6 Nutrition and metabolic therapy

Malnutrition leads to an increased risk of infection due to immune compromise (related to decreased intake of trace elements, amino acids and vitamins, plus decreased production of leptin), increased fatigability and inability to wean/mobilise due to loss of muscle bulk, and poor wound healing. Gut mucosal atrophy occurs within days of non‐feeding and may compromise the ability to feed enterally.

Adequate nutritional support should, in general, be provided early during critical illness. Improved outcomes from early nutritional support exist for patients with trauma and burns. Enteral feed is also a gastric protectant. However, the patient should be resuscitated and stabilised before enteral feeding is contemplated as gut hypoperfusion will compromise the ability to absorb, and feeding may render the gut more ischaemic. Increasing abdominal distension, pain/discomfort, large gastric aspirates, and diarrhoea suggest the need for a period of bowel rest rather than persisting with feeding and addition of prokinetics.

Enteral nutrition is indicated when swallowing is inadequate or impossible but GI function is otherwise intact. Parenteral nutrition is indicated when the GI tract cannot be used to provide adequate nutritional support, e.g. obstruction, ileus, high small bowel fistula, or malabsorption. Parenteral nutrition may be used to supplement enteral nutrition.

As with nitrogen requirements below, this is inexact and optimal day‐to‐day intake is not known for individual patients. Various formulae can calculate basal metabolic rate but are misleading in critical illness. Metabolic rate can be measured by indirect calorimetry, but most patients are assumed to require 2000–2700Cal/d or less if starved or underweight. Burn‐injured patients generally receive more feed.

Nitrogen excretion can be calculated in the absence of renal failure according to the 24h urea excretion.

However, as with most formulae, this method lacks accuracy. Most patients require 7 – 14g/d.

The normal requirements of substrates, vitamins, and trace elements are tabled opposite. Most long‐term, critically ill patients require folic acid and vitamin supplementation during nutritional support. Trace elements are usually supplemented in parenteral formulae but should not be required during enteral nutrition.

Enteral nutrition, p128; Parenteral nutrition, p130.

Routes include nasogastric, nasoduodenal/jejunal, gastrostomy, and jejunostomy. Nasal tube feeding should be via a soft, fine‐bore tube to aid patient comfort and avoid ulceration of the nose or oesophagus. Prolonged enteral feeding may be accomplished via a percutaneous/per‐operative gastrostomy or jejunostomy. Enteral feeding provides a more complete diet than parenteral nutrition, maintains structural integrity of the gut, improves bowel adaptation after resection, and reduces infection risk.

Most patients tolerate iso‐osmolar, non‐lactose feed. Carbohydrates are provided as sucrose or glucose polymers; protein as whole protein or oligopeptides (may be better absorbed than free amino acids in ‘elemental’ feeds); fats as medium chain or long chain triglycerides. Medium chain triglycerides are better absorbed. Standard feed is formulated at 1Cal/mL. Special feeds are available, e.g. high fibre, high protein‐calorie, restricted salt, high fat or concentrated (1.5 or 2Cal/mL) for fluid restriction. Immune‐enhanced feeds (e.g. glutamine‐enriched or Impact^®, a feed supplemented with nucleotides, arginine, and fish oil) may reduce nosocomial infections, but no evidence of outcome benefit has yet been shown from large prospective studies.

Once a decision is made to start enteral nutrition, 30mL/h full strength standard feed may be started immediately. Starter regimens incorporating dilute feed are not necessary. After 4h at 30mL/h, the feed should be stopped for 30min prior to aspiration of the stomach. Since gastric juice production is increased by the presence of a nasogastric tube, it is reasonable to accept an aspirate of <200mL as evidence of gastric emptying, and therefore, to increase the infusion rate to 60mL/h. This process is repeated until the target feed rate is achieved. Thereafter, aspiration of the stomach can be reduced to 8‐hourly. If gastric aspirate volume >200mL, the infusion rate is not increased though feed is continued. If aspirates remain at high volume, consider either prokinetics to promote gastric emptying (e.g. metoclopramide, erythromycin), bowel rest (especially if abdominal distension or discomfort increases), nasoduodenal/jejunal or parenteral feeding.

Nutrition—use and indications, p126; Gut motility agents, p294; Vomiting/gastric stasis, p406; Diarrhoea, p408.

Carbohydrate is normally provided as concentrated glucose. 30–40% of total calories are usually given as lipid (e.g. soya bean emulsion). The nitrogen source is synthetic, crystalline L‐amino acids which should contain appropriate quantities of all essential and most non‐essential amino acids. Carbohydrate, lipid, and nitrogen sources are usually mixed into a large bag in a sterile pharmacy unit. Vitamins, trace elements, and appropriate electrolyte concentrations can be achieved in a single infusion, thus avoiding multiple connections. Volume, protein and calorie content of the feed should be determined on a daily basis in conjunction with the dietician.

A dedicated catheter (or lumen of a multi‐lumen catheter) is placed under sterile conditions. For long‐term feeding, a subcutaneous tunnel is often used to separate skin and vein entry sites. This probably reduces the risk of infection and clearly identifies the special purpose of the catheter. Ideally, blood samples should not be taken nor other injections or infusions given via the feeding lumen. The central venous route allows infusion of hyperosmolar solutions, providing adequate energy intake in reduced volume.

Parenteral nutrition via the peripheral route requires a solution with osmolality <800mOsm/kg. Either the volume must be increased or the energy content (particularly from carbohydrate) reduced. Peripheral cannulae sites must be changed frequently.

Nutrition—use and indications, p126; Indirect calorimetry, p234; Electrolyte management, p482; Hypophosphataemia, p498; Metabolic acidosis, p502; Hyperglycaemia, p508.

Hyperglycaemia and insulin resistance occur commonly in critically ill patients and are associated with an increased risk of mortality. This may be related to immune compromise, an increased rate of bacterial growth, and the effects of glycation and free radical production on protein, lipid and mitochondrial function and integrity.

In two landmark papers by van den Berghe et al., a combination of tight glucose control (aiming for blood glucose levels of 4.5–6.1mmol/L) plus additional glucose and insulin administration reduced mortality and morbidity in both surgical and medical critical care patients. Benefit was only seen in those receiving >3–4 days’ therapy.

Controversy has since existed regarding how tight the glucose control should be, with some advocating a 5–8mmol/L target range to reduce the risk of potentially injurious hypoglycaemia, particularly as regular testing introduces a significant nurse workload. The introduction of (semi‐) continuous, (semi‐) automated blood glucose monitoring devices should facilitate closer maintenance of normoglycaemia.

Several protocols and algorithms have been devised by different groups. None are perfect, but suit the particular circumstances of their units in terms of staffing levels and expertise.

Hypoglycaemia, p506.