CONTENTS
- Rapid Reference: treatment for severe hyperkalemia 🚀
- Diagnosis of hyperkalemia
- Severity & risk stratification
- Causes of hyperkalemia
- Investigation of the etiology of hyperkalemia
- Treatment: Moderate hyperkalemia
- Treatment of severe hyperkalemia
- Sodium zirconium cyclosilicate
- Podcast
- Questions & discussion
- Pitfalls
volume resuscitation if hypovolemic
- Bicarb <22 mM ➡️ use isotonic bicarbonate. 💉
- Bicarb >22 mM ➡️ use lactated Ringers or plasmalyte.
- ⚠️ Don't give normal saline (it will increase the potassium).
temporizing measures
- IV calcium ⚡️ (1 gram of calcium chloride, or 3 grams of calcium gluconate).
- Dextrose/insulin: ⚡️
- 5 units regular insulin as an intravenous bolus.
- If glucose <250 mg/dL (<14 mM), give ~two ampules of D50W (100 ml total) –or– ~500 ml of D10W infused over four hours.
- Beta-2 agonist: ⚡️
- Albuterol: 10-20 mg nebulized (e.g., 4-8 standard nebs back-to-back, or a continuous neb).
- Terbutaline 7 mcg/kg s.q. (or ~0.5 mg).
- Epinephrine gtt if hypotensive/bradycardic.
kaliuresis for patients who can produce urine ⚡️
- Relatively normal renal function: IV loop diuretic alone may be sufficient (e.g., 60-160 mg IV furosemide).
- Moderate/severe renal dysfunction with possible need for emergent dialysis: Attempt to avoid dialysis using aggressive diuretics:
- 💣 Loop diuretic (e.g., 160-250 mg IV furosemide or 4-5 mg IV bumetanide).
- 💣 Thiazide (500-1,000 mg IV chlorothiazide, or 5-10 mg metolazone).
- 💣 +/- Acetazolamide (250-1,000 mg IV/PO).
- 💣 +/- Fludrocortisone 0.2 mg PO (esp. patients on ACEi/ARB, tacrolimus).
- Replace urine losses with crystalloid to avoid hypovolemia.
- Bicarb <22 mM ➡️ use isotonic bicarbonate. 💉
- Bicarb >22 mM ➡️ use lactated Ringers.
sodium zirconium cyclosilicate ⚡️
- This is only mildly effective, so it shouldn't be relied upon as the sole treatment.
- May help avoid or delay dialysis in borderline cases.
- Dose is 10 grams PO q8hrs.
dialysis indications
- (1) Chronic hemodialysis.
- (2) Failure of other measures (no response to diuretic bomb and not a candidate for large-volume expansion with isotonic bicarbonate).
hyperkalemia is usually asymptomatic
- Most patients are asymptomatic (even with severe hyperkalemia).
- Left untreated, hyperkalemia may manifest in the following ways:
- Bradycardia.
- Neuromuscular weakness (uncommonly seen; may cause muscle fasciculations, paresthesias, depressed reflexes, and ascending weakness). (32852924)
- Ventricular tachycardia/fibrillation (syncope, palpitations), sudden cardiac death.
ECG in hyperkalemia
- Hyperkalemia can cause a very wide range of ECG changes.
- The textbook sequence of changes illustrated above often doesn't occur. (29244647) Instead, hyperkalemia can mimic a wide variety of pathologies (including STEMI and all varieties of bundle/conduction blocks).
- Severe hyperkalemia (e.g. K>7 mM) can occur without obvious ECG changes.
- The following patterns are highly suggestive of hyperkalemia. In an unstable patient, it may be reasonable to give IV calcium based on patterns #2-4 below while awaiting a potassium level.
- [1] Peaked T-waves:
- Narrow, pointy, prominent T-waves.
- Often this is the most notable finding on the ECG (may be visible on bedside monitor as well).
- [2] Ventricular tachycardia mimic:
- QRS wave widens and P-waves may disappear. If patient is tachycardic, this may look like ventricular tachycardia.
- Useful clues: Compared to ventricular tachycardia, T-waves can be sharper than would be usual and heart rate is often slower than would be typical.
- [3] Sine-wave pattern:
- Profound widening of QRS complex and peaked T-waves mimics a sine wave.
- [4] Bradycardia:
- Hyperkalemia can manifest with bradycardia (often in the context of other drugs that slow down the AV node).
- There should always be a high suspicion for hyperkalemia in any bradycardic patient, especially if there are other ECG findings to suggest hyperkalemia.
laboratory diagnosis & pseudohyperkalemia
Hyperkalemia is variably defined as potassium >5.5 mM or >5.0 mM, differing between various guidelines and publications. (38425037)
pseudohyperkalemia refers to artificially elevated potassium due to:
- [1] In vitro hemolysis.
- Most hemolysis occurs as an in vitro artefact. In this case the patient isn't truly hyperkalemic. Repeating the lab test will usually yield a lower potassium value.
- Sometimes patients have true intravascular hemolysis. In this case the hyperkalemia is real! Repeating the lab test will yield the same results (positive hemolysis & hyperkalemia).
- ⚠️ Point-of-care testing is generally accurate, but it cannot detect hemolysis. (32852924)
- [2] Severe polycythemias causing potassium release during clotting (e.g., platelets >1 million or WBC count >50,000). This can be avoided by point-of-care testing or measuring labs in a heparinized tube.
- [3] Prolonged tourniquet application or fist clenching during blood draw.
- [4] Delayed sample processing.
elevated potassium → look at the ECG
- The first response to a lab report of hyperkalemia should be to look at the telemetry tracing and obtain an ECG.
- If the telemetry/ECG shows features of hyperkalemia, this confirms the diagnosis.
- If the lab reports severe hyperkalemia but the ECG is normal, consider the possibility of pseudohyperkalemia and repeat the lab.
The first step of treatment requires determining whether hyperkalemia is life-threatening (severe). No evidence-based definition for “severe” hyperkalemia exists. Clinical judgement is needed, with attention to the following factors:
- Potassium level: >6.5-7 mM is more worrisome.
- Chronicity:
- Chronic hyperkalemia is better tolerated (e.g., dialysis patients who frequently have hyperkalemia).
- Acute hyperkalemia is more dangerous.
- ECG changes: are worrisome, in particular: (28874951)
- Bradycardia or junctional rhythm.
- QRS widening.
- Ongoing potassium release (e.g., by tumor lysis syndrome or rhabdomyolysis) increases the likelihood of progressive deterioration.
Below is a consensus definition of severe hyperkalemia from a KDIGO conference. (31706619) The European Resuscitation Council has similarly defined severe hyperkalemia as >6.5 mM. (30820692)
💡 Critically ill patients often develop hyperkalemia due to a combination of several factors (e.g. hypovolemia plus renal dysfunction plus an ACE-inhibitor). Successful treatment may require addressing many of these problems simultaneously.
medications
- Potassium supplements.
- ACEi / ARB, aliskiren (renin-inhibitor).
- NSAIDs.
- Nonselective beta-blockers (e.g., labetalol).
- Potassium-sparing diuretics:
- Amiloride, triamterene.
- Spironolactone, eplerenone, finerenone, drospirenone.
- Antibiotics:
- Ketoconazole.
- IV penicillin G-potassium.
- Pentamidine.
- Trimethoprim.
- Heparin (induces suppression of aldosterone synthesis)
- Calcineurin inhibitors (cyclosporine, tacrolimus) (May down-regulate mineralocorticoid receptors and also impair principal cell Na/K-ATPase inhibitors).
- Rarely:
- Aminocaproic acid.
- Baxdrostat (aldosterone synthase inhibitor).
- Digoxin toxicity.
cellular lysis releasing potassium
- Hemolysis, hematoma (severe hemolysis may cause persistent hemolysis with repeated laboratory measurements).
- Red blood cell transfusion.
- Rhabdomyolysis.
- TLS (tumor lysis syndrome).
- Tissue necrosis of other etiologies:
- Trauma.
- Infarction.
abnormal renal potassium handling
- Renal failure of any etiology with GFR below ~15 ml/min (usually, compensatory mechanisms can maintain potassium equilibrium until the GFR is very low).
- Hyporeninemic hypoaldosteronism (impaired renin synthesis in renal juxtaglomerular cells; renal function is often mild-moderately impaired):
- Chronic renal insufficiency due to diabetes and/or HTN (most common).
- Tubulointerstitial diseases.
- HIV.
- Nephrosclerosis.
- Aldosterone resistance due to diseases involving the tubulointerstitium:
- Obstructive uropathy.
- Sickle cell disease.
- Lupus nephritis.
- Kidney transplant rejection.
- Amyloidosis.
- Multiple myeloma or monoclonal gammopathy.
adrenal insufficiency, e.g.:
- Addison disease.
- Bilateral adrenal gland injury (e.g., Waterhouse-Friderichsen syndrome).
other
- DKA and/or hyperglycemic hyperosmolar nonketotic syndrome (HHS).
- Hyperkalemic periodic paralysis.
hyperkalemia laboratory package
- Every hyperkalemic patient doesn't need these labs. However, if you're in a rush and want to fire off a lot of labs, here are some to consider:
- 📦 Electrolytes including Ca/Mg/Phos.
- 📦 CK (creatinine kinase).
- 📦 LDH (lactate dehydrogenase).
- 📦 Random cortisol level.
- 📦 Urine potassium level, urine creatinine level.
[1] review medication list and consider clinical context
- The etiology of hyperkalemia is often clear based on a history and medication review.
- Renal failure is a very common etiology and this will be rapidly diagnosed.
[2] consider the possibility of cellular lysis
- Context is often suggestive (e.g., malignancy or risk for rhabdomyolysis).
- With normal renal function, cellular lysis will usually cause a transient elevation in potassium. If the potassium has remained stably elevated for several days, this suggests an alternative etiology.
- Laboratory constellation: may see hyperkalemia, hyperphosphatemia, hypocalcemia.
- Evaluation: check CK and LDH levels.
[3] consider the possibility of adrenal insufficiency
- Context is often suggestive (e.g., discontinuation of steroid, or chronic features of Addison disease, relatively low blood pressure).
- Laboratory constellation: may see hyperkalemia, NAGMA, hypoglycemia.
- Evaluation: start with random cortisol level.
[4] patients who have hyperkalemia plus NAGMA
- The differential diagnosis here centers around different forms of type IV RTA.
- Evaluation of this combination is discussed further in the chapter on NAGMA here: 📖
[1] treat any definable causes
- Treat all identifiable causes of hyperkalemia.
- Discontinue any nephrotoxins and establish a state of euvolemia with adequate perfusion.
- Consider a renal diet with limited potassium intake.
[2] gentle kaliuresis (renal excretion of potassium)
- Potassium excretion can generally be promoted using diuretic among patients able to produce urine (otherwise dialysis will be needed).
- Moderate hyperkalemia can generally be treated with a single diuretic (e.g. IV furosemide), followed by volume replacement with Lactated Ringer's to maintain a net even fluid balance. 🌊
- If this regimen fails, more aggressive therapies may be utilized with additional medications discussed below.
indications for IV calcium
- [1] ECG changes, especially:
- Bradycardia or other dysrhythmia.
- Conduction delays.
- (For patients with isolated peaked T-waves, use of calcium is controversial.)(34890894)
- [2] Acute hyperkalemia with K>6.5 mM is often considered an indication for intravenous calcium. (32852924) However, in the absence of ECG changes this is controversial and it may be reasonable to withhold IV calcium. (34890894)
- Patients with chronic renal failure on dialysis are often adapted to mild hyperkalemia. Such patients may also be at increased risk of complications following IV calcium administration (e.g., calcium-phosphate precipitation causing calciphylaxis). Consequently, in the context of chronic renal failure without ECG changes, it may often be wise to cautiously withhold IV calcium.
initial dose
- ⚠️ Rapid administration of IV calcium may cause abdominal discomfort, flushing, nausea, and vomiting.
- Peripheral access: 3 grams IV calcium gluconate over 10 minutes.
- Central access: 1 gram IV calcium chloride over 10 minutes.
- For persistent, dangerous arrhythmias (e.g., ongoing bradycardia with hypoperfusion) higher doses may be needed.
- Hyperkalemia is generally more dangerous than hypercalcemia, so you're probably better off erring on the side of hypercalcemia. If you have a point-of-care electrolyte monitor available, check calcium levels and avoid pushing the ionized calcium >3 mM.
repeat doses?
- Calcium only lasts for about 30-60 minutes, so the dose may need to be repeated.
- The ideal strategy for re-dosing is unknown. An expert guideline recommended re-dosing once or twice if needed, while admitting the lack of evidence. (28976587)
dosing
- Insulin dose: 5 units IV insulin (must be given IV). (27693804)
- Dextrose dose:
- Traditionally, 2 ampules of D50W has often been used (100 ml total, providing 50 grams of dextrose). Only one ampule of D50W may be inadequate to prevent hypoglycemia. (31084947)
- D10W may be used instead (e.g., 500 ml infused over 4 hours). D10W has the advantages of causing less rebound hypoglycemia and less irritation of veins.
- Dextrose administration may be omitted if the baseline glucose level is already >250 mg/dL (14 mM). (27148740) If the baseline glucose is high (e.g. ~180-250 mg/dL or 10-14 mM) then the dose of dextrose might be cut in half, to 25 grams.
subsequent monitoring
- Observe for the occurrence of hypoglycemia
- The potassium shift lasts for ~4 hours. (38425037) Consequently, this may need to be redosed periodically if there is a delay to definitive therapy (e.g., diuresis or dialysis).
albuterol
- ⚠️ In reality, albuterol is nearly always underdosed for hyperkalemia. The real-world efficacy of this intervention is consequently minimal.
- Albuterol causes a small shift of potassium into cells for ~2-4 hours.
- This requires a lot of albuterol (10-20 mg, equal to about 4-8 nebulizer treatments back-to-back). Logistically, the best way to achieve this dose is to provide albuterol as a continuous nebulized therapy.
- The reduction in plasma potassium is typically ~0.6-1 mEq/L, but the efficacy is roughly 50% lower in end-stage renal disease. (38425037)
- Onset occurs within 30 minutes, with a peak effect at 90-120 minutes. (38425037)
subcutaneous terbutaline 💊
- Terbutaline is arguably superior to albuterol.
- The advantage of terbutaline is that it is logistically feasible to administer a meaningful dose.
- The dose of terbutaline is 7 ug/kg s.q. (or ~0.5 mg). (15957133)
- ⚠️ Terbutaline does increase the heart rate, so this may be contraindicated for patients with myocardial ischemia or baseline tachycardia.
IV epinephrine
- Epinephrine should not be used solely for hyperkalemia. However, if the patient does require a vasopressor, then epinephrine may be a sensible choice.
- Epinephrine is phenomenal for hyperkalemia-induced bradycardia, because it simultaneously treats both the hyperkalemia and the bradycardia.
hypertonic bicarbonate doesn't work
- Ampules of hypertonic bicarbonate have been proven to be ineffective in several RCTs. (3052050, 1552710, 8852501, 9170015)
- Why? The hypertonic nature of the fluid pulls potassium out of the cells due to osmotic shifts (“solvent drag”). (2402122) This counteracts the effect of increasing the pH, with an overall neutral effect on the potassium.
isotonic bicarbonate does work in metabolic acidosis
- Isotonic bicarbonate 💉 is generally obtained by adding three amps of bicarbonate to a liter of D5W (this creates a 150 mM solution of bicarbonate).
- Isotonic bicarbonate decreases the potassium in three ways: (18936701)
- [1] Dilution.
- [2] Shifting of potassium into muscle cells.
- [3] Renal potassium excretion is promoted by alkalosis.
- Isotonic bicarbonate infusions have been demonstrated to work, but only for patients with metabolic acidosis. (1552710, 24132, 1668124) This requires giving 1-2 liters of fluid, so it is not a viable treatment for patients with volume overload.
- Substantial volumes of isotonic bicarbonate can cause a sustained reduction in potassium levels.
isotonic bicarbonate should often be used as a resuscitative crystalloid
- Many patients present with renal failure and hyperkalemia due to volume depletion. Isotonic bicarbonate is the preferred resuscitative fluid for hyperkalemic patients with metabolic acidosis (bicarbonate below ~20 mM).
- For patients with significant hypovolemia, bicarbonate should be infused rapidly (e.g., 500-1,000 ml/hour). This should be administered instead of another resuscitative crystalloid (such as normal saline or lactated ringers).
- A common mistake is to administer isotonic bicarbonate at 100-150 ml/hour alongside with another IV crystalloid. This is an error that will prevent achieving the full benefit of isotonic bicarbonate volume expansion. 📖
- The isotonic bicarbonate may be dosed with the goal of bringing the patient's serum bicarbonate level back to a high-normal level (24-28 mM). The dose can be estimated by calculating the patient's bicarbonate deficit. 🧮 Divide the bicarbonate deficit by 150 to estimate the number of liters of isotonic bicarbonate needed. The dose is usually 1-2 liters. (Of course, the ability to provide large volumes of bicarbonate may be limited if the patient becomes volume overloaded.)
- If the patient remains hypovolemic after receiving enough sodium bicarbonate to increase the bicarbonate level >24 mEq/L, then any residual hypovolemia can subsequently be treated with lactated ringers.
dialysis vs. kaliuresis
- Ultimately, most patients will require elimination of excess potassium from the body. This may be achieved either via the kidneys (kaliuresis) or via dialysis.
- Patients with end-stage renal disease on chronic dialysis will require emergent dialysis (attempting kaliuresis is futile). For most other patients, kaliuresis should be attempted prior to emergent dialysis, using the following steps:
kaliuresis step #1 = volume resuscitation if hypovolemic
- Patients with metabolic acidosis should be resuscitated with isotonic bicarbonate as discussed above. 📖
- If bicarbonate level is normal/elevated, lactated ringers or plasmalyte are the preferred resuscitative fluids.
kaliuresis step #2 = diuretics +/- fludrocortisone
general concept of kaliuresis
- Kaliuresis involves using potassium-wasting diuretics to stimulate potassium excretion in the urine.
- Higher diuretic doses and more diuretics should be utilized in:
- More severe hyperkalemia.
- More severe renal dysfunction (which causes diuretic resistance).
- In life-threatening hyperkalemia, it's often better to err on the side of giving excessive diuretic. If the patient experiences a large-volume diuresis, this can be easily corrected by giving back crystalloid. Alternatively, if in inadequate diuretic dose is given, this may lead to arrhythmias or unnecessary dialysis. For maximum potency, a combination of three diuretics may be used (when given at maximal doses this is termed the nephron bomb).
agents & dosing:
- 💣 Loop diuretic (e.g., 80-250 mg IV furosemide or 2-5 mg IV bumetanide).
- 💣 +/- Thiazide (500-1,000 mg IV chlorothiazide, or 5-10 mg metolazone).
- 💣 +/- Acetazolamide (250-1,000 mg IV/PO).
- 💣 +/- Fludrocortisone 0.2 mg PO:
- Fludrocortisone may help stimulate the kidneys to secrete potassium. This is most effective among patients with known or potential type IV RTA such as ACEi/ARB or NSAIDs (etiologies listed here: 📖)
- Consider fludrocortisone if the patient starts producing lots of urine, but the potassium level isn't falling (i.e., the potassium content of the urine is inadequately low).
kaliuresis step #3 = determine response to diuretic
- If the patient doesn't produce urine in response to diuretic, then kaliuresis has failed. Dialysis will generally be required.
- If the patient does produce urine:
- Urine volume should generally be replaced with crystalloid to prevent volume depletion.
- Bicarb <22 mM ➡️ use isotonic bicarbonate. 💉
- Bicarb >22 mM ➡️ use lactated Ringers.
- Electrolytes (including magnesium) should be checked frequently and repleted as needed.
- Urine volume should generally be replaced with crystalloid to prevent volume depletion.
sodium zirconium cyclosilicate
- Sodium zirconium cyclosilicate is an oral potassium binder that is safe and somewhat effective (essentially a next-generation version of Kayexalate). 🌊
- Sodium zirconium cyclosilicate causes about ~0.2 mM reduction in potassium within 4 hours and ~0.4 mM reduction within 24 hours. This effect size is small. Whether this is clinically beneficial depends on the context:
- For an anuric patient with severe hyperkalemia, sodium zirconium cyclosilicate will predictably fail. Such patients require emergent dialysis. Don't delay dialysis while hoping that sodium zirconium cyclosilicate will treat the hyperkalemia.
- For patients on the borderline of requiring dialysis, a small reduction in potassium might be beneficial. In some situations, this could stave off dialysis for long enough that kidney function could recover.
- The dose is 10 grams PO q8hrs.
(kayexalate or patiromer)
- ⚠️ Kayexalate is currently antiquated and should not be utilized:
- Patiromer:
- Patiromer is less effective than sodium zirconium cyclosilicate for acute management of hyperkalemia.
- A single oral dose of patiromer may decrease potassium by ~0.23 mM within seven hours of administration. (38425037)
- Patiromer should only be used for acute hyperkalemia in hospitals without access to sodium zirconium cyclosilicate. It's OK to use patiromer in that context, but you shouldn't have high hopes about its efficacy.
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- The following therapies should be avoided: kayexalate, hypertonic bicarbonate (bicarbonate ampules), normal saline.
- Don't provide temporizing measures without definitive therapy (e.g. patient is given insulin/glucose but no other treatment). This will temporarily make the potassium look better, but the hyperkalemia will inevitably recur later on.
- Insulin dosing errors: 5 units must be given intravenously (not subcutaneously).
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