Hyper Kale Mia is a Potentially Life

8/3/2019 Hyper Kale Mia is a Potentially Life

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Hyperkalemia is a potentially life-threatening illness that can be difficult to diagnose

because of a paucity of distinctive signs and symptoms. The physician must be

quick to consider hyperkalemia in patients who are at risk for this disease process.

Because hyperkalemia can lead to sudden death from cardiac arrhythmias, any

suggestion of hyperkalemia requires an immediate ECG to ascertain whether

electrocardiographic signs of electrolyte imbalance are present.

http://emedicine.medscape.com/article/766479-overview

Pathophysiology

Potassium is a major ion of the body. Nearly 98% of potassium is intracellular, with the

concentration gradient maintained by the sodium- and potassium-activated adenosinetriphosphatase (Na+/K+ ATPase) pump. The ratio of intracellular to extracellular potassium is

important in determining the cellular membrane potential. Small changes in the extracellular

potassium level can have profound effects on the function of the cardiovascular and

neuromuscular systems. The normal potassium level is 3.5-5.0 mEq/L, and total body potassiumstores are approximately 50 mEq/kg (3500 mEq in a 70-kg person).

Minute-to-minute levels of potassium are controlled by intracellular to extracellular exchange,

mostly by the sodium-potassium pump that is controlled by insulin and beta2 receptors. A

balance of GI intake and renal potassium excretion achieves long-term potassium balance.

Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L.[1] Ranges are as follows:

5.5-6.0 mEq/L - Mild

6.1-7.0 mEq/L - Moderate

7.0 mEq/L and greater - Severe

Hyperkalemia results from the following:

Decreased or impaired potassium excretion - As observed

with acute orchronic renal failure[2] (most common),

potassium-sparing diuretics, urinary obstruction, sickle cell

disease, Addison disease, and systemic lupus

erythematosus (SLE) Additions of potassium into extracellular space - As

observed with potassium supplements (eg, PO/IV

potassium, salt substitutes), rhabdomyolysis, and hemolysis

(eg, blood transfusions, burns, tumor lysis)
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Transmembrane shifts (ie, shifting potassium from the

intracellular to extracellular space) - As observed with

acidosis and medication effects (eg, acute digitalis toxicity,

beta-blockers, succinylcholine) Factitious or pseudohyperkalemia - As observed with

improper blood collection (eg, ischemic blood draw from

venipuncture technique), laboratory error, leukocytosis, and

thrombocytosis

Epidemiology

Frequency

United States

Hyperkalemia is diagnosed in up to 8% of hospitalized patients.

Mortality/Morbidity

The primary cause of morbidity and death is potassium's effect on cardiac function.[3]

The mortality rate can be as high as 67% if severe hyperkalemia is not treated rapidly. [4]

Sex

The male-to-female ratio is 1:1

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History

Hyperkalemia can be difficult to diagnose clinically because complaints may be vague. Thehistory is most valuable in identifying conditions that may predispose to hyperkalemia.

Hyperkalemia frequently is discovered as an incidental laboratory finding.

Cardiac and neurologic symptoms predominate.

Patients may be asymptomatic or report the following:

Generalized fatigue
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Weakness

Paresthesias

Paralysis

Palpitations

Hyperkalemia is suggested in any patient with a predisposition toward elevated potassium level.Potential potassium level elevation is observed in the following:

Acute or chronic renal failure, especially in patients who are on dialysis

Trauma, including crush injuries (rhabdomyolysis), or burns

Ingestion of foods high in potassium (eg,bananas, oranges, high-

protein diets, tomatoes, salt substitutes). This alone is not likelyto cause clinically significant hyperkalemia in most people; it is often a contributing

factor to an acute potassium elevation.

Medications - Potassium supplements, potassium-sparing diuretics, nonsteroidal anti-

inflammatory drugs (NSAIDs), beta-blockers, digoxin, succinylcholine, and digitalisglycoside

Medication combinations (ie, spironolactone, ACE inhibitors)[5]

Redistribution - Metabolic acidosis (diabetic ketoacidosis [DKA]), catabolic states

http://emedicine.medscape.com/article/766479-clinical

Physical

Evaluation of vital signs is essential to determine hemodynamic stability and presence of cardiac

arrhythmias related to the hyperkalemia.[1]

Cardiac examination may reveal extrasystoles, pauses, orbradycardia.

Neurologic examination may reveal diminished deep tendon reflexes or decreased motorstrength.

In rare cases, muscular paralysis and hypoventilation may be observed.

Search for the stigmata of renal failure, such as edema, skin changes, and dialysis sites.

Look for signs of trauma that could put the patient at risk for rhabdomyolysis

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Causes
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Pseudohyperkalemia

Hemolysis (in laboratory tube) most common Thrombocytosis Leukocytosis Venipuncture technique (ie, ischemic blood draw from prolonged tourniquet

application)

Redistribution

Acidosis Insulin deficiency Beta-blocker drugs Acute digoxin intoxication or overdose Succinylcholine[6]

Arginine hydrochloride Hyperkalemic familial periodic paralysis???????????

Excessive endogenous potassium load

Hemolysis Rhabdomyolysis Internal hemorrhage

Excessive exogenous potassium load

Parenteral administration Excess in diet

Potassium supplements Salt substitutes

Diminished potassium excretion

Decreased glomerular filtration rate (eg, acute or end-stage chronic renalfailure)

Decreased mineral corticoid activity Defect in tubular secretion (eg, renal tubular acidosis II and IV) Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics)

http://emedicine.medscape.com/article/766479-clinical#a0218

Laboratory Studies

Potassium level

The relationship between the serum potassium level and symptoms is not consistent. For

example, patients with a chronically elevated potassium level may be asymptomatic at much
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higher levels than other patients. The rapidity of change in the potassium level influences the

symptoms observed at various potassium levels.

BUN and creatinine level

For evaluation of renal status

Calcium level

If patient has renal failure (because hypocalcemia can exacerbate cardiac rhythm disturbances)

Glucose level

In patients with diabetes mellitus

Digoxin level

If patient is on a digitalis medication

Arterial or venous blood gas

If acidosis is suspected

Urinalysis

If signs of renal insufficiency without an already known cause are present (to look for evidence

of glomerulonephritis)

http://emedicine.medscape.com/article/766479-workup

Other Tests

Continuous cardiac monitoring

Indicated for evaluation of rhythm disturbances

ECG

ECG is essential and may be instrumental in diagnosing hyperkalemia in the appropriate clinicalsetting. ECG changes have a sequential progression of effects, which roughly correlate with the

potassium level.

ECG findings may be observed as follows:
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Early changes of hyperkalemia include peaked T waves, shortened QTinterval, and ST-segment depression (see the images below).

Peaked T waves in hyperkalemia.

Peaked T waves in hyperkalemia. These changes are followed by bundle-branch blocks causing a widening of

the QRS complex, increases in the PR interval, and decreased amplitude of

the P wave (see the images below). Widened QRS

complexes in hyperkalemia. Widened QRScomplexes in a patient whose serum potassium level was 7.8 mEq/L.

These changes reverse with appropriate treatment (see the image below).

ECG of a patient with pretreatment potassiumlevel of 7.8 mEq/L and widened QRS complexes after receiving 1 ampule ofcalcium chloride. Notice narrowing of QRS complexes and reduction of Twaves.

Without treatment, the P wave eventually disappears and the QRSmorphology widens to resemble a sine wave. Ventricular fibrillation orasystole follows.
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ECG findings generally correlate with the potassium level, but potentially life-threatening arrhythmias can occur without warning at almost any level ofhyperkalemia.

Cortisol and aldosterone levels

To check for mineralocorticoid deficiency when other causes are eliminated

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Prehospital Care

A patient with known hyperkalemia or a patient with renal failure with suspected hyperkalemiashould have intravenous access established and should be placed on a cardiac monitor.[8] In the

presence of hypotension or marked QRS widening, intravenous bicarbonate, calcium, and insulin

given together with 50% dextrose may be appropriate as discussed in Medication. Avoid calcium

if digoxin toxicity is suspected. Magnesium sulfate (2 g over 5 min) may be used alternatively inthe face of digoxin-toxic cardiac arrhythmias.

http://emedicine.medscape.com/article/766479-treatment

Perform continuous ECG monitoring with frequent vital sign checks when hyperkalemia issuspected or when laboratory values indicative of hyperkalemia are received.

Initial management includes assessment of the ABCs and prompt evaluation of the patient's

cardiac status with an ECG.

Discontinue any potassium-sparing drugs or dietary potassium.

If the hyperkalemia is severe (potassium >7.0 mEq/L) or if the patient is symptomatic, begintreatment before diagnostic investigation of the underlying cause. Individualize treatment based

upon the patient's presentation, potassium level, and ECG. Not all patients should receive every

medication listed in Medication s. Patients with mild hyperkalemia, for example, may need onlyexcretion enhancement.

Some studies are emerging that suggest sodium polystyrene sulfonate (SPS), also known as

Kayexalate, may be unhelpful in hyperkalemia and may increase the chance of colonic necrosis

(especially when used with sorbitol).[9, 31, 32, 33]

http://emedicine.medscape.com/article/766479-treatment#a1126

Electrolyte supplements
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Class Summary

These agents are used to treat hyperkalemia and to reduce the risk of ventricular fibrillationcaused by hyperkalemia. They act quickly and can be lifesaving, thus they are the first-line

treatment for severe hyperkalemia when the ECG shows significant abnormalities (eg, widening

of QRS interval, loss of P wave, cardiac arrhythmias). Calcium usually is not indicated when theECG shows only peaked T waves.

Calcium chloride or calcium gluconate (Kalcinate)

Calcium increases threshold potential, thus restoring normal gradient between threshold potential

and resting membrane potential, which is elevated abnormally in hyperkalemia. One ampule of

calcium chloride has approximately 3 times more calcium than calcium gluconate. Onset ofaction is < 5 min and lasts about 30-60 min. Doses should be titrated with constant monitoring of

ECG changes during administration; repeat dose if ECG changes do not normalize within 3-5

min.

Antidotes

Class Summary

Insulin is administered with glucose to facilitate the uptake of glucose into the cell, bringingpotassium with it.

View full drug information

Dextrose (D-Glucose)

Glucose and insulin temporarily shift K+ into cells; effects occur within first 30 min of

administration.


Insulin (Humulin, Humalog, Novolin)

Stimulates cellular uptake of K+ within 20-30 min; administer glucose along with insulin toprevent hypoglycemia (monitor blood glucose levels closely).

http://emedicine.medscape.com/article/766479-medication#3

Alkalinizing agents
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Class Summary

These agents increase the pH, which results in a temporary potassium shift from the extracellularto the intracellular environment. These agents enhance the effectiveness of insulin in patients

with acidemia.


Sodium bicarbonate (Neut)

Bicarbonate ion neutralizes hydrogen ions and raises urinary and blood pH. Onset of action

within minutes, lasts approximately 15-30 min. Only likely to be efficacious if underlyingacidosis present. Monitor blood pH to avoid excess alkalosis.

Use 8.4% solution in adults and children, 4.2% solution in infants.

http://emedicine.medscape.com/article/766479-medication#4

Beta2-adrenergic agonists

Class Summary

These agents promote cellular reuptake of potassium, possibly via the cyclic gAMP receptorcascade.


Albuterol (Ventolin, Proventil)

Adrenergic agonist that increases plasma insulin concentration, which may in turn help shift K+

into intracellular space. Lowers K+ level by 0.5-1.5 mEq/L. Can be very beneficial in patientswith renal failure when fluid overload is concern. Onset of action is 30 min; duration of action is

2-3 h

Diuretics

Class Summary

These agents cause the loss of potassium through the kidney.

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Furosemide (Lasix)

Effects are slow and frequently take an hour to begin. Lowers potassium level by inconsistent

amount. Large doses may be needed in renal failure.


Ethacrynic acid (Edecrin)

Increases excretion of water by interfering with chloride-binding cotransport system, which in

turn inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Binding resins

Class Summary

These agents promote exchange of potassium for sodium in GI system.


Sodium polystyrene sulfonate (Kayexalate)

Exchanges Na+ for K+ and binds it in gut, primarily in large intestine, decreasing total body

potassium. Onset of action after PO ranges from 2-12 h (longer when administered rectally).

Lowers K+ over 1-2 h with duration of action of 4-6 h. Potassium level drops by approximately0.5-1 mEq/L.

Multiple doses usually necessary.

Electrolytes

Class Summary

These agents have been successfully used in the treatment of acute SLOW released oral

potassium overdose.


Magnesium sulfate
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Nutritional supplement in hyperalimentation; cofactor in enzyme systems involved in

neurochemical transmission and muscular excitability. In adults, 60-180 mEq of potassium, 10-

30 mEq of magnesium, and 10-40 mmol of phosphate per day may be necessary for optimummetabolic response. Give IV for acute suppression of torsade. Repeat doses are dependent upon

continuing presence of patellar reflex and adequate respiratory function.

Complications

Life-threatening cardiac arrhythmias may ensue.

Hypokalemia may result from the treatment of hyperkalemia.

Prognosis

Expect full resolution with correction of the underlying etiology.

Reduction of plasma potassium should begin within the first hour of initiation of treatment.

http://emedicine.medscape.com/article/766479-followup#a2650

Patient Education

Pursue diet modification.

Discontinue use of medications that may worsen hyperkalemia.

Encourage adherence to dialysis schedule if patient is noncompliant.

Hyperkalemia Symptoms

Hyperkalemia is a relatively common disturbance ofelectrolytes, and up to 8% of hospitalizedpatients in the U.S. are diagnosed with hyperkalemia. Most cases of hyperkalemia are mild and

may not produce any symptoms at all. Typically, hyperkalemia that develops slowly over time

produces fewer symptoms than a sudden rise in potassium levels.

Usually, symptoms do not become apparent until potassium levels are very high (7.0 mEq/l orgreater). Sometimes people with hyperkalemia report nonspecific symptoms such as muscle

weakness, tiredness, tingling sensations, ornausea.

A slow heartbeat and weak pulse are more serious symptoms, since these may signal an effect on

the electrical activity of the heart. Potassium is responsible for maintaining normal heart rhythmand hyperkalemia can have potentially life-threatening effects. While mild hyperkalemia
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probably has a limited effect on the heart, moderate hyperkalemia can changes in the

electrocardiogram(EKG, ECG) recording (EKG is an electrical reading of the activity of the

neuromuscularactivity of the heart), and severe hyperkalemia can cause the heart to stop beating.

Hyperkalemic periodicparalysis is a rare inherited disorder that can result in sudden

hyperkalemia accompanied by muscle paralysis.

http://www.emedicinehealth.com/hyperkalemia/page2_em.htm

Hyperkalemia Overview

Hyperkalemia is an excessive level ofpotassiumin the bloodstream. Potassium has severalimportant functions in the body. It is essential for the normal functioning of the muscles, heart,

and nerves. Potassium helps the body regulate activity of muscle, including thesmooth muscle

(involuntary muscles, such as the muscles found in the digestive tract), skeletal muscle(voluntary muscles, such as muscles of the extremities and torso), and the muscle of the heart. It

is also important for maintaining normal heart electrical rhythm and for normal electrical signals

in the nervous system.

The normal potassium level in the blood is 3.5-5.0 milliEquivalents perliter (mEq/L).

Potassium levels between 5.1 mEq/L to 6.0 mEq/L are considered to be mildhyperkalemia.

Potassium levels of 6.1 mEq/L to 7.0 mEq/L are moderate hyperkalemia, andlevels above 7 mEq/L reflect severe hyperkalemia.

Hyperkalemia Causes

Excess potassium in the bloodstream can result from diseases of the kidneys or adrenal glands as

well as from certain medications. Hyperkalemia can also be the result of potassium moving out

of its usual location within cells into the bloodstream.

The majority of potassium within the body (about 98%) is located within cells, with only 2%located in the bloodstream. A number of conditions can cause potassium to move out of the cells

into the blood circulation, thereby increasing the measured level of potassium in the blood, even

though the total amount of potassium in the body has not changed. Diabetic ketoacidosis, anemergency that can develop in people with type I diabetes, is an example of a condition in which

potassium is drawn out of cells and into the bloodstream.

Similarly, any condition in which there is massive tissue destruction can result in elevated levels

of blood potassium as the damaged cells release their potassium. Examples of tissue destructioninclude:

trauma,
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burns,

surgical procedures,

destruction oftumor cells or red blood cells, and

rhabdomyolysis (a condition involving destruction of muscle cells that issometimes associated with muscle injury, alcoholism, or drug abuse).

Moreover, difficulty in drawing blood from veins for testing can traumatize red blood cells,

releasing potassium into the serum of the blood sample to cause a falsely elevated reading of

hyperkalemia on the blood test.

Any condition that decreases kidney function can result in hyperkalemia, since the kidneys ridthe body of excess potassium by excreting it in the urine. Examples of conditions that decrease

kidney function are glomerulonephritis,acute orchronic renal failure, transplant rejection, and

obstructions within the urinary tract (such as the presence of stones).

The adrenal glands secrete many hormones important for proper body function. Among these is

aldosterone, which regulates the retention ofsodium and fluid in the kidneys along with the

excretion of potassium in the urine. Diseases of theadrenal gland (such as Addison's disease, that

causes a decreased aldosterone secretion) lead to a decrease in kidney excretion of potassiumresulting in hyperkalemia.

Examples of medications that may lead to elevated potassium levels include:

nonsteroidal antiinflammatory drugs,

ACE inhibitors,

Angiotensin II receptor blockers (ARBs), and

some types of diuretics.

http://www.emedicinehealth.com/hyperkalemia/article_em.htm#causes

Medications

Medications for hyperkalemia can include:

Diuretics to increase potassium excretion in the urine.

Drugs such as epinephrine and albuterol (Ventolin, Proventil, AccuNeb,Vospire, ProAir) that act on beta-2 adrenergic receptors have been used todecrease potassium levels in the blood by increasing its movement back intocells.

Cation-exchange resins are drugs that bind potassium and lead to itselimination via the gastrointestinal tract.
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http://www.emedicinehealth.com/hyperkalemia/page8_em.htm#medications

Hyperkalemia Treatment

The treatment of hyperkalemia is based upon the underlying cause of the hyperkalemia and the

severity of symptoms (or the presence of EKG abnormalities) as well as upon the overall healthstatus of the patient. Mild hyperkalemia in a healthy individual may be treated on an outpatient

basis. Emergency treatment is necessary if hyperkalemia is severe and has caused changes in the

EKG, suggesting an effect on heart function. Severe hyperkalemia is usually treated in thehospital, frequently in an intensive careunit.

http://www.emedicinehealth.com/hyperkalemia/page5_em.htm#treatment

Prevention

It is not possible to prevent the majority of causes of hyperkalemia. However, maintaining ahealthy lifestyle and following your healthcare professional's instructions for management of any

chronic medical conditions can help slow or prevent progression of many diseases that may be

associated with hyperkalemia.

http://www.emedicinehealth.com/hyperkalemia/page10_em.htm#prevention

Disorders of Potassium

Hyperkalemia and Hypokalemia Due to Failed Body

Regulation

Apr 5, 2009 Anthony Lee

Potassium - BigStockPhoto

Potassium is an important electrolyte in the body that can be problematic in

excessive or inadequate amounts.

Potassium is an electrolyte substance that is necessary for survival. It facilitates various cellular

functions and is especially important for nerves, muscles, and the heart's electrical system. In
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order to maintain these functions, the body regulates the amount of potassium in the body. Even

so, consequences may ensue when there is too much or too little potassium.

Regulation of Potassium

Potassium is obtained from one's diet in foods such as various fruits and meats. It is entirelyabsorbed into the bloodstream from the digestive system and predominantly stays within the

body's cells. Normally, the human body maintains a serum potassium level between 3.5 and 5.3milliequivalents per liter (mEq/L).

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Most excess potassium is eliminated from the body through the kidneys. When blood passes

through these organs, fluid and small substances, including potassium, are filtered into the

tubules of the kidneys. Most of this filtrate is reabsorbed back into the blood. If potassium needsto be excreted, the kidneys can secrete it into their own collecting ducts, mediated by a hormone

called aldosterone. Meanwhile; a small amount of potassium is excreted from the body by

secretion into the colon of the gastrointestinal tract.

Hyperkalemia

Hyperkalemia is defined as a serum potassium level greater than 5.3 mEq/L. This often occurs

with kidney failure, particularly when the patient increases his or her intake of potassium. Inaddition, hyperkalemia can result from drugs that inhibit potassium excretion (e.g., potassium-

sparing diuretics) and conditions that shift potassium out of cells, such as destruction of skeletal

muscle (rhabdomyolysis) and destruction of tumor cells following chemotherapy (tumor lysis).

Read This Next

Benefits and Too Much Potassium in Foods Drugs that Cause High Potassium Functions, Sources and Deficiency of Potassium

Symptoms of hyperkalemia stem from effects on skeletal muscles and the heart, includingfatigue, weakness, and palpitations. Treatment of hyperkalemia first requires restriction of

potassium intake. From there, methods to lower serum potassium include glucose and insulin to

stimulate cellular uptake of potassium, saline and diuretics to increase urine production and renal

potassium excretion, Kayexalate to increase gastrointestinal secretion of potassium, and, as a lastresort, emergency dialysis.
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omSep.com%26adT%3DAscom%2BSeparation%26adU%3Dwww.ultraspin.com.au/oil-skimmer%26adT%3DUltraspin%2BOily%2BWater%26adU%3Dwww.Tcmtreatment.com%26adT%3DParkinsons%2BHospital%2BChina%26gl%3DID&usg=AFQjCNHgmp_D2WXj2VQz3xAigqkbBDWsfghttp://googleads.g.doubleclick.net/aclk?sa=L&ai=BH9qy3eJ6TtCBHq-JiAet2qmSDrnwzu0C0ZC3gDPAjbcBwJoMEAEYASD1rvYBKBQ4AFCVtYuyBGDpquKD5A2yARB3d3cuc3VpdGUxMDEuY29tyAEB2gE-aHR0cDovL3d3dy5zdWl0ZTEwMS5jb20vY29udGVudC9kaXNvcmRlcnMtb2YtcG90YXNzaXVtLWExMDc1MDiAAgGpArVx_eDg8Lk-yAKZyfUnqAMB6AOjA-gDsAr1AwAAAAT1AyAAAAA&num=1&sig=AOD64_12-3ijzc0oef2OmSRemuvqMvtbwg&client=ca-pub-7332027313721357&adurl=http://www.thewhiteroom.info/main.faceshttp://googleads.g.doubleclick.net/aclk?sa=L&ai=BH9qy3eJ6TtCBHq-JiAet2qmSDrnwzu0C0ZC3gDPAjbcBwJoMEAEYASD1rvYBKBQ4AFCVtYuyBGDpquKD5A2yARB3d3cuc3VpdGUxMDEuY29tyAEB2gE-aHR0cDovL3d3dy5zdWl0ZTEwMS5jb20vY29udGVudC9kaXNvcmRlcnMtb2YtcG90YXNzaXVtLWExMDc1MDiAAgGpArVx_eDg8Lk-yAKZyfUnqAMB6AOjA-gDsAr1AwAAAAT1AyAAAAA&num=1&sig=AOD64_12-3ijzc0oef2OmSRemuvqMvtbwg&client=ca-pub-7332027313721357&adurl=http://www.thewhiteroom.info/main.faceshttp://googleads.g.doubleclick.net/aclk?sa=L&ai=BTJic3eJ6TtCBHq-JiAet2qmSDujW98kCwNvZkTbAjbcBsJ8aEAIYAiD1rvYBKBQ4AFDkj_WF_v____8BYOmq4oPkDbIBEHd3dy5zdWl0ZTEwMS5jb23IAQHaAT5odHRwOi8vd3d3LnN1aXRlMTAxLmNvbS9jb250ZW50L2Rpc29yZGVycy1vZi1wb3Rhc3NpdW0tYTEwNzUwOKgDAegDowPoA7AK9QMAAAAE9QMgAAAA&num=2&sig=AOD64_3330lutEepFKqg9_rXVPpL8Gpo7w&client=ca-pub-7332027313721357&adurl=http://www.parathyroid.com/parathyroid-surgery.htmhttp://googleads.g.doubleclick.net/aclk?sa=L&ai=BTJic3eJ6TtCBHq-JiAet2qmSDujW98kCwNvZkTbAjbcBsJ8aEAIYAiD1rvYBKBQ4AFDkj_WF_v____8BYOmq4oPkDbIBEHd3dy5zdWl0ZTEwMS5jb23IAQHaAT5odHRwOi8vd3d3LnN1aXRlMTAxLmNvbS9jb250ZW50L2Rpc29yZGVycy1vZi1wb3Rhc3NpdW0tYTEwNzUwOKgDAegDowPoA7AK9QMAAAAE9QMgAAAA&num=2&sig=AOD64_3330lutEepFKqg9_rXVPpL8Gpo7w&client=ca-pub-7332027313721357&adurl=http://www.parathyroid.com/parathyroid-surgery.htmhttp://www.suite101.com/content/kidney-failure-a22315http://www.suite101.com/content/benefits-and-too-much-potassium-in-foods-a80461http://www.suite101.com/content/drugs-that-cause-high-potassium-a331349http://nita-mukherjee.suite101.com/functions-sources-and-deficiency-of-potassium-a311976http://www.suite101.com/content/dialysis-a22417


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Hypokalemia

Hypokalemia is when the serum potassium level is less than 3.5 mEq/L. Many causes ofhypokalemia are the reverse of those of hyperkalemia. For example, patients with hypokalemia

may have inadequate intake of potassium coupled with use of diuretic drugs or excessive

aldosterone (hyperaldosteronism). A common cause of hypokalemia is diarrhea because ofpotassium loss via the gastrointestinal tract.

The symptoms of hypokalemia are similar to those of hyperkalemia: fatigue, weakness, and

palpitations. Treatment involves stopping any medications that contribute to hypokalemia and

providing potassium supplementation orally or through an intravenous line.

Read more at Suite101: Disorders of Potassium: Hyperkalemia and Hypokalemia

Due to Failed Body Regulation | Suite101.com

http://www.suite101.com/content/disorders-of-potassium-a107508#ixzz1YfIx32Ie

http://www.suite101.com/content/disorders-of-potassium-a107508

Low Potassium (Hypokalemia) Overview

Low potassium levels (hypokalemia), can cause weakness as cellular processes are impaired.

Potassium is a mineral (electrolyte) in the body. Almost 98% of potassium is found inside the

cells. Small changes in the level of potassium that is present outside the cells can have severeeffects on the heart, nerves, and muscles.

Potassium is important to maintain several bodily functions:

Muscles need potassium to contract.

The heart muscle needs potassium to beat properly and regulate bloodpressure.

The kidney is the main organ that controls the balance of potassium by removing excess

potassium into the urine.

When potassium levels are low (hypokalemia), you can become weak as cellular processes areimpaired.

The normal potassium level is 3.5-5.0 mEq/L (mEq/L stand for milliequivalentsper liter of blood and this is a measure used to evaluate the level). Lowpotassium is defined as a potassium level below 3.5 mEq/L.

Almost one out of five people hospitalized in the United States has a lowpotassium level.
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People with eating disorders such as anorexia nervosa and bulimia, patientswith AIDS, alcoholics, and those who have had bariatric surgery have a higherincidence of hypokalemia than others.

http://www.emedicinehealth.com/low_potassium/article_em.htm

Potassium homeostasis

Potassium, the most abundant intracellular cation, is essential for the life of the organism.Potassium is obtained through the diet, and common potassium-rich foods include meats, beans,

fruits, and potatoes.

Gastrointestinal absorption is complete, resulting in daily excess intake of approximately 1

mEq/kg/d (60-100 mEq). Ninety percent of this excess is excreted through the kidneys, and 10%is excreted through the gut. Potassium homeostasis is maintained predominantly through the

regulation of renal excretion. The most important site of regulation is the collecting duct, where

aldosterone receptors are present.

Excretion is increased by (1) aldosterone, (2) high sodium delivery to the collecting duct (eg,diuretics), (3) high urine flow (eg, osmotic diuresis), (4) high serum potassium level, and (5)

delivery of negatively charged ions to the collecting duct (eg, bicarbonate).

Excretion is decreased by (1) absence or relative deficiency of aldosterone, (2) low sodiumdelivery to the collecting duct, (3) low urine flow, (4) low serum potassium level, and (5) renal

failure.

Kidneys adapt to acute and chronic alterations in potassium intake. When potassium intake is

chronically high, potassium excretion likewise is increased. In the absence of potassium intake,

obligatory renal losses are 10-15 mEq/d. Thus, chronic losses occur in the absence of anyingested potassium. The kidney maintains a central role in the maintenance of potassium

homeostasis, even in the setting of chronic renal failure. Renal adaptive mechanisms allow the

kidneys to maintain potassium homeostasis until the glomerular filtration rate drops to less than15-20 mL/min. Additionally, in the presence of renal failure, the proportion of potassium

excreted through the gut increases. The colon is the major site of gut regulation of potassium

excretion. Therefore, potassium levels can remain relatively normal under stable conditions, evenwith advanced renal insufficiency. However, as renal function worsens, the kidneys may not be

capable of handling an acute potassium load.

Serum potassium level

Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a

very poor indicator of total body stores. Because potassium moves easily across cell membranes,

serum potassium levels reflect movement of potassium between intracellular and extracellularfluid compartments, as well as total body potassium homeostasis.

Mechanisms for sensing extracellular potassium concentration are not well understood. Evidence

suggests that adrenal glomerulosa cells and pancreatic beta cells may play a role in potassium
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sensing, resulting in alterations in aldosterone and insulin secretion.[1, 2]As both of these

hormonal systems play important roles in potassium homeostasis, these new findings are no

surprise; however, the molecular mechanisms by which these potassium channels signal changesin hormone secretion and activity have still not been determined.

Muscle contains the bulk of body potassium, and the notion that muscle could play a prominentrole in the regulation of serum potassium concentration through alterations in sodium pump

activity has been promoted for a number of years. Insulin stimulated by potassium ingestionincreases the activity of the sodium pump in muscle cells, resulting in an increased uptake of

potassium. Studies in a model of potassium deprivation demonstrate that acutely, skeletal muscle

develops resistance to insulin-stimulated potassium uptake even in the absence of changes inmuscle cell sodium pump expression. However, long term potassium deprivation results in a

decrease in muscle cell sodium-pump expression, resulting in decreased muscle uptake of

potassium.[3, 4, 5]

Thus, there appears to be a well-developed system for sensing potassium by the pancreas and

adrenal glands, resulting in rapid adjustments in immediate potassium disposal and for long-termpotassium homeostasis. High potassium states stimulate cellular uptake via insulin-mediated

stimulation of sodium-pump activity in muscle and stimulate potassium secretion by the kidneyvia aldosterone-mediated enhancement of distal renal expression of secretory potassium channels

(ROMK). Low potassium states result in insulin resistance, impairing potassium uptake into

muscle cells, and cause decreased aldosterone release, lessening renal potassium excretion.

Several factors regulate the distribution of potassium between the intracellular and extracellularspace, as follows:

Glycoregulatory hormones: (1) Insulin enhances potassium entry into cells,and (2) glucagon impairs potassium entry into cells.

Adrenergic stimuli: (1) Beta-adrenergic stimuli enhance potassium entry intocells, and (2) alpha-adrenergic stimuli impair potassium entry into cells.

pH: (1) Alkalosis enhances potassium entry into cells, and (2) acidosis impairspotassium entry into cells.

An acute increase in osmolality causes potassium to exit from cells. An acute cell/tissuebreakdown releases potassium into extracellular space.

http://emedicine.medscape.com/article/242008-overview

Hypokalemia can occur due to 1 of 3 pathogenetic mechanisms.

The first is deficient intake. Poor potassium intake alone is an uncommon cause of hypokalemia

but occasionally can be seen in very elderly individuals unable to cook for themselves or unable

to chew or swallow well. Over time, such individuals can accumulate a significant potassium

deficit. Another clinical situation where hypokalemia may occur due to poor intake is in patientsreceiving total parenteral nutrition (TPN), where potassium supplementation may be inadequate

for a prolonged period of time.
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The second is increased excretion. Increased excretion of potassium, especially coupled with

poor intake, is the most common cause of hypokalemia. The most common mechanisms leading

to increased renal potassium losses include enhanced sodium delivery to the collecting duct, aswith diuretics; mineralocorticoid excess, as with primary or secondary hyperaldosteronism; or

increased urine flow, as with an osmotic diuresis.

Gastrointestinal losses, most commonly from diarrhea, also are common causes of hypokalemia.

Vomiting is a common cause of hypokalemia, but the pathogenesis of the hypokalemia iscomplex. Gastric fluid itself contains little potassium, approximately 10 mEq/L. However,

vomiting produces volume depletion and metabolic alkalosis. These 2 processes are

accompanied by increased renal potassium excretion. Volume depletion leads to secondaryhyperaldosteronism, which, in turn, leads to enhanced cortical collecting tubule secretion of

potassium in response to enhanced sodium reabsorption. Metabolic alkalosis also increases

collecting tubule potassium secretion due to the decreased availability of hydrogen ions forsecretion in response to sodium reabsorption.

The third is due to a shift from extracellular to intracellular space. This pathogenetic mechanismalso often accompanies increased excretion, leading to a potentiation of the hypokalemic effect

of excessive loss. Intracellular shifts of potassium often are episodic and frequently are self-limited, for example, with acute insulin therapy for hyperglycemia.

Regardless of the cause, hypokalemia produces similar signs and symptoms. Because potassium

is overwhelmingly an intracellular cation and because a variety of factors can regulate the actual

serum potassium concentration, an individual can incur very substantial potassium losses withoutexhibiting frank hypokalemia. Conversely, hypokalemia does not always reflect a true deficit in

total body potassium stores.

http://emedicine.medscape.com/article/242008-overview#a0104

Frequency

United States

In the general population, data are difficult to estimate; however, probably fewer than 1% of

people on no medications have a serum potassium level of lower than 3.5 mEq/L. Potassium

intake varies according to age, sex, ethnic background, and socioeconomic status. Whether these

differences in intake produce different degrees of hypokalemia or different sensitivities tohypokalemic insults is not known. Up to 21% of hospitalized patients have serum potassium

levels lower than 3.5 mEq/L, with 5% of patients achieving potassium levels lower than 3

mEq/L. Of elderly patients, 5% demonstrate potassium levels lower than 3 mEq/L.

In patients on non potassium-sparing diuretics, hypokalemia is present in20-50%. African Americans and females are more susceptible. Risk isenhanced by concomitant illness such as heart failure or nephrotic syndrome.

Other groups with a high incidence of hypokalemia include individuals witheating disorders, published incidence ranging from 4.6%[6] to 19.7%[7] in anoutpatient setting; patients with AIDS, of which 23.1% of hospitalized patients
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are hypokalemic; and patients with alcoholism, where the incidence ofhypokalemia in the inpatient setting is reportedly as high as 12.6%[8] and islikely due to a hypomagnesemia-induced decrease in tubular reabsorption ofpotassium. A relatively new and emerging group of individuals who are athigh risk for hypokalemia are patients who have undergone bariatric surgery.[9]

Mortality/Morbidity

Hypokalemia generally is associated with higher morbidity and mortality,especially due to cardiac arrhythmias or sudden cardiac death. However, anindependent contribution of hypokalemia to increased morbidity/mortalityhas not been conclusively established.

Patients who develop hypokalemia often have multiple medical problems,making the separation and quantitation of the contribution by hypokalemia,per se, difficult. For further details, see Complications.

Race

Some suggestion is observed of increased frequency of diuretic-inducedhypokalemia in African Americans. The higher frequency of hypokalemia inthis group may be due to the lower intake of potassium among AfricanAmerican men (approximately 25 mEq/d) than in their white counterparts(70-100 mEq/d).

Sex

Some suggestion also is observed of increased frequency of diuretic-inducedhypokalemia in women.

Age

With age, frequency increases, due to increased use of diuretics and poordiet, which often is low in potassium.

Symptoms are nonspecific and predominantly are related to muscular or cardiac function.

o Weakness and fatigue are the most common complaints. The muscular weakness

that occurs with hypokalemia can manifest in protean ways, ie, dyspnea,

constipation or abdominal distention, or exercise intolerance. Rarely, muscle

weakness progresses to frank paralysis.o Occasionally, a patient may complain of worsening diabetes control or polyuria

due to a recent onset of hyperglycemia or nephrogenic diabetes insipidus.

o The patient also may complain of palpitations.

o With severe hypokalemia or total body potassium deficits, muscle cramps and

pain can occur with rhabdomyolysis.

When the diagnosis of hypokalemia is discovered, investigate potential pathophysiologicmechanisms.

o Poor intake may result from the following:


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Eating disorders

Dental problems

Povertyo Increased excretion may be due to the following:

Medications, including diuretics, AIDS therapy, or antibiotics

Polyuria Vomiting or diarrhea

o Shift of potassium into the intracellular space may occur due to the following:

Recurrent episodes of paralysis Use of high doses of insulin

High-dose beta agonist therapy (eg, for chronic obstructive pulmonary

disease)

http://emedicine.medscape.com/article/242008-clinical

Vital signs generally are normal, except for occasional tachycardia or tachypnea due to

respiratory muscle weakness.o Hypertension may be a clue to primary hyperaldosteronism, renal artery stenosis,

licorice ingestion, or the more unusual forms of genetically transmitted

hypertensive syndromes such as congenital adrenal hyperplasia, glucocorticoid

remediable hypertension, or Liddle syndrome.o Relative hypotension should suggest occult laxative use, diuretic use, bulimia, or

one of the unusual tubular disorders such as Bartter syndrome or Gitelman

syndrome (see Bartter Syndrome). Bear in mind that occult diuretic use is farmore common than either congenital tubular disorder and is, in fact, also called

"pseudo Bartter."

Muscle weakness and flaccid paralysis may be present.

Patients may have depressed or absent deep-tendon reflexes.

Pathophysiologic mechanisms include poor intake, increased excretion, or a shift of potassium

from the extracellular to the intracellular space. Mechanisms causing increased excretion are the

most common. Singly, poor intake or an intracellular shift is a distinctly uncommon cause.Often, several disorders are present simultaneously.

Poor intake

o Eating disorders: Anorexia, bulimia, starvation, pica, and alcoholism

o Dental problems: Inability to chew or swallow

o Poverty: Lack of food, ie, "tea-and-toast" diet of elderly individuals

o Hospitalization: Potassium-poor TPN Increased excretion

o Endogenous mineralocorticoid excess

Cushing disease Primary hyperaldosteronism, most commonly due to adenoma or bilateral

adrenal hyperplasia

Secondary hyperaldosteronism due to volume depletion, congestive heart

failure, cirrhosis, or vomiting
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Adrenocortical carcinoma

Tumor that is producing adrenocorticotropic hormone

Congenital disorders - Congenital adrenal hyperplasia (11-betahydroxylase or 17-alpha hydroxylase deficiency) or glucocorticoid-

remediable hypertension

o

Hyperreninism due to renal artery stenosiso Exogenous mineralocorticoid excess

Steroid therapy for immunosuppression

Glycyrrhizic acid - Inhibits 11-beta hydroxysteroid dehydrogenase;contained in licorice and Chinese herbal preparations

Renal tubular disorders - Type I and type II renal tubular acidosis

Hypomagnesemia

o Congenital disorders

Bartter syndrome: This is a group of autosomal-recessive disorders

characterized by hypokalemic metabolic alkalosis and hypotension.

Mutations in 6 different renal tubular proteins in the loop of Henle have

been discovered in individuals with clinical Bartter syndrome.[10, 11]

Theyare the NaKCl (NKCC2) transporter; the ROMK1 potassium channel; the

chloride channel CLCKa either alone or in combination with the chloridechannel CLCKb; the calcium sensing receptor; and barttin, a protein

required for the surface expression of the chloride channels. The most

severe cases present antenatally or neonatally with profound volumedepletion and hypokalemia. Less severe cases present in childhood or

early adulthood with persistent hypokalemic metabolic alkalosis that is

resistant to replacement therapy. Type IV, a variant to the classic Barttersyndrome, is associated with sensorineural hearing loss.

Gitelman syndrome: This is an autosomal-recessive disorder characterized

by hypokalemic metabolic alkalosis and low blood pressure. It is causedby a defect in the thiazide-sensitive sodium chloride transporter in thedistal tubule. Compared to Bartter syndrome, it generally is milder,

presents later, and is complicated by hypomagnesemia. In contrast,

patients with Bartter syndrome generally do not develophypomagnesemia. Hypocalciuria is also frequently found in Gitelman

syndrome, while the patients with Bartter syndrome are more likely to

have increased urinary calcium excretion. Liddle syndrome: This syndrome is an autosomal-recessive disorder

characterized by a mutation in the epithelial sodium channel in the

aldosterone-sensitive portion of the nephron, leading to unregulated

sodium reabsorption, hypokalemic metabolic alkalosis, and severehypertension.

o Osmotic diuresis: Mannitol and hyperglycemia can cause osmotic diuresis.

o Increased gastrointestinal losses: Losses can result from diarrhea or small

intestine drainage. The problem can be particularly prominent in tropical illnesses,

such as malaria or leptospirosis.[12]Severe hypokalemia has also been reported

with villous adenoma or VIPomas.[13]

o Drugs


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Diuretics (carbonic anhydrase inhibitors, loop diuretics, thiazide

diuretics): Increased collecting duct permeability or increased gradient for

potassium secretion can result in losses. Some penicillins

Exogenous bicarbonate ingestion

Amphotericin B, azole class of antifungal agents, echinocandin class ofantifungal agents[14]

Gentamicin

Cisplatin Stacker 2[15]

Beta-agonist intoxication[16]

Shift of potassium from extracellular to intracellular space

o Alkalosis, metabolic or respiratory

o Insulin administration or glucose administration: This stimulates insulin release.

o Intensive beta-adrenergic stimulation

o Hypokalemic periodic paralysis is a rare disorder with recurrent periods of

hypokalemic paralysis between periods of normal serum potassium levels. Inmost cases, it is due to an abnormality in the alpha 1 subunit of the

dihydropyridine-sensitive calcium channel in the skeletal muscle. How a defect ina calcium channel produces hypokalemic paralysis is not well understood.

o Thyrotoxic periodic paralysis is an acquired form of hypokalemic periodic

paralysis and is most common in Asian males. The mechanism by whichhyperthyroidism produces hypokalemic paralysis is not yet understood, but

theories include increased Na-K-ATPase activity, which has been found in

patients with both thyrotoxicosis and paralysis.o Refeeding: This is observed in prolonged starvation, eating disorders, and

alcoholism.

The history may be vague. Patients are often asymptomatic, particularly with mild hypokalemia.

Symptoms are often due to the underlying cause of the hypokalemia rather than the hypokalemiaitself. Hypokalemia should be suggested by a constellation of symptoms that involve the GI,

renal, musculoskeletal, cardiac, and nervous systems. The patient's medications should be

reviewed to ascertain whether any of them could cause hypokalemia.

Common symptoms include the following:

Palpitations

Skeletal muscle weakness or cramping

Paralysis, paresthesias Constipation[4]

Nausea or vomiting

Abdominal cramping

Polyuria, nocturia, or polydipsia Psychosis, delirium, or hallucinations

Depression


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Findings that are consistent with severe hypokalemia may include the following:

Signs of ileus

Hypotension

Ventricular arrhythmias[5]

Cardiac arrest Bradycardia or tachycardia

Premature atrial or ventricular beats Hypoventilation, respiratory distress

Respiratory failure

Lethargy or other mental status changes

Decreased muscle strength, fasciculations, or tetany

Decreased tendon reflexes

Cushingoid appearance (eg, edema)

Renal losses

o Renal tubular acidosis

o

Hyperaldosteronismo Magnesium depletion

o Leukemia (mechanism uncertain)

GI losses (source may be medical or psychiatric[6] , ie, anorexia or bulimia)o Vomiting or nasogastric suctioning

o Diarrhea

o Enemas or laxative use

o Ileal loop

Medication effects

o Diuretics (most common cause)

o Beta-adrenergic agonists

o Steroidso Theophylline

o Aminoglycosides

Transcellular shift

o Insulin

o Alkalosis

Malnutrition or decreased dietary intake, parenteral nutrition

Urine potassium: This test is of vital importance because it establishes thepathophysiologic mechanism and, thus, helps formulate the differential diagnosis.

o A spot urine potassium measurement is, for obvious reasons, the easiest and most

commonly obtained test. Low urine potassium (< 20 mEq/L) suggests poor intake,

a shift into the intracellular space, or gastrointestinal loss. High urine potassium(>40 mEq/L) suggests renal loss.

o A spot urine sodium and osmolality test obtained simultaneously with a spot urine

potassium test can help refine the interpretation of the urine potassium level. A

low urine sodium level (< 20 mEq/L) with a high urine potassium level suggests

the presence of secondary hyperaldosteronism. If the urine osmolality is high(>700 mOsm/kg), then the absolute value of the urine potassium concentration

can be misleading and can suggest that the kidneys are wasting potassium.


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For example, suppose the serum potassium level is 3 mEq/L and the urine

potassium level is 60 mEq/L. The high urine potassium level would

suggest renal potassium loss. However, the final concentration ofpotassium in the urine is dependent not only on the quantity of potassium

secreted in response to sodium reabsorption, but also on the concentration

of the urine. In the above example, if urine osmolality is 300 mOsm/kg, ie, not

concentrated relative to serum, then a measured urine potassium of 60

mEq/L indeed suggests renal potassium loss. However, if the urineosmolality is 1200 mOsm/kg, ie, concentrated 4-fold relative to serum,

then the potassium concentration in the urine, in the absence of urinary

concentration due to water reabsorption, is 15 mEq/L, ie, very low.

The conclusion would then be that the kidneys are not responsible for thelow serum potassium.

o To account for the potentially confounding effect of urine concentration on the

interpretation of the urine potassium concentration, a calculation called the

transtubular potassium gradient (TTKG) has been developed.

[17, 18]

This test, ineffect, back-calculates what the serum-to-tubular fluid ratio of potassium would

be at the level of the cortical collecting tubule, where potassium is secreted beforeurine concentration has occurred.

Performing this test requires measuring serum and urine potassium levels

and osmolality according to the following equation: TTKG = (Urine potassium X serum osm )/(serum potassium X urine osm)

A value less than 3 suggests that the kidney is not wasting excessive

potassium, while a value greater than 7 suggests a significant renal loss.

This test cannot be applied when the urine osmolality is less than theserum osmolality.

Urine potassium in 24 h: While more cumbersome to obtain, a 24-hour urinemeasurement of potassium excretion yields more precise data on exactly how muchpotassium is being lost through renal excretion.

o Because the kidneys are able to conserve potassium up to approximately 10-15

mEq/d, a value of less than 20 mEq/24-hour urine specimen suggests appropriaterenal conservation of potassium, while values above that indicate some degree of

renal wasting.

o To ensure that a full and accurate 24-hour urine sample has been collected, urine

creatinine should be measured simultaneously.

Basic metabolic profile: Measure electrolytes, BUN, and creatinine.

Serum sodium level

o

Low serum sodium suggests thiazide diuretic use or marked volume depletionfrom gastrointestinal losses.

o High serum sodium might suggest that nephrogenic diabetes insipidus has

occurred secondary to hypokalemia. This could indicate that the hypokalemia is along-standing problem. A high serum sodium level also might suggest the

presence of primary hyperaldosteronism, especially if hypertension also is

present.

Serum bicarbonate level


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o A low serum bicarbonate level might suggest renal tubular acidosis, diarrhea, or

the use of carbonic anhydrase inhibitors.

o A high serum bicarbonate level is consistent with either primary

hyperaldosteronism or secondary hyperaldosteronism. Causes of secondary

hyperaldosteronism could be exogenous prednisone therapy, vomiting, or the use

of thiazide or loop diuretics. A high serum bicarbonate level is also consistentwith Bartter, Gitelman, or Liddle syndrome.

Hyperglycemia might suggest that the hypokalemia has been of sufficient severity and

duration to impair glucose tolerance.

Creatine kinase: Occasionally, hypokalemia will be of sufficient severity to produce not

only muscle weakness but also frank rhabdomyolysis. This most often occurs in the

setting of alcoholism, where total body potassium stores may be quite low due toprolonged periods of poor intake. Severe rhabdomyolysis can lead to renal failure and

subsequent severe hyperkalemia.

Magnesium: Often, severe hypokalemia is associated with significant magnesium losses

and cannot be corrected unless the hypomagnesemia is corrected.

Algorithm for evaluation of hypokalemia: Complete history and physical examinationcan reveal the cause in most cases, negating the need for extensive testing.

o Urine potassium level less than 20 mEq/L suggests gastrointestinal loss, poor

intake, or shift of potassium into cells. Question the patient regarding (1) diarrhea

and use of laxatives; (2) diet and TPN contents; and (3) the use of insulin,

excessive bicarbonate supplements, and episodic weakness.o A urine potassium level higher than 40 mEq/L suggests renal loss.

Examine the patient's medication list. Question the patient regarding the

use of diuretics. Look at the acid-base balance; alkalosis suggests vomiting, Bartter

syndrome, Gitelman syndrome, diuretic abuse, or mineralocorticoid

excess. Acidosis suggests renal tubular acidosis types I or II or Fanconisyndrome (as is observed with paraproteinemias, amphotericin use,gentamicin use, or glue sniffing [toluene abuse]).

Measure the magnesium level; if low, correct it before attempting to

correct the potassium level. Measure the patient's blood pressure. Elevated blood pressure suggests

primary hyperaldosteronism, Cushing syndrome, congenital adrenal

hyperplasia, glucocorticoid-remediable hypertension, renal artery stenosis,or Liddle syndrome. Low blood pressure suggests diuretic abuse or a renal

tubular disorder such as Bartter syndrome, Gitelman syndrome, or renal

tubular acidosis.

o

If the urine potassium level is higher than 20 mEq/L but lower than 40 mEq/L,calculate the TTKG.

A TTKG of less than 3 suggests that renal loss is not a cause of

hypokalemia. A TTKG greater than 7 suggests mineralocorticoid excess.

A middle value may indicate a mixed disorder.


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Perform an ECG to determine whether the hypokalemia is affecting cardiac function or to

detect digoxin toxicity. ECG may show atrial or ventricular tachyarrhythmias, decreased

amplitude of the P wave, or appearance of a U wave.

In most cases, the cause of hypokalemia is apparent from the history and physical

examination and is confirmed by the measurement of urine potassium. By far the most

common causes are losses due to diuretics or gastrointestinal disorders. Depending onhistory, physical examination findings, clinical impressions, and urine potassium results,

the following tests may be appropriate, but they should not be first-line tests unless the

clinical index of suspicion for the disorder is high.

o Diuretic screen in urine and/or serum

o Serum renin, aldosterone, and cortisol

o 24-hour urine aldosterone, cortisol, sodium, and potassium

o Pituitary imaging to evaluate for Cushing syndrome

o Adrenal imaging to evaluate for adenoma

o Renal angiogram to evaluate for renal artery stenosis

o Enzyme assays for 17-beta hydroxylase deficiency

Cushing Syndrome Hypocalcemia

Hypomagnesemia

Medical Care

Orient medical care toward 4 different aims: (1) decreasing potassium losses, (2) replenishing

potassium stores, (3) evaluating for potential toxicities, and (4) determining the cause to preventfuture episodes.

In treating hypokalemia, the first step is to identify and stop ongoing losses of potassium.

o Discontinue diuretics/laxatives.o Use potassium-sparing diuretics if diuretic therapy is required (eg, severe heart

failure).

o Treat diarrhea or vomiting.

o Use H2 blockers to decrease nasogastric suction losses.

o Control hyperglycemia if glycosuria is present.

Repletion of potassium losses is the second step.

o As a first approximation, for every decrease in serum potassium of 1 mEq/L, the

potassium deficit is approximately 200-400 mEq. However, bear in mind that

many factors in addition to the total body potassium stores contribute to the serum

potassium concentration. Therefore, this calculation could either overestimate orunderestimate the true potassium deficit.

o Oral potassium is absorbed readily. Relatively large doses can be given safely.

Oral administration is limited by patient tolerance because some individualsdevelop nausea or even gastrointestinal ulceration with enteral potassium

formulations.

o Intravenous potassium is less well tolerated because it can be highly irritating to

veins and can be given only in relatively small doses, generally 10 mEq/h. Under
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close cardiac supervision in emergent circumstances, as much as 40 mEq/h can be

administered through a central line.

o Oral and parenteral potassium can be used safely simultaneously.

o Take ongoing potassium losses into consideration by measuring the volume and

potassium concentration of body fluid losses.

o If the patient is severely hypokalemic, avoid glucose-containing parenteral fluidsto prevent an insulin-induced shift of potassium into the cells.

o If the patient is acidotic, correct the potassium first to prevent an alkali-induced

shift of potassium into the cells.o Replete magnesium if low.

o Tailor treatment to the individual patient. For example, if diuretics cannot be

discontinued due to an underlying disorder such as congestive heart failure,institute potassium-sparing therapies such as a low-sodium diet, potassium-

sparing diuretics, ACE inhibitors, and angiotensin receptor blockers. The low-

sodium diet and potassium-sparing diuretics limit the amount of sodiumreabsorbed at the cortical collecting tubule, thus limiting the amount of potassium

secreted. ACE inhibitors and angiotensin receptor blockers inhibit the release ofaldosterone, thus blocking the kaliuretic effects of that hormone.

Monitor for toxicity of hypokalemia. Generally, the toxicity of hypokalemia is cardiac in

nature. Monitor the patient if evidence of cardiac arrhythmias is observed, and institute

very aggressive replacement parenterally under monitored conditions.

Determine the underlying cause to treat and prevent further episodes.o Again, history and physical examination findings clarify the cause in the vast

majority of cases.

o Look for clues to the etiology.

Urine potassium concentration

Presence of hypertension or hypotension

Acid-base disturbances Family history

Tooth erosion; melanosis coli; obsession with body image; high-risk

behaviors such as cheerleading, wrestling, or modeling; or evidence ofalcohol abuse

o Tailor the workup to the individual patient if the cause is not completely apparent.

4.2. Diagnosis Gangguan Keseimbangan Kalium4.2.1. Diagnosis Hipokalemia

Diagnosis hipokalemia didasarkan kepada hasil pengukuran kalium serum kecil dari 3,5

mmol/L. Untuk mengetahui penyebab, dilanjutkan dengan pengukuran kalium urin, status

asam basa dan Transtubular Kalium Consentration Gradient (TTKG). Indeks ini

menggambarkan konservasi kalium pada duktus koligentes di korteks ginjal. Diukurdengan perhitungan :1,2,17

TTKG=(K urin)/(K plasma) (Osmolalitas Urin)/(Osmolalitas Plasma)Etiologi hipokalemia dapat berupa1,2,17 :Hipokalemia dengan ekskresi kalium pada urin meningkat menunjukkan adanya

pembuangan yang berlebihan

Hipokalemia dengan ekskresi kalium rendah dengan asidosis metabolik menunjukkanadanya pembuangan kalium yang berlebihan pada saluran cerna seperti pada diare.


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Hipokalemia dengan ekskresi kalium rendah dengan alkalosis metabolik menunjukkan

adanya muntah kronik atau pemberian diuretik jangka lama.

Hipokalemia dengan ekskresi kalium rendah dengan alkalosis metabolik dan disertaihipotensi, merupakan pertanda Sindroma Bartter

Hipokalemia dengan ekskresi kalium tinggi dengan alkalosis metabolik dan disertai

tekanan darah tinggi merupakan pertanda hiperaldosteronisme primerGejala hipokalemia dapat berupa kembung, otot kram, mialgia dan mudah lelah. Bisa

didapatkan hipertensi, dan perubahan pada EKG, yaitu gelombang u, QT memanjang,

bahkan aritmia.2,17

Gbr. 4. Algoritma pernelusuran etiologi hipokalemia berdasarkan ekskresi kalium urin17

Gbr. 5. Contoh EKG pada pasien dengan Hipokalemia7

4.2.2. Diagnosis Hiperkalemia

Diagnosis ditegakkan berdasarkan nilai kalium serum diatas 5,1 mmol/L denganmanifestasi klinis kelemahan otot sampai paralisis, sehingga pasien merasa sesak nafas.

Pemeriksaan EKG mutlak dilakukan untuk melihat adanya gelombang T yang tinggi dan

runcing (T tall), AV Blok, QRS melebar atau aritmia ventrikel. Untuk mencari penyebab

hiperkalemia, perlu diukur TTKG.2,20 Gbr. 6. Algoritma penelusuran etiologi hiperkalemia17

Gbr. 6. Gambaran T tall pada EKG17

4.3. Diagnosis Gangguan Keseimbangan Kalsium

4.3.1. Diagnosis Hipokalsemia

Diagnosis dibuat berdasarkan kepada hasil pemeriksaan laboratorium, dimana kalsium

serum < 8,8 mmol/L, setelah nilai dikoreksi sesuai albumin serum. Nilai koreksi :Ca serum+ (0,8 [albumin serum normal-albumin aktual] )

Gejala klinis dapat berupa19,22:

Terutama gejala neurologik, yaitu bingung, ensefalopati, depresi, psikosisTanda Chovstek, yaitu Kontraksi otot wajah yang dirangsang dengan mengetuk ringan

nervus fasialis pada lokasi lokasi tertentu

Gbr. 7. Tanda Chovstek22Tanda Trousseau, yaitu spasme karpopedal. Dapat dicetuskan dengan pemasangan

torniket selama 3 menit.

Gbr. 8. Tanda Trousseau22

5.2 Penatalaksanaan Gangguan Keseimbangan Kalium

5.2.1. Penatalaksanaan Hipokalemi

Dalam melakukan koreksi kalium, perlu diperhatikan indikasinya, yaitu 2,14 :

Indikasi mutlak, yaitu pada pasien dalam keadaan pengobatan digitalis, KAD, pasien

dengan kelemahan otot nafas dan hipokalemia berat.

Indikasi kuat, yaitu diberikan dalam waktu yang tidak terlalu lama yaitu padakeadaan insufisiensi koroner, ensefalopati hepatik dan penggunaan obat-obat

tertentu.

Indikasi sedang, dimana pemberian Kalium tidak perlu segera seperti pada

hipokalemia ringan dengan nilai K antara 3-3,5 mmol/L.

Pemberian Kalium dapat melalui oral. Pemberian 40-60 mmol/L dapat

meningkatkan kadar Kalium sebesar 1-1,5 mmol/L. Pemberian Kalium intravena

diberikan dalam larutan KCl dengan kecepatan 10-20 mmol/jam. Pada keadaan


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dengan EKG yang abnormal, KCl diberikan dengan kecepatan 40-100 mmol/jam. KCl

dilarutkan dalam NaCl isotonik dengan perbandingan 20 mmol KCl dalam 100 ml

NaCl isotonik melalui vena besar. Jika melalui vena perifer, KCl maksimal 60 mmol

dilarutkan dalam NaCl isotonik 1000 ml. Bila melebihi kadar ini, dapat menimbulkan

rasa nyeri dan sklerosis vena. Kebutuhan Kalium dapat dihitung dengan rumus :

7,21(K yang diinginkan-K serum )/3 x BB

5.2.2. Penatalaksanaan Hiperkalemia

Penatalaksaan meliputi pemantauan EKG yang kontinu jika ada kelainan EKG atau

jika kalium serum lebih dari 7 mEq/L. Untuk mengatasi hiperkalemia dalam

membran sel, diberikan kalsium intravena, yang diberikan dalam bentuk kalsium

glukonat melalui intravena dengan sediaan 10 ml larutan 10% selama 10 menit. Hal

ini berguna untuk menstabilkan miokard dan sistem konduksi jantung. Ini bisa

diulang dengan interval 5 menit jika tidak ada respon. 1,2

Memacu kalium kembali dari ekstrasel ke intrasel dengan cara pemberian 10 unit

insulin dalam 50 ml glukosa 40% secara bolus intravena. Pemberian natrium

bikarbonat yang dapat meningkatkan pH sistemik yang akan merangsang ion H

keluar dari dalam sel dan menyebabkan ion K masuk ke dalam sel. Bikarbonat

diberikan sebanyak 50 mEq intravena selama 10 menit. Hal ini dalam keadaan

tanpa asidosis. Kemudian pemberian Beta 2 agonis baik secara inhalasi maupun

drip intravena. Obat ini akan merangsang pompa NaK-ATPas dan Kalium masuk ke

dalam sel. Mengeluarkan kelebihan Kalium dari dalam tubuh dengan cara

pemberian diuretik, resin penukar, atau dialisis.14,22

Tabel 2. Opsi Penatalaksanaan hiperkalemia9

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Diagnosis dan Penatalaksanaan Keseimbangan Elektrolit

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BAB I

PENDAHULUAN

Tubuh manusia merupakan suatu sistem yang terdiri dari berbagai proses fisikokimia yangmenunjang kehidupan sehari hari. Tubuh selalu berusaha agar segala sesuatu yang adadidalamnya berada dalam rentang konstan agar tercapai keadaan homeostasis. Seluruh sistem

metabolisme bekerja sama dengan harmonis satu sama lain dalam menjalankan fungsinya

masing masing. 1,2

Elektrolit dan cairan merupakan salah satu faktor yang berperan dalam menjaga keseimbanganini. Secara kimiawi, elektrolit adalah unsur unsur yang berperan sebagai ion dalam larutan dan

memiliki kapasitas untuk konduksi listrik. Dan keseimbangan elektrolit merupakan suatu hal

yang penting agar sel dan organ dapat berfungsi secara normal. Elektrolit terdiri atas kation dananion. Di dalam tubuh ada beberapa kation yang penting yaitu, natrium, kalium, kalsium dan

magnesium. Sedangkan anion yang penting adalah klorida, bikarbonat, dan fosfat.1,2,3

Gangguan keseimbangan elektrolit diartikan sebagai suatu keadaan dimana kadar elektrolit didalam darah berada dalam rentang nilai yang tidak normal. Bisa melebihi nilai normal atau

dibawah nilai normal. Implikasi dari keadaan ini berpengaruh dalam hal keseimbangan cairan

dan fungsi fungsi organ tubuh lainnya. Berbagai macam hal dapat menyebabkanketidakseimbangan ini. Ketidakseimbangan antara kebutuhan dengan asupan serta ekskresi

adalah penyebab utamanya. Adanya gangguan dari sistem regulasi yang berperan, juga

memberikan dampak dalam keseimbangan elektrolit.1,3

Dalam praktek klinik sehari hari gangguan elektrolit merupakan kelainan yang sangat seringdijumpai. Keadaan ini biasanya merupakan bagian manifestasi klinis dari penyakit dasar yang

diderita pasien. Hampir 20 % pasien rawat inap mengalami gangguan elektrolit, yang disebabkan

oleh bermacam hal, sehingga dalam pembiayaanpun menjadi hal yang diperhitungkan.4,5

Gangguan elektrolit seringkali terdiagnosis saat pasien dirawat di rumah sakit, terutama padapasien pasien dengan penyakit kritis. Keadaan ini berhubungan dengan meningkatnya risiko

mortalitas di rumah sakit. Insidensi gangguan elektrolit terbanyak adalah gangguan kalium dannatrium. Sebanyak lebih dari 21 % pasien di rumah sakit mengalami hipokalemia dan 15 20 %

mengalami hiponatremia. Pasien pasien dengan hiperkalemia mencapai 1 10 %, sedangkan

hipernatremia 0,3 5,5 % dari seluruh pasien yang dirawat. Hiperkalsemia terjadi pada lebih dari

70 % kasus keganasan. Hipomagnesemia muncul pada lebih dari 12% pasien, yang terkadangsering diabaikan oleh para klinisi. 6,7,8,9,10,11
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8/3/2019 Hyper Kale Mia is a Potentia

Hyper Kale Mia is a Potentially Life

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