must be passed into the stomach, a complete oesophageal obstruction will be an absolute contraindication, as are ascites, sepsis, abnormal clotting and peritoneal dialysis. The patient should have no intake for 8 hours before the procedure. The basic gastrostomy is fashioned in a retrograde manner from within the stomach. A suture is placed through the anterior abdominal and gastric wall and brought out through the mouth. A catheter with a tapered tip is then fixed to the oral end of the suture from the abdominal wall. The catheter is then delivered through the abdominal wall. The holding sutures are removed from the abdominal wall after 1 week.
There is a 3 per cent incidence of major complications, sepsis, puncture of another viscus such as the colon or the need for a laparotomy. Minor complications in 7 percent of cases include wound infection and circum stomal drainage.
A tract forms within 2 weeks and, if the catheter is removed, another of similar size may he inserted within a few hours.
There are two types of feeding jejunostomy: a Witzel jejunostomy with formation of a serosal tunnel, and a needle jejunostomy using a catheter of a small gauge. The ease of jejunostomy as an adjunct to an intraabdominal surgical procedure has increased in popularity.
It is of importance to control infusion rates of nutrients, particularly with a jejunal feed. The perceived benefits of an enteral pump infusion system include:
• more efficient nutrient delivery;
• reduced abdominal discomfort;
• decreased incidence of osmotic diarrhoea.
A particular advantage is the pump alarm system indicating an empty bag, line occlusion or a failing pump battery system. This safety mechanism promotes mobility for the patient, a more continuous energyintake than an intermittent feeding regimen and a mechanism providing security and confidence for the patient, and nursing and medical staff.
Parenteral nutrition by intravenous feeding is used in less than 4—5 per cent of all hospital admissions, either when enteral feeding is not possible, or to supplement deficient enteral feeding. It has been suggested that although the incidence of serious, noninfectious complications is lower in patients receiving total parenteral nutrition, the incidence of septic complications is substantially higher and only in severely malnourished patients do the benefits outweigh the risks.
Total parenteral nutrition is particularly complicated by displacement of the catheter, sepsis, mechanical problems and metabolic derangements — which occur in up to 10 per cent of postoperative patients.
Intravenous (i.v.) fat has many immunosuppressive effects:
i.v. long-chain triglycerides reduce the functions of the reticuloendothelial system and neutrophils and the ratio of Thelper to T-suppressor cells. Contraindications include cardiac failure, severe liver disease, disorders of fat metabolism, uncontrolled diabetes, shock and severe blood dyscrasias. It must be remembered that total parenteral nutrition is not to be undertaken lightly. It is potentially hazardous and can be dangerous in inexperienced hands. The formation of multidisciplinary nutritional care teamsincluding dieticians and pharmacists is a major advance and their advice should be sought.
When planning an intravenous feeding regimen, first
weigh the patient and calculate the fluid needs for the next
24 hours. Energy and nitrogen intake should be calculated on
a body weight basis, remembering that daily needs may
change. Daily biochemical patient monitoring is essential
Most feeding teams decide on the nitrogen and energy requirements of their patients, and tailor-make the feeds from the wide variety of amino acid solutions with and without electrolytes, and the various concentrations of dextrose and fat available (Table 5.5).Typically, these are mixed under laminar flow sterile conditions in the pharmacy into 3-litre bags giving sufficient for 24 hours or, better still, supplied to specifications by one of the companies involved in the manufacture of i.v. solutions. Twenty per cent glucose is equivalent to 3200 kJ/litre (770 kcal/litre) and Intralipid 20 per cent (KabiVitrum) is equivalent to 8400 kJ/litre (2000 kcal).
As most glucose solutions are hypertonic and irritant, they are usually given through central veins, the cannulation of which requires technical finesse. In the short term, the nutritional requirements in aseptic patients can be adequately met with mixtures of amino acids, fat and glucose given peripherally. Fat buffers the vein wall and sometimes subtherapeutic doses of heparin and hydrocortisone are given to act locally in the prevention of thrombophlebitis. The energy requirements of surgical patients have often been overestimated; few will require more than 8400 kJ (2000 kcal) per day (Macfie).
Technique for central venous catheter insertion with a skin tunnel
Percutaneous catheter insertion requires expertise to prevent the complications which may occur in one in five attempts. These are air embolism, pneumothorax and injury to the subclavian artery or brachial plexus because of significant variation in relationship of the subclavian vein to the clavicle and first rib. A suhclavian vein cutdown technique may be employed to allow cannulation of the vein under direct vision. A silicone rubber catheter of 1 mm diameter (Vygon, Vygon UK Ltd, Uxbridge, UK) is inserted by intraclavicular approach, the introducer inserted under local anaesthetic through a 1-cm skin incision (A) 2 cm below the midclavicular point. The position of the catheter is checked radiologically, ensuring the tip is in the superior vena cava or right atrium. The catheter hub is removed and the introducer withdrawn. The introducer is now inserted through the skin puncture at (B) about 7 cm below and medial to (A); it is passed through the subcutaneous tissue toemerge at (A) and the catheter threaded through the introducer at (A) until it is seen within the transparent introducer at (B). The introducer is partially withdrawn and cut at X—X so that 2 cm remains in the tunnel and 2 cm protrudes, and the catheter pushed fully through the 4-cm sleeve, avoiding kinks at (A). (A) and (B) are cleaned with chlorhexidine in alcohol and sprayed with povidone iodine powder. Incision (A) is closed with a stitch and covered with a sterile dressing. Caution: it is possible for the catheter tip to perforate the vein wall. If this occurs in the pleural cavity a pneumothorax can be caused. Before the infusion is started, it is essential to confirm by a free backflow of blood that the catheter remains in the lumen of the vessel.
Commence feeding using half-strength solution and increase to the desired daily intake over days. Additives to solutions should be avoided and given through a separate line, although central mixing in pharmacy allows addition under sterile conditions into a 3-litre bag delivery system.
Catheter-related sepsis may occur in up to a third of patients fed parenterally. Skin flora are important in the pathogenesis of this sepsis and the skin at the site of the catheter insertion should be swabbed on alternate days. Bacteriological skin culture shows a strong association between microbial growth, usually Staphylococcus epidermidis, and the development of catheter-related infection. Factors known to increase the risk of infection include variation from the strict nursing protocol for care of the catheter, the age of the patient and the duration of hospital stay before the institution of parenteral nutrition.
Home parenteral nutrition
Chronic intestinal failure results in a failure of adequate nutrient absorption from the gut to maintain body weight. This may follow extensive bowel resection, multiple high output fistulas, motility disorders and extensive Crohn’s disease. Such patients require prolonged nutritional management by a skilled and experienced team. Long-term home parenteral nutrition depends upon suitable case selection andextensive patient training by experienced nurses, together with a comprehensive hospital pharmaceutical service: the patient will live at home and manage his or her own parenteral feeding. With successful treatment, many patients are able to return to work or care for the home and family unaided or with minimum help.
Notes on solutions. Fructose, sorbitol or alcohol solutions are potentially disadvantageous owing to an associated lactic acidosis or hepatocellular damage. Fat, isotonic preparations of vegetable oils in water with an emulsification agent or purified egg phospholipid in lntralipid (to stabilise the mixture) should not be used 12 hours before blood sampling as they interfere with analysis. The rate of clearance of intravenous fat is increased after surgery or when energy demands are high (Feggetter).
The nitrogen sources are either casein hydrolysates, or laevorotatory isomers of amino acids. In such solutions, all essential amino acids should be present with a broad spectrum of the nonessential amino acids. No single amino acid should predominate since, if its use is inefficient, this will interfere with the use of the others (Tweedle). In sepsis, renal failure and hepatic failure, the use of solutions containing only essential amino acids, isoleucine, leucine, valine, phenylalanine, lysine and tyrosine is under investigation.
Complications. The initial complications of parenteral feeding arise from malposition of the catheter tip and radiographic confirmation of the site of the catheter tip is mandatory before infusion. Infection, particularly septicaemia, arises from continuous direct vascular access and immune depression in malnourished patients, together with the solutions being ideal bacterial and fungal culture media. Catheter insertion with strict asepsis, daily care of the entry site cleaned with 1—2 per cent tincture of iodine and alcohol solutions, and the strict use of the line only for nutrient solutions all contribute to prevention. However, if a patient develops an unexplained fever, hypotension, vomiting, diarrhoea, confusion or seizures, a full clinical examination with appropriate radiology and bacteriological culture of blood, sputum, urine and swabs of the catheter site are indicated. If a source of infection is discovered it is treated, but if no source is found and the fever persists for 24 hours, remove the catheter and send the tip for bacteriological and fungal culture, Candida albicans, staphylococci or Klebsiella frequently being isolated. Recommence the parenteral regimen using a new catheter at a fresh site.
Prolonged use of amino acids and glucose alone will result in essential fatty acid deficiency, with dermatitis, anaemia and increased capillary permeability, a complication avoided by the use of intravenous fat solutions or essential fatty acids rubbed into the skin weekly. Similarly, hypophosphataemia is seen with such regimens and accentuated by the use of insulin, resulting in enzyme defects, adenosine-5’-triphosphate (ATP) deficiency and a shift to the left in the oxygen dissociation curve. This is prevented by a daily intake of 13 mmol of potassium dihydrogen phosphate. Table 5.6 lists some clinical syndromes and biochemical disorders resulting from drug—nutrient interactions and Table 5.7 lists other biochemical complications. Jaundiceoccurring during parenteral nutrition is cholestatic, perhaps the result of sepsis, malnutrition and hypoxia.
Severe hepatic steatosis is rare during total parenteral nutrition. However, transient hepatic abnormalities are so common that some authorities regard it as the most frequent metabolic complication. A cholestatic picture tends to predominate with increases in alkaline phosphatase and bilirubin. Elevations of serum transaminases may also be found. Hepatic biopsy performed in the jaundice phase shows histological evidence of fatty infiltration, periportal lymphocytic infiltration with bile duct proliferation and intrahepatic cholestasis or biliary sludging resulting in extrahepatic obstruction.
The syndrome differs somewhat between infants and adults. In the former, typical morphological changes and jaundice, fatty metamorphosis and even cirrhotic transformation are described, whereas older patients predominantly have enzyme derangements.
The patho physiology of hepatic dysfunction is not entirely understood.
Up to 40 per cent of surgical patients have an elevation of alkaline phosphatase, particularly if the feeding solution contains more than 214 kJ/kg daily, while it has been suggested that reduction in carbohydrate intake by increased use of a fat solution reduces liver dysfunction. In the vast majority of patients, hepatic function disturbance is both mild and self-limiting and spontaneous recovery is invariable after cessation of total parenteral nutrition.
In the patient with jaundice, it is proposed that cyclical nocturnal total parenteral nutrition reverses abnormalities when replacing continuous parenteral nutrition. Metabolic acidosis, much less common if fructose and alcohol are avoided, may arise from infusion of available hydrogen ions in amino acid solutions and is simply corrected with sodium bicarbonate solution.
Steroids. Anabolic steroids (e.g. Durabolin 25 mg i.m. weekly) may be used to improve nitrogen balance, but the effect may not be observed for some days.
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