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<div class="noeditbox">Welcome to [[Pathophysiology of Complex Patient Problems|PT 635 Pathophysiology of Complex Patient Problems]] This is a wiki created by and for the students in the School of Physical Therapy at Bellarmine University in Louisville KY. Please do not edit unless you are involved in this project, but please come back in the near future to check out new information!!</div><div class="editorbox">
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'''Original Editors '''-Courtney Ahlers &amp; Jessica Ketterer [[Pathophysiology of Complex Patient Problems|from Bellarmine University's&nbsp;Pathophysiology of Complex Patient Problems project.]]  
'''Original Editors '''-Courtney Ahlers &amp; Jessica Ketterer [[Pathophysiology of Complex Patient Problems|from Bellarmine University's&nbsp;Pathophysiology of Complex Patient Problems project.]]  


'''Lead Editors''' - Your name will be added here if you are a lead editor on this page.&nbsp; [[Physiopedia:Editors|Read more.]]
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== Definition/Description  ==
== Definition/Description  ==
[[File:Membrane potential ions (id).jpg|right|frameless]]
Potassium is an important nutrient and [[Electrolytes|electrolyte]], it helps muscles work, including those [[Muscles of Respiration|involved in breathing]] and keeping the [[Anatomy of the Human Heart|heart]] beating. But too much potassium in our system, known as hyperkalemia, can cause serious health problems. And people with [[Chronic Kidney Disease|kidney disease]] are more prone to developing hyperkalemia.<ref>Healthline [https://www.healthline.com/health/high-potassium/hyperkalemia-facts 5 Things to Know About Hyperkalemia for National Kidney Month] Available: https://www.healthline.com/health/high-potassium/hyperkalemia-facts<nowiki/>(accessed 18.9.2021)</ref>


Hyperkalemia is characterized by an elevated serum potassium level greater than 5.5 mmol/L and is classified as an electrolyte abnormality.&nbsp;<ref name="Raymond et al.">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;amp;amp;amp;amp;db=c8h&amp;amp;amp;amp;amp;amp;amp;amp;amp;AN=2010782358&amp;amp;amp;amp;amp;amp;amp;amp;amp;site=ehost-live (accessed 22 Mar 2013)</ref>&nbsp; Acute hyperkalemia is often preceded by issues such as illness, dehydration, or introduction of medications that affect potassium levels. <ref name="Hollander-Rodriguez and Calvert" />&nbsp;
Hyperkalemia is defined as a serum or plasma potassium level above the upper limits of normal, usually greater than 5.0 mEq/L to 5.5 mEq/L. While mild hyperkalemia is usually asymptomatic, high levels of potassium may cause life-threatening [[Heart Arrhythmias: Assessment|cardiac arrhythmias]], muscle weakness or paralysis. Symptoms usually develop at levels higher levels, 6.5 mEq/L to 7 mEq/<ref name=":0">Simon LV, Hashmi MF, Farrell MW. [https://www.ncbi.nlm.nih.gov/books/NBK470284/ Hyperkalemia]. StatPearls [Internet]. 2020 Dec 1.Available:https://www.ncbi.nlm.nih.gov/books/NBK470284/ (accessed 18.9.2021)</ref>


== Prevalence ==
Image 1: Illustration of the way that differences in ion concentration on opposite sides of a cell membrane produce a voltage difference. Potassium is usually an intracellular cation.


Approximately 1 to 10 percepnt of hospital patients are affected by hyperkalemia.&nbsp; <ref name="Hollander-Rodriguez and Calvert">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)</ref>  
For patients with mild transient hyperkalemia, the prognosis is excellent if the inciting cause is addressed and treated. Sudden onset, extreme hyperkalemia can cause cardiac arrhythmias that can be lethal in up to two-thirds of cases if not rapidly treated. Hyperkalemia is an independent risk factor for death in hospitalized patients.<ref name=":0" />


The mortality rate for patients with hyperkalemia is approximately 1 in 1000. <ref name="Raymond et al." />
== Etiology ==
Often a report of high blood potassium isn't true hyperkalemia. Instead, it may be caused by the rupture of [[Blood Physiology|blood cells]] in the blood sample during or shortly after the blood draw. The ruptured cells leak their potassium into the sample. This falsely raises the amount of potassium in the [[Blood Tests|blood sample]], even though the potassium level in your body is actually normal. When this is suspected, a repeat blood sample is done.
[[File:Dialysis.jpg|right|frameless]]
The most common cause of genuinely hyperkalemia is related to the kidneys, eg:


<br>
* Acute kidney failure
* [[Chronic Kidney Disease|Chronic kidney disease]]
Other causes of hyperkalemia include:
* [[Addison's Disease|Addison's disease]] (adrenal insufficiency)
* Angiotensin II receptor blockers
* Angiotensin-converting enzyme ([[ACE Inhibitors: Congestive Heart Failure|ACE]]) inhibitors
* [[Beta-Blockers|Beta blockers]]
* [[Dehydration]]
* Destruction of red blood cells due to severe injury or [[Burns Overview|burns]]
* Excessive use of potassium supplements
* [[Diabetes Mellitus Type 1|Type 1 diabetes]]<ref>Mayo clinic [https://www.mayoclinic.org/symptoms/hyperkalemia/basics/causes/sym-20050776 Hyperkalemia] Available: https://www.mayoclinic.org/symptoms/hyperkalemia/basics/causes/sym-20050776 (accessed 18.9.2021)</ref>
Image 2: Dialysis for Chronic Kidney Disease.
 
== Epidemiology ==
Hyperkalemia is unusual in the general population, reported in less than 5% of the population, worldwide.
 
* Affects up to 10% of all hospitalized patients, most cases in hospitalized patients are due to medications and renal insufficiency.
* Diabetes, malignancy, extremes of age, and acidosis are other important causes in inpatients.
* Hyperkalemia is rare in children but may occur in up to 50% of premature infants.
* Hyperkalemia is more commonly reported in men than women perhaps due to increased muscle mass and higher rates of [[rhabdomyolysis]] and increased prevalence of [[Neuromuscular Disorders|neuromuscular disease]].
 
Today there is a risk that empirical use of ACE inhibitors may cause hyperkalemia, which can be of concern in high risk populations eg diabetics, those with heart failure, and peripheral vascular disease<ref name=":0" />.


== Characteristics/Clinical Presentation  ==
== Characteristics/Clinical Presentation  ==
[[File:Ecg_thing.gif|alt=|right|frameless|524x524px]]Hyperkalemia most commonly occurs in patients with [[Chronic Kidney Disease|chronic renal failure]] and is also correlated with [[diabetes]]. <ref name="Hollander-Rodriguez and Calvert">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)</ref>&nbsp;<ref name="Spiro">Tamirisa KP, Aaronson KD, Koelling TM. Spironolactone-induced renal insufficiency and hyperkalemia in patients with heart failure, American Heart J 2004; 148(6):971-978. Available from: Europe Pubmed Central. http://www.sciencedirect.com/science/article/pii/S0002870304007501 (Accessed 4 April 2013)</ref>


Hyperkalemia most commonly occurs in patients with chronic renal failure. <ref name="Hollander-Rodriguez and Calvert" />
Image 3: [[Electrocardiogram|ECG]] is monitored in patients with hyperkalemia:


Signs and Symptoms  
Signs and Symptoms  
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#palpitations
#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. &nbsp;Some signs and symptoms listed above are a result of the impaired nerve conduction and muscle contraction dysfunction. &nbsp;Muscular dysfunction includes the cardiac system and can lead to life threatening ventricular arrhythmias. &nbsp;Electrocardiogram (ECG) dysfunction is more common in patients with acute hyperkalemia.<ref name="Raymond et al." />  
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. &nbsp;Some signs and symptoms listed above are a result of the impaired nerve conduction and muscle contraction dysfunction. &nbsp;Muscular dysfunction includes the cardiac system and can lead to life threatening ventricular arrhythmias. &nbsp;Electrocardiogram ([[Electrocardiogram|ECG]]) dysfunction is more common in patients with acute hyperkalemia.<ref name="Raymond et al.">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;db=c8h&amp;AN=2010782358&amp;site=ehost-live (accessed 22 Mar 2013)</ref>  
 
== Associated Co-morbidities  ==
 
{| style="width: 547px; height: 451px" border="1" cellspacing="1" cellpadding="1" width="547"
|-
| colspan="2" | '''&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Table 1 '''
'''&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; 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
|
|}
 
<ref name="Hollander-Rodriguez and Calvert" />
 
== Medications  ==
 
{| style="width: 849px; height: 480px" border="1" cellspacing="1" cellpadding="1" width="849"
|-
| colspan="6" | '''TABLE 5<br>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
|-
| &nbsp;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:&nbsp;
 
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:&nbsp;
 
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.<ref name="Hollander-Rodriguez and Calvert" /><br>


== Diagnostic Tests/Lab Tests/Lab Values  ==
== Diagnostic Tests/Lab Tests/Lab Values  ==
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Initial diagnosis is initiated with patient history, medication review, and physical examination.&nbsp;  
Initial diagnosis is initiated with patient history, medication review, and physical examination.&nbsp;  


Laboratory tests include:  
[[Blood Tests|Laboratory tests]] include:  


#serum electrolytes (especially potassium and glucose <ref name="Raymond et al." />)  
#serum electrolytes (especially potassium and glucose <ref name="Raymond et al." />)  
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#trial of oral fludrocortisone (Florinef)<ref name="Hollander-Rodriguez and Calvert" />
#trial of oral fludrocortisone (Florinef)<ref name="Hollander-Rodriguez and Calvert" />


Patients will likely not present with symptoms of hyperkalemia until potassium levels have exceeded 7 mmol/L.&nbsp; HOwever, immediate medical attention is required when potassium level exceed 6.5 mmol/L or exceed 6.0 mmol/L&nbsp;with ECG changes consistent with hyperkalemia.<ref name="Raymond et al." />  
Patients will likely not present with symptoms of hyperkalemia until potassium levels have exceeded 7 mmol/L.&nbsp; However, immediate medical attention is required when potassium level exceed 6.5 mmol/L or exceed 6.0 mmol/L&nbsp;with ECG changes consistent with hyperkalemia.<ref name="Raymond et al." />
 
ECG is monitored in patients with hyperkalemia:<br>
 
[[Image:Ecg thing.gif]]<br>
 
<ref name="Raymond et al." />
 
== Etiology/Causes  ==
 
Hyperkalemia is typically caused when the kidneys can no longer excrete potassium, when the body is unable to effectively&nbsp;distribute potassium between the extracellular and intracellular space, or the effects of medications (including increased potassium intake).&nbsp; 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.&nbsp; For medication induced hyperkalemia, a combination of ACE inhibitors and spironolactone or the&nbsp;use of NSAIDs in patients with impaired kidney function or diabetes can predispose the patient.&nbsp; Adrenal insufficiency is another potential cause, particularly when the patient also presents with hyponatremia and muscular weakness.&nbsp; Congenital&nbsp;factors that can produce hyperkalemia include pseudohypoaldosteronism and aldosterone synthesis abnormalities.<ref name="Hollander-Rodriguez and Calvert" />
 
Many factors influence the aforementioned causes of hyperkalemia:
 
{| style="width: 688px; height: 826px" border="1" cellspacing="1" cellpadding="1" width="688"
|-
| '''Table 1. Causes of Hyperkalemia''' <ref name="Raymond et al." />
|-
|
'''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&nbsp;
 
|-
|
'''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&nbsp;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
 
|}
 
== &nbsp;&nbsp;Systemic Involvement&nbsp;&nbsp;  ==
== &nbsp;&nbsp;Systemic Involvement&nbsp;&nbsp;  ==


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|}
|}


== Medical Management (current best evidence)  ==
== Treatment ==
The urgency with which hyperkalemia should be managed depends on how rapidly the condition developed, the absolute serum potassium level, the degree of symptoms, and the cause.<ref name=":0" />


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.&nbsp; Although ECG changes are common indicators for severe hyperkalemia, the patient may still have life threatening hyperkalemia even if ECG readings are normal.&nbsp; The intent of immediate medical intervention is to stabilize the myocardium to prevent arrhythmias.&nbsp; In addition to the medications listed in Table 5, total body potassium levels can be lowered through kidney excretion, gastrointestinal (GI) elimination, or dialysis.&nbsp; Lowering via kidney excretion is achieved&nbsp;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.&nbsp; Long term management is focused on addressing the underlying cause, which can be achieved by discontinuing medications or consuming low potassium diets.<ref name="Hollander-Rodriguez and Calvert" />  
* 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.&nbsp;  
* Although ECG changes are common indicators for severe hyperkalemia, the patient may still have life threatening hyperkalemia even if ECG readings are normal.&nbsp;  
* The intent of immediate medical intervention is to stabilize the myocardium to prevent arrhythmias.&nbsp;  
 
In addition to the medications listed in Table 5, total body potassium levels can be lowered through kidney excretion, gastrointestinal (GI) elimination, or dialysis.&nbsp; Lowering via kidney excretion is achieved&nbsp;by the use of [[diuretics]], while lowering via GI elimination occurs with the use of Kayexalate.&nbsp; Long term management is focused on addressing the underlying cause, which can be achieved by discontinuing medications or consuming low potassium diets.<ref name="Hollander-Rodriguez and Calvert" />  


[[Image:Afp20060115p283-f2.gif]]  
[[Image:Afp20060115p283-f2.gif]]  
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Figure 2:&nbsp; Algorithm for the management of hyperkalemia.<ref name="Hollander-Rodriguez and Calvert" />  
Figure 2:&nbsp; Algorithm for the management of hyperkalemia.<ref name="Hollander-Rodriguez and Calvert" />  


== Physical Therapy Management (current best evidence)  ==
Foods high in potassium can also be implicated in the development of hyperkalemia.&nbsp;


Potassium levels &lt; 3.2 mEq/L or &gt; 5.1 mEq/L are contraindicated for physical therapy intervention due to the potential for arrhythmia and tetany.&nbsp; When potassium levels are not within the normal range (3.5-5.0 mEq/L) exercise is not effective due to decreased muscle pH and action potentials&nbsp;as well as&nbsp;inhibition of motor neurons.&nbsp; With a patient who has marginal potassium levels, vital signs (including pulse rhythm) and any signs of dizziness, muscle weakness or cramping, numbness or tingling, and changes in balance should be closely monitored.&nbsp; At this time, no research addresses the change in potassium level that occurs with exercise.&nbsp; However, it is known that patients with hyperkalemia are at risk for ventricular arrhythmias which can result in reduced exercise tolerance.<ref name="Goodman">Goodman CC &amp;amp;amp;amp;amp;amp; 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</ref>  
{| style="width: 698px; height: 326px" border="1" cellspacing="1" cellpadding="1" width="698"
|-
|
Table 2. High-potassium foods<ref name="Raymond et al." />  


Hyperkalemia is a disorder that is not managed primarily by a physical therapist, however physical therapists should be aware of signs and symptoms of this disorder and should refer the patient to a medical doctor when indicated.
(National Kidney foundation, 2010)


== Alternative/Holistic Management (current best evidence)  ==
|-
|
- salt substitutes and salt free broth


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


== Differential Diagnosis  ==
- molasses


Pseudohyperkalemia occurs when lab reports indicate elevated serum potassium levels but the patient does not actually have elevated serum potassium.&nbsp; This phenomenon occurs most commonly with destruction of red blood cells with collection of blood specimen.<ref name="Hollander-Rodriguez and Calvert" />
- seaweed


== Case Reports/ Case Studies  ==
- chocolate


Case Study 1
- bran cereal, wheat germ, granola


[http://search.proquest.com/docview/1288361388/fulltextPDF/13D36C908586D89710A/1?accountid=6741 Colonic ulceration in a patient with renal disease and hyperkalemia]&nbsp;<ref>Chelcum JL, Sable RA, Friedman K. Colonic ulceration in a patient with renal disease and hyperkalemia, J of American Academy of Physician Assistants 2012; 25(10):34-38. Available from: ProQuest. http://search.proquest.com/docview/1288361388/fulltextPDF?accountid=6741 (Accessed 22 Mar 2013)</ref>
- vegetables (acorn squash, artichoke, bamboo shoots, beets, broccoli, brussel sprouts, chinese cabbage, carrots, greens (except kale), kohlrabi, mushrooms (canned), parsnips, potatoes, pumpkin, rutabagas, spinach, tomatoes, vegetable juices)  


51 year old male who developed large GI ulcer following pharmacological management of hyperkalemia
- dried fruit (apricot, dates, figs, raisins, prunes)


<br>
- nuts and seeds, (peanut butter)


Case Study 2
- dried peas and beans (lima beans, black beans, refried beans, lentils, legumes)


[http://search.proquest.com/docview/1030946274/fulltextPDF/13D368764547F8F25FD/1?accountid=6741 Beating the odds--surviving extreme hyperkalemia]&nbsp;<ref name="Beating">Muck PM, Letterer S, Lindner U, et al. Beating the odds-surviving extreme hyperkalemia. The American J of Emergency Medicine 2012; 30:250.e1 - 250.e4. Available from: ProQuest. http://search.proquest.com/docview/1030946274/fulltext/13D368764547F8F25FD/1?accountid=6741 (Accessed 22 Mar 2013)</ref>
- fruit and juice (apricot, avocado, banana, cantaloupe, grapefruit, honeydew, kiwi fruit, mango, nectarine, orange, papaya, pomegranate, prune)  


58 year old woman who survived severe hyperkalemia (&gt; 10 mmol/L)
<br>


<br>
|}


== Resources <br> ==
== Physical Therapy Management  ==
 
Hyperkalemia is a disorder that is not managed primarily by a physical therapist, however physical therapists should be aware of signs and symptoms of this disorder and should refer the patient to a medical doctor when indicated.  
[http://www.mayoclinic.com/health/hyperkalemia/MY00940 High Potassium (Hyperkalemia)--Mayo Clinic]
 
[http://www.nlm.nih.gov/medlineplus/ency/article/001179.htm High Potassium Levels--Medline Plus]


== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed])  ==
* Potassium levels &lt; 3.2 mEq/L or &gt; 5.1 mEq/L are contraindicated for physical therapy intervention due to the potential for arrhythmia and tetany.&nbsp; 
* When potassium levels are not within the normal range (3.5-5.0 mEq/L) exercise is not effective due to decreased muscle pH and action potentials&nbsp;as well as&nbsp;inhibition of motor neurons.&nbsp; 
* With a patient who has marginal potassium levels, [[Vital Signs|vital signs]] (including pulse rhythm) and any signs of dizziness, muscle weakness or cramping, numbness or tingling, and changes in balance should be closely monitored.&nbsp;  


<br>
At this time, no research addresses the change in potassium level that occurs with exercise.&nbsp; However, it is known that patients with hyperkalemia are at risk for ventricular arrhythmias which can result in reduced exercise tolerance.<ref name="Goodman">Goodman CC &amp; 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</ref>  
<div class="researchbox"><rss>http://www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1l_vN2os9ImhzaE9-baJnk6gPwsC9cuWxeJQLrj8c6qE8IPYB1|charset=UTF-8|short|max=10</rss></div>
== References ==
== References ==


see [[Adding References|adding references tutorial]].  
see [[Adding References|adding references tutorial]].  
Line 327: Line 168:
<references />&nbsp;  
<references />&nbsp;  


[[Category:Bellarmine_Student_Project]]
[[Category:Bellarmine Student Project]]
[[Category:Conditions]]

Latest revision as of 06:42, 8 February 2023

Definition/Description[edit | edit source]

Membrane potential ions (id).jpg

Potassium is an important nutrient and electrolyte, it helps muscles work, including those involved in breathing and keeping the heart beating. But too much potassium in our system, known as hyperkalemia, can cause serious health problems. And people with kidney disease are more prone to developing hyperkalemia.[1]

Hyperkalemia is defined as a serum or plasma potassium level above the upper limits of normal, usually greater than 5.0 mEq/L to 5.5 mEq/L. While mild hyperkalemia is usually asymptomatic, high levels of potassium may cause life-threatening cardiac arrhythmias, muscle weakness or paralysis. Symptoms usually develop at levels higher levels, 6.5 mEq/L to 7 mEq/[2]

Image 1: Illustration of the way that differences in ion concentration on opposite sides of a cell membrane produce a voltage difference. Potassium is usually an intracellular cation.

For patients with mild transient hyperkalemia, the prognosis is excellent if the inciting cause is addressed and treated. Sudden onset, extreme hyperkalemia can cause cardiac arrhythmias that can be lethal in up to two-thirds of cases if not rapidly treated. Hyperkalemia is an independent risk factor for death in hospitalized patients.[2]

Etiology[edit | edit source]

Often a report of high blood potassium isn't true hyperkalemia. Instead, it may be caused by the rupture of blood cells in the blood sample during or shortly after the blood draw. The ruptured cells leak their potassium into the sample. This falsely raises the amount of potassium in the blood sample, even though the potassium level in your body is actually normal. When this is suspected, a repeat blood sample is done.

Dialysis.jpg

The most common cause of genuinely hyperkalemia is related to the kidneys, eg:

Other causes of hyperkalemia include:

Image 2: Dialysis for Chronic Kidney Disease.

Epidemiology[edit | edit source]

Hyperkalemia is unusual in the general population, reported in less than 5% of the population, worldwide.

  • Affects up to 10% of all hospitalized patients, most cases in hospitalized patients are due to medications and renal insufficiency.
  • Diabetes, malignancy, extremes of age, and acidosis are other important causes in inpatients.
  • Hyperkalemia is rare in children but may occur in up to 50% of premature infants.
  • Hyperkalemia is more commonly reported in men than women perhaps due to increased muscle mass and higher rates of rhabdomyolysis and increased prevalence of neuromuscular disease.

Today there is a risk that empirical use of ACE inhibitors may cause hyperkalemia, which can be of concern in high risk populations eg diabetics, those with heart failure, and peripheral vascular disease[2].

Characteristics/Clinical Presentation[edit | edit source]

Hyperkalemia most commonly occurs in patients with chronic renal failure and is also correlated with diabetes. [4] [5]

Image 3: ECG is monitored in patients with hyperkalemia:

Signs and Symptoms

  1. muscular weakness
  2. flaccid paralysis
  3. ileus
  4. ECG changes[4]
  5. nausea
  6. slow, weak or irregular pulse
  7. sudden collapse (heart rate too slow or stops)[6]
  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.[7]

Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]

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

Laboratory tests include:

  1. serum electrolytes (especially potassium and glucose [7])
  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)[4]

Patients will likely not present with symptoms of hyperkalemia until potassium levels have exceeded 7 mmol/L.  However, immediate medical attention is required when potassium level exceed 6.5 mmol/L or exceed 6.0 mmol/L with ECG changes consistent with hyperkalemia.[7]

  Systemic Involvement  [edit | edit source]

Table 5-10 Clinical Features of Various Electrolyte Imbalances[8]

Potassium Imbalance (hyperkalemia) System Dysfunction
Cardiovascular tachycardia and later bradycardia, ECG changes, cardiac arrest (with levels .7.0 mEq/L)
GI nausea, diarrhea, abdominal cramps
Musculoskeletal muscle weakness, flaccid paralysis
Genitourinary oliguria, anuria
Central nervous system areflexia progressing to weakness, numbness, tingling, and flaccid paralysis
Acid-base balance metabolic acidosis

Treatment[edit | edit source]

The urgency with which hyperkalemia should be managed depends on how rapidly the condition developed, the absolute serum potassium level, the degree of symptoms, and the cause.[2]

  • 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.  Long term management is focused on addressing the underlying cause, which can be achieved by discontinuing medications or consuming low potassium diets.[4]

Afp20060115p283-f2.gif

Figure 2:  Algorithm for the management of hyperkalemia.[4]

Foods high in potassium can also be implicated in the development of hyperkalemia. 

Table 2. High-potassium foods[7]

(National Kidney foundation, 2010)

- salt substitutes and salt free broth

- yogurt, milk

- molasses

- seaweed

- chocolate

- bran cereal, wheat germ, granola

- vegetables (acorn squash, artichoke, bamboo shoots, beets, broccoli, brussel sprouts, chinese cabbage, carrots, greens (except kale), kohlrabi, mushrooms (canned), parsnips, potatoes, pumpkin, rutabagas, spinach, tomatoes, vegetable juices)

- dried fruit (apricot, dates, figs, raisins, prunes)

- nuts and seeds, (peanut butter)

- dried peas and beans (lima beans, black beans, refried beans, lentils, legumes)

- fruit and juice (apricot, avocado, banana, cantaloupe, grapefruit, honeydew, kiwi fruit, mango, nectarine, orange, papaya, pomegranate, prune)


Physical Therapy Management[edit | edit source]

Hyperkalemia is a disorder that is not managed primarily by a physical therapist, however physical therapists should be aware of signs and symptoms of this disorder and should refer the patient to a medical doctor when indicated.

  • Potassium levels < 3.2 mEq/L or > 5.1 mEq/L are contraindicated for physical therapy intervention due to the potential for arrhythmia and tetany. 
  • When potassium levels are not within the normal range (3.5-5.0 mEq/L) exercise is not effective due to decreased muscle pH and action potentials as well as inhibition of motor neurons. 
  • With a patient who has marginal potassium levels, vital signs (including pulse rhythm) and any signs of dizziness, muscle weakness or cramping, numbness or tingling, and changes in balance should be closely monitored. 

At this time, no research addresses the change in potassium level that occurs with exercise.  However, it is known that patients with hyperkalemia are at risk for ventricular arrhythmias which can result in reduced exercise tolerance.[8]

References[edit | edit source]

see adding references tutorial.

  1. Healthline 5 Things to Know About Hyperkalemia for National Kidney Month Available: https://www.healthline.com/health/high-potassium/hyperkalemia-facts(accessed 18.9.2021)
  2. 2.0 2.1 2.2 2.3 Simon LV, Hashmi MF, Farrell MW. Hyperkalemia. StatPearls [Internet]. 2020 Dec 1.Available:https://www.ncbi.nlm.nih.gov/books/NBK470284/ (accessed 18.9.2021)
  3. Mayo clinic Hyperkalemia Available: https://www.mayoclinic.org/symptoms/hyperkalemia/basics/causes/sym-20050776 (accessed 18.9.2021)
  4. 4.0 4.1 4.2 4.3 4.4 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)
  5. Tamirisa KP, Aaronson KD, Koelling TM. Spironolactone-induced renal insufficiency and hyperkalemia in patients with heart failure, American Heart J 2004; 148(6):971-978. Available from: Europe Pubmed Central. http://www.sciencedirect.com/science/article/pii/S0002870304007501 (Accessed 4 April 2013)
  6. 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
  7. 7.0 7.1 7.2 7.3 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&db=c8h&AN=2010782358&site=ehost-live (accessed 22 Mar 2013)
  8. 8.0 8.1 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