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Nutrition

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Refeeding syndrome

Nutrition

Assessment

Enteral nutrition

Parenteral nutrition

Controversies

Indications for nutritional support

Failure to achieve adequate oral intake or mechanical or physiological GI failure

- severe post-operative GI failure (eg fistulae, short bowel)
- borderline malnutrition, pre-op nutritional support

NB paucity of evidence supporting the value of nutritional support in critically ill

Nutritional assessment

The complexity and heterogeneity of diet and multiple effects that nutrients have on tissue and organ structure and function make it inevitable that there can be no definitive test of nutritional status. In particular there is no single test or technique that has been found to be both sensitive and specific test of protein energy malnutrition

Weight loss

Surprisingly this is a poor guide to dangerous malnutrition

Subjective global assessment

- incorporates information from patient’s history and from physical examination. Includes information on weight change, dietary intake compared to patient’s usual pattern, metabolic demands of patient’s underlying disease, extent of ascites or peripheral oedema, loss of subcutaneous fat and muscle bulk
- although this assessment has been validated in a general hospital population it has not be evaluated in the critically ill

Anthropometry

- easy to use but relatively inaccurate. Arm muscle circumference, arm circumference and triceps skinfold thickness can be measured. Skinfold thickness can indicate a loss of muscle bulk but is better as a trend measurement than as an isolated measurement
- limited value in the critically ill

Biochemistry

Plasma proteins

- acute disease increases transcapillary escape of these proteins and has a much more profound effect on plasma concentration than malnutrition

- also the synthesis of acute-phase proteins occurs preferentially over that of visceral proteins regardless of nutritional state. Concentration of acute phase proteins such as CRP and fibrinogen rise in association with a drop in serum albumin, pre-albumin and transferrin. Thus measurement of CRP may aid interpretation of albumin, pre-albumin and transferrin levels as markers of nutritional state
- a quantitative way of monitoring this relationship has been proposed: Prognostic inflammatory and nutritional index is calculated from:

CRP (mg/L) x a 1 acid glycoprotein (mg/L)/albumin (g/L) x prealbumin (mg/L)

- use of albumin as a nutritional marker is further handicapped by its long plasma half-life of 20 days. Of the plasma proteins used as nutritional markers albumin is the worst indicator of nitrogen balance

Functional

  • hand grip dynamometry probably the best indicator or malnutrition and of all the nutritional measurements is the best predictor of post-operative complications

Practical approach

  • based on history and examination
  • important elements of history:
  • diseases associated with increased risk of malnutrition
  • recent severe weight loss
  • history of chronic low food intake
  • examination:
  • signs of disease associated with catabolic state (eg multiple trauma, burns, sepsis)
  • signs of malnutrition (eg cachexia, oedema, muscle atrophy)
  • body mass index ((weight/height2) <20 kg/m2

Enteral nutrition

Requirments

- iso-osmolar (to prevent osmotic diarrhoea)
- lactose free (starvation and malnutrition results in a relative lactase deficiency)
- 2000 kCal daily in fat and carbohydrate (30-35 kcal/kg). Giving excess energy, particularly as CHO increases fat synthesis with fat deposition in the liver, and increases CO2 production. Approx 2/3 of daily energy provision should be in form of CHO, although ideal ratio not known.
- 75g protein daily (1.5-2 g/kg)
- use of oligosaccharides allows an increase in the carbohydrate content of the feed without an increase in osmolarity
- sodium adjustment to the patient's requirements often necessary

Constituents

Protein

  • principally milk derived
  • most commercial feeds contain 100-180 kcal/ g of protein
  • provided in 3 forms: intact native proteins (polymeric diets), small peptides (semi-elemental) or amino acids (elemental)
  • intact proteins doe not have a significant impact on osmolality but require normal levels of pancreatic enzymes for complete digestion
  • peptides are better absorbed than either intact protein or amino acids by both healthy and diseased gut. However no advantage over standard feed has been demonstrated in controlled trials in the severely ill in terms of tolerance or outcome.

Lipid

  • vegetable oil containing saturated and unsaturated fats, essential fatty acids (eg linoleic and arachadonic acid), predominantly long chain but also medium chain triglycerides.
  • deficiency of essential fatty acids results in rash and neuropathy
  • lipids allow a reduction in osmolality of the feed and provide a substantial amount of energy in a small volume

Carbohydrate

  • polysaccharides most common form. Well tolerated but require pancreatic enzymes for digestion
  • disaccharides require specific disaccharidases in small bowel mucosa for hydrolysis and digestion
  • monosaccharides do not require hydrolysis but tolerance may be limited by absorptive capacity of the small bowel
  • metabolism of carbohydrates associated with greater CO2 production than metabolism of lipids. The clinical significance of this is unclear

Other

  • electrolytes
  • trace elements
  • vitamins
  • insoluble fibre increases faecal mass through water absorption. This regulates intestinal transit which may decrease diarrhoea. Although efficacy is not clearly established
  • most mixtures contain 1 kCal/ml

Special nutrients

There is some experimental evidence that particular nutrients improve immunologic function, gut mucosal function or alter inflammatory response and some enteral preparations contain some of these substances (eg Impact). Supplements which have been studied include glutamine, arginine, nucleotides, medium chain triglycerides, W 3 fatty acids and fibre. There is some evidence that feeding with Immun-Aid (supplemented with glutamine, arginine and branched chain amino acids) is associated with a lower incidence of septic complications. Similar finding in trauma patients fed with enteral feed supplemented with glutamine only.

Glutamine

  • energy substrate in rapidly replicating cells (enterocytes and immune cells)
  • glucose pre-cursor in intestine and liver
  • counteracts acidosis in kidney
  • partly responsible for regulaton of intracellular water content in skeletal muscle
  • in animals:
    • maintains intestinal integrity, prevents deterioration of gut permeability, exerts trophic effects in ileum and in colon – prevents gut translocation of bacteria and endotoxin
  • some data to suggest that enteral and also intravenous glutamine supplementation reduces morbidity

Arginine

  • substrate for nitric oxide synthesis
  • anabolic effects

Nucleotides

  • immunostimulant properties in vitro on natural killer cells and T lymphocytes
  • associated with improved outcome in animal septic models

Omega-3- fatty acids

  • shift prostaglandin and leukotriene synthesis from PGE2 and LTB4 to the less active PGE3 and LTB5

Growth factor

  • recombinant GH consistently improves nitrogen balance, rate of protein synthesis in critically ill patients and enhances the healing of burns. An adequate source of glutamine appears to be important for it to be effective. Commonly used dose is 10 mg/day SC. Effects may be mediated by stimulation of insulin-like growth factor. Adverse effects include glucose intolerance and hypercalcaemia
  • insulin-like growth factor improves nitrogen balance in critically ill patients. Can cause hypoglycaemia
  • however recent data show that routine administration of growth hormone to critically ill patients results in an increase in mortality and morbidity

Routes

Gastric

  • nasal preferable to oral because of better patient tolerance. Contraindications include # of base of skull. Complications include trauma and bleeding on insertion, erosion of nares and sinusitis
  • in early stages large bore tubes preferable to fine bore as they allow aspiration of gastric contents and detection of gastric stasis
  • later fine bore are preferable because of increased comfort and decreased incidence of sinusitis. Complications of insertion include
    Pharyngeal
    - trauma and bleeding
    - perforation of retropharyngeal space
    - abscess
    Chest
    - oesophageal perforation
    - pneumomediastinum
    - pneumothorax
    - pulmonary haemorrhage
    - pneumonitis
    - pleural effusion
    - empyema
    Abdominal
    - gastric perforation
    - bowel perforation
  • gastrostomy (usually percutaneous endoscopic) usually reserved for patients needing long term enteral feeding (³ 4-6 weeks) when oral intake is impossible or insufficient but when gastric emptying is normal. Relative contraindications include ascites, gastric carcinoma or ulcer, previous laparotomy, coagulation disorders Complications occur in 1/4 of patients and are similar to those associated with jejunostomy

Enteric

  • nasoenteric tube: fine bore if aspiration not required. Spontaneous transpyloric passage of enteric tubes is uncommon even with the aid of prokinetics. Usually placed with fluoroscopic or endoscopic guidance
  • feeding jejunostomy usually created as an additional procedure during a laparotomy for other indications. Relatively high frequency of complications including leaks, wound infection and peritonitis. Percutaneous endoscopic jejunostomy is an alternative.

Complications of enteral feeding

Related to feeding tubes

  • complications of insertion
  • failed insertion
  • patient discomfort
  • erosion of nares
  • sinusitis
  • tube displacement (infusion to inappropriate site)
  • tube obstruction
  • surgical complications of gastrostomy and jejunostomy
  • aerophagy

Related to enteral feeding

  • nosocomial infection from bacterial contamination of feed
  • nausea, abdominal discomfort and distension
  • regurgitation or vomiting. If aspirated gastric residue is >200-300 ml decrease rate of administration by 50% for 4-6 h and then resume progressively over 24-48 h. Prokinetics may be helpful.
  • pulmonary aspiration of feed
  • diarrhoea. If this occurs check stool for Clostridia toxin and decrease rate of administration
  • intestinal pseudo-obstruction
  • interactions with enteral medication

Related to feed contents

  • hyperglycaemia
  • uraemia
  • hypercarbia
  • electrolyte abnormalities
  • specific deficiency disorders with long term use

Enteral feeding in patients with organ failure

Severe hepatic encephalopathy

  • transiently decrease protein intake to 0.5 g/kg/day

Renal failure

  • patients on renal replacement therapy: no restriction
  • those not on renal replacement therapy: protein 0.3 g/kg/day until renal function improves. However protein restriction should not be undertaken in order to prevent the need for renal replacement therapy.

Pancreatitis

  • enteral feed is traditionally witheld. However there is no evidence to support this practice. Patients may actually benefit from early enteral feeding. Jejunal feeding has been suggested but again there is no direct evidence to support this approach

Timing

  • start as early as possible
  • delay of 5-7 days is probably acceptable
  • if there is evidence of prior malnutrition or the patient is highly catabolic this interval should be reduced to 1-2 days

Parenteral nutrition

Indications

- patients who cannot be fed via GI tract for more than a few days
- no absolute contraindications but renal and hepatic failure both require careful attention to use of amino acids and lipid
- severe disturbances of lipid metabolism preclude use of IV lipid
- need for TPN should be reviewed daily

Requirements

Adult allowance/kg body wt/day

  • Water 30 ml
  • Energy 125 kJ (30 kcal)
  • Nitrogen 0.1-0.2 g
  • Glucose 3 g
  • Lipid 2 g
  • Sodium 1-2 mmol
  • Potassium 0.7-1 mmol
  • Calcium 0.1 mmol
  • Magnesium 0.1 mmol
  • Phosphorus 0.4 mmol

Water

- extra water required to replace losses from vomiting, diarrhoea, sweating and fever (approx 150 ml/day per 1ºC rise)

Protein and energy requirements

- protein requirements can be estimated by measuring nitrogen excretion:

Urinary urea (mmol/day) = Nitrogen (g)/day
            30

1 g of nitrogen = 6.25 g protein

Unfortunately there is often delay between collection of urine and obtaining results and then any change in the constitution of the bag cannot be made until the next bag made up. As a result some doubt the usefulness of measuring urinary urea or nitrogen excretion
- daily nitrogen requirements can be estimated more crudely according to the following criteria:

  • Major trauma or burns 20 g N/day*
  • Major sepsis 15 g N/day
  • Uncomplicated surgery 9 g N/day

- most effective mixture thought to be one that contains all the essential and most of the non-essential amino acids. A high content of a single non-essential amino acid, especially glycine, should be avoided. Cysteine and histidine are necessary in children. Formulas enriched with branched-chain amino acids (isoleucine, leucine and valine) slightly improve nitrogen balance in postoperative and trauma patients, but don't alter outcome
- glutamine has a peculiar role in nutrition in that the depletion of glutamine in muscle occurs relatively rapidly but replacement is slow. If glutamine is added to TPN appears to promote muscle anabolism and may be an important intestinal growth factor. Clinical value not established.
- there is no need to alter the amino acid composition for patients with liver failure
- energy requirements can be assessed using a metabolic cart but this is only really of value in research. In practice, give 125 kCal/g N.
- whole body protein balance not affected by energy source but metabolism of glucose results in a higher respiratory quotient than fat and therefore an increased need to excrete CO2. Also, use of glucose as the sole energy source is associated with the development of fatty change in the liver and Intralipid provides a useful vehicle for the administration of fat-soluble vitamins. Give 30-40% of non-protein energy as lipid whenever possible
- some evidence that GH results in increased protein anabolism. However not clear whether this is useful in clinical terms or simply reflects an increased synthesis of acute phase proteins

Carbohydrate

- glucose carbohydrate of choice. Physiological substrate required by brain and metabolized by all body tissues. Prerequisite of protein anabolism. When insulin production reduced, as in early post-traumatic and septic state, infusion of excessive glucose results in lipogenesis with a marked increase in CO2 production. If hyperglycaemia occurs consider reducing glucose infusion rate rather than adding insulin
- fructose. Supposed advantages:

  • insulin-independent
  • less irritant to veins
  • more rapidly metabolized by liver
  • better nitrogen sparing effect

But only first few steps of metabolism are insulin-independent and conversion of substrates to glucose requires insulin. In susceptible patients, especially children, and at high infusion rates can cause severe lactic acidosis
- sugar alcohols (eg sorbitol, xylitol) have no advantages over glucose and may cause lactic acidosis, hyperuricaemia, osmotic diuresis

Lipid

- provides more energy per ml than CHO
- avoids complications of excess glucose
- lipid necessary for cell wall integrity, PG synthesis, function of lipid-soluble vitamins
- essential FFA deficiency causes dermatitis, alopecia, fatty liver, defective immune response
- Intralipid particles are the same size as chylomicrons and are cleared by body as such
- infusion rate should not exceed 0.5 g/kg/h so as not to exceed maximum rate of lipid uptake
- emulsions are isotonic and can be given via a peripheral vein
- in patients likely to be lipid intolerant serum lipids should be monitored
- if lipid cannot be given daily it should be given twice weekly to avoid development of essential fatty acid deficiency
- may cause alterations of immune function but have not been established to have any clinically important deleterious effects in immune response. However the daily inclusion of lipid in TPN appears to be associated with a worse outcome.

Electrolytes

- potassium essential for protein synthesis with about 6 mmol/g nitrogen required for optimal amino acid utilization. Requirement for potassium usually greatest during first few days of TPN
- hypophosphataemia occurs early in phosphorus-free TPN. Principal dangers are decrease in 2,3-DPG with decreased oxygen delivery and muscle weakness
- chloride and acetate. Some of the amino acid solutions contain large amounts of acetate. If chloride:acetate ratio of salts not balanced acid:base problems may result.

Vitamins

- most common reported deficiencies are folate, thiamine and vitamin K
- recommended daily IV intake (IV requirements greater than oral) = 10 ml of MVI-12 (Rorer):

  • Vitamin A 1 mg
  • Vitamin D 5 mcg
  • Vitamin E 10 mcg
  • Vitamin C 100 mg
  • Folic acid 400 mcg
  • Nicotinamide 40 mg
  • Riboflavin 3.6 mg
  • Thiamine 3 mg
  • Pyridoxine 4 mg
  • Cyanocobalamin 5 mcg
  • Pantothenic acid 15 mg
  • Biotin 60 mcg

Trace elements

- zinc essential part of many enzymes (eg carbonic anhydrase). Deficiency leads to poor healing and dermatitis and can develop within a few weeks
- copper important for RBC maturation and lipid metabolism
- manganese important in calcium/phosphorus metabolism, reproduction and growth
- cobalt essential constituent of B12
- chromium necessary for normal glucose utilization
- molybdenum component of oxidases
- selenium component of glutathione peroxidase
- exact requirements of trace elements in TPN not clear. Following have been recommended:

  mcg/day
Chromium 10-15
Copper 500-1500
Fluoride 950
Iodine 130-910
Iron 1100
Manganese 150-800
Molybdenum 20
Selenium 200
Zinc 2500-6400

Composite bags

- TPN now usually given in this form, in which all the necessary constituents mixed together in one bag under sterile conditions
- advantages are reduced risk of infection, decreased variability in blood glucose (reaches equilibrium 30 mins after starting infusion), less risk of missing out trace elements (eg Zn, Fe, Cu, manganese, Co, I, chromium, molybdenum) and vitamins (thiamine and folate especially important)
- lipid emulsion stable provided divalent ion concentration not excessive
- infuse at a constant rate by infusion pump over 24 hrs. Claimed that there may be advantages in infusing over 18 hrs but there is little objective evidence to support this contention
- contains fat in the form of Intralipid, protein as amino acids and carbohydrate as glucose

Monitoring

- daily electrolytes and glucose
- urinary urea
- Mg and trace elements weekly

Complications

Re-feeding syndrome

- acute cardiopulmonary and neurological dysfunction manifested as cerebral and pulmonary oedema
- thought to be due to severe hypophosphataemia (£ 0.32 mmol/l)
- when severely malnourished patient is fed, the incorporation of glucose into the Kreb's cycle requires large amounts of phosphate. However this cannot be mobilised sufficiently quickly from bone with a resulting exacerbation of hypophosphataemia, leading to increased membrane leakiness
- metabolic monitoring is crucial at commencement of TPN in severe malnutrition
- introduction of feeding should be gradual, building up to total requirement over 3-5 days

Selenium deficiency

- may develop after prolonged home TPN
- results in a syndrome similar to osteomalacia

Infection

- no evidence that tunnelling feeding lines results in a reduction in infection rate

Hyperglycaemia

- may accentuate hyperglycaemic response of stressed patient
- insulin infusion may be required. However if excessive glucose is infused insulin may result in lipogenesis
- renal threshold for glucose often exists in ITU patients and as a result there may be an osmotic diuresis and the development of hypernatraemia
- may result in hyperosmolar dehydration

Others

- complications of CVP lines
- electrolyte imbalance, especially hypokalaemia in first 24-48 h, hypomagnesaemia in patient with GI fluid loss and hypophosphataemia in first 24-48 h
- hyperammonaemia has been described, particularly in infants and patients with liver failure and in association with solutions containing excessive glycine or inadequate arginine
- rebound hypoglycaemia if TPN stopped abruptly

Controversies

Does provision of short-term TPN improve outcome?

There is no evidence that provision of TPN is superior to no nutritional support (in patients unable to eat for < 14 days). While there are some data to suggest that TPN is positively detrimental in ICU patients, the patients studied were not very ill by ICU standards.

Does provision of short term enteral nutrition improve outcome?

Early enteral nutrition probably leads to improved wound healing, better nutritional outcome and improved gastrointestinal permeability. In adult surgical patients early introduction of enteral feeds was associated with a reduction in complications and possibly shorter hospital stay. Early enteral nutrition is recommended.

Is the very early introduction of enteral feed associated with improved outcome?

Apart from a single unblinded study in trauma patients there is no evidence that starting enteral nutrition as soon as possible improves outcome.

Is feeding into the small bowel preferable to gastric feeding?

Feeding into small bowel increases tolerance of feeds but does not effectively reduce the risk of aspiration and pneumonia.

References

Heyland DK. Nutritional support in the critically ill patient. A critical review of the evidence. Crit Care Clinics 14(3): 423-40; 1999.

Heyland DK, MacDonald S, Keefe L, Drover JW. Total parenteral nutrition in the critcally ill patient: a meta-analysis. JAMA 280:2013-9, 1998

Jolliet, P., Pichard, C., Biolo, G., et al. Enteral nutrition in intensive care patients: a practical approach. Intens.Care Med. 24:848-859, 1998.

Koretz R.L. Nutritional supplementation in the ICU. How critical is nutrition for the critically ill? AJRCCM, 1995; 151:570-3

Takala J, Ruokonen E, Webster NR, Nielsen MS, Zandstra DF, Vundelinckx G et al. Increased mortality associated with growth hormone treatment in critically ill adults. N Engl J Med 1999;341:785-792

Last updated March 2000

 


© Charles Gomersall December 1999, March 2000

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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