Nutrition in the Surgical Patient

Surgical illness, trauma and sepsis throw the body into a catabolic, hypermetabolic state where adequate nutrition is not a luxury but a determinant of wound healing, immune competence and survival. This chapter covers nutritional assessment, the enteral-versus-parenteral decision, indications and complications of TPN, refeeding syndrome, immunonutrition and ERAS — all recurrent themes in postoperative and critical-care surgery MCQs.

The metabolic response to injury (why nutrition matters)

Sir David Cuthbertson described the biphasic metabolic response to trauma. Knowing this framework anchors every nutrition question.

Phase	Timing	Features
Ebb phase	First 24–48 h	Hypovolaemia, ↓cardiac output, ↓body temperature, ↓metabolic rate, hyperglycaemia (stress), insulin resistance
Flow phase	Days to weeks	Hypermetabolism, ↑cardiac output, ↑oxygen consumption, catabolism, negative nitrogen balance, ↑glucose turnover, fever

During the flow phase the body preferentially mobilises skeletal muscle protein for gluconeogenesis (glutamine and alanine are the principal carriers). Counter-regulatory hormones — catecholamines, cortisol, glucagon — and cytokines (TNF-α, IL-1, IL-6) drive this. Unlike simple starvation, the catabolism of injury is not suppressed by giving glucose; this is the key distinction.

High-yield: In simple starvation the body adapts to ketosis and spares protein. In the injured/septic patient, catabolism continues despite feeding because of the hormonal/cytokine milieu — hence aggressive nutritional support is required.

The respiratory quotient (RQ) is testable: carbohydrate oxidation RQ = 1.0, fat = 0.7, protein = 0.8, mixed diet ≈ 0.85. Overfeeding (RQ >1.0) reflects lipogenesis and increases CO₂ production — dangerous in a patient being weaned off the ventilator.

Nutritional assessment

There is no single perfect marker; assessment combines history, anthropometry, biochemistry and validated tools.

Clinical/anthropometric

• Unintentional weight loss — the single most useful bedside indicator. >10% loss over 6 months (or >5% in 1 month) is significant.
• BMI = weight (kg) / height (m²). <18.5 underweight; <16 indicates severe malnutrition.
• Triceps skinfold thickness — estimates fat stores; mid-arm muscle circumference — estimates lean muscle.
• Hand-grip dynamometry — functional measure of muscle.

Biochemical markers

Marker	Half-life	Use / caveat
Albumin	~20 days	Prognostic, NOT a sensitive nutrition marker; falls in inflammation (negative acute-phase reactant), fluid overload. <3.0 g/dL = ↑surgical risk; <2.0 g/dL = severe
Prealbumin (transthyretin)	~2 days	Best for monitoring short-term nutritional response/repletion
Transferrin	~8–10 days	Affected by iron status
Retinol-binding protein	~12 h	Very short half-life; affected by renal function

High-yield: Albumin reflects severity of illness and is a prognostic marker, but prealbumin is the better marker to track the response to nutritional therapy because of its short half-life. Nitrogen balance is the gold-standard dynamic index of adequacy.

Nitrogen balance = (protein intake in g/6.25) − (24-h urinary urea nitrogen + 4). A positive balance means anabolism. 1 g nitrogen = 6.25 g protein = ~30 g lean tissue.

Validated scoring tools

• Subjective Global Assessment (SGA) — history (weight change, intake, GI symptoms, function) + physical exam; classes A (well-nourished), B (moderate), C (severe).
• NRS-2002 (Nutritional Risk Screening) — recommended by ESPEN for hospitalised patients; score ≥3 = at risk, ≥5 = high risk.
• MUST (Malnutrition Universal Screening Tool) — BMI + weight loss + acute disease effect.

Estimating requirements

A simple stepwise estimate: assess weight → estimate energy → estimate protein → add micronutrients → reassess.

• Energy: 25–30 kcal/kg/day for most surgical/ICU patients. The Harris–Benedict equation estimates basal energy expenditure, multiplied by stress factors (1.2 elective surgery, 1.3–1.5 sepsis/trauma, up to 2.0 major burns). Indirect calorimetry is the gold standard for measuring actual energy expenditure.
• Protein: 1.0–1.5 g/kg/day (up to 2.0 in burns/critical illness). Non-protein calorie : nitrogen ratio ≈ 150 : 1 (lower, ~100:1, in severe stress).
• Carbohydrate: glucose is the main calorie source; maximum oxidation ~4–5 mg/kg/min — exceeding this causes hyperglycaemia and hepatic steatosis.
• Fat: 20–30% of calories; provides essential fatty acids and is calorie-dense (9 kcal/g).

High-yield: Permissive underfeeding / euvolaemic hypocaloric feeding (with adequate protein) is favoured early in critical illness. Overfeeding causes hyperglycaemia, hepatic steatosis, hypercapnia and azotaemia.

Enteral versus parenteral nutrition

This is the most heavily tested decision. The governing principle:

High-yield: "If the gut works, use it." Enteral nutrition is always preferred over parenteral when the GI tract is functional and accessible — it is cheaper, more physiological, maintains gut mucosal integrity, reduces bacterial translocation, and is associated with fewer infectious complications.

Enteral nutrition (EN)

Routes: nasogastric, nasojejunal, percutaneous endoscopic gastrostomy (PEG), surgical/needle-catheter jejunostomy. Choice depends on anticipated duration (>4–6 weeks → consider a tube ostomy such as PEG) and aspiration risk (post-pyloric/jejunal feeding for high aspiration risk or gastroparesis).

Timing: Early EN within 24–48 h of admission/surgery improves outcomes. The presence of bowel sounds or flatus is not required to start feeding after most abdominal surgery.

Contraindications to EN: intestinal obstruction, paralytic ileus, high-output enterocutaneous fistula, intractable vomiting/diarrhoea, short bowel with inadequate absorptive surface, severe shock/bowel ischaemia.

Complications of EN:

• Mechanical — tube blockage, malposition, nasal erosion.
• GI — diarrhoea (most common), bloating, cramps.
• Aspiration pneumonia — the most feared; reduce risk by head-up 30–45°, post-pyloric feeding, prokinetics.
• Metabolic — hyperglycaemia, electrolyte shifts, refeeding syndrome.

Parenteral nutrition (PN/TPN)

Intravenous delivery of all macronutrients and micronutrients, used when the gut cannot be used or is inaccessible.

Indications for TPN:

1. Prolonged paralytic ileus
2. Short bowel syndrome (massive resection)
3. High-output enterocutaneous fistula
4. Severe acute pancreatitis when enteral access fails (note: jejunal EN is now preferred in pancreatitis when tolerated)
5. Prolonged inability to use the gut (e.g., severe mucositis, prolonged obstruction, intractable vomiting)
6. Severe malnutrition with non-functioning gut before major surgery

Access: Central venous catheter (subclavian preferred for long-term, dedicated lumen) because of the high osmolarity of the solution. Peripheral parenteral nutrition (PPN) is possible only with dilute, low-osmolarity (<900 mOsm/L) solutions for short periods.

Feature	Enteral	Parenteral
Prerequisite	Functioning, accessible gut	Reliable venous access
Cost	Low	High
Gut mucosa	Maintained (trophic)	Atrophy, ↑translocation
Infection risk	Lower	Higher (catheter sepsis)
Major risks	Aspiration, diarrhoea	Line sepsis, hyperglycaemia, cholestasis, refeeding
Preferred?	Yes, first choice	Only if EN impossible

Complications of TPN:

• Catheter-related: insertion (pneumothorax, arterial puncture), catheter-related bloodstream infection (CRBSI) — most common serious complication; thrombosis.
• Metabolic: hyperglycaemia (most common), hypoglycaemia (abrupt stoppage), electrolyte disturbances, refeeding syndrome, hypertriglyceridaemia.
• Hepatobiliary: steatosis (early), cholestasis and intestinal-failure-associated liver disease (IFALD) with prolonged use; acalculous cholecystitis / gallstones from biliary stasis (no enteral stimulation of CCK).
• Gut: mucosal atrophy, bacterial translocation.

High-yield: The commonest serious complication of TPN is catheter-related bloodstream infection; the commonest metabolic complication is hyperglycaemia. Long-term TPN causes hepatic steatosis/cholestasis and acalculous cholecystitis/gallstones. Always wean TPN gradually to avoid rebound hypoglycaemia.

Refeeding syndrome

A potentially fatal set of fluid and electrolyte shifts when nutrition (especially carbohydrate) is reintroduced to a chronically starved or severely malnourished patient. This is one of the single most examined topics.

Mechanism: Starvation → depleted intracellular stores despite "normal" serum levels → carbohydrate refeeding → surge of insulin → cellular uptake of phosphate, potassium and magnesium → drop in serum levels; glucose load also consumes phosphate to form ATP and 2,3-DPG.

The biochemical hallmark is HYPOPHOSPHATAEMIA. Also: hypokalaemia, hypomagnesaemia, thiamine deficiency, and fluid retention.

High-yield: The defining/most characteristic abnormality of refeeding syndrome is hypophosphataemia. Thiamine (vitamin B1) must be given before/with carbohydrate to prevent Wernicke's encephalopathy.

At-risk patients: chronic alcoholism, anorexia nervosa, prolonged starvation/fasting, marasmus/kwashiorkor, prolonged ICU stay, post-bariatric surgery, malabsorption.

Clinical consequences: cardiac arrhythmias and failure, respiratory failure (weak diaphragm), rhabdomyolysis, seizures, haemolysis, delirium, sudden death.

Prevention/management — stepwise:

1. Identify risk (NICE criteria: BMI <16, weight loss >15% in 3–6 months, little intake >10 days, low baseline K/PO₄/Mg).
2. Start low, go slow → begin at ~10 kcal/kg/day (5 kcal/kg in extreme risk) and increase over 4–7 days.
3. Give thiamine (and B-complex) before feeding and for the first several days.
4. Replace and monitor phosphate, potassium and magnesium daily; correct before/during feeding.
5. Monitor fluid balance, cardiac rhythm.

Immunonutrition and special substrates

• Glutamine — the principal fuel for enterocytes and lymphocytes; a "conditionally essential" amino acid in catabolic states. Supplementation may preserve gut integrity. (Caution: the REDOXS trial showed harm with high-dose parenteral glutamine in patients with multi-organ failure/renal failure — a frequently tested nuance.)
• Arginine — substrate for nitric oxide and a stimulus for T-cell function and wound healing; debated/avoided in severe sepsis.
• Omega-3 (n-3) fatty acids — anti-inflammatory eicosanoid precursors.
• Nucleotides — support rapidly dividing immune cells.
• Branched-chain amino acids (BCAAs) — relevant in hepatic encephalopathy.

High-yield: Glutamine is the major energy source for the small-bowel enterocyte (and a key fuel for immune cells). Arginine + glutamine + omega-3 + nucleotides constitute classic "immunonutrition" formulae used in selected major elective GI/oncologic surgery.

ERAS — Enhanced Recovery After Surgery

ERAS (originally "fast-track surgery," pioneered by Henrik Kehlet) is a multimodal, evidence-based pathway to attenuate the surgical stress response and accelerate recovery. Nutrition is central.

Key nutritional/perioperative elements:

• No prolonged fasting: clear fluids allowed up to 2 hours before surgery; solids up to 6 hours.
• Carbohydrate loading the night before and 2–3 h pre-op (oral complex carbohydrate drink) reduces insulin resistance and protein loss.
• Avoid routine bowel preparation (in many colorectal pathways).
• Early oral/enteral feeding within 24 h postoperatively.
• Multimodal opioid-sparing analgesia, early mobilisation, early removal of catheters/drains/NG tubes, avoidance of fluid overload, maintenance of normothermia, PONV (nausea) prophylaxis.

High-yield: ERAS abolishes traditional "nil by mouth from midnight" — clears up to 2 h, solids up to 6 h pre-op, plus pre-operative carbohydrate drinks to reduce post-op insulin resistance and catabolism.

Key differentials / distinctions to keep clear

Entity	Discriminator
Marasmus vs Kwashiorkor	Marasmus = total calorie deficit, severe wasting, no oedema, normal-ish albumin; Kwashiorkor = protein deficit, oedema, fatty liver, low albumin
Starvation vs stress catabolism	Starvation adapts (ketosis, protein-sparing); stress = obligatory protein breakdown not suppressed by glucose
Marker of severity vs marker of repletion	Albumin = severity/prognosis; prealbumin = response monitoring
EN diarrhoea vs C. difficile	Reduce feed rate/osmolarity, exclude infection; not always the formula

Wound healing nutrients (commonly asked one-liners)

• Vitamin C — collagen hydroxylation (proline/lysine); deficiency → poor healing, scurvy.
• Zinc — cofactor for many enzymes; deficiency impairs healing.
• Vitamin A — counteracts the inhibitory effect of steroids on healing.
• Protein and arginine — substrate for collagen and immune function.
• Copper — lysyl oxidase (collagen cross-linking).

Recently asked / exam angle

• Best marker to monitor short-term nutritional repletion → prealbumin (transthyretin) (short half-life ~2 days). Albumin is for prognosis/severity.
• Most characteristic electrolyte abnormality in refeeding syndrome → hypophosphataemia. Give thiamine before feeding.
• Preferred route of nutrition when gut is functional → enteral ("if the gut works, use it").
• Commonest serious complication of TPN → catheter-related bloodstream infection; commonest metabolic complication → hyperglycaemia.
• Long-term TPN → hepatic steatosis/cholestasis and acalculous cholecystitis/gallstones (biliary stasis from lack of enteral CCK stimulus).
• Main fuel of the enterocyte → glutamine.
• ERAS pre-op fasting → clears 2 h, solids 6 h, plus carbohydrate loading; early post-op feeding within 24 h.
• Maximum glucose oxidation rate ≈ 4–5 mg/kg/min; overfeeding raises RQ >1 and CO₂ (problematic in ventilator weaning).
• Non-protein calorie : nitrogen ratio ≈ 150:1 (lower in severe stress).
• Cuthbertson's ebb (hypometabolic) and flow (hypermetabolic) phases of the metabolic response to trauma.
• REDOXS trial: high-dose parenteral glutamine harmful in multi-organ/renal failure.

Mnemonics

• Refeeding watch — "PKM down": Phosphate, Kpotassium, Magnesium all fall; give thiamine first.
• TPN trouble — the 3 S's: Sepsis (line), Sugar (hyper/hypoglycaemia), Steatosis/cholestasis (liver).
• ERAS "2-4-6" memory cue: carbohydrate drink up to 2 h, early feed by ~24 h, solids until 6 h pre-op.

Rapid revision

1. Metabolic response to injury is biphasic — ebb (hypometabolic) then flow (hypermetabolic catabolic); catabolism is not suppressed by glucose.
2. Unintentional weight loss >10% in 6 months is the most useful bedside malnutrition marker; BMI <18.5 underweight, <16 severe.
3. Albumin = prognostic/severity; prealbumin = best for monitoring repletion (half-life ~2 days).
4. Nitrogen balance is the dynamic gold standard; 1 g N = 6.25 g protein.
5. Energy ~25–30 kcal/kg/day, protein 1–1.5 g/kg/day; indirect calorimetry is the gold standard for measuring energy expenditure.
6. Enteral is always preferred when the gut works — cheaper, trophic to mucosa, fewer infections.
7. Start early enteral feeding within 24–48 h; bowel sounds are not a prerequisite.
8. TPN indications: prolonged ileus, short bowel, high-output fistula, prolonged non-functioning gut.
9. Commonest serious TPN complication = catheter-related sepsis; metabolic = hyperglycaemia; long-term = cholestasis + acalculous cholecystitis/gallstones.
10. Refeeding syndrome = hypophosphataemia (+ low K, low Mg); give thiamine before carbohydrate; start low and go slow.
11. Glutamine fuels enterocytes/immune cells; avoid high-dose parenteral glutamine in multi-organ failure (REDOXS).
12. ERAS: clear fluids to 2 h, solids to 6 h pre-op, carbohydrate loading to cut insulin resistance, early post-op feeding and mobilisation.