Hyperkalemia

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Original Editors -Courtney Ahlers & Jessica Ketterer from Bellarmine University's Pathophysiology of Complex Patient Problems project.

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Definition/Description

Hyperkalemia is characterized by an elevated serum potassium level greater than 5.5 mmol/L and is classified as an electrolyte abnormality.   Acute hyperkalemia is often preceded by issues such as illness, dehydration, or introduction of medications that affect potassium levels.  

Prevalence

Approximately 1 to 10 percepnt of hospital patients are affected by hyperkalemia. 

The mortality rate for patients with hyperkalemia is approximately 1 in 1000.

Characteristics/Clinical Presentation

Hyperkalemia most commonly occurs in patients with chronic renal failure.

Signs and Symptoms

1. muscular weakness
2. flaccid paralysis
3. ileus
4. ECG changes
5. nausea
6. slow, weak or irregular pulse
7. sudden collapse (heart rate too slow or stops)
8. paraestesias
9. fatigue
10. palpitations

Potassium is regulated through excretion via the renal system. When this system's function declines, the extracellular potassium concentration increases and can lead to membrane excitability.  Some signs and symptoms listed above are a result of the impaired nerve conduction and muscle contraction dysfunction.  Muscular dysfunction includes the cardiac system and can lead to life threatening ventricular arrhythmias.  Electrocardiogram (ECG) dysfunction is more common in patients with acute hyperkalemia.

Associated Co-morbidities

Table 1                                 Disorders Causing Hyperkalemia
Disorders leading to hyperkalemia caused by impaired renal excretion of potassium	Disorders leading to hyperkalemia caused by shift of potassium into the extracellular space
acquired hyporeninemic hypoaldosteronism	acidosis
Addison's disease	damage to tissue from rhabdomyolysis, burns, or trauma
congenital adrenal hyperplasia (recessive or autosomal dominant)	familial hyperkalemic periodic paralysis
mineralocorticoid deficiency	hyperosmolar states (uncontrolled diabetes, glucose infusions)
primary hypoaldosteronism or hyporeninemia	tumor lysis syndrome
pseudohypoaldosteronism	insulin deficiency or resistance
renal insufficiency or failure
systemic lupus erythematosus
type IV renal tubular acidosis

Medications

TABLE 5 Medications Used in Acute Treatment of Hyperkalemia
Medication	Dosage	Onset	Length of Effect	Mechanism of Action	Cautions
Calcium gluconate	10 to 20 mL of 10 percent solution IV over two to three minutes	immediate	30 minutes	Protects myocardium from toxic effects of calcium; no effect on serum potassium level	Can worsen digoxin toxicity
Insulin	Regular insulin 10 units IV with 50 mL of 50 percent glucose	15 to 30 minutes	two to six hours	Shifts potassium out of the vascular space and into the cells; no effect on total body potassium	Consider 5 percent dextrose solution infusion at 100 mL per hour to prevent hypoglycemia with repeated doses. Glucose unnecessary if blood sugar elevated above 250 mg per dL (13.9 mmol per L)
Beta agonists: Albuterol (Ventolin)	10 to 20 mg by nebulizer over 10 minutes (use concentrated form, 5 mg per mL)	15 to 30 minutes	two to three hours	Shifts potassium into the cells, additive to the effect of insulin; no effect on total body potassium	May cause a brief initial rise in serum potassium
Diuretics:  Furosemide (Lasix)	20 to 40 mg IV, give with saline if volume depletion is a concern	15 minutes to one hour	four hours	Increases renal excretion of potassium	Only effective if adequate renal response to loop diuretic
Potassium binding resins:  Sodium polystyrene sulfonate (Kayexalate)	Oral: 50 g in 30 mL of sorbitol solution Rectal: 50 g in a retention enema	one to two hours (rectal route is faster)	four to six hours	Removes potassium from the gut in exchange for sodium	Sorbitol may be associated with bowel necrosis. May lead to sodium retention

IV = intravenously

--Medications listed from most to least urgent.

Diagnostic Tests/Lab Tests/Lab Values

Initial diagnosis is initiated with patient history, medication review, and physical examination. 

Laboratory tests include:

1. serum electrolytes
2. creatinine
3. blood urea nitrogen (BUN)
4. spot urine test (potassium, creatinine, and osmoles)
5. transtubular potassium gradient (assessment of renal potassium handling)
6. trial of oral fludrocortisone (Florinef)

Patients will likely not present with symptoms of hyperkalemia until potassium levels have exceeded 7 mmol/L.

ECG is monitored in patients with hyperkalemia:

FIGURE 1

Etiology/Causes

Hyperkalemia is typically caused when the kidneys can no longer excrete potassium, when the body is unable to effectively distribute potassium between the extracellular and intracellular space, or the effects of medications (including increased potassium intake).  For hyperkalemia caused by decreased excretion of potassium, there is an insufficient delivery of sodium and water in the kidney and the presence of aldosterone.  For medication induced hyperkalemia, a combination of ACE inhibitors and spironolactone or the use of NSAIDs in patients with impaired kidney function or diabetes can predispose the patient.  Adrenal insufficiency is another potential cause, particularly when the patient also presents with hyponatremia and muscular weakness.  Congenital factors that can produce hyperkalemia include pseudohypoaldosteronism and aldosterone synthesis abnormalities.

Many factors influence the aforementioned causes of hyperkalemia:

Table 1. Causes of Hyperkalemia

Factitious hyperkalemia (laboratory value higher than serum value) - hemolysis due to specimen handling or collection error - laboratory error

Increased intake of potassium - potassium supplements - penicillin G potassium - nutritional supplements

Increased shift of potassium from intracellular space - exercise - tissue destruction (e.g., tumour lysis syndrome, rhabdomyolysis, trauma) - normal anion gap acidosis - lack of insulin - hyperosmolality - hyperkalemic periodic paralysis - medications (succinylcholine, beta blockers, digitoxin intoxication, intravenous amino acids)

Impaired renal potassium excretion - decreased flow (e.g. from decreased effective circulating volume, chronic or acute renal failure, nonsteroidal anti-inflammatories) - hypoaldosterone - primary adrenal insufficiency - medications (e.g. spironolactone, triamterene, amiloride, ACE inhibitors, ARBs, trimethoprim, pentamidine, cyclosporine, tacrolimus, heparin) - primamry renin insufficiency - pseudohypoaldosteronism - distal renal tubular acidosis - congenital adrenal hyperplasia - interstitial renal disease

Unknown mechanism - herbal medicine (e.g. alfalfa, dandelion, noni juice, horsetail, milkweed, thistle)

ACE = angiotensin-converting enzyme ARB = angiotensin receptor blocker

Systemic Involvement

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Medical Management (current best evidence)

The presence of ECG changes, a rapid rise of serum potassium, indications of decreased kidney function, or significant acidosis require immediate medical treatment for hyperkalemia.  Although ECG changes are common indicators for severe hyperkalemia, the patient may still have life threatening hyperkalemia even if ECG readings are normal.  The intent of immediate medical intervention is to stabilize the myocardium to prevent arrhythmias.  In addition to the medications listed in Table 5, total body potassium levels can be lowered through kidney excretion, gastrointestinal (GI) elimination, or dialysis.  Lowering via kidney excretion is achieved by the use of diuretics, while lowering via GI elimination occurs with the use of Kayexalate, both of which are explained in greater detail in Table 5.  Long term management is focused on addressing the underlying cause, which can be achieved by discontinuing medications or comsuming low potassium diets.

Figure 2:  Algorithm for the management of hyperkalemia.

Physical Therapy Management (current best evidence)

Potassium levels < 3.2 mEq/L or > 5.1 mEq/L contraindicated for physical therapy intervention due to the potential for arrhythmia and tetany.

Alternative/Holistic Management (current best evidence)

No research indicates there is an effective method to manage hyperkalemia via alternative or hoistic medicine.

Differential Diagnosis

Pseudohyperkalemia occurs when lab reports indicate elevated serum potassium levels but the patient does not actually have elevated serum potassium.  This phenomenon occurs most commonly with destruction of red blood cells with collection of blood specimen.

Case Reports/ Case Studies

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Resources

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Recent Related Research (from Pubmed)

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References

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