Medicine chapters
Sodium and potassium disorders
A practical approach to low and high sodium and low and high potassium: causes sorted by volume status and urine tests, the symptoms and ECG changes, safe correction rates and emergency treatment.
- Hyponatraemia (Na below 135) is the commonest electrolyte problem; first check osmolality (exclude pseudohyponatraemia), then sort by volume status and urine sodium; correct chronic cases slowly (no more than about 8–10 mmol/L in 24 hours) to avoid osmotic demyelination.
- Hypernatraemia means water deficit; replace water slowly over about 48 hours.
- Hyperkalaemia with ECG changes is an emergency: IV calcium gluconate to protect the heart, insulin with glucose (and salbutamol) to shift K into cells, then remove K. Hypokalaemia (diuretics, vomiting, diarrhoea, hyperaldosteronism) causes weakness and U waves; replace K and check magnesium.
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Overview
Sodium and potassium disorders are among the commonest problems on medical and surgical wards.
- Sodium problems are really problems of water balance. They mainly affect the brain (cells swell or shrink).
- Potassium problems affect excitable tissues: the heart (arrhythmias) and muscle (weakness).
Usual reference ranges: sodium 135–145 and potassium 3.5–5.0 mmol/L (laboratories differ slightly).
Plasma osmolality
Calculated osmolality ≈ 2 × (Na + K) + glucose + urea, with every value entered in mmol/L; the normal result is about 280–295 mOsm/kg.
Na 120, K 3.5, glucose 6, urea 4 (mmol/L)
Osmolality = 2 × (120 + 3.5) + 6 + 4 = 247 + 10 = 257 → low → true (hypotonic) hyponatraemia
Hyponatraemia
Definition: Na below 135 mmol/L; severe below about 125. It is the commonest electrolyte disorder in hospital patients.
Step 1: exclude false or non-hypotonic hyponatraemia
- Pseudohyponatraemia: very high lipids or proteins (e.g. myeloma) take up plasma volume; the lab reports low sodium but osmolality is normal. No treatment needed.
- High glucose (or mannitol) draws water out of cells and dilutes sodium; osmolality is high. Treat the glucose.
- Drip-arm sample: blood taken from an arm receiving low-sodium fluid.
Step 2: assess volume status (and urine sodium)
| Volume status | Urine Na | Causes |
|---|---|---|
| Hypovolaemic (dry) | Below 20 mmol/L | Extrarenal loss: vomiting, diarrhoea, burns, pancreatitis, haemorrhage |
| Hypovolaemic | Above 20 mmol/L | Renal loss: diuretics (especially thiazides), Addison disease, osmotic diuresis (glucose, urea), salt-losing nephropathy, cerebral salt wasting |
| Euvolaemic | Usually above 20 | SIADH, hypothyroidism, glucocorticoid deficiency (pituitary), drugs (carbamazepine, SSRIs, chlorpropamide), psychogenic polydipsia (urine dilute), beer potomania, post-operative hypotonic fluids, exercise-associated (marathon runners) |
| Hypervolaemic (oedematous) | Usually below 20 (unless on diuretics) | Heart failure, cirrhosis, nephrotic syndrome, kidney failure |
Diuretics can produce a picture of hyponatraemia with hypokalaemia in an older patient with heart failure. Addison disease gives hyponatraemia with hyperkalaemia.
SIADH is diagnosed in a euvolaemic patient with low plasma osmolality, inappropriately concentrated urine (urine osmolality above plasma) and urine sodium above about 30 mmol/L, after excluding hypothyroidism, adrenal insufficiency and diuretics. Its causes (lung cancer, especially small cell; pneumonia; CNS disease; drugs) and treatment are covered in the SIADH and diabetes insipidus chapter.
Clinical features
Due to water moving into brain cells as plasma osmolality falls.
- Mild or chronic: often none; nausea, malaise, unsteadiness and falls in the elderly, poor concentration.
- Severe or rapid: headache, confusion, vomiting, drowsiness, seizures, coma, respiratory arrest (cerebral oedema).
- Symptoms depend more on speed of fall than on the absolute level. Symptoms are uncommon above 125 mmol/L.
- Higher risk of brain swelling: children, premenopausal women, hypoxia.
Management
Acute (under 48 hours) or severely symptomatic (seizures, coma):
- Hypertonic (3%) saline in small boluses (Kumar suggests about 1 mL/kg over 1 hour, repeated if needed), in a high-dependency setting.
- Aim to raise sodium by about 4–6 mmol/L quickly; this is usually enough to stop seizures.
- Check sodium every 1–2 hours.
Rule of thumb: 1 mL/kg of 3% saline raises plasma Na by about 1 mmol/L (body water taken as 50% of weight)
Woman of 60 kg with seizures and Na 112: 60 mL of 3% saline over 1 hour → expected rise about 1 mmol/L per 60 mL; repeat and recheck until symptoms stop (target rise 4–6 mmol/L)
Chronic or mildly symptomatic: treat the cause.
- Hypovolaemic: 0.9% saline; stop diuretics.
- Euvolaemic (SIADH): fluid restriction (about 500–1000 mL a day); stop causative drugs; then options include oral urea, demeclocycline or a vasopressin V2 antagonist (tolvaptan).
- Hypervolaemic: fluid and salt restriction, loop diuretics, treat the heart, liver or kidney disease.
- Correct potassium and magnesium deficits (note that giving potassium also raises sodium).
Osmotic demyelination syndrome (ODS)
In chronic hyponatraemia the brain has adapted by losing solutes. If sodium is then raised too fast, brain cells shrink and myelin in the pons (and elsewhere) is damaged.
- Safe limit: raise sodium by no more than about 8–10 mmol/L in 24 hours (Kumar advises keeping within 8 mmol/L in the first day and 18 mmol/L over 48 hours), and less in high-risk patients.
- High-risk: alcohol misuse, malnutrition, cirrhosis, hypokalaemia, elderly women on thiazides.
- Features appear 2–6 days later: dysarthria, dysphagia, spastic quadriparesis, "locked-in" state, coma. MRI changes may take 2 weeks to show.
- Overcorrection often comes from a sudden water diuresis (e.g. after volume repletion, cortisol replacement or stopping a drug). If sodium rises too fast, give 5% glucose and/or desmopressin to bring it back.
Acute hyponatraemia kills by brain swelling (treat fast); chronic hyponatraemia kills by overcorrection (treat slowly).
"From low to high, your pons will die."
Hypernatraemia
Definition: Na above 145 mmol/L. It almost always means too little water relative to sodium. Because thirst is so powerful, it occurs mainly when a person cannot drink: infants, the elderly, confused or unconscious patients.
Causes
- Water loss without replacement: fever, sweating, burns, diarrhoea, vomiting, hyperventilation.
- Renal water loss: diabetes insipidus (cranial or nephrogenic: lithium, hypercalcaemia, hypokalaemia, demeclocycline), osmotic diuresis (hyperglycaemia, HHS, urea after relief of obstruction).
- Sodium gain (iatrogenic): hypertonic saline, 8.4% sodium bicarbonate, high-sodium drugs; rarely primary hyperaldosteronism (mild).
Features
Thirst, lethargy, irritability, confusion, seizures, coma; brain shrinkage can tear bridging veins (intracranial bleeding).
Investigations
Plasma and urine osmolality: dilute urine (osmolality below plasma) despite high sodium suggests diabetes insipidus; a rise after desmopressin points to cranial DI. Concentrated urine suggests extrarenal losses or solute load.
Management
- Replace water slowly, over about 48 hours, aiming for a fall of no more than about 10 mmol/L a day; too rapid a fall causes cerebral oedema and seizures.
- Oral water if possible; otherwise 5% glucose or 0.45% saline. If the patient is shocked or the sodium is extreme (above about 170), start with 0.9% saline to restore circulation (it is still hypotonic compared with the patient's plasma).
- Desmopressin for cranial DI; stop lithium where possible.
Man of 70 kg, Na 160 mmol/L; total body water ≈ 0.6 × 70 = 42 L
Water deficit = 42 × (160 ÷ 140 − 1) = 42 × 0.143 ≈ 6 L
Replace about 6 L (plus ongoing losses) over 48 hours, checking sodium often
Potassium: background
About 98% of potassium is inside cells. Serum K depends on:
- Shift into cells: insulin, β2-agonists (salbutamol, adrenaline), alkalosis.
- Shift out of cells: acidosis, insulin lack, cell breakdown, digoxin toxicity, suxamethonium.
- Renal excretion: driven by aldosterone and sodium delivery to the collecting duct.
In diabetic ketoacidosis, total body potassium is low even if the serum level is normal or high; insulin drives K into cells and the level can crash, so potassium is added to fluids once K falls below the upper normal range and urine is flowing.
Hypokalaemia
Causes
| Mechanism | Examples |
|---|---|
| Renal loss (urine K above about 20 mmol/day) | Thiazide and loop diuretics (commonest), primary hyperaldosteronism, Cushing syndrome, ectopic ACTH, liquorice, renal tubular acidosis types 1 and 2, amphotericin, hypomagnesaemia, Bartter, Gitelman, Liddle |
| Gut loss (urine K low) | Diarrhoea, laxative abuse, villous adenoma, fistulae, ileostomy. Vomiting causes hypokalaemia mainly through renal loss (alkalosis and secondary aldosteronism) |
| Shift into cells | Insulin (DKA treatment), salbutamol, alkalosis, refeeding, hypokalaemic periodic paralysis, treatment of B12 deficiency |
| Low intake | IV fluids without K, starvation |
The commonest cause of chronic hypokalaemia is diuretic therapy; next think of hyperaldosteronism, vomiting and diarrhoea.
Inherited tubular syndromes
| Syndrome | Defect (mimics) | Blood pressure | Renin/aldosterone | Clue |
|---|---|---|---|---|
| Bartter | Thick ascending limb, NKCC2 (like a loop diuretic) | Normal or low | High | High urinary calcium; presents in childhood |
| Gitelman | Distal tubule NCC (like a thiazide) | Normal or low | High | Low urinary calcium, low magnesium; often young adults with cramps |
| Liddle | Overactive ENaC (collecting duct) | High | Low | Responds to amiloride, not spironolactone |
| Primary hyperaldosteronism | Adrenal | High | Aldosterone high, renin low | Responds to spironolactone |
Features
- Muscle weakness, cramps, fatigue; paralysis when severe (below about 2.5 mmol/L); ileus and constipation.
- Arrhythmias (atrial and ventricular ectopics, more so with heart disease); increases digoxin toxicity.
- Polyuria (nephrogenic DI) and metabolic alkalosis.
- ECG: flattened or inverted T waves, ST depression, prominent U waves, apparent long QT (QU).
Management
- Treat the cause; stop or reduce diuretics, or add a potassium-sparing diuretic (amiloride, spironolactone).
- Oral potassium (slow-release or effervescent) for mild cases.
- IV potassium chloride for severe hypokalaemia, arrhythmias, weakness or DKA: added to 0.9% saline (not glucose, which drives K into cells), given slowly with monitoring; use lower rates in renal impairment. Never give potassium as a bolus.
- Check and correct magnesium: hypokalaemia will not correct while magnesium is low (magnesium lack causes renal K wasting).
Hyperkalaemia
Causes
| Mechanism | Examples |
|---|---|
| Reduced renal excretion (commonest) | Acute kidney injury, advanced CKD; drugs: ACE inhibitors, ARBs, spironolactone, amiloride, triamterene, NSAIDs, trimethoprim, heparin, ciclosporin; Addison disease; hyporeninaemic hypoaldosteronism (type 4 RTA, diabetes) |
| Shift out of cells | Acidosis, DKA (insulin lack), rhabdomyolysis, tumour lysis, burns, haemolysis, digoxin toxicity, suxamethonium |
| Increased intake | K supplements, salt substitutes, massive transfusion of stored blood |
| Spurious (pseudohyperkalaemia) | Haemolysed sample, delayed processing, fist clenching, very high white cell or platelet counts, EDTA contamination |
An unexpectedly high potassium in a well patient with a normal ECG is often a haemolysed or delayed sample. Repeat it urgently, but do not delay treatment if the ECG is abnormal.
The combination of an ACE inhibitor (or ARB) with spironolactone or NSAIDs, especially in kidney impairment, is a classic cause of dangerous hyperkalaemia.
Features
- Often no symptoms until cardiac arrest; muscle weakness; Kussmaul breathing if acidotic.
- K above 6.5–7 mmol/L or any ECG change = emergency.
ECG changes (roughly in order)
- Tall, peaked (tented) T waves
- Flattened or absent P waves, long PR interval
- Widened QRS
- Sine-wave pattern
- Ventricular fibrillation or asystole
Emergency management
| Step | Treatment | Purpose and notes |
|---|---|---|
| 1. Protect the heart | 10 mL of 10% calcium gluconate IV over about 5 minutes (or calcium chloride); repeat if ECG changes persist | Stabilises the myocardium within minutes; does not lower K; effect lasts under an hour |
| 2. Shift K into cells | Soluble insulin (10 units) given IV together with 50% glucose (50 mL) over 10–15 minutes | Lowers K by about 1 mmol/L within an hour; monitor glucose for hypoglycaemia for several hours |
| Nebulised salbutamol (high dose) | Adds to insulin; may cause tremor and tachycardia | |
| Sodium bicarbonate only if severely acidotic | Limited effect | |
| 3. Remove K from the body | Potassium binders (calcium resonium or newer agents such as patiromer or sodium zirconium cyclosilicate); loop diuretics if passing urine | Slower (hours) |
| Haemodialysis | Refractory hyperkalaemia, especially in kidney failure | |
| 4. Stop the cause | Stop K supplements, ACE inhibitors, ARBs, spironolactone, NSAIDs; treat AKI, DKA | Prevent recurrence |
"C BIG K Drop": Calcium, Beta-agonist, Insulin and Glucose, Kayexalate (binder), Dialysis.
Calcium does not lower potassium. It only buys time; insulin–glucose must follow. Give calcium cautiously in digoxin toxicity, where it may worsen arrhythmias.
Expect: pseudohyponatraemia with normal osmolality; calculating osmolality; classifying hyponatraemia by volume status and urine sodium; thiazides and Addison disease as renal causes; SIADH criteria and fluid restriction; 3% saline for seizures; the safe correction limit and osmotic demyelination in an alcoholic (quadriparesis, dysphagia); hypernatraemia as water deficit and slow correction; DKA and insulin shifting potassium; Bartter (high urinary calcium) versus Gitelman (low calcium, low magnesium) versus Liddle (hypertension, low renin, amiloride); hypokalaemia ECG (U waves) and magnesium; hyperkalaemia causes (ACE inhibitors, spironolactone, AKI, Addison) and ECG sequence; calcium gluconate first, then insulin–glucose, salbutamol, binders and dialysis.
Quick revision
- Osmolality ≈ 2(Na + K) + glucose + urea; normal osmolality with low Na = pseudohyponatraemia.
- Hyponatraemia: dry (urine Na below 20 = gut; above 20 = diuretics, Addison), euvolaemic (SIADH, hypothyroid, polydipsia), oedematous (heart, liver, kidney failure, nephrotic).
- Seizures: 3% saline boluses, raise Na 4–6 mmol/L. Chronic: no more than about 8–10 mmol/L in 24 hours; risk of ODS.
- Hypernatraemia: water deficit; 5% glucose or 0.45% saline over 48 hours.
- Hypokalaemia: diuretics, vomiting, diarrhoea, hyperaldosteronism, insulin; weakness, U waves; IV KCl in saline; correct magnesium.
- Bartter = loop-like (high urine Ca); Gitelman = thiazide-like (low urine Ca, low Mg); Liddle = hypertension, low renin.
- Hyperkalaemia: AKI, ACE inhibitor + spironolactone, Addison, acidosis, haemolysed sample; peaked T, wide QRS, sine wave.
- Treat: calcium gluconate 10 mL 10% IV → IV insulin (10 units) with 50% glucose (50 mL) → salbutamol → binders → dialysis.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
Why must chronic hyponatraemia be corrected slowly?
The brain has already adapted by losing solutes; a rapid rise in sodium pulls water out of brain cells and damages myelin, causing osmotic demyelination.
What is pseudohyponatraemia?
A falsely low sodium reading caused by very high lipids or proteins in the sample; the plasma osmolality is normal and no treatment is needed.
Why is calcium given first in hyperkalaemia if it does not lower potassium?
It quickly stabilises heart muscle membranes and reduces the risk of a fatal arrhythmia while other treatments move potassium into cells.
Why should IV potassium not be mixed in glucose?
Glucose stimulates insulin release, which drives potassium into cells and can make hypokalaemia worse.
How do Bartter and Gitelman syndromes differ?
Both cause hypokalaemic alkalosis with normal blood pressure, but Bartter (loop-like) has high urinary calcium and Gitelman (thiazide-like) has low urinary calcium and low magnesium.