Metabolic emergencies - hypo- and hyperkalaemia
Description
- 98% of body potassium is intracellular - the plasma level is a poor guide to total body stores
- Normal 3.5-5.2 mmol/L
| Threshold | Severity | |
|---|---|---|
| Hyperkalaemia | >5.5 mild, >6.0 moderate, >6.5 severe | Or any level with ECG change - the ECG outranks the number |
| Hypokalaemia | <3.5 mild, 2.5-3.0 moderate, <2.5 severe |
- Pseudohyperkalaemia - always exclude before treating
- Haemolysed sample, fist clenching with tourniquet, delayed processing, marked thrombocytosis (>1000) or leucocytosis, sampling above a drip
- Clue: high K+ with a completely normal ECG and no cause. Repeat as a free-flowing or plasma (lithium heparin) sample
Epidemiology
- Hyperkalaemia in ~1-10% of inpatients; ~50% of patients with CKD stage 4-5
- Hypokalaemia in ~20% of inpatients, mostly diuretic-related
- Drug-induced causes dominate both - RAAS inhibitors, MRAs, trimethoprim for high; thiazides and loops for low
Aetiopathogenesis
Hyperkalaemia
A. Reduced excretion (the commonest mechanism)
- CKD/AKI - the dominant cause
- Hypoaldosteronism: Addison disease, type 4 RTA (diabetic hyporeninaemic hypoaldosteronism)
- Drugs: ACE inhibitors, ARBs, spironolactone/eplerenone/amiloride, NSAIDs, trimethoprim (blocks ENaC like amiloride), heparin, calcineurin inhibitors, digoxin toxicity, beta-blockers
B. Transcellular shift out of cells
- Metabolic acidosis (mineral acidosis - not lactic or ketoacidosis, where the anion enters the cell)
- Insulin deficiency / hyperglycaemia and hyperosmolality - the mechanism in DKA
- Rhabdomyolysis, tumour lysis, massive haemolysis, burns
- Suxamethonium (contraindicated in burns, denervation, prolonged immobility)
- Hyperkalaemic periodic paralysis
C. Increased intake - rarely alone; salt substitutes, transfusion of old blood, IV supplements
Hypokalaemia
A. Renal loss (urinary K+ >20 mmol/L or K+/creatinine >1.5 mmol/mmol)
- Diuretics - thiazide and loop, the commonest cause
- Hyperaldosteronism (hypokalaemia + hypertension + metabolic alkalosis -> Conn syndrome), Cushing, liquorice, renal artery stenosis
- RTA type 1 and 2 (hypokalaemia with a normal anion gap acidosis)
- Bartter (loop-like) and Gitelman (thiazide-like, with hypomagnesaemia and hypocalciuria)
- Amphotericin, aminoglycosides, cisplatin
- Hypomagnesaemia - refractory hypokalaemia until magnesium is replaced
B. GI loss (urinary K+ <20)
- Diarrhoea (with a normal anion gap acidosis), laxative abuse, villous adenoma, fistula
- Vomiting/NG loss - loses H+ and Cl-, driving renal K+ loss via secondary hyperaldosteronism and bicarbonaturia (metabolic alkalosis)
C. Transcellular shift into cells
- Insulin, beta-2 agonists, alkalosis, refeeding syndrome, thyrotoxic periodic paralysis, theophylline
Diagnosis
Hyperkalaemia - ECG changes, roughly in order
1. Tall, peaked, narrow-based T waves (earliest)
2. PR prolongation, flattened/absent P waves
3. Widening QRS
4. Sine wave -> VF/asystole
- ECG changes correlate poorly with the level, and a normal ECG never excludes danger - but any change mandates immediate calcium
- Also: bradycardia, junctional rhythm, ECG mimicking STEMI or Brugada pattern
Hypokalaemia - ECG
- Flattened T waves, ST depression, prominent U waves, prolonged QU
- Ventricular ectopy, torsades, digoxin toxicity potentiation
Workup
- Repeat sample to exclude pseudohyperkalaemia; 12-lead ECG immediately
- UEC, glucose, magnesium, calcium, phosphate, CK, venous gas with lactate
- Urinary potassium and creatinine, urine osmolality (TTKG largely abandoned) - separates renal from extrarenal loss
- Acid-base pattern is highly discriminating
- Second-line: aldosterone/renin ratio, short synacthen, urinary chloride (vomiting <20 vs diuretics/Bartter >20)
Management
Hyperkalaemia - four steps, in order
### 1. Stabilise the myocardium
- IV calcium - gluconate 10% 10-30 mL, or calcium chloride 10% 10 mL via central access
- Indicated for any ECG change, or K+ >6.5
- Onset 1-3 min, duration only 30-60 min - repeat as needed
- *No potassium-lowering effect whatsoever* - it buys time
- Traditional caution in digoxin toxicity is now regarded as overstated; give it if the ECG demands
### 2. Shift potassium into cells
- Insulin + glucose: 10 units actrapid with 50 mL of 50% dextrose
- Onset 15-30 min, lasts 4-6 h, falls ~0.6-1.2 mmol/L
- Monitor BSL hourly for 6 hours - hypoglycaemia is the commonest iatrogenic complication; omit dextrose only if BSL >15
- Nebulised salbutamol 10-20 mg - additive to insulin, falls ~0.5-1 mmol/L; tachycardia, ~30% do not respond
- Sodium bicarbonate has only a modest and unreliable potassium-lowering effect, except with significant metabolic acidosis - not a primary agent
### 3. Remove potassium from the body - the only step that actually treats it
- Loop diuretic +/- IV fluid if the patient makes urine and is not volume-depleted
- Potassium binders
- Sodium zirconium cyclosilicate (SZC) - onset ~1 h; or patiromer - onset ~7 h
- Resonium (calcium/sodium polystyrene sulfonate) is slow, poorly evidenced and causes colonic necrosis with sorbitol - largely superseded
- Dialysis - definitive; for refractory hyperkalaemia, oligoanuric AKI, or established ESKD
### 4. Prevent recurrence
- Cease the culprit drug - trimethoprim, NSAID, MRA, potassium supplement, salt substitute
- Dietary potassium restriction and dietitian review
- Binders now allow RAAS inhibition to be continued in heart failure and CKD rather than abandoned - prefer this to withdrawing prognostic therapy
- Treat the underlying cause: fludrocortisone in hypoaldosteronism, insulin in DKA
Hypokalaemia
- Replace magnesium first or simultaneously - hypokalaemia is refractory until Mg is corrected
- Oral replacement wherever possible - safer and faster than IV
- IV: maximum 10 mmol/h peripherally; up to 20 mmol/h centrally with continuous cardiac monitoring
- Never give undiluted; never as a rapid bolus
- Severe (<2.5) or symptomatic (arrhythmia, weakness, paralysis, rhabdomyolysis) -> IV + monitored bed
- Correct the cause: change diuretic, add a potassium-sparing agent, treat vomiting/diarrhoea
- In thyrotoxic and hypokalaemic periodic paralysis, potassium is redistributed not depleted - replace cautiously to avoid rebound hyperkalaemia
- Recheck K+ and Mg after each replacement episode
Associations
- CKD and AKI
- Diabetes - DKA, type 4 RTA, insulin therapy
- Heart failure on RAAS inhibitors and MRAs
- Addison disease, congenital adrenal hyperplasia
- Primary hyperaldosteronism, Cushing syndrome
- Rhabdomyolysis, tumour lysis syndrome, massive transfusion
- Alcohol use disorder and refeeding syndrome (hypokalaemia, hypophosphataemia, hypomagnesaemia)
- Digoxin therapy - hypokalaemia potentiates toxicity, hyperkalaemia marks acute toxicity
Natural history & complications
- Hyperkalaemia >6.5 or with ECG change is an immediate arrhythmic risk - VF or asystole without warning
- Rate of rise matters more than the absolute level - a dialysis patient at 6.5 is often stable; an acute rise to 6.0 in rhabdomyolysis is not
- Hyperkalaemia in CKD and heart failure is chronic and recurrent, and its main harm is often under-treatment of the underlying disease through RAAS inhibitor withdrawal
- Hypokalaemia: chronic depletion -> nephrogenic diabetes insipidus, hypokalaemic nephropathy, rhabdomyolysis, ileus, arrhythmia
- Over-rapid correction of either direction causes harm - check frequently and reassess the cause
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