NephrologyTier 1Disease (DEADMAN)

Hyperkalaemia

Description

K+ >5.5 mmol/L; severe >6.5, or any level with ECG changes
98% of body potassium is intracellular - the serum level is a poor guide to total body stores
Two questions, always in this order:
- 1. Is it real? (pseudohyperkalaemia)
- 2. Is it a shift, or a failure of excretion?

Severity

~2-3% of hospital inpatients; up to 10% of those with CKD
CKD, diabetes and RAS-blocking drugs account for the great majority
Hyperkalaemia is the commonest reason RAS blockade and MRAs are stopped or under-dosed - and stopping them worsens long-term outcomes

1. Pseudohyperkalaemia - exclude first

Haemolysed sample; fist clenching or prolonged tourniquet; delayed processing; sample from above a drip arm
Marked thrombocytosis or leucocytosis (K+ released during clotting) - serum high, plasma normal. Send a plasma (heparin) tube
Familial pseudohyperkalaemia (red cell membrane leak, worse when cold)
*A high K+ with no clinical explanation is a repeat sample until proven otherwise*

2. Transcellular shift

Metabolic acidosis (mineral acids - HCl, NH4Cl - shift K+ out; organic acidoses like lactic and ketoacidosis shift less)
Insulin deficiency / hyperglycaemia - DKA and HHS present with a high serum K+ but a large total body deficit
Beta blockers (non-selective), digoxin toxicity (Na-K ATPase inhibition)
Tissue breakdown - rhabdomyolysis, tumour lysis, haemolysis, burns, crush injury, GI bleed
Suxamethonium (contraindicated in burns, denervation, prolonged immobility), hyperkalaemic periodic paralysis
Hyperosmolality (mannitol, hypertonic saline)

3. Reduced renal excretion - the commonest chronic mechanism

CKD, especially eGFR <30; AKI (particularly oliguric)
Hypoaldosteronism
- Type 4 RTA (hyporeninaemic hypoaldosteronism) - diabetic nephropathy, chronic interstitial disease, NSAIDs, calcineurin inhibitors
- Adrenal insufficiency (Addison disease) - hyperkalaemia + hyponatraemia
- Congenital adrenal hyperplasia (21-hydroxylase deficiency)
Reduced distal Na delivery - severe volume depletion, heart failure
Gordon syndrome (pseudohypoaldosteronism type 2) - hyperkalaemia, hypertension, metabolic acidosis, thiazide-responsive

4. Drugs - the list to recite

Mechanism	Drugs
RAAS blockade	ACEi, ARB, ARNI, aliskiren
Aldosterone antagonism	Spironolactone, eplerenone (finerenone less)
ENaC blockade	Amiloride, triamterene, trimethoprim, pentamidine
Tubular / other	Calcineurin inhibitors (also cause hyperuricaemia, metabolic acidosis, hypophosphataemia and hypomagnesaemia), NSAIDs, heparin (inhibits aldosterone synthesis), digoxin, beta blockers, suxamethonium
Load	K+ supplements, salt substitutes (KCl), stored blood, penicillin G potassium

*Trimethoprim is amiloride in disguise* - it blocks the ENaC and also raises creatinine without changing GFR

ECG - do it immediately; it drives the treatment

Progression is roughly sequential but not reliable - a normal ECG does not exclude dangerous hyperkalaemia**

Assess

Repeat the sample (plasma tube if thrombocytosis/leucocytosis suspected)
Volume status, urine output, medication list including OTC and salt substitutes
UEC, VBG (rapid K+ and pH), glucose, CK, urate, LDH, calcium, phosphate, FBE
Renin, aldosterone and cortisol if unexplained hyperkalaemia with normal eGFR
Transtubular potassium gradient (TTKG) - historical, now rarely used; urine K+/creatinine ratio is preferred
- Urine K+ <20 mmol/L with hyperkalaemia -> impaired renal excretion

The three steps - in this order

1. Protect the myocardium - if ECG changes or K+ >=6.5

IV calcium gluconate 10% 10-30 mL (or calcium chloride 10% 10 mL via central access)
- Onset 1-3 min; lasts only 30-60 min - repeat if changes recur
- *Does not lower the potassium at all* - it stabilises the myocardial membrane
- Caution in digoxin toxicity - give slowly, diluted (the old 'stone heart' concern is now regarded as overstated, and calcium should not be withheld in a life-threatening rhythm)

2. Shift K+ into cells - buys 2-6 hours

Insulin 10 units actrapid + 50 mL of 50% glucose IV (or 25 g dextrose)
- Onset 15-30 min, lasts 4-6 h; lowers K+ ~0.5-1.2 mmol/L
- *Monitor BSL hourly for 6 hours - late hypoglycaemia is the commonest iatrogenic harm*; omit or reduce glucose if BSL >15
Salbutamol 10-20 mg nebulised (4-8 times the asthma dose)
- Onset 30 min; lowers K+ ~0.5-1 mmol/L; additive with insulin
- Up to 20-40% are non-responders; tachycardia and tremor limit use in ischaemic heart disease
Sodium bicarbonate - only if there is a significant metabolic acidosis; not effective as a standalone K+-lowering therapy

3. Remove K+ from the body - the only definitive step

Dialysis - fastest and definitive; for refractory hyperkalaemia, anuria, or severe ECG changes
- Intermittent HD removes K+ far faster than CRRT
Loop diuretic +/- IV fluid if volume replete and urine output preserved
Potassium binders
- Sodium zirconium cyclosilicate (SZC) - onset ~1 h; also useful acutely
- Patiromer - onset ~7 h; binds other oral drugs - separate doses by 3 h
- Sodium polystyrene sulfonate (resonium) - slow, poorly evidenced acutely; *do not give with sorbitol - colonic necrosis*

4. Treat the cause and prevent recurrence

Stop or reduce the culprit drugs; review salt substitutes
Dietary potassium restriction and dietitian referral
Fludrocortisone for hypoaldosteronism; treat adrenal insufficiency
Correct acidosis - NaHCO3 to HCO3- >=22 mmol/L
*In CKD, use a potassium binder to keep the patient on their ACEi/ARB and MRA rather than stopping the drugs* - the drugs give the long-term cardiorenal benefit
Written sick-day rules

Cardiac arrest can be the presenting feature - there is no reliable warning
The rate of rise matters more than the absolute level - a chronically dialysed patient tolerates 6.5 that would arrest an acutely anuric patient
Chronic hyperkalaemia in CKD is recurrent unless the driver is fixed - each episode risks the drugs that most benefit the patient being stopped
Mortality of severe hyperkalaemia in hospital is high, largely reflecting the underlying illness

After treatment

Recheck K+ at 2, 4 and 6 hours - insulin and salbutamol effects wear off and K+ rebounds
Monitor BSL for 6 hours after insulin
Reconcile the medication list before discharge and document which drugs were stopped, why, and when they should be restarted
Repeat UEC within 1-2 weeks of restarting or up-titrating any RAS-blocking drug

6 more sections, plus exam facts

Premium unlocks every note across every specialty, and the full exam fact library behind it.