Metabolic response to trauma
Metabolic response to trauma, burns, IV fluids and electrolytes (FCPS Part 1)
Ebb and flow phases, stress hormones, IV fluids, burns and the Parkland formula, sodium, potassium and acid-base disorders for FCPS Part 1. Each disorder is explained from its mechanism so the treatment order makes sense.
Phases of the response to injury
| Phase | Timing | Features |
|---|---|---|
| Ebb | First 24–48 hours | Lower metabolic rate, oxygen use and temperature; hypovolaemia; high catecholamines; the task is resuscitation |
| Flow (catabolic) | Days to weeks | Raised metabolic rate and cardiac output, hyperglycaemia with insulin resistance, protein breakdown (negative nitrogen balance), lipolysis, fever |
| Anabolic | Weeks | Protein and fat stores rebuilt; positive nitrogen balance |
- Hormones raised: cortisol and ACTH, ADH (water retention, oliguria), aldosterone (sodium retained, potassium lost), catecholamines, glucagon, growth hormone. Insulin action falls, and T3 falls (sick euthyroid).
- IL-6 is the main driver of the acute phase response (CRP rises); IL-1 and TNF add fever.
- Skeletal muscle responds by proteolysis, releasing alanine and glutamine for hepatic gluconeogenesis and gut fuel, so patients waste muscle.
- Post-operative sodium and water retention means hypotonic fluids readily cause hyponatraemia.
- The same hormones (ADH, aldosterone, thirst) are maximal in severe dehydration. The kidney must still pass about 400–500 mL of urine a day to excrete the daily solute load, even at maximal concentration. Pre-renal dehydration raises urea out of proportion to creatinine (for example urea 70 mg/dL with creatinine 0.8 mg/dL).
- Enhanced recovery (regional anaesthesia, minimally invasive surgery, early feeding, warming, good analgesia) blunts the response.
Body fluids and maintenance
- Total body water is about 60% of weight (42 L in a 70 kg man): two-thirds intracellular (28 L), one-third extracellular (14 L), of which about three-quarters is interstitial and one-quarter plasma (3.5 L). Blood volume is about 70 mL/kg in adults.
- Daily maintenance: water 25–30 mL/kg; sodium and potassium about 1 mmol/kg each; 50–100 g glucose to prevent ketosis. Children: 4-2-1 mL/kg/h rule.
- Insensible loss is about 500–800 mL a day and rises about 10–15% for each degree of fever.
| Fluid | Na+ | K+ | Cl− | Other | Use |
|---|---|---|---|---|---|
| 0.9% saline | 154 | 0 | 154 | None | Resuscitation; large volumes cause hyperchloraemic metabolic acidosis |
| Hartmann's (Ringer's lactate) | 131 | 5 | 111 | Lactate 29, calcium 2 | Balanced resuscitation and burns; lactate becomes bicarbonate in the liver |
| 5% dextrose | 0 | 0 | 0 | Glucose 50 g/L | Free water; not for resuscitation |
| 0.18% saline with 4% dextrose | 30 | 0 | 30 | Glucose | Maintenance; hyponatraemia risk |
- Of 1 L of 0.9% saline about 250 mL stays in the plasma (it spreads through the extracellular fluid); of 1 L of 5% dextrose only about 70–100 mL stays, because water spreads through all compartments.
Burns
- Oedema in the first hours is caused mainly by increased capillary permeability: heat damage and histamine, prostaglandins and kinins open endothelial gaps, so protein-rich fluid leaks into tissue. Hypoproteinaemia adds to it later. Fluid loss is greatest in the first 8–12 hours.
| Depth | Look | Blanching | Pain | Healing |
|---|---|---|---|---|
| Superficial (epidermal) | Red, dry, no blisters | Yes | Painful | Days |
| Superficial partial thickness | Red, moist, blisters, upper dermis | Yes, brisk | Very painful | About 2 weeks, little scar |
| Deep partial thickness | Blotchy red and white, fixed staining | No | Reduced | Slow; often needs grafting |
| Full thickness | White, leathery or charred | No | Painless (nerve endings destroyed) | Grafting |
- Pain means nerves survive: a painless burn is deeper, not milder.
- Rule of nines (adult): head 9%, each arm 9%, front of trunk 18%, back of trunk 18%, each leg 18%, perineum 1%. Front of trunk plus one arm = 27%. The patient's palm with fingers is about 1%. Children have relatively larger heads.
- Parkland formula: 4 mL × weight (kg) × %TBSA of Hartmann's in 24 hours, half in the first 8 hours from the time of the burn (not arrival) and half in the next 16. A 70 kg man with 30% burns needs 8,400 mL, so 4,200 mL in the first 8 hours. Titrate to urine output of about 0.5 mL/kg/h in adults.
Crush injury and rhabdomyolysis
- Crushed muscle releases myoglobin, potassium, phosphate and CK. Myoglobin precipitates in acidic, concentrated urine and is toxic to tubules, causing acute kidney injury; dark urine with CK of tens of thousands confirms it.
- The most important kidney-protecting step is generous IV fluid early (ideally started before release), aiming for high urine output. Releasing the crush can cause sudden hyperkalaemic cardiac arrest, so monitor ECG and potassium.
Sodium
- Hyponatraemia (under 135 mmol/L): assess volume. Hypovolaemic (vomiting, diuretics, Addison disease): give saline. Euvolaemic (SIADH, hypothyroidism, post-operative ADH with hypotonic fluids): restrict fluid. Hypervolaemic (heart failure, cirrhosis, nephrotic): restrict ± diuretic. Seizures: hypertonic 3% saline bolus. Correct chronic hyponatraemia by no more than 8–10 mmol/L in 24 hours to avoid osmotic demyelination.
- Hypernatraemia: water deficit (elderly, diabetes insipidus); correct slowly to avoid cerebral oedema.
- Hyperglycaemia draws water out of cells and lowers sodium; hyperlipidaemia and paraproteins cause pseudohyponatraemia.
Potassium
- Hypokalaemia: vomiting, diarrhoea, fistulas, diuretics, insulin, beta-2 agonists, alkalosis, low magnesium. Weakness, ileus, arrhythmia; ECG flat T waves and U waves. Give IV KCl no faster than 10 mmol/h peripherally.
- Hyperkalaemia: AKI, ACE inhibitors, potassium-sparing diuretics, rhabdomyolysis, burns, tumour lysis, massive transfusion, acidosis, suxamethonium; haemolysed sample. ECG: tall tented T, flat P, wide QRS, sine wave.
- Treatment order: IV calcium gluconate first to stabilise the myocardium (it does not lower potassium); insulin with dextrose and nebulised salbutamol shift potassium into cells; then remove it (binders, dialysis). Refractory hyperkalaemia or fluid overload in AKI needs dialysis.
Calcium
- Hypercalcaemia of malignancy (PTHrP, bone metastases), for example 3.6 mmol/L (14.4 mg/dL): patients are dehydrated because calcium causes nephrogenic diabetes insipidus. First rehydrate with IV 0.9% saline; the most effective next step is an IV bisphosphonate (zoledronic acid or pamidronate), which inhibits osteoclasts and acts over 2–4 days. Calcitonin acts within hours but briefly.
Gastrointestinal losses and acid–base
| Fluid lost | Main ions lost | Result |
|---|---|---|
| Gastric (vomiting, outlet obstruction) | H+ and Cl−, K+ | Hypochloraemic hypokalaemic metabolic alkalosis |
| Pancreatic, small bowel, diarrhoea | HCO3− (pancreatic about 115 mmol/L), K+ | Normal anion gap metabolic acidosis |
- In gastric outlet obstruction the kidney first retains sodium. Once potassium is depleted, it exchanges sodium for H+ instead, producing paradoxical aciduria despite alkalosis. Treat with 0.9% saline plus KCl.
| Disorder | pH | Primary change | Surgical causes |
|---|---|---|---|
| Metabolic acidosis | Low | Low HCO3− | Shock (lactate), ischaemic bowel, DKA, AKI, fistulas, excess saline |
| Metabolic alkalosis | High | High HCO3− | Vomiting, NG aspiration, diuretics, massive transfusion |
| Respiratory acidosis | Low | High PaCO2 | Hypoventilation: head injury with slow breathing, opioids, pain splinting |
| Respiratory alkalosis | High | Low PaCO2 | Pain, anxiety, PE, early sepsis |
- Anion gap = Na+ − (Cl− + HCO3−), normally about 8–12. Raised: lactate, ketones, uraemia, salicylate, methanol. Normal: diarrhoea, fistulas, renal tubular acidosis, ureterosigmoidostomy, excess saline.
Access and nutrition
- In a shocked patient with no venous access, use intraosseous access (proximal tibia or humerus).
- Feed enterally where possible. Parenteral nutrition risks line sepsis, hyperglycaemia, refeeding hypophosphataemia and cholestasis.
Remember Calcium protects the heart, insulin moves potassium, only dialysis or binders remove it.
Exam trap Parkland's first half is given in the first 8 hours from the burn, not from arrival.
Exam trap A painless, white, leathery burn is full thickness; blistered, painful, blanching skin is superficial partial thickness.
How FCPS asks about this
- Oedema after major burns: increased capillary permeability.
- Parkland for 70 kg with 30% burns: 8,400 mL in 24 hours, 4,200 mL in the first 8 hours from the burn.
- Rule of nines for front of trunk and one arm: 27%.
- Fluid with potassium, calcium and lactate: Hartmann's solution.
- Crush injury with CK 60,000 and dark urine: generous IV fluids to protect the kidneys.
- Hypercalcaemia of malignancy after rehydration: IV bisphosphonate.
- Vomiting from pyloric obstruction: hypochloraemic hypokalaemic metabolic alkalosis with paradoxical aciduria; replace with saline and potassium.
Test yourself on this topic
5 of the 29 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
In Cuthbertson's description of the metabolic response to injury, which feature characterises the flow phase?
Answer: Hypermetabolism, negative N balance
Ebb phase (first 24–48 hours): hypovolaemia, reduced metabolic rate and oxygen consumption, low cardiac output, hypothermia—aimed at survival. Flow phase (days to weeks): a hypermetabolic catabolic state with increased oxygen consumption, raised cardiac output, fever, muscle protein breakdown (negative nitrogen balance), lipolysis and hyperglycaemia. Recovery is followed by an anabolic phase of protein synthesis and weight gain. Early feeding, pain control and minimally invasive surgery blunt the response.
Phases after injury
- Ebb (24–48 h): low metabolism, shock
- Flow: hypermetabolic, catabolic, negative N balance
- Anabolic: rebuilding
Remember Ebb is low tide, flow is high tide.
Why the other options are wrong
- Low metabolic rate, hypothermia Ebb phase.
- Reduced oxygen consumption Ebb phase.
- Anabolic weight gain Anabolic (recovery) phase.
- Fall in cardiac output Ebb phase; cardiac output rises in the flow phase.
An alcoholic with sodium 108 mmol/L for several days is corrected rapidly to 130 mmol/L within 24 hours. Two days later he develops quadriparesis and difficulty swallowing and speaking. What has happened?
Answer: Osmotic demyelination
In chronic hyponatraemia (over 48 hours) brain cells lose organic osmolytes to avoid swelling. If sodium is then raised quickly, water shifts out of brain cells and oligodendrocytes in the pons (and elsewhere) are damaged, causing demyelination days later: spastic quadriparesis, dysarthria, dysphagia, locked-in syndrome. Risk is higher in alcoholics, malnutrition and hypokalaemia. Limit correction to 8–10 mmol/L in 24 hours. Rapid fall in sodium, in contrast, causes cerebral oedema.
Sodium correction speed
- Chronic hyponatraemia: correct ≤ 8–10 mmol/L per 24 h
- Too fast → osmotic demyelination (pons)
- Too fast a fall → cerebral oedema
Remember Low to high, brain will fry.
Exam trap The damage appears 2–6 days after correction, so the link is easy to miss.
Why the other options are wrong
- Cerebral oedema from low sodium That occurs when sodium falls, not when it is corrected.
- Wernicke encephalopathy Confusion, ophthalmoplegia, ataxia; from thiamine deficiency.
- Brainstem vasospasm infarct Not the mechanism.
- Guillain–Barré syndrome Ascending weakness after infection, no link to sodium.
On the first day after a laparotomy, a patient has a temperature of 37.9 °C, is comfortable and has reduced breath sounds at both bases. What is the most likely cause?
Answer: Inflammatory response, atelectasis
A low-grade fever in the first 24–48 hours after surgery is usually the normal inflammatory response to tissue injury, often with basal atelectasis; treatment is early mobilisation, breathing exercises and analgesia. Later causes follow a rough timeline: chest infection (days 2–3), urinary infection (days 3–5), wound infection and anastomotic leak (days 5–7), DVT (days 7–10). A very sick patient on day 1 still needs full assessment.
Postoperative fever
- Day 1–2: inflammation, atelectasis
- Day 2–3: chest infection
- Day 3–5: urinary infection
- Day 5–7: wound, leak
- Day 7–10: DVT
Remember Timing of fever points to its cause.
Exam trap Day 1 fever with a very sick patient may be a missed injury or early necrotising infection.
Why the other options are wrong
- Anastomotic leak Usually days 5–7.
- Deep wound infection Usually days 5–7.
- Deep vein thrombosis Usually later.
- Catheter-related urinary infection Usually days 3–5.
Why is 5% dextrose a poor choice for restoring blood volume in haemorrhage?
Answer: It acts as free water
Fluid distribution follows its effective tonicity. Colloids stay mainly in the plasma. Isotonic saline or Hartmann's distributes through the extracellular fluid, so about a quarter remains in plasma (plasma is about a quarter of ECF). 5% dextrose is effectively free water once the glucose is metabolised; it spreads through total body water (two-thirds into cells), so only about 1/12 remains intravascular. Dextrose is used for maintenance water, not resuscitation, and large volumes cause hyponatraemia.
Where fluid goes
- Colloid: mostly plasma
- Saline / Hartmann's: ECF, ~1/4 stays in plasma
- 5% dextrose: total body water, ~1/12 in plasma
Remember Dextrose is water in disguise.
Why the other options are wrong
- It contains too much sodium It contains no sodium.
- It stays in vessels, overloading It leaves the vessels quickly.
- It causes hyperkalaemia It does not contain potassium.
- It is hypertonic, dehydrating cells It is isotonic in the bag but behaves as free water.
A burn on the forearm is white and leathery, does not blanch and is painless to pinprick. What is its depth?
Answer: Full thickness
Superficial (epidermal) burns are red and painful without blisters. Superficial partial-thickness burns are pink, blistered, moist and very painful with brisk capillary refill. Deep partial-thickness burns are blotchy red, with sluggish or absent blanching and reduced sensation. Full-thickness burns destroy the whole dermis with its nerve endings: white, waxy, leathery or charred, non-blanching and painless. They need excision and grafting.
Burn depth
- Epidermal: red, painful
- Partial thickness: blisters, painful
- Deep dermal: blotchy, less sensation
- Full thickness: white, leathery, painless
- Full thickness needs grafting
Remember No pain, no blanching: full thickness.
Exam trap Pain means nerves survive; a painless burn is deeper, not milder.
Why the other options are wrong
- Superficial (epidermal) Red and painful, no blisters.
- Superficial partial thickness Pink, blistered and very painful.
- Deep partial thickness with blisters Blotchy, some sensation remains.
- Superficial dermal Painful with blisters.
Where this sits in the CPSP syllabus
- Paper 1: General pathology, Metabolic response to trauma; fluid and electrolyte disorders
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