Feeding in ICU

Feeding in intensive care: Alice Springs 2009

Minimize wasting of lean body mass
Treat any existing malnutrition
Maintain correct water and electrolyte balance
Provide essential elements such as protein and vitamins

Timing of feeds:
• Early feeding (within 72 hours at latest) can reduce morbidity and mortality. Enteral feeding should be considered within 24 hours of admission to ICU if there are no complicating factors (such as abdominal surgery).
• Bowel sounds provide some indication of stomach and colon function only. It is common for bowel sounds to be reduced in intubated patients, due to decrease in swallowed air. Bowel sounds do not need to be present to commence feeding, as the small bowel may still have normal motility and absorptive function.
Estimate feeding requirements:
The dietician will calculate the feeding requirements of the patients.
This is based on the likely basal metabolic rate (BMR), adjusted for stress, activity and diet induced thermogenesis.
A rough guide to BMR:
Age (years)            Female                              Male
15-18                    13.3W+690                       17.6W+656
18-30                    14.8W+485                       15W+690
30-60                     8.1W+842                        11.4W+870
>60                        9W+656                           11.7W+585
Severe sepsis you will need to add 25-50%.

Route of feeding:
Enteral: Preferred as less complications, helps GIT protection, is cheaper and easier.
Type of feed depends on renal function, diabetes, liver disease and feed intolerance.

 Appropriate choice of feeding product and route
Standard feed in ICU. 1 Cal/mL. High protein and micronutrient content.
Nutrisen Multifibre
fibre added try when diarrhoea a problem
For strict fluid restriction with reduced electrolytes (eg renal). 2 Cal/mL. Moderate protein content, very low electrolyte content, small amount of fibre.
Elemental formula (no digestion required) Use when absorption difficult e.g pancreatic insufficiency prolonged starvation.
Carbohydrate is monosaccharides, protein is amino acids, fat is mostly medium-chain triglyceride. Made up from powder, usually to 1 Cal/mL. Normal protein content, low electrolyte content, low fat, minimal residue.
Hepatamine+Vivonex mix
Branched-chain amino acid formula, for encephalopathy. Branched-chain amino acid supplement mixed with Vivonex (see above for Vivonex details)

Appropriate management
• See nursing flow chart for feed advancement
• Large gastric aspirates should be assessed in the light of other tolerance indicators (abdominal distension or pain, bowel activity, previous tolerance, abdo xray).
• If NG feeding is likely to be required for more than two weeks, a fine-bore tube is recommended once feeding tolerance has been established. Salem sump tubes are associated with mucosal irritation and ulceration, swallowing difficulties and discomfort.
Interruption of feeding should be minimised.
• Radiology: unless fasting is required, feeds should be continued until patient is ready for transport.
• Extubation: feeding should be continued until MO makes decision regarding extubation. MO will request that the feed stops, and will plan extubation time accordingly.
• Surgical procedures: MOs to document the time that feeds should stop before theatre. In general, six hours should be adequate for surgery, and can often be less.
• Take care with insulin infusions when feeds stop. Perform hourly blood sugar levels initially after stopping feeds. Insulin sliding scale may need to be reviewed.
• If feeds have been stopped for less than 6 hours, they can be recommenced at the previously tolerated rate.
• If feeds have been stopped for more than 6 hours, use Enteral Feeding Protocol to start feeding again.
• In particular cases (eg respiratory patients with frequently-interrupted feeds) the goal feed rate may be increased to compensate for the missed feed. Dietitian or MO will indicate the new goal rate and the duration of “catch-up” feeding. Overfeeding should be avoided.
• Vomiting: should be treated as a large gastric aspirate, i.e prokinetic agent added metoclopromide 10mg qid ivi or erythromycin 250mg bd ivi. If the patient is distressed, or if vomiting is continuous, feeds can be stopped but should be restarted after two hours or as soon as possible.
If high aspirates or vomitting consider placement of a traspyloric tube. Need to still have a NG tube in place for 24 hours to monitor aspirates.
Hints in placing transpyloric tubes: Use of the tiger tubes is discouraged as often nasal bleeding occurs with insertion and removal
100 cm feeding tube with a soft tip.
Insert into stomach
Turn patient to their right side
Fill the stomach with 500mls of air via a 3 way tap close off
Give 250mg of erythromycin iv.
Advance the feeding tube slowly at least 10cm.
If wish to check more accurately give 10mls of gastrograffin via feeding tube and do a lower chest/ upper abdominal Xray.

• Diarrhoea: is not an indication for stopping enteral feeds. This is common in ICU and is often multifactorial, need to:
Change to nutisen multifibre
Ensure no contamination of feeds
If patient has been on broad spectrum antibiotics it is not C difficle
Ensure no feacl impaction- causes overflow diarrhoea
Malabsorption- consider pancreatic insufficieny, consider changing to elemental feed
Stop prokinetics
Stop oral magnesium if possible
Review all drugs as some have large amounts of sorbitol

• Refeeding Syndrome: see Policy & Procedure for Refeeding Syndrome.
• Abdominal distension: This must be taken seriously. Need to:
Check stool chart for last bowel action
Check an abdominal X ray
Consider C difficile infection
Cease lactulose unless good indication e.g hepatic encephalopathy
Consider SBP in patients with cirhosis
Abdominal girth measurement should be taken if increasing distension is suspected. Record the girth at umbilicus, in the patient’s medical record. Increasing distension should be viewed very seriously.
If bowel very distended i.e >8 cm large bowel diameter needs surgical review, consider NG on suction, bowel rest and starting TPN.

• Suspected aspiration of the feed: Prevention of aspiration, by monitoring patient position and ensuring that the head of the bed is adequately raised, may be more important than detecting aspiration once it has already occurred. If aspiration of the feed is suspected, stop the feed. Blue food colouring has been used in the past, for assessment of aspiration, however it may be ineffective in detecting aspiration, and fatal complications from its use have been reported. Blue food colouring may still be used at MO’s risk (eg for detection of GIT leak/fistula)
• Blocked feeding tube: prevent blockages by flushing well before and after giving medications through tube. This prevents medications reacting with the feed and with one another, causing clots. Ensure that medications are well crushed. If the tube can be flushed slowly, and flushing does not seem to improve the flow, then the tube may be kinked rather than blocked. (Replace or Xray tube.) If tube appears to be blocked:
o Use the smallest syringe available that fits onto tube.
o Suck out as much of tube content as possible.
o Fill the syringe with warm water and flush into tube using moderate pressure.
o Clamp tube, wait 10 minutes, and then suck out as much of tube content as possible.
o Repeat.
§ Soft drinks should not be used for unblocking tubes, as they can make the tube prone to block again, and their acid content can worsen the blockage.
§ If this does not work, pancreatic enzyme can be used, but this is expensive – check with MO whether it would be more appropriate just to replace the tube. Pancrelipase+sodium bicarbonate is available from pharmacy in ready-to-use form: just add 20mL water for injection, shake well and flush into tube using the warm-water procedure described above. The bottle should be labelled with the date and time of use.
• Additional water or salt may be required, eg for neurosurgical patients. These should not be mixed with feeds but instead prescribed as tube-flushes on the med chart. Extra salt can be given as salt tablets (10mmol Na+ each) or as ordinary food service salt sachets (17mmol Na+ each) which are cheaper and less bulky.
Proceedings of the North American Summit on Aspiration in the Critically Ill Patient, 2002 JPEN 26(6):S1-S85
McClave et al (1992). Use of residual volume as a marker for enteral feeding intolerance: prospective blinded comparison with physical examination and radiographic findings. JPEN 16(2):99-105.
Lin H & Citters G (1997). Stopping enteral feeding for arbitrary gastric residual volume may not be physiologically sound: results of a computer simulation model. JPEN 21(5):286-289.
Pinilla et al (2001). Comparison of gastrointestinal tolerance to two enteral feeding protocols in critically ill patients: a prospective, randomised controlled trial. JPEN 25(2):81-86
Burd R & Lentz C (2001). The limitations of using gastric residual volumes to monitor enteral feedings: a mathematical model. NCP 16:349-354.
Freedland et al (1989). Microbial contamination of continuous drip feedings. JPEN 13(1):18-22
Kohn C (1991). The relationship between enteral formula contamination and length of enteral delivery set usage. JPEN 15(5): 567-571
Guenter et al (1991). Tube feeding-related diarrhea in acutely ill patients. JPEN 15(3):277-280.
Homann et al (1994). Reduction in diarrhea incidence by soluble fibre in patients receiving total or supplemental enteral nutrition. JPEN 18(6):486-490.
Belknap et al (1990). Microorganisms and diarrhea in enterally fed intensive care unit patients. JPEN 14(6):622-628.
Krupp K & Heximer B (1998). Going with the flow: how to prevent feeding tubes from clogging. Nursing98 (April):54-55.
Frankel et al (1998). Methods of restoring patency to occluded feeding tubes. NCP 13:129-131.
Maloney J et al (2002). Food dye use in enteral feedings: a review and a call for a moratorium. NCP 17:169-181.
Meissner W, Dohrn B, Reinhart K. Enteral naloxone reduces gastric tube reflux and frequency of pneumonia in critical care patients during opioid analgesia. Crit Care Med 2002;31:776-779
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Refeeding syndrome is the term used to describe the adverse metabolic effects and clinical complications when a starved or seriously malnourished individual commences refeeding.
The following patients can be classified at extreme risk:
• Patients with anorexia nervosa
• Patients with chronic alcoholism
• Patients who are extremely emaciated or have chronic malnutrition
eg energy intake <500Cal/day for more than a week (eg fluids only, or modified texture)
or who meet the definitions of kwashiorkor (adequate energy but deficient in protein), or
marasmus (deficient energy and protein)
• Patients with with BMI<14
• Patients who have lost >1kg weight per week for last 3 months
• Patients presenting with low levels of K+, PO42-, Mg2+
(check for signs of dehydration, eg raised urea, which might mask low levels)
The following patients can be classified at high risk:
• Frail elderly patients assessed by dietitian as being at nutritional risk
• Patients not coping with difficult economic circumstances, eg homeless
• Morbidly obese patients with rapid weight loss (eg after gastric ballooning or banding)
• Patients who have not been fed for 7 – 10days with evidence of stress and depletion
• Patients who have been fasted and/or given only IV fluids for a prolonged period
Risk is increased in patients who are given TPN or IV dextrose, as these are forms of carbohydrate that are rapidly administered parenterally - this speeds the metabolic effects. However, patients receiving enteral feeding or oral diet can also be at risk.
Refeeding syndrome may show up as late as 3-5 days after feeding starts.
How refeeding syndrome occurs:
During starvation the following changes occur:
• Decrease in BMR (mediated by hormonal changes)
• Decrease in heart rate
• Breakdown of lean body tissue, producing K+, PO42-, Mg2+, Zn2+ which are cleared by increased urinary excretion
• Decrease in serum proteins as production decreases
• Decreased gut enzyme activity
• Decreased gut motility
Rapid refeeding causes the following changes:
• Increase in BMR
• Increase in heart rate
• Rapid change in hormone levels (eg increase in insulin, thyroid hormones)
• Glucose becomes the dominant fuel
• Anabolic protein synthesis is stimulated
• Replenishment of body energy stores (ATP, glycogen)
• Rapidly increased cellular uptake of glucose and minerals, reducing the available serum levels of K+, PO42-, Mg2+, Zn2+
• Retention of Na+ and fluid
Effects of these changes:
Total body stores are depleted during starvation, and cells take up circulating PO42-, resulting in hypophosphataemia.
↓ PO42- → ↓ATP
→ less ATP available for muscle contraction (including heart and respiratory muscles)
→ reduced oxygenation of tissues, ventilation difficulties
cardiac arrhythmias
sensory disturbances, confusion
Refeeding causes a shift of K+ into the cell → ↓ K+ → cardiac arrhythmias
cardiac arrest
GI changes (constipation, ileus)
glucose intolerance, polyuria
neuromuscular weakness
respiratory depression
Refeeding causes a shift of Mg2+ into the cell → ↓ Mg2+ →cardiac arrhythmias
GI changes (constipation, ileus)
neuromuscular weakness
depression, irritability, confusion
Thiamine is an essential coenzyme in carbohydrate metabolism. Carbohydrate loading in a patient whose thiamine stores are depleted will cause thiamine deficiency, eg Wernicke’s encephalopathy
Insulin levels are depressed during starvation. Sudden refeeding with carbohydrate can cause hyperglycaemia.
Procedure for management of refeeding patients
1. Assessment – assign patient to risk category
Anthropometry – weight and weight history
Biochemistry – nutritional indicators (albumin, prealbumin, haemoglobin, lymphocytes, urea)
refeeding syndrome indicators (K+, PO42-, Mg2+, Zn2+, Na+)
request the above indicators if not yet done
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Clinical signs associated with starvation (↑risk): shortness of breath/ poor exercise tolerance
2. Prophylactic supplementation for extreme-risk patients
  IV (preferable)oralthiaminethiamine 100mgthiamine 100mgmultivitaminIntravite 1x2mL vialVitaminorum 2 tabletszinczinc chloride
2mL ampoule, given over 1h in 100mL normal saline or 5% dextrose
(= 5mg Zn2+ = 76.5μmol Zn2+)zinc sulphate 1 capsule
(zinc sulphate 50mg = 20mg Zn2+= 306μmol Zn2+)phosphatepotassium dihydrogen phosphate
1x10mL ampoule, given over 1h in 100mL normal saline or 5%dextrose
(= 14.5mmol PO42- + 25mmol K+)Phosphate-Sandoz 1 tablet
(elemental PO42- 500mg
= 16.1mmol PO42- + 20.4mmol Na+ + 3.1mmol K+)3. Monitoring
Check serum levels of K+, PO42-, Mg2+, 2-4 hours after commencing feed and then several times daily for first week, and then at least second-daily until stabilised.
NOTE: Feed will need to be stopped if PO42- levels fall to critically low range, until replacement has occurred and levels are approaching normal.
Once patient has stable biochemistry and is tolerating feeding at the goal rate, risk of refeeding syndrome no longer exists and close monitoring can be ceased. Serum levels should be checked three days after supplementation is discontinued.
4. Feed and supplementation
If patient is on an oral diet, small meals should be ordered and patient should be monitored closely.
Parenteral feeding should be initiated very slowly, with constant monitoring. See TPN Protocol for advice on appropriate infusion rates for the different TPN products, as these vary.
For enteral feeding, use a standard feed as follows:
Extreme risk patientsHigh risk patientsStart with 0.5 x estimated BEE
ie start as low as 20mL/hStart with 0.8 – 1.0 x estimated BEE
ie start with about 1000Cal/day = 40mL/hIncrease by 200-300Cal every two to three days only if tolerated and biochem is stabilisedIncrease rate daily or second-daily, 20 – 40mL/h at a time, only if tolerated and biochem is stabilisedMay take two weeks to reach goal rateMay reach goal rate in a weekFluid requirements will need to be met via IV or extra water flushes while patient on low feed rate. Continue monitoring and supplementing as needed.
• Use IV supplementation, or the higher dose in the oral dose range, for extreme risk patients, changing to oral form/moving to lower dose when biochem reaches top end of normal range
Continue supplementation until patient is receiving feed at the goal rate, AND biochemical indicators are stable and in normal range

100mg/day for first five days
IVoralthiamine 100mgthiamine 100mgMULTIVITAMIN
Daily for first three weeks or until stable
IVoralIntravite 1x2mL vialVitaminorum 2 tablets dailyPHOSPHATE
Normal range 0.6 – 1.3mmol/L RDI 32mmol
IVoralpotassium dihydrogen phosphate
1x10mL ampoule, given over 1h in 100mL normal saline or 5%dextrose
(= 14.5mmol PO42- + 25mmol K+)
Repeat over next 12h if serum level not sufficiently changed.Phosphate-Sandoz 1-6 tablets daily
(elemental PO42- 500mg
= 16.1mmol PO42- + 20.4mmol Na+ + 3.1mmol K+)
Start with 1 tablet and increase if needed.
Wait 2h before giving any calcium supplements.MAGNESIUM
Normal range: 0.72 – 0.92mmol/L RDI 11mmol
IV supplementation recommended if pt presents with low Mg2+ levels, as this indicates total body depletion. Serum levels should be monitored for 2 weeks even if normal, as blood levels do not necessarily reflect total body store, and fluctuations can occur.
IVoralmagnesium sulphate
1x5mL ampoule, given over 1h in 100mL normal saline or 5% dextrose
(= 10mmol Mg2+)
Repeat over next 12h if serum level not sufficiently changed.Magmin 1-6 tablets daily
(magnesium aspartate 500mg = 1.7mmol Mg2+
Start with 1 tablet and increase if needed.
Wait 2h before giving any calcium supplements.ZINC
Normal range: 10 - 18μmol/L RDI 12mg, ie 183μmol
IVoralzinc chloride
2mL ampoule, given over 1h in 100mL normal saline or 5% dextrose
(= 5mg Zn2+ = 76.5μmol Zn2+)
Usually given 3 times per week (M,W,F)zinc sulphate 1 capsule daily
(zinc sulphate 50mg = 20mg Zn2+= 306μmol Zn2+)POTASSIUM
Normal range: 3.5 – 5.0mmol/L Normal diet intake: 50 – 140mmol
IVoraluse the existing ward protocol for K+ replacement.
10mL vial contains 10mmol K+* SlowK 1-6 tablets (600mg tab = 8mmol K+)
* Chlorvescent 1-6 tablets (14mmol K+)
* KCl elixir 1-6 doses (15mL dose = 20mmol K+)
Start with one tablet/dose and increase if needed.REFERENCES
Crook et al (2001). The importance of the refeeding syndrome. Nutrition 17:632-637.
Solomon S & Kirby D (1990). The refeeding syndrome: a review. JPEN 14(1):90-97.
Brooks M & Melnik G (1995). The refeeding syndrome: an approach to understanding its complications and preventing its occurrence. Pharmacotherapy 15(6):713-726.
Bowling T & Silk D (1995). Refeeding remembered. Nutrition 11(1):32-34.
Birmingham et al (1996). Anorexia nervosa: refeeding and hypophosphatemia. International Journal of Eating Disorders 20(2):211-213
Vaszar et al (1998). Refeeding syndrome induced by cautious enteral alimentation. The Gastroenterologist 6(1):79-81.
Havala T & Shronts E (1990). Managing the complications associated with refeeding. Nutrition in Clinical Practice 5:23-29.
Fisher et al (2000). Hypophosphatemia secondary to oral refeeding in anorexia
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