How to "De-potash" a Patient (Treatment of Hyperkalemia)

"Depotashing" refers to lowering an elevated serum potassium (hyperkalemia, K+ > 5.0 mEq/L). Management follows three sequential pillars:

Approach to treatment of hyperkalemia - NKF Primer

Step 0 - Immediate Assessment

12-lead ECG immediately - look for peaked T waves, prolonged PR, wide QRS, sine wave pattern, or VF.
Any ECG change OR K+ ≥ 6.5-7.0 mEq/L = medical emergency requiring admission and continuous cardiac monitoring.
Exclude pseudo-hyperkalemia (hemolyzed sample, extreme leukocytosis/thrombocytosis).

Pillar 1 - Stabilize the Heart (Membrane Protection)

Intravenous Calcium - does NOT lower K+, but protects the myocardium immediately.

Preparation	Dose	Route	Onset	Duration
Calcium gluconate 10%	10 mL (repeat if needed)	IV over 2-3 min	1-3 min	30-60 min
Calcium chloride 10%	3-4 mL	IV over 2-3 min	1-3 min	30-60 min

Repeat if ECG changes persist or recur after initial improvement.
Caution in digoxin toxicity: hypercalcemia potentiates digoxin toxicity. If needed, dilute in 100 mL D5W and infuse over 20-30 min.
Do NOT mix calcium with bicarbonate (precipitates calcium carbonate).

Pillar 2 - Shift K+ Into Cells (Temporizing)

These buy time; they do not remove K+ from the body.

A. Insulin + Glucose (most reliable)

10 units regular insulin IV + 50 mL of 50% dextrose (D50) bolus immediately.
Effect: starts in 10-20 min, peaks at 30-60 min, lasts 4-6 hours. Drops K+ by ~0.5-1.2 mEq/L.
Follow with 5-10% dextrose infusion at 50-100 mL/hr to prevent hypoglycemia (occurs in up to 75% without ongoing glucose).
If blood glucose > 200-250 mg/dL: give insulin alone, monitor glucose closely.
Never give dextrose without insulin - may paradoxically worsen hyperkalemia in insulin-deficient patients.

B. Beta-2 Agonists (additive to insulin)

Albuterol (salbutamol) 20 mg nebulized over 10 minutes.
Onset ~30 min; effect is additive to insulin and also reduces risk of hypoglycemia.
Note: the dose for hyperkalemia is far higher than asthma dosing.
IV albuterol 0.5 mg is equivalent (available in Europe, not the US).

C. Sodium Bicarbonate (controversial)

Useful only if severe metabolic acidosis is present (HCO3 < 10 mmol/L) or in patients with residual kidney function.
Does NOT enhance the K+-lowering effect of insulin or albuterol.
Little benefit in ESKD/dialysis patients without residual renal function.
Do not give in same IV line as calcium.

Pillar 3 - Remove K+ from the Body (Definitive)

A. Loop Diuretics

Furosemide (or bumetanide): effective if patient has adequate residual kidney function.
Useful for hypervolemic, non-oliguric patients.

B. Dialysis

Most effective method but cannot usually be initiated fast enough to skip the above steps.
Indications: severe AKI, ESKD, oliguric hyperkalemia unresponsive to medical management.
Hemodialysis preferred over peritoneal dialysis for speed.

C. Potassium Binders (adjuncts, not emergency monotherapy)

Drug	Mechanism	Onset	Dose	Key Adverse Effects
Sodium polystyrene sulfonate (SPS / Kayexalate)	Na+-K+ exchange resin	Hours to days	50 g PO or PR in sorbitol	Diarrhea, metabolic alkalosis, rare colonic necrosis (FDA black box)
Patiromer (Veltassa)	Binds K+ in exchange for Ca2+ in colon	~7 hours	8.4 g once daily PO	Constipation, hypomagnesemia; separate from other oral meds by 3 h
Sodium zirconium cyclosilicate (Lokelma)	Binds K+ in exchange for H+/Na+ across entire GI tract	~1 hour	10 g TID x 48h, then 5 g daily	Constipation, edema (high sodium content); raises gastric pH

Patiromer and zirconium cyclosilicate are approved for chronic management and are the preferred binders for long-term use. SPS is not approved for chronic use.

Non-Emergent / Chronic Hyperkalemia Management

Dietary counseling: restrict K+ to ~60 mEq/day; avoid salt substitutes (KCl).
Medication review: stop/reduce ACE inhibitors, ARBs, NSAIDs, potassium-sparing diuretics, heparin if possible.
Ensure effective diuretic therapy: loop diuretics are especially important when eGFR < 30 mL/min.
Oral NaHCO3: corrects metabolic acidosis, enhances renal K+ excretion in patients with residual kidney function.
Potassium binders (patiromer or zirconium cyclosilicate): can also facilitate continued use of RAASi at recommended doses in CKD/heart failure patients.

Quick Reference Summary

Intervention	Goal	K+ Drop	Onset	Duration
IV Calcium	Membrane stabilization	None	1-3 min	30-60 min
Insulin + Glucose	Cell shift	0.5-1.2 mEq/L	10-20 min	4-6 h
Nebulized Albuterol 20 mg	Cell shift	0.5-1.0 mEq/L	30 min	2-4 h
NaHCO3	Cell shift (+ renal excretion)	Variable	30-60 min	Variable
Loop diuretics	Removal	Variable	30-60 min	Hours
Dialysis	Removal	1-2+ mEq/L/session	1-2 h setup	Rapid
K+ binders	Removal (GI)	0.5-1.0 mEq/L	Hours-days	Chronic

Sources: Brenner & Rector's The Kidney (9th ed.), p. 773-774 | NKF Primer on Kidney Diseases, 8e, p. 128-129 | Fischer's Mastery of Surgery, 8th ed., p. 218

Recent evidence note: A 2025 network meta-analysis (PMID 40542996) confirms novel K+ binders (patiromer and zirconium cyclosilicate) are superior to SPS in CKD/heart failure patients needing RAASi, reinforcing the current shift away from SPS for chronic management.

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