Category Archives: Nutrition

Appropriate nutrition is integral to patient care (Nestle Health Science sponsored session)

Smart nutrition not more nutrition

(Zudin A. Puthucheary)

Muscle wasting is common in critical illness, significantly greater in the sickest pts 

Intramuscular hypoxia in critical illness

  • unlikely to use glucose as fuel
  • fat can be used but decreased mitochondrial beta-oxidation leads to build up of fat within muscle
  • Increasing CHO / lipid delivery unlikely to be useful in acute critical illness

In ALL pts, ATP levels decreased in 1st week of critical illness, but chronic illness depletes ATP more quickly than in previously well individuals

ASICS trial: considers if ketogenesis can provide alternative substrate for energy

 

Altered protein homeostasis in critical illness: body attempts to increase anabolism but fails.  Can pts exercise to stimulate protein homeostasis? –> low tolerance for exercise during critical illness

 

Smarter use of protein is required

  • with continuous amino acid provision, protein synthesis drops off after 2 hours
  • not all proteins created equally – 10g leucine per 100g whey protein
  • no other amino acid stimulates muscle protein synthesis like leucine, but despite muscle growth, strength is not improved without exercise

 

In practice, cannot separate energy requirement from protein requirement

  • both are necessary
  • the ability of nutritional protein or calories to modulate muscle metabolism is likely to depend on quality and type of nutrition rather than quantity

 

Relevance of outcome measures: only 1% of trials since 2000 measure muscle function as a primary outcome – more trials needed which focus on functional outcome

 

Can nutrition be used to target mitochondrial dysfunction?

(Mervyn Singer)

Mitochondria are important

 

Lactate becomes important fuel source in critical illness – autocannibalism to feed other organs: is muscle wasting adaptive?

Long term Rodent model of critical illness (faecal peritonitis) – rats do not restore diurnal rhythm of metabolism by day 7

 

Strict blood glucose control using insulin- protects hepatocyte mitochondrial structure and function in critically ill pts

 

Fatty acids stimulate production of uncoupling protein –> more heat generated, but mitochondrial membrane potential decreases –> decreased ATP, decreased ROS generation

Oleic acid induces fatty acid oxidation and decreases organ dysfunction and mortality in experimental sepsis (raised IL-6 production in septic mice, but decreased upon addition of oleic acid)

Coenzyme Q10: No difference in clinical outcomes between ubiquinol (reduced Coenzyme Q10) and placebo in pts with severe sepsis / septic shock. No difference in vascular endothelial biomarkers, inflammatory biomarkers, or biomarkers related to mitochondrial injury.

Succinate: in septic rats, succinate increases mitochondrial oxygen consumption –> buildup of succinate during ischaemia causes reperfusion injury through mitochondrial ROS

Supplementing with antioxidants: if the pt is in MOF and damage has already been done, have we missed the boat?

  • Multiple means of modulating mitochondrial function via nutrition with no clear guide on what to do, but one-size-fits-all approach unlikely to benefit anyone

 

Update 2018 ESPEN guidelines

(Mette Berger)

Nutritional Risk Screening tool – quick scoring, screen within first 48 hours of admission

Exact timing of phases of critical illness is less important than the concept of Varying nutritional needs with each phase

  • If oral intake is not possible, early enteral nutrition (EN) is better than delayed EN
  • If EN / oral intake both not possible, implement PN within 3-7 days
  • If pt is very sick, the gut will be affected – don’t give full dose EN in septic shock pts –> risk of severe complications including vomiting, diarrhoea, bowel ischaemia, acute colonic pseudo-obstruction
  • Hypocaloric nutrition (not exceeding 70% energy expenditure) should be administered in early phase of acute illness

 

No strong evidence for high protein delivery – 1.3g protein / kg / day should be given progressively + physical activity may improve the beneficial effects

 

In healthy individuals, consuming breakfast will stop endogenous glucose production

  • this process carries on in sick pts, resulting in a protein loss of ~ 120g / day to generate 1200kcal /day

 

Slow progression in feeding may allow early detection of refeeding syndrome which can be treated

 

Increased protein delivery while decreasing carbohydrate loads

(Juan B. Ochoa)

 

Paradigm: Substitute for what the patient is unable to eat

  • but even 10% hyper caloric overfeeding will worsen outcomes in sick pt

 

No benefit to meeting caloric goals in the first 7 days, and in fact this will have undesirable consequences

 

Belief that 50% of caloric intake should be from carbohydrates is an outdated concept – it is a method of cheap food provision in 19th century prisons

  • regrettably most commercial formulae consist of mostly simple sugar, without complex CHO

 

Ideally use indirect calorimetry to estimate requirements; predictive equations tend to result in overfeeding

 

Protein delivery is affected by choice of feeding formula; hypocaloric high-protein nutrition is safe metabolically and clinically

 

Nutrition in Challenging Conditions

Continuing Professional Education Session

 

Nutrition in patients with CRRT

(Pierre Singer)

 

AKI – metabolic modifications, hypercatabolism, hyperglycaemia

Nutrients and solutes levels affected by haemodialysis/haemofiltration

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Equations to calculate energy expenditure (EE) can be misleading in CRRT, likely to result in overfeeding – measure EE by indirect calorimetry after 6 hours stabilisation

 

Pts use more fat than carbohydrates, therefore give 50% fat + 50% carbs

 

Amino acids lost through convection and ultrafiltration: 8g/day, total loss including catabolism: 10-15g/day, therefore give at least 1.3g/kg/day protein and more to compensate for losses

 

Loss of micronutrients in effluent: Selenium, Copper, Zinc –replace with trace element solutions

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Hypophosphataemia in AKI treated with haemodialysis is associated with adverse events

 

Nutrition of obese patients

(Mette Berger)

 

BMI poor indicator of body composition / obesity, doesn’t account for muscle loss in ageing and disease, and does not detect sarcopenia (measured on cross sectional CT imaging at Lumbar L3 level)

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Obesity associated with increased all-cause mortality in hospitalised pts (increased prevalence of hypertension, Type 2 DM, hypercholesterolaemia)

 

High rates of central obesity and sarcopenia in CKD irrespective of RRT

 

Obesity and trauma:

  • Relative block on lipolysis and fat oxidation
  • Shift to preferential use of proteins and carbohydrates
  • Resultant catabolism

 

Glucose handling in obesity:

  • Relative insulin resistance and risk of Type 2 DM
  • Sepsis/trauma induces post-receptor insulin resistance
  • Significant risk of hyperglycaemia (conventional feeds use carbohydrates as predominant energy source)

 

Obesity can co-occur with malnutrition – MDT approach to handle various aspects of obesity

 

How much to feed obese pts?

  • Penn State Equations: 80% validity in predicting resting metabolic rate in critically ill pts at extremes of BMI

(Prediction of resting metabolic rate in critically ill patients at the extremes of body mass index.)

 

Simple guide:

  • Assess nutritional need and develop plan within 48hrs of ICU admission (pt usually has little reserves)
  • Will need Indirect Calorimetry or Penn State Equations for more accurate calculation of energy expenditure
  • Feeding should not be hypocaloric, but rather Aim for Iso-caloric for lean mass
  • Ideal body weight used to calculate protein needs (2-2.5 g/kg)
  • Careful attention to micronutrients, B12, Cu, Fe to avoid anaemia / neurological problems
  • Convert to Enteral feeding as soon as pt is stabilised

 

 

Nutrition during non-invasive ventilation

(Steffen Weber-Carstens)

 

Reasons NOT to feed enterally during NIV:

  • Potential need for intubation
  • NGT presence may cause air leakage, compromising effectiveness of NIV
  • Gastric distension associated diaphragmatic splinting
  • Removal of mask to consume oral diet may cause deterioration

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In this group of pts, TPN is in fact preferred to EN – no increase in mortality / gastrointestinal infection rate with TPN compared to EN; EN associated with significantly more GI infections

Enteral versus parenteral early nutrition in ventilated adults with shock: a randomised, controlled, multicentre, open-label, parallel-group study (NUTRIREA-2).

 

Nutrition in necrotising pancreatitis

(Valentin Fuhrmann)

 

Severe acute pancreatitis

  • shock, respiratory failure, AKI, delirium, abdominal compartment syndrome
  • mortality 20%
  • Early enteral nutrition (EN) important in the multimodal therapy

 

Recommendations:

Mild- oral feed once pain / vomiting resolved

Severe- Early EN – ESPEN 2018; Parenteral nutrition only when EN route not available / not tolerated / not meeting energy requirements (ACG 2013)

 

NG tube feeding safe and well-tolerated compared to NJ feeding

Nasogastric or nasojejunal feeding in predicted severe acute pancreatitis: a meta-analysis

 

Feeding intolerance is common in acute pancreatitis (nausea, vomiting, ileus, diarrhoea)

Early versus on-demand nasoenteric tube feeding in acute pancreatitis.

 

Managing feeding intolerance:

  • Start EN early to avoid extended ileus
  • Re-assess GI function early
  • Slow start, do not aim for full energy needs
  • Prokinetics
  • Post-pyloric feeding is an option if prokinetics not helping
  • Diagnose and manage of intraabdominal hypertension
  • Consider parenteral route

 

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ESICM guidelines:  DELAY enteral feeding in cases of

  • Uncontrolled shock
  • Uncontrolled hypoxia / hypercapnoea / acidosis
  • Abdominal compartment syndrome
  • Gastric aspirates > 500mls / 6hrs

 

 

 

Nutrition in elderly frail patients

(Jean-Charles Preiser)

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Nutritional management in frailty:

  • Acute phase: refeeding risk
  • Recovery phase: Need adequate calories, high protein intake, exercise, selected pharmaconutrients

 

ESPEN Recommendations for refeeding hypophosphataemia

  • Measure electrolytes 2-3x/day, supplement if needed
  • Restrict energy supply for 48hrs then gradually increase

 

Positive energy balance is associated with accelerated muscle atrophy (Positive energy balance is associated with accelerated muscle atrophy and increased erythrocyte glutathione turnover during 5 wk of bed rest)

 

Burden of critical illness in frail pts lasts for long period after d/c from ICU and hospital

  • huge task of rebuilding
  • Vit D deficiency associated with muscle loss (type 2 myocytes), supplementation increases muscle protein synthesis in non-critically ill
  • Selected amino acids, in particular leucine, can stimulate muscle protein synthesis
  • Combination of increased protein intake, amino acid supplementation and exercise

 

 

Nutrition in malnourished patients

(Michael Hiesmayr)

 

Risk factors for malnutrition include:

  • Unintentional weight loss >5% in 1 month
  • Starvation >7days
  • Prolonged hypocaloric feeding / chronic swallowing difficulties
  • Idiosyncratic diets (qualitative malnutrition)
  • Nutrient losses / reduced absorption e.g. GI condition, chronic pancreatitis, chronic antacid use (by binding minerals), chronic high-dose diuretics, post bariatric surgery

 

Malnourished pts do not always look thin (e.g. bariatric surgery); low BMI does not mean malnourishment (e.g. endurance sports)

 

Those who tend to eat less in hospital are either the elderly or pts <39 yrs of age: ? related to unusual situation of being hospitalised at this age / history of chronic illness

 

Measurements:

  • BMI – fluctuates with fluid resuscitation
  • Muscle mass – visualisation by CT / Ultrasound (degree of subjectivity)
  • Muscle function – MRC grading of strength, Dynamometer
  • Bioimpedance

 

Muscle layer thickness is dynamic and fluid-sensitive

  • up to 15% apparent increase in muscle mass after 8-hr surgical procedure
  • reflects lean tissue, but also fluid, impaired venous return and inflammation

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Nutrition risk assessment:

 

Estimate body weight if unknown

Investigate nutrition history

  • history from pt / family
  • If malnourished, start slow feed and increase progressively
  • Prophylactic thiamine
  • Supplement K+, Mg++, PO4- (measure)

Observe pt for GI tolerance, cardio/pulmonary tolerance

 

Sensible take home messages:

  • Due to loss of autonomy, ICU pts are often dependent on nutrition care
  • Always consider malnutrition once the pt has been on ICU >7 days even if body size appears fine
  • Look at the patient, not just the numbers – muscle bulk, hands, overall appearance
  • NO reason not to feed early once condition stabilised
  • If the pt is ‘eating independently’ on ICU, always monitor intake to avoid false reassurances of adequate nutrition
  • Aim to retrain pt to eat while on ICU + swallowing test before discharge to the ward, where there is less direct nursing care and risk of further malnutrition

Nutrition Masterclass (20/10/2018)

Energy Needs and Nutritional Status

Heleen Ondemans-Van Straaten (The Netherlands)

Assess nutritional status

  • Hx unintended weight loss / decreased physical performance before admission
  • Physical exam
  • Body Composition
    • Bio-impedance analysis 
    • Phase angle calculation 

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  • Ultrasound / CT manual measurement of muscle diameter / circumference 

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Low muscle mass and low phase angle = increased risk of mortality 

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BMI does not reflect nutritional status – obese patient can be malnourished

Assess energy needs

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Energy needs vary with time, phase of illness

  • ESPEN guidelines recommend Hypocaloric nutrition no more than 70% energy expenditure in acute phase   

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Early overfeeding definitely not beneficial, likely harmful

GI Dysfunction

Annika Reintam Blaser (Estonia)

No tool or marker to measure GI function in critically ill; GI dysfunction not usually obvious early on

Motility can be assessed, but does not reflect digestion / absorption

Sometimes the best early indicator comes from asking the surgeon about condition of the bowel during surgery!IMG_0007

Terminology: Acute GI injury (AGI) with grading of severity, to guide enteral feeding 

Feeding Intolerance can be at level of stomach (obvious: vomiting, large volume aspirates) and also small bowel / colon (less easy to monitor: distension / diarrhoea)

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Use of Enteral feeding and pro kinetics

  • Start Slow
  • Review daily for response
  • Clear plan of action as if managing drug prescription

How to Monitor Nutrition

Jan Wernerman (Sweden)

Assess calorie and protein intake

  • hourly record of intake and GI losses
  • identify non-nutrition calories, non-nutrition proteins
  • consider GI response to previous day’s feeding plan

Indirect Calorimetry early and reliable in mechanical ventilation, more difficult in spontaneous breathing

  • measures energy expenditure (different from energy requirement)
  • guides feeding decisions but EE changes with time, therefore needs repeat measurement

Protein:

  • how much to give? Do sick pts need more?
  • no hard evidence
  • practicality of measuring urinary urea
  • difficulty of interpreting Nitrogen balance data
  •  high protein dose early on in illness is better retained than higher protein dose given late

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Triglycerides:

  • stay with recommended limits
  • upper reference 2mmol/L
  • limited evidence of harm in humans when TGs 5-10mmol/L over a few days, but in practice, the response is usually to decrease fat intake
  • is pt on prolonged propofol infusion? Known to raise TGs
  • some pts will have raised TGs regardless of what we do

Glucose: ESPEN (2018) recommends monitoring at least 4-hourly, using insulin when BM > 10mmol/L

Phosphate:

  • may decrease in response to feeding
  • ESPEN (2018) recommends restricting caloric intake but limited evidence for duration of restriction

Specific nutrients: Trace elements, vitamins, Selenium, Glutamine, Growth hormone, Thyroxine

  • difficult to advise on measurements
  • even if levels known, controversial as to relation to illness
  • no clear guidelines on when to supplement 
  • prudent to look at overall clinical picture

Advantages of Enteral Nutrition vs Parenteral Nutrition in critical illness

Arthur RH van Zanten (The Netherlands)

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Early Enteral Nutrition (EEN): initiated within 24-48 hours of admission, trauma, injury

  • aim to maintain condition of gut (microvilli health, intestinal barrier, intestinal mucosal immunity)
  • provide nutrients to deal with metabolic stress
  • reduce morbidity compared with parenteral nutrition
  • reduce cost compared with parenteral nutrition

Usual post-operative organ recovery time

  • Stomach 24-48hrs
  • Small intestine 12-24hrs (recovers most quickly, consider post-pyloric feeding with prokinetics)
  • Colon 48-120hrs (therefore do not wait for bowel sounds before commencing feeding)

Fewer post-op complications with EEN in major upper GI resection

  • the anastomosis needs Oxygen, Blood flow and Nutrition to heal

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Early EN vs delayed EN: no difference in mortality, but significantly reduced risk of infection

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Few situations where EN should be delayed

  • unstable shock
  • acute GI bleed
  • bowel ischaemia
  • abdominal compartment syndrome

** use of vasopressors not a contraindication unless harm-dynamically unstable

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EN has limited risk of overfeeding compared to parenteral feeding, however EN is also less likely to achieve feeding targets due to interruption in feeding times

EuAsia Day 3: Metabolic issues

Hyponatraemia: European guidelines (E Hoste)

Proportion of ICU pts with hypoNa (<135) – 14 to 27%

Acute hypoNa – < 48hrs

Symptoms variable

Guideline recommends treating for severe symptomatic hypoNa with 150mls of 3%NaCl over 20 minutes, aim for Na increase of 5mmol/L

Aim to correct severe hypoNa by 10mmol/L in D1 (8mmol/L D2) until pt asymptomatic or Na >130

IF corrected too quickly – add in 5% dextrose and/or consider desmopressin 2mcg (per 8hr)

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References:

Clinical practice guideline on diagnosis and treatment of hyponatraemia

 

Nutrition in ICU (Ostermann)

Malnutrition is associated with poor outcome

Critically ill patients lose 10-20% of body protein within a week

Resting energy expenditure – Estimation/Harris and Benedikt/Indirect calorimetry

TICACOS trial – enteral feeding with energy target determined by estimation (control) vs indirect calorimetry

  • Improved survival in pts where targets were met
  • Better outcomes in control group (estimation 25kcal/kg/day)

CALORIES Trial (TPN)

  • No significant difference in groups

ESICM Guidelines (2017)

  • Early enteral nutrition as a default
  • Delay enteral nutrition in specific cases e.g. uncontrolled shock, bowel ischaemia, life threatening hypoxaemia/hypercapnia/acidosis
  • Not to delay EN in prone position

ASPEN (2016)

  • PN initiated ASAP in high risk groups if EN not feasible
  • PN can be considered in low risk pts after 7-10 days if unable to meet >60% energy goal
  • Immune0modulating enteral formulation should be considered in pts with severe trauma or TBI or post-operatively

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References:

The tight calorie control study (TICACOS): a prospective, randomized, controlled pilot study of nutritional support in critically ill patients.

Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient

Early enteral nutrition in critically ill patients: ESICM clinical practice guidelines

 

Liver failure: how to support (Gruber)

Liver dysfunction common but acute liver failure is rarer

Liver dysfunction post immunotherapy (as part of cancer treatment) is not uncommon

  • Supportive care
  • Steroids 1-2mg/kg/day

Commonest cause on ICU – sepsis

Cirrhotic pts have vascular hypo-reactivity due to increase NO levels

Relative adrenal insufficiency is common

Septic liver pts

  • Supportive
  • Prophylaxis – encephalopathy, GI bleeds, infection
  • High risk of fungal infection

Acute variceal haemorrhage

  • oesophageal varices common
  • Peak re-bleed day 5
  • Endoscopic and interventional radiology interventions
  • Reduction of portal pressure – octreotide, somastatin etc

AKI common but majority is NOT hepato-renal syndrome (HRS)

  • 2 types of HRS: type 1 rapid and poorer outcomes
  • Specifically for HRS: albumin/terlipressin
  • RRT as a bridge (consider citrate)

Liver support systems

  • MARS, RELIEF, PROMETHIUS
  • Failed to show mortality benefits

References:

Acute-on-chronic liver failure definitions

Acute esophageal variceal bleeding: Current strategies and new perspectives