Hyperkalemia: Difference between revisions
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#sudden collapse (heart rate too slow or stops)<ref name="NIH">Dugdale DC, Zieve D. MedlinePlus. [homepage on the Internet]. 2011 [cited 2013 Mar 22]. Available from: U.S. National Library of Medicine, National Institutes of Health Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001179.htm</ref> | #sudden collapse (heart rate too slow or stops)<ref name="NIH">Dugdale DC, Zieve D. MedlinePlus. [homepage on the Internet]. 2011 [cited 2013 Mar 22]. Available from: U.S. National Library of Medicine, National Institutes of Health Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001179.htm</ref> | ||
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 ventricular | 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.<ref name="Raymond et al." /> | ||
== Associated Co-morbidities == | == Associated Co-morbidities == |
Revision as of 03:26, 27 March 2013
Original Editors -Courtney Ahlers & Jessica Ketterer from Bellarmine University's Pathophysiology of Complex Patient Problems project.
Lead Editors - Your name will be added here if you are a lead editor on this page. Read more.
Definition/Description[edit | edit source]
Hyperkalemia is characterized by an elevated serum potassium level greater than 5.5 mmol/L and is classified as an electrolyte abnormality. [1] Acute hyperkalemia is often preceded by issues such as illness, dehydration, or introduction of medications that affect potassium levels. [2]
Prevalence[edit | edit source]
Approximately 1 to 10 percepnt of hospital patients are affected by hyperkalemia. [2]
The mortality rate for patients with hyperkalemia is approximately 1 in 1000. [1]
Characteristics/Clinical Presentation[edit | edit source]
Hyperkalemia most commonly occurs in patients with chronic renal failure. [2]
Signs and Symptoms
- muscular weakness
- flaccid paralysis
- ileus
- ECG changes[2]
- nausea
- slow, weak or irregular pulse
- sudden collapse (heart rate too slow or stops)[4]
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.[1]
Associated Co-morbidities[edit | edit source]
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[edit | edit source]
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) |
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 |
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 |
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.[2]
Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]
Initial diagnosis is initiated with patient history, medication review, and physical examination.
Laboratory tests include:
- serum electrolytes
- creatinine
- blood urea nitrogen (BUN)
- spot urine test (potassium, creatinine, and osmoles)
- transtubular potassium gradient (assessment of renal potassium handling)
- trial of oral fludrocortisone (Florinef)[2]
Patients will likely not present with symptoms of hyperkalemia until potassium levels have exceeded 7 mmol/L.[1]
Etiology/Causes[edit | edit source]
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.[2]
Systemic Involvement[edit | edit source]
add text here
Medical Management (current best evidence)[edit | edit source]
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.[2]
Figure 2: Algorithm for the management of hyperkalemia.[2]
Physical Therapy Management (current best evidence)[edit | edit source]
Potassium levels < 3.2 mEq/L or > 5.1 mEq/L contraindicated for physical therapy intervention due to the potential for arrhythmia and tetany.[5]
Alternative/Holistic Management (current best evidence)[edit | edit source]
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Differential Diagnosis[edit | edit source]
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.[2]
Case Reports/ Case Studies[edit | edit source]
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Resources
[edit | edit source]
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Recent Related Research (from Pubmed)[edit | edit source]
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References[edit | edit source]
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- ↑ 1.0 1.1 1.2 1.3 Raymond C, Sood A, Wazny L. Treatment of hyperkalemia in patients with chronic kidney disease--a focus on medications. CANNT Journal [serial on the Internet]. (2010, July), [cited March 22, 2013]; 20(3): 49-54. Available from: CINAHL with Full Text. http://search.ebscohost.com/login.aspx?direct=true&amp;amp;amp;amp;amp;db=c8h&amp;amp;amp;amp;amp;AN=2010782358&amp;amp;amp;amp;amp;site=ehost-live (accessed 22 Mar 2013)
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Hollander-Rodriguez JC, Calvert, Jr. JF. Hyperkalemia. American Family Physician 2006; 73(2):283-290. Available from: PubMed. http://www.ncbi.nlm.nih.gov/pubmed/16445274 )22 March 2013)
- ↑ Cite error: Invalid
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- ↑ Dugdale DC, Zieve D. MedlinePlus. [homepage on the Internet]. 2011 [cited 2013 Mar 22]. Available from: U.S. National Library of Medicine, National Institutes of Health Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001179.htm
- ↑ Goodman CC & Fuller KS. In K Falk editor. Pathology: Implications for the Physical Therapist. St. Louis: Saunders Elsevier; 2009. pp.150, 157, 187-189, 480, 558, 927, 1243, 1640-1641