fluid and electrolyte disorders

Potassium disorders, hypernatraemia, diabetes insipidus, and inherited tubulopathies. For hyponatraemia, see the dedicated note. Potassium is the most immediately dangerous electrolyte — ECG changes drive urgency, not the serum level alone.

severe hyperkalaemia — C BIG K

ECG immediately — do not wait for repeat K⁺
stop offending agents now: ACEi/ARB, MRA, K-sparing diuretics, NSAIDs, trimethoprim, K⁺ supplements
Calcium gluconate 10 mL of 10% IV over 2–3 min if ECG changes or K⁺ ≥6.5 mmol/L (repeat if ECG changes persist; lasts ~30–60 min — may need redosing); alternative: CaCl₂ 10 mL of 10% via central line. Stabilises myocardium but does not lower K⁺. Caution with digoxin — give slowly/diluted
Beta-agonist: salbutamol 10–20 mg nebulised
Insulin: 10 units regular insulin IV + 25 g dextrose (D50W 50 mL) given together; use 5 units if eGFR <30; withhold dextrose if glucose >14 mmol/L
Glucose monitoring: BSL q1h × 6 h post-insulin
shift agents (insulin, salbutamol) are temporising — K⁺ rebounds in 2–6 h; definitive lowering requires binders, diuresis, or dialysis
K⁺ binders: sodium zirconium cyclosilicate (Lokelma) 10 g PO or patiromer 8.4 g PO (onset 1–6 h — not emergency monotherapy; avoid sodium polystyrene sulfonate)
NaHCO₃ only if concurrent metabolic acidosis — minimal K⁺-lowering effect alone
loop diuretic if volume-replete with adequate renal function
repeat K⁺ and ECG at 1–2 h
if refractory or anuric → emergency haemodialysis

do not miss

Hyperkalaemia with ECG changes (peaked T waves, widened QRS, sine wave) → IV calcium immediately, do not wait for a repeat level
Severe hypokalaemia (K⁺ <2.5 mmol/L) → arrhythmia risk; replace IV before insulin in DKA
Acute hypernatraemia with obtundation → free water deficit correction; too-rapid correction of chronic hypernatraemia causes cerebral oedema

hyperkalaemia

ECG progression

Peaked T waves → PR prolongation → loss of P waves → widened QRS → sine wave → VF/asystole. ECG changes typically appear at K⁺ >6.5 mmol/L but can be absent even at high levels — a normal ECG does not exclude dangerous hyperkalaemia. Always get an ECG.

emergency management — C BIG K

Indications for emergency treatment: ECG changes or K⁺ ≥6.5 mmol/L.

step	intervention	mechanism	onset
Cardiac membrane	calcium gluconate 10 mL of 10% (1 g) IV over 2–3 min; repeat if ECG changes persist (or CaCl₂ 10 mL via central line)	stabilises myocardium	1–3 min
Beta-agonist	salbutamol 10–20 mg nebulised	shifts K⁺ intracellularly	15–30 min
Insulin	10 units regular insulin IV + 25 g dextrose (D50W 50 mL)	shifts K⁺ intracellularly	15–30 min
Glucose	monitor BSL q1h × 6 h post-insulin	prevent hypoglycaemia	—
K⁺ binders	sodium zirconium cyclosilicate (SZC/Lokelma) 10 g PO or patiromer 8.4 g PO	GI K⁺ elimination	1–6 h

Stop offending agents — ACEi/ARB, MRA, K-sparing diuretics, NSAIDs, trimethoprim, K⁺ supplements
Sodium polystyrene sulfonate (Kayexalate) — falling out of favour due to questionable efficacy and GI injury risk (colonic necrosis); avoid in bowel-compromised patients
NaHCO₃ — only if concurrent metabolic acidosis; minimal K⁺-lowering effect alone
Loop diuretics — if volume-replete and adequate renal function
Emergency haemodialysis — refractory hyperkalaemia or AKI/CKD with no renal clearance

shift agents are temporary

Insulin, salbutamol, and bicarbonate shift K⁺ intracellularly but rebound within hours. Only calcium (membrane stabilisation) plus definitive removal (dialysis, binders, diuresis) address the underlying problem.

insulin-induced hypoglycaemia

Hypoglycaemia occurs in ~15% of patients given IV insulin for hyperkalaemia. Give dextrose with (not after) insulin. Use 5 units if eGFR <30 (prolonged insulin clearance). Monitor glucose for ≥6 hours.

hypokalaemia

ECG changes

Flat/inverted T waves → ST depression → prominent U waves → prolonged QT → torsades de pointes.

causes

Renal losses: diuretics (thiazides > loops), RTA type I/II, hypomagnesaemia, hyperaldosteronism, Bartter/Gitelman
GI losses: diarrhoea, vomiting (renal loss from metabolic alkalosis, not gastric K⁺ loss), laxative abuse
Transcellular shift: insulin, beta-agonists, alkalosis, refeeding syndrome

management

Always check and replace Mg²⁺ — hypokalaemia is refractory until Mg²⁺ is corrected (Mg²⁺ normally inhibits ROMK-mediated K⁺ secretion)
Mild (3.0–3.4): oral KCl 40–80 mmol/day
Moderate (2.5–2.9): oral KCl 80–120 mmol/day; IV if symptomatic or nil per os
Severe (<2.5): IV KCl — max 20 mmol/h peripherally, 40 mmol/h centrally with cardiac monitoring
In DKA: replace K⁺ before starting insulin if K⁺ <3.3 mmol/L

hypernatraemia

Na⁺ >145 mmol/L. Almost always a water access problem — the thirst mechanism is intact in most patients, so hypernatraemia implies inability to drink (intubated, altered LOC, extremes of age) or massive water losses.

classification by mechanism

mechanism	examples	urine osmolality
water loss — renal	diabetes insipidus, osmotic diuresis (glucose, urea, mannitol)	low (DI) or variable (osmotic)
water loss — extrarenal	insensible (fever, burns), GI (diarrhoea)	>700 mOsm/kg (appropriate concentration)
inadequate intake	restricted access, impaired thirst (geriatric, hypothalamic)	>700 mOsm/kg
sodium gain	hypertonic saline, NaHCO₃ infusion, salt poisoning	variable

free water deficit

$\text{Free water deficit (L)} = \text{TBW} \times \frac{\text{serum Na} - 140}{140}$

TBW = 0.5 × weight (women/elderly) or 0.6 × weight (men). Add ongoing losses.

correction

Chronic (>48 h or unknown duration): max 0.5 mmol/L per hour, ≤10–12 mmol/L per 24 h — faster risks cerebral oedema (brain has accumulated idiogenic osmoles). In adults, recent data suggest failure to correct within 72 h worsens mortality, so do not under-correct either
Acute (<48 h, iatrogenic): can correct faster (1–2 mmol/L per hour) safely
Enteral free water preferred (oral or NG); IV D5W if not feasible
Monitor Na⁺ q4–6h during active correction

diabetes insipidus

Inappropriately dilute urine (urine osmolality <300 mOsm/kg) in the setting of elevated serum Na⁺ or serum osmolality.

	central DI	nephrogenic DI
defect	insufficient ADH production	renal resistance to ADH
causes	pituitary surgery, craniopharyngioma, infiltrative (sarcoid, Langerhans), traumatic brain injury, idiopathic	lithium (most common drug cause), hypercalcaemia, hypokalaemia, tubulointerstitial disease, congenital (V2R/AQP2 mutations)
DDAVP challenge	urine osmolality rises >50% and urine volume drops	minimal/no response
treatment	desmopressin (DDAVP) — intranasal 10–20 µg or oral 100–400 µg	treat underlying cause; thiazide (paradoxical antidiuresis via volume contraction → proximal reabsorption); amiloride for lithium-induced (blocks lithium entry via ENaC); low-sodium diet

Copeptin (C-terminal pro-vasopressin) is emerging as the diagnostic standard for the polyuria-polydipsia workup, largely superseding the water deprivation test in accuracy. Canadian availability remains limited but expanding.

post-pituitary surgery — triphasic response

Day 1–5: DI (axonal shock → low ADH). Day 5–10: SIADH (dying neurons release stored ADH). Day 10+: permanent DI if >80% of magnocellular neurons destroyed. Monitor sodium closely through all three phases.

inherited tubulopathies

	Bartter	Gitelman	Liddle
site	TAL (thick ascending limb)	DCT (NaCl cotransporter)	collecting duct (ENaC)
mimics	loop diuretic	thiazide	mineralocorticoid excess
inheritance	AR	AR	AD
K⁺	low	low	low
metabolic	alkalosis	alkalosis	alkalosis
Mg²⁺	low	low	normal
urine Ca²⁺	high (nephrocalcinosis risk)	low (key distinguishing feature)	normal
BP	normal/low	normal/low	hypertension
renin/aldo	high/high	high/high	low/low
treatment	K⁺/Mg²⁺ supplementation, NSAIDs (↓ PGE₂-mediated losses), spironolactone	K⁺/Mg²⁺ supplementation, spironolactone, amiloride	amiloride or triamterene (block ENaC directly); spironolactone ineffective

Gitelman vs Bartter — the calcium trick

Low urine calcium = Gitelman (thiazide effect → enhanced proximal Ca²⁺ reabsorption). High urine calcium = Bartter (loop effect → impaired paracellular Ca²⁺ reabsorption in TAL). This distinction is clinically testable and frequently examined.

traps

Repeating a haemolysed K⁺ without an ECG — if K⁺ is reported as >6.0, get an ECG immediately regardless of haemolysis suspicion. Treat the ECG, not the number.
Forgetting Mg²⁺ in refractory hypokalaemia — K⁺ will not stay corrected until Mg²⁺ is replaced. This is the single most common reason for “refractory” hypokalaemia.
Correcting chronic hypernatraemia too fast — brain has accumulated idiogenic osmoles over days; rapid correction → cerebral oedema. Slow and steady.
Assuming polyuria = DI — osmotic diuresis (hyperglycaemia, post-obstructive, urea) is far more common than DI. Check urine osmolality: if >300, it is not DI.
Liddle syndrome treated with spironolactone — the defect is a gain-of-function ENaC mutation, not excess aldosterone. Spironolactone blocks MR, which is upstream; amiloride blocks ENaC directly and is the correct treatment.

fluid and electrolyte disorders

hyperkalaemia

ECG progression

emergency management — C BIG K

hypokalaemia

ECG changes

causes

management

hypernatraemia

classification by mechanism

free water deficit

correction

diabetes insipidus

inherited tubulopathies

traps

Key references