4. Fluid Balance and Electrolytes
Fluid Balance and Electrolytes
Sri Lankan Surgery MD Part One — exam-directed master note
This topic commonly appears through:
Perioperative fluid prescriptions.
Postoperative oliguria.
Vomiting, diarrhoea, intestinal obstruction and fistulae.
Sodium and potassium interpretation.
ECG changes.
Emergency electrolyte correction.
Burns, sepsis, trauma and renal failure.
Data interpretation and OSCE prescribing stations.
The central principle is:
Do not treat a fluid chart or electrolyte value in isolation. Treat the patient, the physiological disturbance and its cause.
1. Essential physiology
Body-fluid compartments
In a typical non-obese adult:
Total body water: approximately 60% of body weight in a younger man and 50–55% in a woman.
It is lower in older people and obesity.
Intracellular fluid: approximately two-thirds of total body water.
Extracellular fluid: approximately one-third.
Extracellular fluid is divided into:
Interstitial fluid: approximately three-quarters.
Plasma: approximately one-quarter.
Therefore, in a 70 kg young man:
Total body water ≈ 42 L.
Intracellular water ≈ 28 L.
Extracellular water ≈ 14 L.
Plasma volume ≈ 3–3.5 L.
Major ions
| Compartment | Main cation | Main anions |
|---|---|---|
| Extracellular | Sodium | Chloride, bicarbonate |
| Intracellular | Potassium, magnesium | Phosphate, proteins |
Important concept
Serum sodium is mainly a marker of water balance—not simply total body sodium.
A hyponatraemic patient may have:
Low total body sodium: vomiting.
Normal total body sodium: SIADH.
Increased total body sodium: heart failure or cirrhosis.
Similarly, oedema does not prove adequate intravascular volume. A patient with cirrhosis may be oedematous but have reduced effective arterial circulating volume.
2. Movement of fluid between compartments
Osmosis
Water moves across cell membranes toward the compartment with the higher effective osmolar concentration.
Important effective osmoles include:
Sodium and its accompanying anions.
Glucose when markedly elevated.
Mannitol.
Urea contributes to measured osmolality but crosses cell membranes relatively freely, so it contributes less to effective tonicity.
Starling forces
Fluid movement across capillaries depends on:
Capillary hydrostatic pressure.
Interstitial hydrostatic pressure.
Plasma oncotic pressure.
Interstitial oncotic pressure.
Capillary permeability.
Lymphatic drainage.
In sepsis, burns and major inflammation, increased endothelial permeability causes fluid to leave the vascular space and produce tissue oedema.
Distribution of administered fluids
One litre of isotonic crystalloid
It mainly remains in the extracellular compartment:
Approximately 750 mL interstitial.
Approximately 250 mL intravascular, although distribution is dynamic and altered in illness.
One litre of 5% dextrose
After glucose metabolism, it behaves approximately as free water:
About two-thirds enters cells.
About one-third remains extracellular.
Only a small amount remains intravascular.
Therefore:
5% dextrose is not a resuscitation fluid.
3. The five questions before prescribing IV fluid
Use NICE’s 5 Rs:
Resuscitation
Routine maintenance
Replacement
Redistribution
Reassessment
NICE recommends 500 mL boluses of a crystalloid containing 130–154 mmol/L sodium over less than 15 minutes when adult fluid resuscitation is required, followed by reassessment. Routine maintenance is different from resuscitation and should not be prescribed using the same fluids or volumes. (NICE)
A useful bedside refinement is:
Need – Responsiveness – Tolerance
Need: Does this patient have tissue hypoperfusion due to volume deficit?
Responsiveness: Will stroke volume increase after fluid?
Tolerance: Can the heart, lungs, kidneys and tissues tolerate the additional fluid?
A patient may be fluid-responsive but already fluid-overloaded. Fluid responsiveness alone is not an indication to keep giving fluid.
4. Clinical assessment of fluid status
History
Ask about:
Oral intake and fasting.
Thirst.
Vomiting and nasogastric losses.
Diarrhoea or high-output stoma.
Urine output.
Fever and sweating.
Bleeding.
Drain, fistula and wound losses.
Diuretics, ACE inhibitors, ARBs and NSAIDs.
Heart, renal and liver disease.
Recent contrast, sepsis or major surgery.
Weight change.
Examination
Assess:
Mental state.
Heart rate and pulse volume.
Blood pressure and postural change.
Capillary refill.
Peripheral temperature.
Mucous membranes.
Jugular venous pressure.
Peripheral and sacral oedema.
Lung crepitations.
Respiratory rate and oxygen requirement.
Daily weight.
Signs of ascites or pleural effusions.
Shock indicators
Hypotension.
Tachycardia.
Cool peripheries.
Prolonged capillary refill.
Altered consciousness.
Oliguria.
Elevated lactate.
Metabolic acidosis.
No single sign is completely reliable.
Investigations
Full blood count.
Sodium, potassium, chloride, bicarbonate.
Urea and creatinine.
Magnesium, calcium and phosphate.
Glucose.
Lactate and blood gas.
Serum and urine osmolality when dysnatraemia is present.
Urine sodium when appropriate.
ECG.
Chest radiograph or lung ultrasound if overload is suspected.
Monitoring
Record:
Hourly urine output when acutely ill.
All oral, enteral and IV input.
Urine, drains, stools, stoma and nasogastric output.
Cumulative balance.
Daily weight.
Electrolyte trends—not isolated measurements.
Important trap
A positive balance of 3 L does not guarantee the patient has retained exactly 3 L because charts often omit:
Oral fluids.
Drug diluents.
Flushes.
Insensible losses.
Unmeasured stool and wound losses.
Daily weight often provides a better estimate; approximately 1 kg acute weight change represents about 1 L water change.
5. Oliguria
A commonly used threshold is:
Urine output below 0.5 mL/kg/hour.
KDIGO includes urine output below 0.5 mL/kg/hour for six hours as one criterion for acute kidney injury.
Causes of postoperative oliguria
Pre-renal or haemodynamic
Hypovolaemia.
Haemorrhage.
Sepsis and vasodilation.
Low cardiac output.
Excessive PEEP.
Abdominal compartment syndrome.
Renal
Acute tubular injury.
Nephrotoxic drugs.
Glomerulonephritis.
Interstitial nephritis.
Pigment nephropathy.
Vascular causes.
Post-renal
Blocked or kinked catheter.
Catheter malposition.
Ureteric obstruction.
Bladder outlet obstruction.
Physiological postoperative response
Pain, nausea, opioids and surgical stress increase ADH and sympathetic activity. Transient oliguria may occur despite adequate circulating volume.
Approach
Check the catheter and bladder.
Review haemodynamics and recent losses.
Examine for hypovolaemia and overload.
Check creatinine, potassium, acid–base status and lactate.
Review nephrotoxins.
Use a fluid challenge only when a volume deficit is plausible.
Reassess immediately after any intervention.
Do not repeatedly give fluid solely because urine output is low.
Diuretics do not treat intrinsic AKI. KDIGO recommends against using diuretics to prevent AKI and suggests using them in AKI only for management of volume overload. (KDIGO)
6. Types of IV fluid
Approximate compositions vary slightly by manufacturer.
| Fluid | Na | Cl | K | Other relevant contents |
|---|---|---|---|---|
| 0.9% saline | 154 | 154 | 0 | No buffer |
| Hartmann’s/lactated Ringer’s | 131 | 111 | 5 | Ca 2, lactate 29 |
| Plasma-Lyte type solution | 140 | 98 | 5 | Mg, acetate and gluconate buffers |
| 5% dextrose | 0 | 0 | 0 | 50 g glucose/L |
| 0.45% saline | 77 | 77 | 0 | Hypotonic |
| 3% saline | 513 | 513 | 0 | Hypertonic |
Values are in mmol/L except glucose.
Balanced crystalloids
Examples:
Hartmann’s.
Lactated Ringer’s.
Plasma-Lyte.
Advantages:
Chloride closer to plasma.
Lower risk of hyperchloraemic metabolic acidosis during large-volume administration.
Often appropriate for general resuscitation and replacement.
Hartmann’s lactate trap
The lactate is sodium lactate, which is metabolised mainly to bicarbonate. It is not the same as infusing lactic acid and does not automatically worsen lactic acidosis.
Potassium trap
Hartmann’s contains approximately 4–5 mmol/L potassium. This small concentration is not by itself an absolute contraindication in every patient with mild hyperkalaemia; the total clinical situation and local protocol matter.
0.9% saline
Useful particularly for:
Hypovolaemic hyponatraemia.
Chloride-responsive metabolic alkalosis.
Significant gastric losses.
Some neurological situations.
Situations where local compatibility requirements favour saline.
Problems with large volumes:
Hyperchloraemia.
Non-anion-gap metabolic acidosis.
Sodium and water overload.
NICE advises daily chloride monitoring when patients receive fluids containing more than 120 mmol/L chloride, such as 0.9% saline, and reassessment if hyperchloraemia or acidaemia develops. (NICE)
Dextrose solutions
5% dextrose is useful for:
Providing free water.
Preventing starvation ketosis as part of maintenance.
Hypernatraemia after circulation is stabilised.
Preventing hypoglycaemia with insulin therapy.
It is unsuitable for:
Shock.
Major haemorrhage.
Raised intracranial pressure.
Initial intravascular resuscitation.
Colloids
Albumin
May have selected indications but is not routinely required for uncomplicated perioperative fluid replacement.
Synthetic starch
Should not be used for routine resuscitation because of safety concerns. NICE specifically recommends against tetrastarch. (NICE)
Blood products
In haemorrhagic shock, the principal lost fluid is blood. Definitive management includes:
Haemorrhage control.
Red cells.
Plasma, platelets and fibrinogen according to the massive haemorrhage protocol.
Prevention of hypothermia, hypocalcaemia and coagulopathy.
Crystalloid cannot replace oxygen-carrying capacity or clotting factors.
7. Fluid resuscitation
General adult approach
Treat airway and breathing.
Stop haemorrhage or other ongoing losses.
Obtain IV or intraosseous access.
Give an appropriate crystalloid bolus.
Reassess:
Blood pressure.
Pulse.
Capillary refill.
Mental state.
Lactate.
Urine output.
Lung signs.
Dynamic stroke-volume response where available.
Repeat only when indicated.
Start vasopressors when vasodilatory shock persists despite an appropriate fluid strategy.
For a frail patient, heart failure or renal impairment, a smaller 250 mL challenge with immediate reassessment may be safer than automatic repeated 500 mL boluses.
Signs the fluid is helping
Improved mentation.
Improved blood pressure and pulse pressure.
Warmer peripheries.
Improved capillary refill.
Reduced lactate over time.
Increased stroke volume.
Appropriate improvement in urine output.
Signs of intolerance or overload
Increasing oxygen requirement.
Crepitations or B-lines.
Raised JVP.
New peripheral or sacral oedema.
Ascites.
Increasing body weight.
Worsening gas exchange.
Abdominal compartment pressure.
Dilutional anaemia or hypoalbuminaemia.
8. Routine maintenance
For adults requiring maintenance alone, NICE initially recommends:
Water: 25–30 mL/kg/day.
Sodium: approximately 1 mmol/kg/day.
Potassium: approximately 1 mmol/kg/day.
Chloride: approximately 1 mmol/kg/day.
Glucose: approximately 50–100 g/day to reduce starvation ketosis.
Consider 20–25 mL/kg/day in older or frail patients, cardiac failure, renal impairment or risk of refeeding syndrome. Use ideal body weight in obesity. (NICE)
Example: 70 kg adult
Approximate initial daily requirements:
Water: 1.75–2.1 L.
Sodium: approximately 70 mmol.
Potassium: approximately 70 mmol.
Chloride: approximately 70 mmol.
Glucose: 50–100 g.
This is only the starting maintenance calculation.
Then modify for:
Oral and enteral intake.
Drug infusions.
Fever.
Ongoing losses.
Renal function.
Heart failure.
Existing sodium or potassium disorder.
Postoperative ADH-driven water retention.
Maintenance traps
Three litres of 0.9% saline is not physiological maintenance.
Maintenance does not replace a pre-existing deficit.
Replacement fluid must be added separately.
Stop IV maintenance once the patient can drink or receive sufficient enteral fluid.
Potassium should be given in premixed solutions according to local policy, not manually injected into a fluid bag. (NICE)
9. Replacement of abnormal losses
Replace:
The measured volume.
With fluid approximating the electrolyte composition of the loss.
While correcting any established deficit.
Common surgical patterns
| Loss | Expected disturbance | Typical replacement principle |
|---|---|---|
| Vomiting/NG aspiration | Chloride, hydrogen and potassium loss; alkalosis | 0.9% saline plus potassium when safe |
| Diarrhoea | Water, sodium, potassium and bicarbonate loss; acidosis | Balanced/isotonic fluid plus potassium |
| Ileostomy | Sodium-rich water loss, magnesium depletion | Sodium-containing fluid/ORS; monitor Mg |
| Pancreatic or biliary fistula | Sodium and bicarbonate loss | Balanced/isotonic replacement; monitor bicarbonate |
| Sweating/burns | Hypotonic salt and water loss | Balanced crystalloid guided by physiology |
| Haemorrhage | Whole blood loss | Haemorrhage control and blood components |
| Polyuria/DI | Free-water loss | Free water plus treatment of cause |
Gastric loss pattern
The classic combination is:
Hypochloraemic, hypokalaemic metabolic alkalosis.
Mechanisms include:
Loss of hydrochloric acid.
Volume contraction.
Secondary aldosterone activation.
Increased renal potassium and hydrogen loss.
Treatment usually requires:
Chloride replacement.
Volume restoration.
Potassium replacement.
Treatment of the obstruction or vomiting.
High-output stoma
Plain water may worsen sodium depletion because intestinal fluid has a relatively high sodium concentration. Management often requires:
Measuring output.
Limiting excessive hypotonic drinks.
Oral glucose-saline solution with adequate sodium.
Antimotility or antisecretory treatment where appropriate.
Monitoring sodium, magnesium and renal function.
10. Postoperative fluid physiology
After major surgery:
ADH rises.
Aldosterone and sympathetic activity rise.
Sodium and water excretion may fall.
Capillary permeability may increase.
Administered fluid may move into the interstitium.
Oliguria may occur without true hypovolaemia.
Therefore, avoid the outdated habit of automatically prescribing extra litres for an assumed “third-space loss.”
Modern principles are:
Avoid unnecessary prolonged fasting.
Use oral or enteral fluid early.
Replace demonstrated losses.
Avoid both hypovolaemia and salt/water overload.
Reassess daily and stop IV fluids promptly.
11. Sodium disorders
Hyponatraemia
Defined as sodium below approximately 135 mmol/L.
First question: is it truly hypotonic?
Hypotonic hyponatraemia
This is true water excess relative to exchangeable sodium and potassium.
Isotonic or pseudohyponatraemia
May occur with extreme:
Hypertriglyceridaemia.
Hyperproteinaemia.
This is mainly an issue with certain indirect laboratory measurement techniques.
Hypertonic hyponatraemia
Caused by another effective osmole drawing water extracellularly:
Hyperglycaemia.
Mannitol.
Serum osmolality
Approximate calculated osmolality in mmol/L units:
[
\text{Osmolality} \approx 2(\text{Na})+\text{glucose}+\text{urea}
]
Approximate effective osmolality or tonicity:
[
2(\text{Na})+\text{glucose}
]
Urea is omitted from effective tonicity.
Corrected sodium in hyperglycaemia
A commonly used approximation is to add about 1.6–2.4 mmol/L to the measured sodium for each 5.6 mmol/L rise in glucose above normal.
Treat the hyperglycaemia and follow measured sodium and osmolality rather than relying entirely on a correction formula.
Classify hypotonic hyponatraemia
Hypovolaemic
Non-renal losses:
Vomiting.
Diarrhoea.
Burns.
Fistulae.
Renal losses:
Diuretics.
Mineralocorticoid deficiency.
Salt-wasting nephropathy.
Cerebral salt wasting.
Euvolaemic
SIADH.
Glucocorticoid deficiency.
Severe hypothyroidism.
Primary polydipsia.
Low-solute intake.
Drugs.
Hypervolaemic
Heart failure.
Cirrhosis.
Nephrotic syndrome.
Advanced renal failure.
Urine investigations
Urine osmolality ≤100 mOsm/kg
Suggests maximally dilute urine:
Primary polydipsia.
Low-solute intake.
Urine osmolality >100 mOsm/kg
Suggests persistent ADH effect.
Urine sodium
Below approximately 30 mmol/L often suggests reduced effective arterial volume.
Above approximately 30 mmol/L may occur with SIADH, adrenal insufficiency, renal salt loss or diuretics.
Interpretation is unreliable after diuretics and must be combined with clinical findings.
SIADH criteria
Typical features include:
Effective serum osmolality below 275 mOsm/kg.
Urine osmolality above 100 mOsm/kg.
Clinical euvolaemia.
Urine sodium above 30 mmol/L with normal intake.
No adrenal, thyroid, pituitary or significant renal insufficiency.
No recent diuretic use.
Symptoms
Severity depends more on the rate of fall than the absolute number.
Mild or chronic:
Nausea.
Headache.
Gait disturbance.
Confusion.
Severe:
Vomiting.
Profound confusion.
Seizures.
Reduced consciousness.
Respiratory arrest.
Cerebral herniation.
Management
Severe neurological symptoms
Treat immediately with hypertonic saline in a monitored environment.
A European guideline regimen is:
150 mL of 3% saline over 20 minutes.
Recheck sodium.
Repeat as required to achieve an initial rise of approximately 5 mmol/L and clinical improvement.
Stop or slow therapy once symptoms improve. Limit the sodium increase to no more than approximately 10 mmol/L in the first 24 hours and 8 mmol/L per 24 hours thereafter; many clinicians use an even lower ceiling in patients at high risk of osmotic demyelination.
High-risk features for osmotic demyelination include:
Very low initial sodium.
Alcohol dependence.
Malnutrition.
Advanced liver disease.
Hypokalaemia.
Cause-specific treatment
Hypovolaemic: isotonic saline and correction of losses.
SIADH: treat cause, stop offending drugs and restrict fluid where appropriate.
Adrenal crisis: glucocorticoid and volume resuscitation.
Hypervolaemic: fluid/sodium restriction and treatment of cardiac, hepatic or renal disease.
Polydipsia: reduce water intake.
Overcorrection
Overcorrection may occur when ADH suddenly falls and the patient produces a large volume of dilute urine.
Management may include, under specialist supervision:
Stop active sodium correction.
Desmopressin.
5% dextrose to relower or stabilise sodium.
Very frequent sodium and urine-output monitoring.
Major exam trap
0.9% saline can worsen sodium in SIADH.
The kidney may excrete the sodium in concentrated urine while retaining part of the administered water—sometimes termed desalination.
Hypernatraemia
Defined as sodium above 145 mmol/L.
Hypernatraemia almost always represents:
Water deficiency relative to body sodium, or less commonly excessive sodium administration.
Causes
Reduced access or intake
Confusion.
Intubation.
Frailty.
Dysphagia.
Impaired thirst.
Lack of available water.
Extrarenal water loss
Fever.
Sweating.
Burns.
Diarrhoea.
Stoma loss.
Renal water loss
Central diabetes insipidus.
Nephrogenic diabetes insipidus.
Osmotic diuresis from glucose, urea or mannitol.
Post-obstructive diuresis.
Recovery phase of AKI.
Sodium gain
Hypertonic saline.
Sodium bicarbonate.
Salt poisoning.
Excessive saline administration with inadequate water.
Assessment
Measure:
Urine volume.
Urine osmolality.
Glucose and urea.
Fluid access.
Recent drugs and surgery.
Interpretation:
Very concentrated urine suggests appropriate renal water conservation and an extrarenal loss.
Very dilute urine with polyuria suggests diabetes insipidus.
Intermediate urine concentration may occur with partial DI or osmotic diuresis.
Water deficit
[
\text{Water deficit} = \text{TBW}\times\left(\frac{\text{current Na}}{140}-1\right)
]
Use a lower TBW fraction in women, older people and obesity.
This calculates only the existing deficit. Add ongoing and normal losses.
Management
If shocked, restore circulation first using isotonic crystalloid.
Then replace free water:
Oral or enteral water is preferred when possible.
5% dextrose IV.
Sometimes 0.45% saline depending on concurrent sodium depletion.
Treat the cause.
Monitor sodium frequently.
For chronic or unknown-duration hypernatraemia, a commonly used target is a fall no faster than about 0.5 mmol/L/hour or 10–12 mmol/L/day. Acute sodium loading may be corrected faster under specialist monitoring. (ScienceDirect)
Diabetes insipidus
Central DI: desmopressin plus controlled water replacement.
Nephrogenic DI: remove the cause, correct potassium/calcium disorders and consider specialist therapies such as thiazides.
12. Potassium disorders
Approximately 98% of potassium is intracellular.
Potassium distribution is influenced by:
Insulin.
Beta-2 stimulation.
Acid–base status.
Plasma osmolality.
Cell breakdown.
Aldosterone.
Distal sodium delivery.
Renal function.
Hypokalaemia
Defined as potassium below 3.5 mmol/L.
Mild: 3.0–3.5.
Moderate: 2.5–2.9.
Severe: below 2.5 mmol/L. (SPS - Specialist Pharmacy Service)
Causes
Reduced intake
Rarely the sole cause but contributes in malnutrition.
Gastrointestinal loss
Vomiting.
Diarrhoea.
Nasogastric suction.
Ileostomy.
Fistulae.
Laxatives.
Renal loss
Loop and thiazide diuretics.
Hyperaldosteronism.
Hypomagnesaemia.
Renal tubular acidosis.
Amphotericin.
Aminoglycosides.
High-dose penicillins.
Intracellular shift
Insulin.
Beta-2 agonists.
Alkalosis.
Refeeding.
Thyrotoxic periodic paralysis.
Effects
Muscle weakness.
Ileus and constipation.
Rhabdomyolysis.
Respiratory weakness.
Increased digoxin toxicity.
Atrial and ventricular arrhythmias.
ECG
Flattened T waves.
ST depression.
Prominent U waves.
Apparent QT or QU prolongation.
Ventricular ectopy and tachyarrhythmias.
Investigation
Repeat potassium if unexpected.
Magnesium.
Acid–base status.
Urine potassium or potassium-to-creatinine ratio.
Blood pressure.
Medication review.
Renin and aldosterone when indicated.
Treatment
Oral potassium
Preferred when:
The patient is stable.
The gut works.
There is no dangerous arrhythmia.
Potassium is not profoundly low.
Intravenous potassium
Required when:
Severe hypokalaemia.
ECG change or arrhythmia.
Severe symptoms.
Inability to use the gastrointestinal tract.
Continuing major losses.
Safety principles:
Never give potassium as an IV push.
Use premixed, labelled solutions.
Check renal function and urine output.
Continuous ECG monitoring for rapid or concentrated replacement.
Peripheral rates are commonly limited to around 10 mmol/hour.
Higher rates, often up to 20 mmol/hour, require a monitored setting and appropriate venous access according to local policy.
Avoid glucose-containing fluid for initial urgent replacement because insulin release may shift potassium intracellularly.
Recheck potassium frequently.
Magnesium rule
Hypokalaemia may remain refractory until magnesium deficiency is corrected.
Hyperkalaemia
Definitions vary slightly by laboratory. Clinically important hyperkalaemia is commonly considered:
Mild: approximately 5.5–5.9.
Moderate: 6.0–6.4.
Severe: ≥6.5 mmol/L.
Causes
Pseudohyperkalaemia
Haemolysed specimen.
Prolonged tourniquet or fist clenching.
Severe thrombocytosis.
Severe leukocytosis.
Delay in processing.
Repeat the sample if the result is unexpected—but do not delay emergency treatment when the ECG is abnormal or the patient is unstable.
Reduced renal excretion
AKI or CKD.
Hypoaldosteronism.
ACE inhibitors or ARBs.
Spironolactone, eplerenone, amiloride.
NSAIDs.
Trimethoprim.
Heparin.
Shift out of cells
Mineral acidosis.
Insulin deficiency.
Hyperosmolality.
Beta-blockade.
Succinylcholine in susceptible patients.
Digoxin toxicity.
Cell destruction
Rhabdomyolysis.
Tumour lysis.
Haemolysis.
Burns.
Crush injury.
Massive transfusion.
ECG progression
Tall, narrow peaked T waves.
Shortened QT.
PR prolongation.
Reduced or absent P waves.
QRS widening.
Sine-wave pattern.
Ventricular fibrillation or asystole.
ECG changes do not correlate perfectly with the potassium level. A normal ECG does not make severe hyperkalaemia safe.
Emergency management: Protect – Shift – Remove – Monitor
1. Protect the myocardium
If ECG changes or peri-arrest:
10 mL of 10% calcium chloride IV over approximately 5 minutes in a resuscitation setting, or
30 mL of 10% calcium gluconate IV over approximately 10 minutes in other settings.
Repeat according to ECG response and protocol.
Calcium:
Stabilises the cardiac membrane.
Acts rapidly.
Does not lower potassium.
UK Kidney Association guidance differentiates calcium chloride for the resuscitation setting from calcium gluconate for most other patients. (UK Kidney Association)
2. Shift potassium into cells
10 units soluble insulin with 25 g glucose IV.
Check glucose before treatment.
Monitor glucose repeatedly for at least several hours.
Additional glucose may be required, particularly when pretreatment glucose is below 7 mmol/L.
Nebulised salbutamol 10–20 mg may be added.
Sodium bicarbonate is not routine but may be considered when significant metabolic acidosis is present. (UK Kidney Association)
3. Remove potassium from the body
Stop potassium administration and causative drugs.
Loop diuretic if producing urine and volume status permits.
Gastrointestinal potassium binders where appropriate.
Dialysis when:
Severe renal failure.
Refractory hyperkalaemia.
Rebound hyperkalaemia.
Severe ECG changes.
Ongoing potassium release.
4. Monitor
Continuous ECG in severe cases.
Repeat potassium after treatment.
Monitor for rebound at four to six hours.
Monitor glucose closely after insulin.
13. Calcium
Physiology
Serum calcium exists as:
Ionised calcium: biologically active.
Albumin-bound calcium.
Complexed calcium.
Alkalosis increases albumin binding and reduces ionised calcium. Therefore a hyperventilating patient may develop tetany despite a normal total calcium.
Corrected calcium
A commonly used formula in mmol/L is:
[
\text{Corrected Ca}
\text{measured Ca}+0.02(40-\text{albumin g/L})
]
This is approximate and can be unreliable in critical illness. Measure ionised calcium when:
Critically ill.
Massive transfusion.
Severe acid–base disorder.
Symptomatic.
Marked hypoalbuminaemia.
Hypocalcaemia
Causes
Post-thyroid or parathyroid surgery.
Vitamin D deficiency.
Renal failure.
Acute pancreatitis.
Sepsis.
Massive transfusion due to citrate.
Hypomagnesaemia.
Tumour lysis.
Hyperphosphataemia.
Features
Perioral and digital paraesthesia.
Muscle cramps.
Tetany.
Chvostek and Trousseau signs.
Laryngospasm.
Seizures.
Hypotension.
Prolonged QT.
Arrhythmias.
Treatment
For symptomatic or severe hypocalcaemia:
IV calcium gluconate with ECG monitoring.
Repeat or continue infusion if necessary.
Correct magnesium.
Treat the cause.
Use calcium chloride preferentially through secure central access when rapid high-dose calcium is required because extravasation is more damaging.
Hypercalcaemia
Causes
The two major causes are:
Primary hyperparathyroidism.
Malignancy.
Other causes include:
Thiazides.
Vitamin D excess.
Granulomatous disease.
Immobilisation.
Thyrotoxicosis.
Adrenal insufficiency.
Milk-alkali syndrome.
Features
“Stones, bones, abdominal groans and psychiatric overtones”:
Polyuria and thirst.
Dehydration.
Renal stones.
Constipation.
Nausea.
Pancreatitis.
Weakness.
Confusion.
Shortened QT.
Arrhythmias.
Management
Stop causative calcium, vitamin D and thiazides.
Restore volume with isotonic crystalloid.
Calcitonin for relatively rapid temporary reduction in severe cases.
IV bisphosphonate or denosumab for malignancy-associated hypercalcaemia.
Glucocorticoids for selected vitamin-D-mediated causes.
Dialysis for severe refractory hypercalcaemia, especially with renal or cardiac failure.
The Endocrine Society recommends an IV bisphosphonate or denosumab for hypercalcaemia of malignancy, with treatment tailored to severity and cause. (Endocrine)
14. Magnesium
Hypomagnesaemia
Causes
Diarrhoea and stoma loss.
Malnutrition and alcohol dependence.
Diuretics.
Proton-pump inhibitors.
Aminoglycosides.
Amphotericin.
Cisplatin.
Pancreatitis.
Refeeding syndrome.
Features
Tremor.
Weakness.
Tetany.
Seizures.
Prolonged QT.
Torsades de pointes.
Refractory hypokalaemia.
Refractory hypocalcaemia.
Treatment
Oral magnesium for mild stable deficiency.
IV magnesium sulphate for severe, symptomatic deficiency or inability to absorb orally.
Torsades is commonly treated with approximately 2 g IV magnesium sulphate, regardless of measured serum magnesium, while correcting precipitating causes.
Hypermagnesaemia
Usually occurs with:
Renal failure.
Excess magnesium antacids or laxatives.
Excess IV magnesium.
Features progress with increasing levels:
Nausea and flushing.
Reduced reflexes.
Weakness.
Hypotension.
Bradycardia.
Heart block.
Respiratory depression.
Cardiac arrest.
Treatment:
Stop magnesium.
IV calcium to antagonise cardiac and neuromuscular effects.
Fluids and loop diuretic when renal function permits.
Dialysis in severe renal failure or toxicity.
15. Phosphate
Hypophosphataemia
Causes
Refeeding syndrome.
Insulin treatment of DKA.
Respiratory alkalosis.
Alcohol dependence.
Malnutrition.
Antacids and phosphate binders.
Diuretics.
Hyperparathyroidism.
Renal tubular loss.
Features
Phosphate is essential for ATP and 2,3-DPG.
Severe deficiency can cause:
Generalised weakness.
Respiratory muscle failure.
Difficulty weaning from ventilation.
Reduced myocardial contractility.
Rhabdomyolysis.
Haemolysis.
Platelet and leukocyte dysfunction.
Confusion, seizures and coma.
Treatment
Oral replacement for mild or moderate deficiency.
IV phosphate for severe, symptomatic deficiency or inability to use the gut.
Monitor calcium, potassium, magnesium and renal function.
Avoid excessive or rapid replacement because of hypocalcaemia, hypotension, arrhythmia and calcium-phosphate precipitation.
Hyperphosphataemia
Causes:
Renal failure.
Tumour lysis.
Rhabdomyolysis.
Haemolysis.
Hypoparathyroidism.
Excess phosphate administration.
Consequences:
Hypocalcaemia.
Tetany.
Soft-tissue and vascular calcification.
Treatment:
Treat cause.
Restrict phosphate.
Phosphate binders.
Dialysis when severe.
16. Chloride
Chloride is often neglected but is highly examinable.
Hypochloraemia
Seen with:
Vomiting.
Nasogastric suction.
Loop or thiazide diuretics.
It often accompanies:
Volume contraction.
Hypokalaemia.
Metabolic alkalosis.
Urine chloride in metabolic alkalosis
Low urine chloride commonly suggests chloride-responsive alkalosis due to vomiting or previous diuretics.
Higher urine chloride suggests ongoing diuretic action, mineralocorticoid excess or renal tubular causes.
Hyperchloraemia
Commonly caused by:
Large-volume 0.9% saline.
Diarrhoeal bicarbonate loss.
Renal tubular acidosis.
It produces or accompanies a normal-anion-gap metabolic acidosis.
17. Acid–base links you must recognise
Anion gap
[
AG = Na-(Cl+HCO_3)
]
Normal is commonly approximately 8–12 mmol/L when potassium is excluded, but laboratory ranges vary.
Albumin correction
Low albumin lowers the expected anion gap.
A useful approximation:
Add approximately 2.5 mmol/L to the measured anion gap for every 10 g/L that albumin is below 40 g/L.
High-anion-gap metabolic acidosis
Think:
Lactate.
Ketoacidosis.
Renal failure.
Toxic alcohols.
Salicylates.
Pyroglutamic acidosis.
Normal-anion-gap metabolic acidosis
Think:
Diarrhoea.
Ileostomy.
Pancreatic/biliary fistula.
Renal tubular acidosis.
Excess saline.
Acetazolamide.
Metabolic alkalosis
Think:
Vomiting or NG suction.
Diuretics.
Mineralocorticoid excess.
Post-hypercapnic alkalosis.
Excess alkali.
Potassium and chloride depletion maintain metabolic alkalosis, so correcting chloride and potassium is often essential.
18. Refeeding syndrome
Refeeding causes insulin release and rapid cellular uptake of:
Phosphate.
Potassium.
Magnesium.
Glucose.
Water.
It may cause:
Arrhythmia.
Heart failure.
Respiratory failure.
Neurological deterioration.
Rhabdomyolysis.
Wernicke encephalopathy.
High-risk criteria
NICE considers a patient high risk with one major criterion such as:
BMI below 16 kg/m².
More than 15% unintentional weight loss.
Little or no intake for more than 10 days.
Low potassium, phosphate or magnesium.
Or two lesser criteria including:
BMI below 18.5.
More than 10% weight loss.
Little or no intake for more than five days.
Alcohol misuse or certain drugs.
Management includes:
Thiamine before and during feeding.
Slow introduction of nutrition, often no more than 10 kcal/kg/day in high-risk patients.
Careful fluid balance.
Daily potassium, magnesium and phosphate initially.
Controlled electrolyte replacement.
NICE advises 5 kcal/kg/day in extreme cases and close cardiac monitoring. (NICE)
19. Burns fluid resuscitation
Traditional exam formula: Parkland
[
4\text{ mL}\times \text{weight in kg}\times%\text{TBSA}
]
Lactated Ringer’s/Hartmann’s.
Total calculated for the first 24 hours.
Half in the first eight hours from the time of burn.
Remaining half over the next 16 hours.
Current practice nuance
The 2024 American Burn Association guideline recommends considering an initial calculation of 2 mL/kg/%TBSA in adults to reduce excessive resuscitation volume, then titrating to physiological endpoints. Therefore, know the classic 4 mL Parkland answer for examinations but recognise that contemporary protocols may start lower. (PubMed)
The formula is only a starting point. Titrate using:
Urine output, commonly around 0.5 mL/kg/hour in adults.
Mental state.
Perfusion.
Lactate/base deficit.
Haemodynamics.
Signs of fluid overload or compartment syndrome.
Avoid fluid creep—giving substantially more than calculated without physiological justification.
20. Important surgical electrolyte syndromes
Intestinal obstruction
May produce:
Vomiting.
Chloride and potassium depletion.
Metabolic alkalosis.
Third-space sequestration.
Hypovolaemia.
AKI.
Later lactic acidosis if strangulation or ischaemia develops.
Pyloric obstruction
Classic:
Hypochloraemia.
Hypokalaemia.
Metabolic alkalosis.
Paradoxical aciduria in advanced volume and potassium depletion.
Why paradoxical aciduria?
Severe sodium and potassium depletion causes the kidney to reabsorb sodium in exchange for hydrogen, producing acidic urine despite systemic alkalosis.
Pancreatitis
May cause:
Hypovolaemia.
Capillary leak.
Hypocalcaemia.
Hyperglycaemia.
AKI.
Lactic acidosis in severe disease.
Massive transfusion
Watch for:
Hypocalcaemia from citrate.
Hyperkalaemia from stored red cells.
Hypomagnesaemia.
Hypothermia.
Dilutional coagulopathy.
Acid–base changes.
Tumour lysis syndrome
Typical pattern:
Hyperkalaemia.
Hyperphosphataemia.
Hypocalcaemia.
Hyperuricaemia.
AKI.
Rhabdomyolysis
Typical pattern:
Hyperkalaemia.
Hyperphosphataemia.
Early hypocalcaemia.
Later possible hypercalcaemia.
Metabolic acidosis.
Pigment-associated AKI.
21. Formulas to memorise
Maintenance water
[
25–30\text{ mL/kg/day}
]
Use 20–25 mL/kg/day in patients prone to overload.
Serum osmolality
[
2Na+\text{glucose}+\text{urea}
]
All in mmol/L.
Effective osmolality
[
2Na+\text{glucose}
]
Free-water deficit
[
TBW\times\left(\frac{Na}{140}-1\right)
]
Anion gap
[
Na-(Cl+HCO_3)
]
Corrected calcium
[
Ca+0.02(40-\text{albumin})
]
Ca in mmol/L; albumin in g/L.
Burn fluid: classic Parkland
[
4\text{ mL}\times kg\times%\text{TBSA}
]
Know that some modern adult protocols start at 2 mL/kg/%TBSA.
22. High-yield examination traps
Oedema does not exclude intravascular depletion.
Oliguria does not automatically mean the patient needs fluid.
5% dextrose does not resuscitate the circulation.
Serum sodium reflects water balance more than total body sodium.
Correct severe symptomatic hyponatraemia based on symptoms, not simply the numerical sodium.
Rapid correction of chronic hyponatraemia causes osmotic demyelination.
Rapid correction of chronic hypernatraemia risks cerebral oedema.
Calcium protects the myocardium in hyperkalaemia but does not reduce potassium.
Insulin lowers potassium temporarily; potassium must still be removed from the body.
Always correct magnesium when hypokalaemia is refractory.
Potassium must never be administered as an IV push.
Large-volume 0.9% saline can cause hyperchloraemic metabolic acidosis.
0.9% saline may worsen SIADH.
Total calcium may be misleading in hypoalbuminaemia or critical illness—check ionised calcium.
Hypophosphataemia can cause failure to wean from ventilation.
Refeeding syndrome is mainly phosphate, potassium, magnesium, thiamine and fluid-shift pathology.
Vomiting produces alkalosis; diarrhoea usually produces normal-anion-gap acidosis.
Postoperative sodium and water retention is common; routine “third-space replacement” causes overload.
A fluid prescription must include a reassessment plan.
Every abnormal electrolyte result should prompt: confirm, assess urgency, ECG when relevant, identify cause, correct safely and recheck.
23. Rapid OSCE answer: prescribing fluids
When shown a fluid chart, say:
“I will first decide whether this patient requires resuscitation, routine maintenance, replacement of abnormal losses, or correction of an existing deficit. I will review oral and IV intake, urine and drain losses, daily weight, haemodynamics, examination for hypovolaemia or overload, renal function, glucose and electrolytes. I will prescribe the smallest appropriate volume with the correct electrolyte composition, document monitoring targets and reassess after administration.”
For an urgent potassium disorder:
“I will place the patient on cardiac monitoring, obtain a 12-lead ECG, repeat the sample if pseudohyperkalaemia is possible without delaying treatment, review renal function and drugs, treat ECG toxicity with IV calcium, shift potassium intracellularly with insulin-glucose and salbutamol, arrange potassium removal and repeat potassium and glucose measurements.”
24. Final memory framework
Fluid prescription: 5 Rs
Resuscitation.
Routine maintenance.
Replacement.
Redistribution.
Reassessment.
Hyperkalaemia: Protect – Shift – Remove – Monitor
Calcium.
Insulin-glucose ± salbutamol.
Diuresis, binders or dialysis.
ECG, glucose and repeat potassium.
Hyponatraemia: Tonicity – Symptoms – Urine – Volume – Cause – Correction limit
Any electrolyte abnormality: C-U-R-E
Confirm and classify.
Urgency and ECG.
Reason or underlying cause.
Electrolyte correction and evaluation afterward.
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