SIGNS AND SYMPTOMS 
History
- Hyperkalemia is often asymptomatic, even at high levels.
- Neuromuscular symptoms, predominantly weakness, which can progress to paralysis.
- Dyspnea owing to respiratory muscle weakness.
- Cardiac dysrhythmias may be the initial manifestation, so patients could also present with chest pain, palpitations, or syncope.
Physical Exam
- Muscular weakness (rare except in severe cases)
- Paralysis has been described
- Cardiac dysrhythmias (see ECG Changes)
ESSENTIAL WORKUP
- Serum potassium > 5 mmol/L
- Collect in heparinized tube if pseudohyperkalemia suspected.
DIAGNOSIS TESTS & INTERPRETATION
Lab
- Electrolytes, BUN, creatinine, glucose:
- Elevated BUN, creatinine in renal failure
- Hyponatremia with mineralocorticoid deficiency
- Mild metabolic acidosis with type IV renal tubular acidosis
- Arterial blood gases:
- Creatinine kinase:
- Rhabdomyolysis can lead to renal insufficiency and result in hyperkalemia
- Ca2+
- For hyperkalemia in face of normal renal function, calculate transtubular potassium gradient (TTKG):
- TTKG = urine K × Posm/plasma K × Uosm
- Posm, plasma osmolality; Uosm, urine osmolality
- TTKG > 8 suggests extrarenal cause; TTKG < 6 indicates renal excretory defect.
Diagnostic Procedures/Surgery
- ECG: Changes correlate with degree of hyperkalemia:
- > 5–6.5: Peaking of T-waves; shortening of QTc interval
- > 6.5–8: PR prolongation; loss of P-waves; widening of QRS complexes
- > 8: Intraventricular blocks; bundle branch blocks; QRS axis shifts; sine wave complex
- Serum potassium cannot be reliably predicted by ECG:
- Some patients (particularly those with chronic renal failure) will tolerate higher potassium levels than others.
- Potassium effects (as seen on ECG) are more important than potassium level
- While unusual, the ECG can be normal in the setting of severe hyperkalemia
DIFFERENTIAL DIAGNOSIS
Pseudohyperkalemia
ALERT
Most common cause of hyperkalemia reported by lab is pseudohyperkalemia owing to hemolysis of red blood cells.
[Outline]
PRE-HOSPITAL
- Treatment of hyperkalemic-induced dysrhythmias/cardiac arrest involves different drugs from usual advanced cardiac life support (ACLS) measures (see Treatment, below):
- Inhaled albuterol can lower potassium temporarily by 1 mmol/L.
- β-agonists can also be administered by metered-dose inhaler or intravenously
- Sodium bicarbonate can be effective in the setting of a metabolic acidosis.
- Calcium chloride or gluconate is available in some prehospital systems and should be considered in the unstable patient when hyperkalemia is suspected.
- Diagnosis suggested by prehospital rhythm strip or in at-risk populations (renal failure)
INITIAL STABILIZATION/THERAPY
- ABCs
- IV access
- Cardiac monitor
ED TREATMENT/PROCEDURES
- Hyperkalemia with ECG changes (widened QRS complexes): Antagonize potassium-mediated cardiotoxicity:
- Administer calcium gluconate (in awake patient) or calcium chloride (in patient without pulse):
- Onset 1–3 min
- 30–60 min duration
- No effect on total serum potassium levels
- Severe (> 7) or moderate (6–7) with ECG changes (heightened T-waves or loss of P-wave): Shift potassium intracellularly:
- Administer combination of insulin and glucose:
- Onset 20–30 min
- 2–4 hr duration
- IV sodium bicarbonate:
- Much more effective in patient who is acidotic
- Onset 20 min
- 2 hr duration
- Caution in patients at risk for volume overload
- Worsens concomitant hypocalcemia and hypernatremia
- Inhaled albuterol:
- Onset within 30 min
- 2–4 hr duration
- Can also be given by metered-dose inhaler or intravenously
- Calcium should be administered if the patient is unstable
- Enhanced excretion for K+ > 6 without ECG changes:
- Administer cation exchange resin:
- All patients:
- Limit exogenous potassium and potassium-sparing drugs.
- Treat underlying cause.
Special Situations
- Renal failure:
- Hemodialysis immediately effective at removing potassium
- Furosemide:
- Effective in the absence of oliguric renal failure
- Causes potassium-losing diuresis
- Cardiac arrest:
- Administer CaCl2 and NaHCO3 with known or suspected hyperkalemia.
- Digoxin toxicity:
- Avoid calcium if possible
- When necessary, administer small doses very slowly.
- Consider Digibind for K+ > 5.5 mmol/L.
- Mineralocorticoid deficiency:
MEDICATION
- Albuterol: 10–20 mg (peds: 2.5 mg if < 25 kg; 5 mg if ≥25 kg) nebulized over 10 min
- Calcium chloride 10%: 10 mL amp (peds: 0.2 mL/kg per dose) IV over 2–5 min
- Calcium gluconate 10%: 10 mL amp (peds: 0.6–1 mL/kg) IV over 2–5 min
- Furosemide: 40–80 mg (peds: 1 mg/kg) IV—modify dose to achieve appropriate diuresis
- Hydrocortisone: 100 mg (peds: 1–2 mg/kg) IV
- Insulin and glucose: 10 U (peds: 0.1 U/kg) regular insulin + 50 mL 50% (peds: 0.5–1 g/kg) dextrose IV
- Sodium bicarbonate: 1–3 amps (44 mEq per amp) IV over 20–30 min (peds: 1–2 mEq/kg per dose)
- Sodium polystyrene sulfonate (Kayexalate) or calcium polystyrene sulfonate (preferred with volume overload):
- Oral: 15 g mixed with water or 50 mL of sorbitol q2h to total of 5 doses
- Rectal enema: 50 g in 200 mL of sorbitol q4–6h
- Peds: 1 g/kg orally or rectally
First Line
- Calcium (under appropriate situations)
- Insulin and glucose
Second Line
- Sodium bicarbonate
- Kayexalate
- Albuterol
[Outline]
DISPOSITION
Admission Criteria
Admit most cases:
- Process of potassium removal is relatively slow.
- Most potassium is intracellular and, therefore, not measured on serum electrolytes.
- Significant changes in levels will take time.
- Levels may continue to rise.
Discharge Criteria
Mild hyperkalemia (< 5.5 mmol/L) provided that:
- Response to treatment has been demonstrated
- Known correctable cause
- Further rises in serum potassium not anticipated
- Early follow-up possible
Issues for Referral
Follow-up to address the underlying cause is important. In many cases, the underlying cause is renal insufficiency and the potassium will become elevated again if this is not addressed. Often this will mean regular hemodialysis.
FOLLOW-UP RECOMMENDATIONS
Many patients with hyperkalemia will be admitted. For those who are not, close follow-up and in many cases access to hemodialysis will be important.
[Outline]
- Alfonzo AV, Isles C, Geddes C, et al. Potassium disorders – clinical spectrum and emergency management. Resuscitation. 2006;70:10–25.
- Freeman K, Feldman JA, Mitchell P, et al. Effects of presentation and electrocardiogram on time to treatment of hyperkalemia. Acad Emerg Med. 2008;15(3):239–249.
- Halperin ML, Kamel KS. Potassium. Lancet. 1998;352:135–140.
- Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med. 2000;18:721–728.
- Rodrguez-Soriano J. Potassium homeostasis and its disturbances in children. Pediatr Nephrol. 1995;9(3):364–374.
- Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36(12):3246–3251.
See Also (Topic, Algorithm, Electronic Media Element)