IV fluids and electrolytes
IV fluids, electrolytes, diuretics and parenteral nutrition in surgery for FCPS
Surgical fluids for FCPS: resuscitation, maintenance, replacing losses, potassium, calcium and magnesium, how diuretics work, and parenteral nutrition. Each rule follows from body water physiology, so post-operative fluid questions can be worked out.
One of the most tested topics in past papers
The five Rs of fluid prescribing
Resuscitation, Routine maintenance, Replacement, Redistribution and Reassessment.
Resuscitation
- Assess heart rate, BP, capillary refill, urine output, lactate, mental state. Lactate rises in shock because tissue hypoxia forces anaerobic glycolysis, turning pyruvate into lactate.
- Give a balanced crystalloid (Hartmann's, Plasma-Lyte) 500 mL over under 15 minutes (250 mL in heart failure or the frail), reassess, repeat to about 2 L, then seek senior help.
- Hartmann's does not worsen lactic acidosis in a perfused patient: its lactate is taken up by the liver and converted to bicarbonate, so it is an alkalinising fluid. It contains a little potassium but is usually safe in mild hyperkalaemia.
- Large volumes of 0.9% saline (154 mmol/L chloride) cause hyperchloraemic normal-anion-gap acidosis: the chloride load lowers bicarbonate (strong ion effect). Saline remains the right fluid for vomiting with hypochloraemic alkalosis.
- Starch colloids (hydroxyethyl starch) increase acute kidney injury and death in sepsis and are no longer used; dextrose is never a resuscitation fluid.
- Haemorrhage: blood and products early, tranexamic acid, permissive hypotension in penetrating trauma (not head injury), stop the bleeding.
| ATLS class | Blood loss | Pulse | BP | Pulse pressure | Urine (mL/h) | Mental state |
|---|---|---|---|---|---|---|
| I | Under 15% | Under 100 | Normal | Normal | Over 30 | Slightly anxious |
| II | 15–30% | 100–120 | Normal | Narrowed | 20–30 | Anxious |
| III | 30–40% | 120–140 | Low | Narrowed | 5–15 | Confused |
| IV | Over 40% | Over 140 | Low | Narrowed | Negligible | Lethargic |
- Hypotension appears only in class III.
Maintenance
- Adults: 25–30 mL/kg/day water, about 1 mmol/kg/day sodium, potassium and chloride, 50–100 g glucose.
- Children (Holliday–Segar): 100 mL/kg/day for the first 10 kg, 50 mL/kg/day for the next 10 kg, 20 mL/kg/day beyond. A 22 kg child needs 1,000 + 500 + 40 = 1,540 mL/day. Use isotonic fluid (0.9% saline with 5% glucose).
- Why hypotonic fluids cause hyponatraemia: pain, nausea, stress and surgery trigger non-osmotic ADH release, so the kidney retains free water; children and post-operative patients have died from it. Headache and vomiting after surgery in a child: check the sodium.
- Fever raises insensible losses from skin and lungs (add about 10–15% per °C); burns and open abdomens add large evaporative losses.
Replacement and redistribution
| Loss | Replace with |
|---|---|
| Vomiting, NG aspirate (H⁺, Cl⁻, K⁺) | 0.9% saline with KCl (hypochloraemic hypokalaemic alkalosis) |
| Diarrhoea, ileostomy, small bowel fistula (Na⁺, K⁺, HCO₃⁻) | Hartmann's with potassium |
| Pancreatic or biliary fistula | Hartmann's, with bicarbonate if needed |
| Third-space loss (ileus, peritonitis, pancreatitis) | Balanced crystalloid (Ringer's lactate) |
| Burns | Parkland: 4 mL × kg × %TBSA Hartmann's in 24 hours, half in the first 8 hours from the burn; urine 0.5 mL/kg/h in adults, 1 mL/kg/h in children |
- Acute pancreatitis needs large early volumes because inflamed tissue and bowel leak fluid into the retroperitoneum and gut lumen; a rising haematocrit and urea mean under-resuscitation. Burn oedema comes from capillary leak with loss of albumin.
- Large-volume paracentesis (over 5 L, here 8 L) in cirrhosis: give IV albumin (about 8 g per litre removed) to prevent post-paracentesis circulatory dysfunction and hepatorenal AKI.
Post-operative oliguria
- Urine under 0.5 mL/kg/h. First check the catheter is not blocked (flush it). If it flushes and the patient is tachycardic with a low-normal BP, the cause is hypovolaemia (prerenal): give a fluid challenge. Never give furosemide to a dry, oliguric patient.
Electrolytes
- Potassium: IV no faster than 10 mmol/h peripherally (20 mmol/h or more centrally with ECG), concentration about 40 mmol/L peripherally, never as a bolus.
- Correct magnesium first: low magnesium lets potassium leak through renal ROMK channels, so hypokalaemia will not correct until magnesium is replaced. Both prolong ileus.
- Hypocalcaemia (after thyroid or parathyroid surgery, massive transfusion, pancreatitis): symptomatic, 10 mL of 10% calcium gluconate IV over 10 minutes with ECG monitoring, then infusion.
- Hyperkalaemia: calcium gluconate stabilises the myocardium; insulin (10 units) with 50 mL of 50% dextrose drives potassium into cells by stimulating the Na⁺/K⁺-ATPase (salbutamol does the same); then remove potassium (dialysis, binders). Monitor glucose for hours, especially in renal failure.
- Hyponatraemia: correct by no more than 8–10 mmol/L in 24 hours. Thiazide-induced hypovolaemic hyponatraemia (sodium 119, low osmolality, clinically dry): stop the thiazide and give 0.9% saline. Hypertonic saline only for severe symptoms. SIADH: fluid restriction.
- Chyle leak after neck dissection (usually left, thoracic duct): low-fat diet with medium-chain triglycerides, which are absorbed straight into the portal blood rather than lymph.
Diuretics: where they act
| Diuretic | Site and mechanism | Key effects and problems |
|---|---|---|
| Loop (furosemide) | Na⁺/K⁺/2Cl⁻ co-transporter in the thick ascending limb | Pulmonary oedema, overload, hypercalcaemia after rehydration; hypokalaemia; ototoxicity with high IV doses (same transporter in the inner ear), worse with gentamicin |
| Thiazide | Na⁺/Cl⁻ co-transporter in the distal tubule | Hyponatraemia, hypokalaemia, hyperuricaemia, hyperglycaemia, hypercalcaemia; reduce lithium clearance (lithium toxicity); rarely thrombocytopenia |
| Spironolactone | Aldosterone receptor antagonist in the collecting duct | First choice for cirrhotic ascites (secondary hyperaldosteronism with very low urine sodium); hyperkalaemia; gynaecomastia from anti-androgen effects (eplerenone avoids it) |
| Amiloride, triamterene | Block epithelial sodium channels (ENaC) in the collecting duct | Potassium-sparing; work in Liddle syndrome (spironolactone does not) |
| Mannitol | Osmotic; filtered, not reabsorbed | Raised ICP, acute glaucoma |
| Acetazolamide | Carbonic anhydrase in the proximal tubule | Glaucoma, altitude sickness, idiopathic intracranial hypertension; metabolic acidosis |
- Mannitol and the brain: it raises plasma osmolality, drawing water out of brain tissue across an intact blood–brain barrier (0.25–1 g/kg). Where the barrier is broken it can leak in and worsen local oedema.
- Mannitol in heart failure: before it causes diuresis it pulls water from cells into the blood, expanding circulating volume, which can precipitate pulmonary oedema; it is also contraindicated in anuria.
- Acute pulmonary oedema with high BP and hypoxia: sit up, oxygen, IV furosemide and a nitrate (venodilator), plus CPAP if needed.
- Potassium-sparing diuretics with ACE inhibitors, or in diabetics with type 4 renal tubular acidosis, cause dangerous hyperkalaemia.
Nutrition in surgical patients
- Screen everyone (MUST: BMI, weight loss, no intake over 5 days). Severely malnourished patients benefit from 7–14 days of feeding before major surgery.
- Enteral first: it keeps the gut mucosa intact, reduces bacterial translocation and infection, and is cheaper. Routes: oral supplements, nasogastric (check aspirate pH 5.5 or less, otherwise chest X-ray), nasojejunal, PEG, feeding jejunostomy.
- Parenteral nutrition when the gut cannot be used for over 5–7 days: prolonged ileus, high-output fistula, short bowel, obstruction, severe pancreatitis intolerant of enteral feeds. Give through a dedicated central line or PICC. About 25–30 kcal/kg/day and 1–1.5 g/kg protein.
| TPN complication | Explanation |
|---|---|
| Line sepsis | Commonest serious complication; Candida in blood culture means remove the line |
| Hyperglycaemia | Commonest metabolic complication; treat with insulin rather than stopping the feed |
| Excess CO₂ and failed weaning | Burning glucose has a respiratory quotient of 1.0 (fat 0.7), and excess carbohydrate drives lipogenesis (RQ above 1), so CO₂ output rises; balance calories with lipid |
| Refeeding syndrome | Insulin drives phosphate, potassium and magnesium into cells; low phosphate weakens muscles (including the diaphragm); start at 10 kcal/kg/day and give thiamine first |
| PN-associated cholestasis | Rising bilirubin and ALP after weeks; also steatosis, gallbladder sludge and stones (no enteral stimulus to empty) |
| Vitamin K deficiency | Weeks of antibiotics plus TPN without vitamin K: bruising with prolonged PT and normal platelets |
| Others | Hypoglycaemia if stopped suddenly, hypertriglyceridaemia, mucosal atrophy, trace element deficiency |
- High-output stoma (over 1.5–2 L/day): oral rehydration solution with sodium 90 mmol/L or more, restrict hypotonic drinks, loperamide, PPI.
Remember Give the fluid that matches what was lost, check the catheter before blaming the kidney, and never give a diuretic to a dry patient.
Exam trap Large volumes of saline cause hyperchloraemic acidosis; Hartmann's lactate becomes bicarbonate in the liver.
Exam trap Mannitol expands blood volume before it causes diuresis, so avoid it in heart failure.
How FCPS asks about this
- Loop diuretics: Na⁺/K⁺/2Cl⁻ co-transporter; ototoxic with high doses and gentamicin.
- Thiazides: reduce lithium excretion; cause hyponatraemia, treated with stopping the drug and giving saline.
- Spironolactone: gynaecomastia from anti-androgen action; first diuretic for cirrhotic ascites; amiloride blocks ENaC.
- Child of 22 kg: 1,540 mL/day by Holliday–Segar; hypotonic fluids risk hyponatraemia through non-osmotic ADH.
- Oliguria after surgery: check the catheter first, then treat hypovolaemia.
- Hyperkalaemia: insulin–dextrose moves potassium into cells via Na⁺/K⁺-ATPase; correct magnesium before potassium.
- TPN: hyperglycaemia commonest metabolic problem; cholestasis after weeks; excess glucose raises CO₂.
Test yourself on this topic
5 of the 65 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
On the first night after a bowel resection, a man's urine output is 15 mL/h for 2 hours. He has a catheter. What should be checked first?
Answer: Whether the catheter is blocked
Low urine output after surgery is common. The first, simplest step is to check the catheter: flush it or look for kinks, since a blocked catheter mimics oliguria. Then assess volume status (pulse, BP, capillary refill, lactate, fluid balance) because hypovolaemia is the commonest cause, and give a fluid challenge if dry. Review drugs (NSAIDs, ACE inhibitors) and check U&E.
Post-op oliguria
- First: check the catheter
- Commonest cause: hypovolaemia
- Target ≥ 0.5 mL/kg/h
- Review nephrotoxins
Remember Flush the catheter before the fluids.
Exam trap Do not give furosemide to a dry, oliguric patient.
Why the other options are wrong
- His serum magnesium level Not the first step.
- A CT scan of the abdomen Premature.
- His urine dipstick for glucose Not helpful here.
- His chest X-ray for pneumonia Not the first step.
Eight hours after a bowel resection, a patient's urine output has been 15 mL/h. The catheter flushes freely, pulse is 110/min and BP 100/65 mmHg. What is the most likely cause?
Answer: Hypovolaemia (prerenal)
Postoperative oliguria (under 0.5 mL/kg/h) is most often prerenal: fluid losses, bleeding, third-space shifts and stress hormones (ADH, aldosterone). After checking the catheter, the patient is assessed for hypovolaemia (tachycardia, low BP, cool peripheries) and given a fluid challenge, with review of losses and drugs. Prolonged hypoperfusion can lead to acute tubular necrosis.
Postoperative oliguria
- Check catheter first
- Commonest: prerenal (hypovolaemia)
- Signs: tachycardia, low BP
- Give fluid challenge, reassess
- Untreated: ATN
Remember Low urine after surgery: fill the tank first.
Exam trap Do not give diuretics to an oliguric hypovolaemic patient.
Why the other options are wrong
- Bladder outlet obstruction Catheter is patent.
- Acute tubular necrosis from the start Possible if hypoperfusion persists, not first.
- Glomerulonephritis Not likely here.
- Syndrome of inappropriate ADH alone Contributes, but tachycardia and low BP point to hypovolaemia.
Which intravenous fluid contains potassium, calcium and lactate in addition to sodium and chloride?
Answer: Hartmann's solution
Hartmann's (compound sodium lactate) per litre: Na⁺ 131, K⁺ 5, Ca²⁺ 2, Cl⁻ 111, lactate 29 mmol. Lactate is converted to bicarbonate by the liver. It is closer to plasma than 0.9% saline (Na⁺ 154, Cl⁻ 154 mmol/L), which in large volumes causes hyperchloraemic metabolic acidosis. Its calcium can clot citrated blood if given through the same line. 5% dextrose contains 50 g glucose per litre and no electrolytes.
Crystalloids
- 0.9% saline: Na 154, Cl 154 → hyperchloraemic acidosis in excess
- Hartmann's: Na 131, K 5, Ca 2, Cl 111, lactate 29
- 5% dextrose: 50 g/L glucose, no salt
Remember Hartmann's has a little of everything.
Why the other options are wrong
- 0.9% sodium chloride Only Na⁺ and Cl⁻ (154 each).
- 5% dextrose Glucose only.
- Dextrose-saline Na⁺, Cl⁻ and glucose only.
- Hydroxyethyl starch Colloid; no lactate.
A 30-year-old motorcyclist has a head injury with GCS 7, a dilated right pupil and CT showing diffuse cerebral oedema. Serum osmolality is 290 mOsm/kg. Intravenous 20% mannitol is given. How does it mainly lower intracranial pressure?
Answer: Osmotic shift of water out of the brain
Mannitol is filtered but not reabsorbed and does not cross an intact blood–brain barrier. It raises plasma osmolality, drawing water out of brain tissue into the circulation and lowering intracranial pressure within minutes. It then causes an osmotic diuresis, so fluid balance and serum osmolality must be watched. Acetazolamide, not mannitol, is the drug that reduces CSF production.
Mannitol in raised ICP
- Osmotic agent, stays in plasma
- Draws water out of brain
- Then osmotic diuresis
- Needs intact blood–brain barrier
Remember Mannitol pulls water out of the brain.
Exam trap Where the blood–brain barrier is broken, mannitol can leak into tissue and worsen local oedema.
Why the other options are wrong
- Reduced CSF production by choroid plexus This is mainly how acetazolamide acts.
- Direct constriction of cerebral arterioles Mannitol has no direct vasoconstrictor action.
- Lower cerebral metabolic oxygen demand Barbiturates and cooling lower metabolic demand.
- Block of Na⁺ uptake in the loop of Henle This is furosemide; mannitol acts osmotically in the proximal tubule and loop.
A 70 kg man has 30% total body surface area burns. Using the Parkland formula, how much crystalloid should he receive in the first 8 hours from the time of the burn?
Answer: 4,200 mL
Parkland formula: 4 mL × weight (kg) × %TBSA burned = total Hartmann's in the first 24 hours (here 4 × 70 × 30 = 8,400 mL). Half is given in the first 8 hours from the time of the burn (not the time of arrival) = 4,200 mL; the other half over the next 16 hours. Only partial- and full-thickness burns count (not simple erythema). The formula is a guide: titrate to urine output 0.5 mL/kg/h in adults (1 mL/kg/h in children). Formal resuscitation is indicated above 15% TBSA in adults and 10% in children.
Parkland formula
- 4 × kg × %TBSA = 24 h volume
- Half in first 8 h from time of burn
- Target urine 0.5 mL/kg/h (adult)
- Resuscitate if >15% adult, >10% child
Remember Four, weight, area; half by eight.
Exam trap The 8 hours start from the time of the burn, not from arrival in hospital.
Why the other options are wrong
- 8,400 mL That is the full 24-hour total.
- 2,100 mL Quarter of the total.
- 6,300 mL Three quarters of the total.
- 2,800 mL Wrong calculation.
Where this sits in the CPSP syllabus
- Surgery & Allied, Paper 2: Drugs in surgical practice, Diuretics, IV fluids and electrolyte replacement; TPN
Read next
Drug dose pages
Doses, cautions and practical tips for drugs in this chapter.