Nutrition in critical illness

Surgical approach (if relevant)

  • Not an operation; however, ICU nutrition often follows a procedural pathway (feeding access and GI evaluation).
    • Assess GI tract usability: bowel sounds not required; focus on haemodynamic stability, abdominal exam, output, imaging if concerned.
    • Establish access: NG/OG tube first-line; consider post-pyloric tube if high aspiration risk or persistent intolerance; consider PEG/PEJ if prolonged feeding anticipated.
    • If enteral route fails/contraindicated: central venous access for PN (or peripheral PN short-term with osmolarity limits).

Anaesthetic management (if relevant)

  • Not a single anaesthetic procedure; considerations apply to ICU patients requiring feeding access (e.g., endoscopic PEG, post-pyloric placement) or surgery while on nutrition support.
    • Type of anaesthesia: usually sedation/GA for PEG or endoscopy; GA for laparotomy; regional rarely primary.
    • Airway: aspiration risk common; ETT often preferred if GA/sedation in high-risk patients; SGA less suitable if full stomach/ileus.
    • Duration: PEG ~30–60 min; post-pyloric placement variable; major surgery variable.
    • Pain: PEG mild–moderate; laparotomy severe; plan multimodal analgesia, consider epidural for major abdominal surgery if appropriate.
    • Peri-procedural nutrition: stop feeds pre-GA per local policy; consider prokinetics; manage glycaemia; continue electrolytes/thiamine if refeeding risk.

Aims and principles

  • Goals: reduce catabolism, preserve lean body mass, support immune function and wound healing, maintain gut integrity, avoid overfeeding and complications.
  • Enteral nutrition (EN) preferred over parenteral nutrition (PN) when GI tract functional: lower infection risk, maintains mucosal barrier, cheaper.
  • Avoid early full-calorie feeding in acute phase of critical illness; consider trophic/low-dose EN initially and advance as stable.

Metabolic response to critical illness (why nutrition is different in ICU)

  • Stress response phases: early acute (ebb/flow overlap), then catabolic flow phase; later anabolic recovery if illness resolves.
    • Neuroendocrine: ↑ catecholamines, cortisol, glucagon; relative insulin resistance.
    • Inflammation: cytokines (IL-1, IL-6, TNF-α) drive proteolysis, lipolysis, acute phase response.
  • Consequences: hyperglycaemia, increased hepatic gluconeogenesis, muscle protein breakdown (negative nitrogen balance), altered lipid handling, micronutrient depletion.
  • Overfeeding risks: hypercapnia (↑ CO2 production), hepatic steatosis/cholestasis, hyperglycaemia, increased infection risk, refeeding complications.

Assessment and when to start

  • Assess nutrition risk and baseline state: weight/BMI trends, recent intake, functional status, comorbidities, frailty, sarcopenia, alcohol use, malabsorption, prior bariatric surgery.
  • Screening tools: MUST (ward), NRS-2002; ICU tools include NUTRIC score (incorporates illness severity).
  • Start EN early when feasible (often within 24–48 h of ICU admission) once haemodynamically stabilising; use caution with escalating vasopressors and signs of gut ischaemia.
    • Contraindications to EN: bowel ischaemia, uncontrolled shock, high-output proximal fistula without distal access, mechanical obstruction, abdominal compartment syndrome (relative), uncontrolled GI bleeding (relative).

Energy targets (calories) and how to estimate

  • Best method: indirect calorimetry (if available) to measure resting energy expenditure; avoids under/overfeeding.
  • If not available: weight-based estimates (institution-dependent). Common pragmatic approach: 20–25 kcal/kg/day early; 25–30 kcal/kg/day later/recovery; adjust for obesity and burns/trauma.
    • Obesity: consider ideal/adjusted body weight; avoid overfeeding; higher protein proportion.
    • Burns/major trauma: higher requirements; specialist input; consider calorimetry.
  • Account for non-nutrition calories: propofol (1.1 kcal/mL as lipid), citrate (CRRT), dextrose infusions.

Protein targets (often the key macronutrient in ICU)

  • Aim to attenuate muscle loss: typical target 1.2–2.0 g/kg/day protein (use ideal/adjusted body weight in obesity).
    • Higher targets often used in burns/trauma; lower may be required temporarily in severe hepatic encephalopathy (individualise).
  • Nitrogen balance: can be estimated using urinary urea nitrogen (UUN) but limited by practicality and non-urinary losses; trend rather than single value.

Enteral nutrition (EN): practical ICU approach

  • Route: NG/OG first-line; post-pyloric (nasojejunal) if high aspiration risk, gastroparesis, recurrent high gastric residuals with intolerance, pancreatitis (select cases).
  • Feeding strategy: continuous infusion often better tolerated in ICU; start low (trophic) and advance every 4–12 h as tolerated to target.
  • Gastric residual volumes (GRV): thresholds vary; interpret with clinical context (vomiting, distension, aspiration). Avoid reflexively stopping feeds for modest GRVs without symptoms.
  • Prokinetics for intolerance: metoclopramide or erythromycin; consider post-pyloric feeding if persistent.
  • Aspiration prevention: head-up 30–45°, oral care, appropriate tube position, consider post-pyloric route in high risk, minimise deep sedation when possible.
  • Formula choice: standard polymeric feeds usually adequate; consider energy-dense if fluid restricted; consider renal/hepatic-specific formulas selectively (evidence mixed).

Parenteral nutrition (PN): indications and key points

  • Indications: non-functional/inaccessible GI tract or EN contraindicated; failure to meet needs with EN over time in high-risk patients (local policy).
    • Examples: short bowel, high-output fistula without distal feeding option, prolonged ileus/obstruction, severe malabsorption, mesenteric ischaemia, severe GI bleeding where EN not possible.
  • Access: central venous catheter preferred for full PN (osmolarity); peripheral PN limited and short-term.
  • Composition: glucose + amino acids + lipids + electrolytes + vitamins/trace elements; tailor to organ dysfunction and labs.
  • Complications: catheter-related bloodstream infection, thrombosis, hyperglycaemia, hypertriglyceridaemia, liver dysfunction (cholestasis/steatosis), electrolyte disturbances, refeeding syndrome.
  • Monitoring: daily U&E, phosphate, Mg, glucose initially; triglycerides; LFTs; fluid balance; line care and asepsis.

Micronutrients and pharmaconutrition

  • Thiamine: give before and during carbohydrate reintroduction in malnourished/alcohol-dependent patients to prevent Wernicke’s and contribute to refeeding prevention.
  • Trace elements/vitamins: ensure daily provision in PN; in EN, standard feeds usually cover once at goal rate; consider extra in burns, CRRT, high-output losses.
  • Glutamine: routine supplementation not recommended in general ICU (signal of harm in some populations); follow local/national guidance.
  • Omega-3/immune-modulating formulas: evidence mixed; may be considered in selected surgical/ARDS contexts per local protocol but not universal.

Glycaemic control and nutrition

  • Critical illness causes insulin resistance; both EN and PN can precipitate hyperglycaemia.
  • Target glucose: avoid tight control; aim for moderate range per ICU policy (commonly ~6–10 mmol/L) balancing hypoglycaemia risk.
  • Practical: insulin infusion protocols; consider reducing carbohydrate load if persistent hyperglycaemia; review sepsis/steroids/vasopressors.

Refeeding syndrome (high-yield viva topic)

  • Definition: potentially fatal shifts in fluids/electrolytes after reintroduction of nutrition in malnourished patients; driven by insulin-mediated cellular uptake.
  • Who is at risk: little/no intake for >5–10 days, significant weight loss, low BMI, alcohol misuse, anorexia, oncology, elderly/frail, post-bariatric, chronic malabsorption, prolonged diuretics/antacids.
  • Biochemistry: hypophosphataemia (hallmark), hypokalaemia, hypomagnesaemia; thiamine deficiency; sodium/water retention → oedema, heart failure.
  • Clinical: arrhythmias, cardiac failure, respiratory failure (diaphragm weakness), rhabdomyolysis, seizures, delirium, haemolysis.
  • Prevention/management: give thiamine (and multivitamins) before feeding; start low calories (e.g., 10 kcal/kg/day or less if very high risk) and increase slowly; aggressive electrolyte replacement; close monitoring (phosphate/Mg/K daily or more).

Special situations

  • Renal failure/CRRT: protein needs often higher with CRRT due to amino acid losses; monitor electrolytes closely; fluid restriction may require energy-dense feeds.
  • Liver failure: avoid protein starvation; manage encephalopathy with standard measures (lactulose/rifaximin) rather than routine protein restriction; consider branched-chain AA in selected cases.
  • Pancreatitis: EN preferred (gastric or jejunal depending on tolerance); PN if EN not possible; avoid prolonged starvation.
  • ARDS/ventilation: avoid overfeeding (↑ CO2 production); permissive underfeeding early may be acceptable; ensure adequate protein.
  • Post-op/major surgery: early EN where possible; consider enhanced recovery principles; treat ileus, minimise opioids, mobilise early.
You are asked to discuss nutrition in critical illness. How would you structure your answer in a viva?

A safe structure is: (1) aims, (2) assess risk and timing, (3) choose route EN vs PN, (4) targets (energy/protein), (5) monitoring/complications, (6) special situations.

  • Aims: preserve lean mass, support recovery, avoid complications of under/overfeeding.
  • Assessment: malnutrition risk (history, weight loss, MUST/NUTRIC), haemodynamic stability, GI function.
  • Route: EN first if gut works; PN if contraindicated or inadequate EN.
  • Targets: estimate energy (prefer calorimetry; otherwise 20–25 kcal/kg/day early), protein 1.2–2.0 g/kg/day; account for propofol calories.
  • Monitoring: glucose, electrolytes (PO4/Mg/K), triglycerides, LFTs, fluid balance; watch for aspiration, line sepsis, refeeding.
Why is enteral nutrition preferred to parenteral nutrition in ICU patients?

Explain physiological and outcome-based reasons, plus practicalities.

  • Maintains gut mucosal integrity and may reduce bacterial translocation.
  • Lower risk of catheter-related bloodstream infection compared with PN.
  • Cheaper, simpler, fewer metabolic complications (though aspiration/intolerance can occur).
  • Still requires vigilance: aspiration prevention, tolerance, and adequate protein delivery.
List indications for parenteral nutrition in critical illness.

PN is for when the gut cannot be used safely/effectively.

  • Mechanical obstruction or prolonged ileus preventing EN.
  • Short bowel syndrome or severe malabsorption.
  • High-output proximal fistula without distal feeding access.
  • Mesenteric ischaemia or bowel discontinuity.
  • Failure to meet nutritional needs with EN over time in high-risk patients (policy-dependent).
How would you estimate calorie requirements in an ICU patient, and what are the pitfalls?

Demonstrate hierarchy of methods and common errors.

  • Best: indirect calorimetry to measure energy expenditure.
  • If unavailable: weight-based estimate (e.g., 20–25 kcal/kg/day early; 25–30 later), adjust for obesity (ideal/adjusted weight).
  • Pitfalls: overfeeding early catabolic phase; not counting propofol/citrate/dextrose calories; using actual weight in morbid obesity; ignoring changing phase of illness.
What protein intake do you aim for in critical illness, and why is protein emphasised?

Protein delivery is central to limiting ICU-acquired weakness and negative nitrogen balance.

  • Typical target: 1.2–2.0 g/kg/day (use ideal/adjusted body weight in obesity).
  • Rationale: stress-induced proteolysis causes rapid skeletal muscle loss; adequate protein supports recovery and wound healing.
  • Caveats: individualise in severe hepatic encephalopathy; higher needs with burns/trauma/CRRT.
Describe refeeding syndrome: pathophysiology, features, and management.

A classic FRCA viva topic: define it, identify high-risk patients, and give a prevention-first plan.

  • Pathophysiology: carbohydrate intake → insulin surge → intracellular shift of phosphate, potassium, magnesium; thiamine demand increases; sodium/water retention.
  • Features: hypophosphataemia (hallmark), hypokalaemia, hypomagnesaemia; arrhythmias, heart failure, respiratory failure, seizures, delirium, rhabdomyolysis.
  • High-risk: prolonged poor intake, low BMI, weight loss, alcohol misuse, frailty, oncology, malabsorption, post-bariatric.
  • Management: thiamine before feeding; start low calories (e.g., ~10 kcal/kg/day or less if very high risk) and increase slowly; replace PO4/Mg/K aggressively; close monitoring.
A ventilated septic patient is on high-dose noradrenaline. Would you start enteral feeding?

The key is balancing benefits of early EN against risk of gut hypoperfusion/ischaemia.

  • Assess haemodynamic trajectory: escalating vasopressors, rising lactate, signs of hypoperfusion increase risk; stabilising/de-escalating supports cautious EN.
  • If unstable: delay or use minimal trophic feeds with extreme caution per local policy; prioritise resuscitation.
  • Monitor for intolerance/ischaemia: abdominal pain/distension, high NG aspirates with clinical deterioration, GI bleeding, rising lactate, increasing vasopressor needs.
What are the complications of parenteral nutrition and how do you monitor for them?

Split into line-related, metabolic, and hepatic complications.

  • Line-related: catheter sepsis, thrombosis, mechanical complications (pneumothorax/arterial puncture at insertion).
  • Metabolic: hyperglycaemia, electrolyte disturbances (including refeeding), hypertriglyceridaemia, fluid overload.
  • Hepatobiliary: cholestasis, steatosis, gallbladder stasis (esp prolonged PN).
  • Monitoring: daily glucose and U&E/PO4/Mg initially; triglycerides; LFTs; strict asepsis and line review; clinical review of fluid balance and infection signs.
How does overfeeding present in ICU and why is it harmful?

Examiners like CO2 production and ventilatory implications.

  • Respiratory: increased CO2 production (especially excess carbohydrate) → harder ventilator wean, respiratory acidosis risk.
  • Metabolic: hyperglycaemia, hypertriglyceridaemia, electrolyte derangements.
  • Hepatic: fatty liver/steatosis, cholestasis (particularly with PN).
  • Infective: hyperglycaemia and PN-related factors associated with infection risk.
An ICU patient on propofol sedation is receiving enteral feeding. What nutritional issue might you miss?

Propofol is delivered in lipid emulsion and contributes significant calories.

  • Propofol provides ~1.1 kcal/mL; high infusion rates can contribute substantial calories leading to overfeeding.
  • Also increases lipid load: monitor triglycerides; consider propofol infusion syndrome risk in appropriate context.
  • Action: account for propofol calories in total energy prescription; adjust feed concentration/rate.
Give a practical approach to feed intolerance in ICU (vomiting/high residuals).

Show a stepwise plan: exclude obstruction/ischaemia, optimise basics, then escalate.

  • Check tube position, head-up positioning, sedation/opioid burden, constipation/ileus; assess abdomen and haemodynamics.
  • Use prokinetics (metoclopramide/erythromycin) and review electrolyte abnormalities (K/Mg).
  • Consider post-pyloric feeding if persistent intolerance or high aspiration risk.
  • If EN not possible: consider PN depending on duration and nutrition risk.

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