Hyperkalemia, Emergency Medicine

Basics

Description

Potassium distribution:
- Extracellular space: 2%
- Intracellular space: 98%
Potassium excretion:
- Renal: 90%
- GI: 10%
Renal (80 " 90%) and extrarenal mechanisms maintain normal plasma concentration between 3.5 and 5 mmol/L.
Renal excretion of potassium affected by:
- Dietary intake
- Distal renal tubular function
- Acid " base balance
- Mineralocorticoids
Regulation between intracellular and extracellular potassium balance is affected by:
- Acid " base balance
- Insulin
- Mineralocorticoids
- Catecholamines
- Osmolarity
- Drugs

Etiology

Decreased potassium excretion:
- Most common cause: Renal failure (acute or chronic)
- Distal tubular diseases:
  - Acute interstitial nephritis
  - Renal transplant rejection
  - Sickle cell nephropathy
  - Renal tubular acidosis (diabetes)
- Mineralocorticoid deficiency:
  - Addison disease
  - Hypoaldosteronism
- Drugs:
  - ACE inhibitors/angiotensin receptor blockers
  - ²-blockers
  - Potassium-sparing diuretics
  - NSAIDs
  - Cyclosporine
  - High-dose trimethoprim
  - Lithium toxicity
Intracellular to extracellular potassium shifts:
- Metabolic acidosis:
  - Serum K+ rises 0.2 " 1.7 mmol/L for each 0.1 U fall in arterial pH.
- Hyperosmolar states
- Insulin deficiency
- Cell necrosis
- Rhabdomyolysis
- Hemolysis
- Chemotherapy
- Drugs:
  - Digitalis toxicity
  - Depolarizing muscle relaxants (e.g., succinylcholine)
  - ²-blockers
  - α-agonists
- Hyperkalemic periodic paralysis
Excess exogenous potassium load:
- Cellular breakdown:
  - Trauma
  - Tumor lysis
- Salt substitutes
- Oral potassium
- Potassium penicillin G
- Rapid transfusions of banked blood
Pseudohyperkalemia:
- Traumatic venipuncture with hemolysis
- Postvenipuncture release of potassium can occur in the setting of:
  - Thrombocytosis (platelets >800,000/mm3)
  - Extreme leukocytosis (WBC >100,000/mm3)
- Prolonged tourniquet time

Diagnosis

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:
- Assess acid " base status
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
Most common cause of hyperkalemia reported by lab is pseudohyperkalemia owing to hemolysis of red blood cells.

Treatment

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.
  - ²-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:
  - 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.

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:
- Administer hydrocortisone

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

Follow-Up

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.

Followup 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.

Pearls and Pitfalls

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.

Additional Reading

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.

Codes

ICD9

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
996.81 Complications of transplanted kidney

ICD10

E87.5 Hyperkalemia
N05.9 Unsp nephritic syndrome with unspecified morphologic changes
N19 Unspecified kidney failure
T86.11 Kidney transplant rejection

SNOMED

14140009 hyperkalemia (disorder)
42399005 renal failure syndrome (disorder)
28689008 Interstitial nephritis (disorder)
236570004 Renal transplant rejection (disorder)
237849008 Drug-induced hyperkalemia (disorder)

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