Rosen & Barkin's 5-Minute Emergency Medicine Consult (363 page)

• Serum potassium >5 mmol/L
  
• Collect in heparinized tube if pseudohyperkalemia suspected.
  

• 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:
  
  • Assess acid–base status
    
• Creatinine kinase:
  
  • Rhabdomyolysis can lead to renal insufficiency and result in hyperkalemia
    
• Ca
  ²⁺
  
• 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.
    

• ECG: Changes correlate with degree of hyperkalemia:
  
  • >5–6.5: Peaking of T-waves; shortening of QT
    _c
    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
    

Pseudohyperkalemia

TREATMENT

• 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)
  

• ABCs
  
• IV access
  
• Cardiac monitor
  

• 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:
    
    • Calcium or sodium polystyrene sulfonate PO or per rectum (PR)
      
    • Avoid in patients with suspected ileus or bowel obstruction.
      
• All patients:
  
  • Limit exogenous potassium and potassium-sparing drugs.
    
  • Treat underlying cause.
    

• Renal failure:
  
  • Hemodialysis immediately effective at removing potassium
    
  • Furosemide:
    
    • Effective in the absence of oliguric renal failure
      
    • Causes potassium-losing diuresis
      
• Cardiac arrest:
  
  • Administer CaCl
    ₂
    and NaHCO
    ₃
    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:
  
  • Administer hydrocortisone
    

• 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
    

• Calcium (under appropriate situations)
  
• Insulin and glucose
  

• Sodium bicarbonate
  
• Kayexalate
  
• Albuterol
  

FOLLOW-UP

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.
  

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
  

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.

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.

• Potassium effect is more important than absolute potassium level. The ECG is the most important determinate of need to treat acutely.
  
• Do not wait for confirmation of the potassium level to treat when the ECG indicates a hyperkalemic emergency
  
• Hyperkalemia is often asymptomatic until late: Obtain an ECG early in patients at risk.
  
• Sodium bicarbonate administration can easily lead to volume overload if not careful.
  

• 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)

• Dialysis Complications
  
• Renal Failure
  

CODES

• 276.7 Hyperpotassemia
  
• 583.89 Nephritis and nephropathy, not specified as acute or chronic, with other specified pathological lesion in kidney
  
• 586 Renal failure, unspecified