Surgery chapters
Fluid, electrolyte and acid-base balance, nutrition and fluid therapy in surgical patients
Daily water and electrolyte needs, what is in common IV fluids, how to replace gut losses, the key sodium, potassium and calcium disorders, a simple approach to acid-base problems, and how to assess and feed surgical patients by the enteral and parenteral routes.
- An adult needs about 30–40 mL/kg of water a day with roughly 1 mmol/kg each of sodium and potassium; Hartmann's is closest to plasma, while large volumes of 0.9% saline cause hyperchloraemic acidosis.
- Loss of gastric juice (vomiting, gastric outlet obstruction) gives hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria; treat with 0.9% saline plus potassium.
- If the gut works, use it: enteral feeding is safer and cheaper than TPN, whose main serious risk is catheter sepsis; restart feeding slowly in the starved to avoid refeeding syndrome (low phosphate).
On this page
Overview
Every surgical patient who cannot eat or drink needs a fluid plan, and many need a feeding plan. Errors are common and harmful: too much salt and water causes oedema, ileus and poor healing; too little causes kidney injury; the wrong fluid causes hyponatraemia, hypokalaemia or acidosis. The UHS TOS says one MCQ on fluids and electrolytes should appear in every paper.
Body water and daily balance
- Total body water is about 60% of lean body weight in men (about 42 L in a 70 kg man): intracellular 28 L, interstitial about 9 L, plasma about 4.6 L.
| Intake (mL/day) | Output (mL/day) | ||
|---|---|---|---|
| Drinks | 1200 | Urine | 1500 |
| Food | 1000 | Insensible (lungs about 400, skin) | 900 |
| Oxidation (metabolic water) | 300 | Faeces | 100 |
| Total | 2500 | Total | 2500 |
- Losses rise with fever, hot climate, hyperventilation and a tracheostomy (no humidification).
- Minimum urine output to clear the daily solute load is about 400 mL/day; postoperatively aim for at least 0.5 mL/kg/hour.
Daily maintenance needs (adult)
| Item | Requirement |
|---|---|
| Water | 30–40 mL/kg/day |
| Sodium | About 50–90 mmol/day (roughly 1 mmol/kg) |
| Potassium | About 50 mmol/day (roughly 1 mmol/kg) |
| Calcium | About 5 mmol/day |
| Magnesium | About 1 mmol/day |
30 mL/kg × 70 kg = 2100 mL
40 mL/kg × 70 kg = 2800 mL
So about 2–2.8 L per day, plus replacement of any extra losses
Intravenous fluids
| Fluid (mmol/L) | Na | K | Ca | Cl | Other |
|---|---|---|---|---|---|
| 0.9% saline | 154 | 0 | 0 | 154 | – |
| Hartmann's (compound sodium lactate) | 131 | 5 | 2 | 111 | Lactate 29 |
| Dextrose saline (4% / 0.18%) | 30 | 0 | 0 | 30 | Glucose 40 g/L |
| 5% dextrose | 0 | 0 | 0 | 0 | Glucose 50 g/L |
| Gelatin colloid (e.g. Gelofusine) | 154 | <1 | – | – | Gelatin 4% |
- 5% dextrose is effectively pure water once the glucose is used; it spreads into all compartments and is poor at restoring blood volume. Each litre has 50 g of glucose (about 200 kcal): enough to spare some protein, not to feed.
- Hartmann's: the lactate is turned into bicarbonate by the liver, so it does not worsen acidosis when the liver is perfused.
- Large volumes of 0.9% saline give a hyperchloraemic metabolic acidosis and salt overload.
- Crystalloid or colloid: no clear survival difference; albumin adds little.
Never give potassium as a rapid IV bolus. Add it to the bag (usually 20–40 mmol/L), mix well, and use saline rather than glucose as the carrier when treating hypokalaemia (glucose drives K+ into cells).
Replacing gastrointestinal losses
| Fluid (mmol/L) | Na | K | Cl | HCO3 |
|---|---|---|---|---|
| Stomach | 50 | 15 | 110 | – |
| Bile | 140 | 5 | 100 | 35 |
| Pancreas | 140 | 5 | 75 | 115 |
| Small bowel (ileum) | 140 | 5 | 100 | 30 |
Most bowel losses (fistulae, NG aspirates, ileostomy) are replaced with 0.9% saline plus potassium, volume for volume, on top of maintenance.
Gastric outlet obstruction and vomiting
Losing gastric juice removes H+ and Cl− (and some K+).
- Hypochloraemic metabolic alkalosis develops; urine at first contains bicarbonate with sodium.
- As dehydration worsens, the kidney (aldosterone) holds sodium and swaps it for K+ and H+.
- Result: hypokalaemia and paradoxically acidic urine despite blood alkalosis.
- Alkalosis lowers ionised calcium, so tetany may occur.
Treatment: IV 0.9% saline with potassium chloride; once chloride and volume are restored, the kidney corrects the alkalosis. Empty the stomach with a wide-bore tube.
Classic MCQ: an elderly man vomiting clear (non-bilious) fluid for days with epigastric swelling has metabolic alkalosis with hypokalaemia and hypochloraemia. The fluid of choice is normal saline with KCl.
Sodium disorders
Hyponatraemia (Na < 135 mmol/L)
- Commonest cause of acute hyponatraemia in hospital: postoperative, from hypotonic fluids (5% dextrose) given while ADH is high after surgery.
- Assess volume status:
- Low volume (vomiting, diarrhoea, fistula, diuretics): give 0.9% saline.
- Normal volume (SIADH): fluid restriction.
- High volume (heart, liver, kidney failure): restrict salt and water.
- Severe symptoms (fits, coma): critical care, hypertonic (3%) saline in small boluses.
- Correct chronic hyponatraemia slowly: no more than 8 mmol/L in the first 24 hours, to avoid osmotic demyelination (central pontine myelinolysis).
Hypernatraemia usually means water loss exceeds salt loss (fever, poor intake, diabetes insipidus); replace water slowly.
Potassium disorders
| Feature | Hypokalaemia | Hyperkalaemia |
|---|---|---|
| Surgical causes | Vomiting, NG suction, diarrhoea, fistulae, villous adenoma, diuretics, IV fluids lacking K+, insulin, alkalosis | Acute kidney injury, tissue damage (crush, burns, ischaemic limb reperfusion), haemolysis, massive transfusion, acidosis, suxamethonium, ACE inhibitors, K-sparing diuretics |
| Symptoms | Muscle weakness, paralytic ileus, hypotonia, hyporeflexia, arrhythmia | Weakness, then sudden arrhythmia or asystole |
| ECG | Flat or inverted T waves, prominent U waves, ST depression, long QT(U) | Tall peaked T waves, flat P, long PR, wide QRS, sine wave, VF |
| Treatment | Oral or IV KCl (in saline); correct magnesium too | See below |
Hypokalaemia that will not correct usually means low magnesium; check and replace it.
Emergency treatment of hyperkalaemia
- Protect the heart: IV 10 mL of 10% calcium gluconate (or chloride). It stabilises the membrane but does not lower K+.
- Shift K+ into cells: IV insulin 10 units with 50 mL of 50% glucose; monitor glucose. Nebulised salbutamol helps; bicarbonate only in severe acidosis.
- Remove K+ from the body: potassium binders, treat the cause, and dialysis if refractory or in renal failure.
- Stop all K+-containing fluids and drugs that raise K+.
Suxamethonium releases potassium from muscle (up to about 1 mmol/L) and can cause dangerous hyperkalaemia after burns, crush injury, denervation or prolonged immobility (from about day 2 onward), so it is avoided in these patients.
Calcium, magnesium and phosphate
- Hypocalcaemia: perioral tingling, carpopedal spasm, Chvostek and Trousseau signs, long QT. Surgical causes: massive transfusion (citrate binds calcium), after thyroid or parathyroid surgery, acute pancreatitis, alkalosis. Treat with IV calcium gluconate.
- Adjust total calcium for a low albumin: for every 1 g/L that albumin falls short of 40 g/L, add 0.02 mmol/L.
Total calcium 2.00 mmol/L, albumin 30 g/L
Corrected Ca = 2.00 + 0.02 × (40 − 30) = 2.00 + 0.20 = 2.20 mmol/L → normal
- Hypomagnesaemia: from diarrhoea, fistulae, diuretics, TPN, alcohol; causes resistant hypokalaemia and hypocalcaemia.
- Hypophosphataemia: typical of refeeding; causes muscle and respiratory weakness, poor cardiac contraction, confusion and fits.
Acid–base balance
Normal arterial ranges: HCO3− 22–26 mmol/L, PaCO2 4.8–6.1 kPa, pH 7.35–7.45.
Approach: (1) Is pH acidaemic or alkalaemic? (2) Does PaCO2 (respiratory) or HCO3− (metabolic) explain it? (3) Is there compensation? (4) In metabolic acidosis, calculate the anion gap.
| Disorder | Primary change | Surgical examples |
|---|---|---|
| Metabolic acidosis, high anion gap | HCO3− falls; unmeasured acid added | Lactic acidosis (shock, ischaemic bowel, sepsis), diabetic ketoacidosis, renal failure |
| Metabolic acidosis, normal anion gap (hyperchloraemic) | HCO3− lost or Cl− gained | Diarrhoea, pancreatic/small bowel fistula, ureterosigmoidostomy, excess 0.9% saline |
| Metabolic alkalosis | HCO3− rises | Vomiting, NG drainage, diuretics, hypokalaemia, mineralocorticoid excess (Cushing's, Conn's) |
| Respiratory acidosis | PaCO2 rises | Hypoventilation: opioids, pain after upper abdominal surgery, COPD, chest wall injury |
| Respiratory alkalosis | PaCO2 falls | Pain, anxiety, early sepsis, PE, hypoxia |
Na 140, K 4, Cl 100, HCO3 12 (mmol/L)
Anion gap = (Na + K) − (Cl + HCO3) = 144 − 112 = 32 → raised (e.g. lactic acidosis from ischaemic bowel)
Normal is about 12–16 mmol/L with this formula
High anion gap causes: GOLD MARK (glycols, oxoproline, L-lactate, D-lactate, methanol, aspirin, renal failure, ketoacidosis).
A low albumin lowers the anion gap and can hide a raised-gap acidosis.
Nutrition in surgical patients
After injury or sepsis, unlike simple starvation, ketosis is blunted and protein breakdown continues even when glucose is given, so energy needs rise (up to about 40 kcal/kg/day) instead of falling.
Assessment
- Unintentional weight loss of more than 10% in 6 months is the most useful simple sign of significant malnutrition.
- BMI < 18.5 = undernutrition; BMI < 15 carries high hospital mortality.
- Serum albumin is not a measure of nutrition in acute illness (it falls with inflammation and fluid shifts), though low albumin predicts a poor outcome.
- MUST (malnutrition universal screening tool) scores BMI, recent weight loss and the acute disease effect (little or no intake for over 5 days); a total of 2 or more is high risk.
- Preoperative feeding must run for at least 2 weeks to change outcome.
Daily requirements (stable adult)
| Nutrient | Amount |
|---|---|
| Energy | About 20–30 kcal/kg/day (often 1300–1800 kcal in bed-bound patients); more after major or complicated surgery |
| Nitrogen | 0.10–0.15 g/kg/day; 0.20–0.25 g/kg/day if hypermetabolic |
| Glucose | About 2 g/kg/day minimum; give energy as a mix of glucose and fat (fat 9 kcal/g) |
| Vitamin C | Rises to 60–80 mg/day after surgery (wound healing) |
1 g nitrogen is contained in 6.25 g protein
70 kg × 0.15 g/kg = 10.5 g nitrogen
10.5 × 6.25 ≈ 66 g protein per day
Overfeeding is the commonest cause of nutritional complications. Excess glucose causes hyperglycaemia, fatty liver and extra CO2 production, which can stop a ventilated patient weaning.
Enteral nutrition: first choice
Why: keeps the gut lining and immune barrier intact, fewer infections, cheaper and safer than TPN.
| Route | Use |
|---|---|
| Oral sip feeds | Patients who can swallow but eat too little |
| Nasogastric tube | Short term (weeks); most patients; check position before use |
| Nasojejunal tube | Gastric stasis, pancreatitis, high aspiration risk |
| Gastrostomy (PEG, radiological or surgical) | Long term (e.g. stroke, head and neck cancer) |
| Feeding jejunostomy | After major upper GI surgery or when the stomach cannot be used |
Complications: tube misplacement or blockage, aspiration, diarrhoea (commonest; slow the rate or dilute the feed, check for C. difficile and drugs), bloating, electrolyte and refeeding problems.
Parenteral nutrition (TPN)
Indications: gut not working or not accessible: short bowel syndrome, high-output enterocutaneous fistula, prolonged ileus or obstruction, severe intestinal failure.
Route: central vein (tunnelled line or PICC) because the mixture is hypertonic; short-term peripheral feeding is possible with lower-osmolarity bags. Use a dedicated lumen and strict asepsis.
| Complication group | Examples |
|---|---|
| Line-related | Catheter sepsis (commonest serious problem; Staphylococci, Candida → remove line), pneumothorax, air embolism, thrombosis, occlusion |
| Metabolic | Hyperglycaemia (commonest metabolic), refeeding syndrome, electrolyte imbalance, hyperchloraemic acidosis, hypertriglyceridaemia |
| Hepatobiliary | Fatty liver, cholestasis (rising bilirubin and ALP), gallbladder sludge and stones (no gut stimulus to contract) |
| Deficiencies | Essential fatty acids; trace elements (below) |
| Trace element deficiency in long-term TPN | Features |
|---|---|
| Zinc | Perioral and acral rash, hair loss, poor wound healing, diarrhoea |
| Copper | Microcytic anaemia, neutropenia, myelopathy like B12 deficiency |
| Chromium | Glucose intolerance |
| Selenium | Cardiomyopathy, muscle weakness |
Refeeding syndrome
When feeding restarts after starvation, insulin drives phosphate, potassium and magnesium into cells and thiamine is used up.
- At risk: severe malnutrition, very low BMI, little intake for many days, alcohol dependence, anorexia nervosa, prolonged fasting (e.g. gastric cancer).
- Results: hypophosphataemia, hypokalaemia, hypomagnesaemia, hypocalcaemia, fluid overload, arrhythmia, respiratory failure, confusion, fits, death.
- Prevention: start at a low calorie rate and build up slowly, give thiamine and vitamins before and during feeding, and check and replace phosphate, potassium and magnesium daily.
With less than about 150 cm of small bowel left, short bowel syndrome is likely; high jejunostomy losses are salt-rich, so restrict plain water and give an oral glucose–salt solution.
Products and protocols vary between Pakistani hospitals; follow the local nutrition team and current national guidance.
Expect: the daily water balance of a 70 kg adult, maintenance needs, composition of saline and Hartmann's, fluid choice for vomiting and peritonitis, the metabolic picture of pyloric obstruction, hypokalaemia ECG and treatment, hyperkalaemia emergency steps and suxamethonium, safe sodium correction, hypocalcaemia after massive transfusion, anion gap causes, the best sign of malnutrition, nitrogen requirements, enteral versus parenteral feeding, managing feed diarrhoea, TPN complications and trace element deficiencies, and refeeding syndrome.
Quick revision
- Water 30–40 mL/kg/day; Na and K about 1 mmol/kg/day; urine at least 0.5 mL/kg/h.
- Hartmann's has lactate (liver → bicarbonate); saline excess → hyperchloraemic acidosis.
- Vomiting/GOO: hypochloraemic hypokalaemic alkalosis, paradoxical aciduria → saline + KCl.
- Hypokalaemia: flat T, U waves; check Mg2+; K+ in saline not dextrose.
- Hyperkalaemia: calcium gluconate, insulin–glucose, salbutamol, then remove K+.
- Chronic hyponatraemia: ≤8 mmol/L rise in 24 h.
- Malnutrition: >10% weight loss in 6 months; albumin is not a nutrition marker.
- Enteral first; TPN for intestinal failure; line sepsis is its main danger.
- Refeeding: low phosphate; start slow, give thiamine.
Written by The House Job from standard references (Bailey & Love; Kumar and Clark's Clinical Medicine).
FAQ
Which IV fluid is best for a patient with prolonged vomiting from gastric outlet obstruction?
0.9% saline with added potassium chloride, which replaces the lost chloride, sodium, water and potassium and lets the kidney correct the alkalosis.
Why is calcium given first in severe hyperkalaemia?
It stabilises the heart muscle membrane within minutes and reduces the risk of arrhythmia, although it does not lower the potassium level; insulin with glucose then moves potassium into cells.
Why is serum albumin a poor measure of nutrition?
Its level falls quickly with inflammation, sepsis and fluid shifts, so it reflects illness severity more than nutritional state.
What should be done for diarrhoea in a patient on nasogastric feeding?
Slow the feed rate or dilute the feed, review drugs such as antibiotics and laxatives, and check stool for C. difficile before stopping enteral feeding.