FCPS Part 1 Pathology and microbiology

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

PhaseTimingFeatures
EbbFirst 24–48 hoursLower metabolic rate, oxygen use and temperature; hypovolaemia; high catecholamines; the task is resuscitation
Flow (catabolic)Days to weeksRaised metabolic rate and cardiac output, hyperglycaemia with insulin resistance, protein breakdown (negative nitrogen balance), lipolysis, fever
AnabolicWeeksProtein 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.
FluidNa+K+Cl−OtherUse
0.9% saline1540154NoneResuscitation; large volumes cause hyperchloraemic metabolic acidosis
Hartmann's (Ringer's lactate)1315111Lactate 29, calcium 2Balanced resuscitation and burns; lactate becomes bicarbonate in the liver
5% dextrose000Glucose 50 g/LFree water; not for resuscitation
0.18% saline with 4% dextrose30030GlucoseMaintenance; 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.
DepthLookBlanchingPainHealing
Superficial (epidermal)Red, dry, no blistersYesPainfulDays
Superficial partial thicknessRed, moist, blisters, upper dermisYes, briskVery painfulAbout 2 weeks, little scar
Deep partial thicknessBlotchy red and white, fixed stainingNoReducedSlow; often needs grafting
Full thicknessWhite, leathery or charredNoPainless (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 lostMain ions lostResult
Gastric (vomiting, outlet obstruction)H+ and Cl−, K+Hypochloraemic hypokalaemic metabolic alkalosis
Pancreatic, small bowel, diarrhoeaHCO3− (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.
DisorderpHPrimary changeSurgical causes
Metabolic acidosisLowLow HCO3−Shock (lactate), ischaemic bowel, DKA, AKI, fistulas, excess saline
Metabolic alkalosisHighHigh HCO3−Vomiting, NG aspiration, diuretics, massive transfusion
Respiratory acidosisLowHigh PaCO2Hypoventilation: head injury with slow breathing, opioids, pain splinting
Respiratory alkalosisHighLow PaCO2Pain, 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.

Question 1Medium

In Cuthbertson's description of the metabolic response to injury, which feature characterises the flow phase?

Question 2Medium

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?

Question 3Medium

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?

Question 4Medium

Why is 5% dextrose a poor choice for restoring blood volume in haemorrhage?

Question 5Easy

A burn on the forearm is white and leathery, does not blanch and is painless to pinprick. What is its depth?

Practise all 29 questions on this topic

Where this sits in the CPSP syllabus

  • Paper 1: General pathology, Metabolic response to trauma; fluid and electrolyte disorders

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