30 Clinical Vignettes: Metabolic Response to Injury & Surgery

• A (Anabolic): This is the recovery/rebuilding phase that develops weeks later after the catabolic phase subsides.
• B (Hypermetabolic flow phase): This phase is characterised by increased cardiac output, raised body temperature, and increased BMR - the opposite of what is seen here.
• D (CARS): This is the anti-inflammatory counterbalance that occurs after the initial pro-inflammatory surge.
• E (SIRS): SIRS corresponds to the hypermetabolic flow phase following resuscitation, not this initial shock state.

• A (Aldosterone/renin): These are activated in the early ebb phase to conserve sodium and circulating volume, not to drive the hypermetabolic flow phase.
• B (Insulin/glucagon): Glucagon contributes to gluconeogenesis, but the primary drivers of this inflammatory phase are cytokines, not these hormones.
• D (GH/IGF-1): Growth hormone is released in response to injury but is not the primary driver of SIRS/flow phase.
• E (Vasopressin/ANP): ADH is released in the ebb phase to conserve water; ANP is a counter-regulatory hormone. Neither drives this hypermetabolic state.

• A (Absolute insulin deficiency): Insulin levels are actually elevated in the flow phase. Absolute deficiency (Type 1-like) does not apply here.
• B (Glycogenolysis from glucagon deficiency): Glucagon is elevated, not deficient. And glycogen stores are depleted within ~24 hours of fasting/injury.
• D (Dietary carbohydrate): Post-operative patients are typically fasting or have reduced oral intake; this is not the mechanism.
• E (Renal glucosuria): Renal glucosuria from tubular dysfunction is not the cause of stress hyperglycaemia.

• A (Harris-Benedict equation): This is the most commonly used predictive equation but is only an estimate and was not validated in morbidly obese patients. It can over- or underestimate needs.
• B (Fick method): Requires a pulmonary artery catheter and estimates cardiac output, not directly metabolic rate.
• D (Urinary nitrogen): Reflects protein catabolism but not total energy expenditure.
• E (Pre-albumin): A marker of nutritional status/acute phase response, not energy expenditure.

• A & B: 10-20 kcal/kg/day is likely to result in underfeeding and prolonged catabolism.
• D & E: 35-50 kcal/kg/day represents overfeeding, which can cause hepatic steatosis, increased lipogenesis, and increased CO2 production requiring greater ventilatory effort.

• A (0.8 g/kg): This is the RDA for healthy adults - wholly insufficient in critical illness.
• B (1.2 g/kg actual weight): This would far exceed appropriate limits when applied to a morbidly obese patient using actual weight.
• C (2.0 g/kg IBW): This is recommended for Class I-II obesity (BMI 30-40), not Class III.
• E (3.0 g/kg IBW): This exceeds current recommendations and is not supported by guidelines.

• Glucose (carbohydrate): RQ = 1.0
• Protein: RQ = 0.8
• Fat (and alcohol): RQ = 0.7

• A (Protein): RQ for protein oxidation is 0.8.
• B (Glucose): RQ for pure carbohydrate oxidation is 1.0 (equal volumes of CO2 produced and O2 consumed).
• C (Amino acids): Covered under protein - RQ ~0.8.
• E (Lactate): Lactate is an intermediate metabolite; it is converted to glucose via the Cori cycle, not directly associated with an RQ of 0.7.

• A & C: The neuroendocrine response and cytokine release are reduced but not eliminated even with laparoscopic surgery.
• D: The ebb phase is triggered by the severity of the injury/shock state, not by the access approach per se.
• E: Cortisol secretion (via HPA axis activation) is attenuated but not specifically blocked by the laparoscopic approach.

• A (Dietary intake): Post-trauma patients are often not eating; even if they were, dietary excess does not cause urinary nitrogen excretion to double.
• B (Hepatic synthesis): While the liver does synthesise acute phase proteins, this is net protein synthesis, not a cause of nitrogen loss.
• D (Renal synthesis): The kidney is not a significant site of protein synthesis in trauma.
• E (Anabolic pathways): Anabolic pathways are suppressed in the catabolic phase; they do not cause increased nitrogen excretion.

• A (Krebs/TCA cycle): This is the intracellular cycle for aerobic energy production from acetyl-CoA.
• B (Pentose phosphate pathway): This pathway generates NADPH and ribose-5-phosphate for nucleotide synthesis and antioxidant defence.
• D (Beta-oxidation): This is the mitochondrial breakdown of fatty acids to acetyl-CoA.
• E (Ornithine cycle): The urea cycle - converts ammonia to urea for excretion; not involved in glucose regeneration.

• A (ATN): Would cause hyperkalaemia and elevated creatinine/urea, not hypokalaemia/hypophosphataemia.
• B (Type 2 DM): Could cause hyperglycaemia but not the electrolyte picture of refeeding syndrome.
• D (Adrenal insufficiency): Causes hyponatraemia and hyperkalaemia, not this pattern.
• E (Primary hyperparathyroidism): Causes hypercalcaemia and hypophosphataemia but not in the context of refeeding and not with hypomagnesaemia/hypokalaemia.

• A & B: 5-15% represents a very modest elevation, not typical for major trauma.
• D: Energy expenditure is clearly elevated above baseline in major trauma; it never equals baseline in the flow phase.
• E: While burns patients may approach 50% above predicted, it is not accurate to state that all trauma patients reach this level. The 15-25% figure applies to most non-burns trauma patients.

• A (Leucine/valine): These are branched-chain amino acids - they are degraded in muscle to provide carbon skeletons for alanine and glutamine synthesis, but are not themselves the primary exported amino acids.
• C, D, E: These are essential amino acids that can be depleted, but they are not the primary amino acids exported from muscle during the stress response.

• A (Insulin/leptin): Insulin levels actually fall during acute shock (despite hyperglycaemia) or remain inappropriately low.
• B (IGF-1/GH): GH is released but its anabolic downstream mediator IGF-1 is reduced during acute stress. Neither predominates in the ebb phase.
• D (Oestrogen/progesterone): Sex hormones play no primary role in the acute metabolic response to injury.
• E (Glucagon/amylin): Glucagon is elevated and promotes gluconeogenesis, but it is not the primary volume-conserving hormone, and amylin is not key here.

• A: Maximising inflammation would increase complications, not improve outcomes.
• B: Prolonging the ebb phase (shock state) is harmful and potentially lethal.
• D: Increasing catecholamines increases cardiac work and metabolic rate unnecessarily.
• E: Complete pharmacological blockade of all hormonal responses would impair wound healing and immune defence.

• A (5%): This would underestimate MODS severity significantly.
• B (10%): Still too low.
• D (50%) & E (75%): These figures are too high for MODS mortality in contemporary trauma systems with modern critical care. Historical mortality may have been higher, but modern care has improved outcomes.

• A (Gluconeogenesis from amino acids): This becomes the predominant substrate after glycogen depletion (>24-48 hours) - not in the first 6 hours.
• C (Ketones): The brain switches to ketoacids only after prolonged fasting (>48 hours).
• D (Fat oxidation): Fat becomes a primary substrate after ~48 hours of fasting.
• E (Muscle proteolysis): This becomes significant in prolonged starvation as the body tries to supply gluconeogenic precursors, not in the first 6 hours.

• A: Sepsis has profound ongoing effects - it does not merely act as a primary trigger.
• C: Sepsis amplifies catabolism; it does not inhibit it.
• D: Sepsis prevents anabolic recovery, not triggers it.
• E: Sepsis dramatically increases proinflammatory cytokines.

• A (Peripheral IV): No effect on IC accuracy.
• B (Urinary catheter): No effect on IC.
• D (NG tube): No effect on IC.
• E (Central line): No effect on IC accuracy.

• A (33%): REE forms a much larger proportion than one-third of total energy expenditure.
• B (50%): An underestimate - REE forms ~67% of total energy expenditure.
• D (75%): An overestimate; activity and thermogenesis account for 25-30%.
• E (90%): This would leave virtually no room for activity or thermogenesis, which is incorrect.

• A (10-14 kcal/kg ABW): This range overlaps but the specific guideline states 11-14, not 10-14.
• C (25-30 kcal/kg actual weight): This is the target for normal/overweight patients, not for obese patients; applying this to an obese patient's actual weight would cause significant overfeeding.
• D (35-40 kcal/kg): Excessive; would cause overfeeding complications.
• E (20-25 kcal/kg IBW): This would be appropriate for normal/overweight patients using IBW, but not the recommended formula for this patient category.

• A: The ebb phase is characterised by decreased cardiac output and reduced BMR - the opposite of maximising cardiac output.
• B: Inflammatory wound healing is a function of the flow phase, not the ebb phase.
• D: Increased nitrogen excretion is a feature of the flow phase (muscle catabolism), not the ebb phase.
• E: Leucocyte migration is part of the inflammatory/flow phase response.

• A (0.8 g/kg): The RDA is for healthy adults; it is grossly insufficient for critically ill patients on CRRT.
• B (1.2-1.5 g/kg): This is the standard critical illness range but does not account for the additional amino acid losses in CRRT.
• C (withhold protein): This is explicitly wrong - protein should not be withheld in dialysis patients.
• E (0.5 g/kg): This would cause severe negative nitrogen balance and worsen outcomes.

• A: This would be the expected physiological response to hyperglycaemia - but it does not occur in severe shock.
• B: Insulin levels are actively suppressed.
• D: No evidence for pulsatile matching; the fundamental point is suppression despite hyperglycaemia.
• E: Alpha cells secrete glucagon, not insulin; this is anatomically incorrect.

• A (Humidity): While humidity affects evaporative heat loss in burns, it is not the primary ICU-based limiter cited.
• C (Enteral vs. parenteral): Route of feeding does not suppress the hypermetabolic response.
• D (Early ambulation): Early mobilisation would actually increase energy expenditure, not limit it.
• E (Antibiotics): Antibiotics treat infection and may reduce sepsis-driven catabolism indirectly, but are not the primary ICU intervention that limits hypermetabolism.

• B (0.80): This would be VCO2/VO2 = 200/250. The actual calculation gives 0.70, not 0.80.
• C (1.00): This would require VO2 = VCO2.
• D (1.40): This would indicate gross overfeeding with active lipogenesis; requires VCO2 > VO2.
• E (0.65): This would suggest extreme starvation/severe ketosis; the calculated value is 0.70, not 0.65.

• Ebb phase: Reduced cardiac output, hypothermia, reduced BMR, lactic acidosis
• Flow phase: Increased cardiac output, raised body temperature, increased BMR, leukocytosis, increased oxygen consumption, increased gluconeogenesis, tissue oedema

• A: This has the features reversed - fever and increased CO are features of the flow phase, not ebb.
• C: Gluconeogenesis is increased in the flow phase (to supply glucose to healing tissues and immune cells), not decreased.
• D: This is partially correct (ebb is catabolic, flow is hypermetabolic) but the flow phase is NOT the anabolic recovery phase - it is still highly catabolic, just with increased metabolism. The true anabolic phase comes later.
• E: This again has features reversed - the flow phase has increased oxygen consumption.

• A (0.1-0.5%): Too low; this turnover rate would mean muscle half-life of years, which does not reflect actual physiology.
• C (5-10%): Too high; this would mean complete muscle turnover in 10-20 days.
• D & E: These are far too high and would represent catastrophic baseline protein turnover.

• A (Primary triggers): The initial injury/tissue damage is the primary trigger; haemorrhage and hypothermia are secondary compounding factors.
• B (Genetic modulators): Genetic variation does influence the metabolic response, but haemorrhage and hypothermia are not genetic.
• D (Anti-inflammatory mediators): These are pro-catabolic, not anti-inflammatory.
• E (Protective mechanisms): These factors worsen outcomes; they are not protective.

• A (0.5 g/kg): This is well below even the standard RDA and would lead to progressive negative nitrogen balance.
• B (0.8 g/kg): This is the RDA for healthy, non-stressed adults and is insufficient in critical illness.
• D (3.0-4.0 g/kg): Excessive; this exceeds even the most aggressive recommended targets and could cause metabolic stress.
• E (withhold protein): There is no evidence to withhold protein pending albumin normalisation. Albumin is an acute phase reactant and will not normalise until the inflammatory response resolves, irrespective of protein provision.