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 adenosine triphosphatase (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 potassium stores 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 or chronic 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)

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

http://emedicine.medscape.com/article/766479-overview#a0199

History
Hyperkalemia can be difficult to diagnose clinically because complaints may be vague. The history 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

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

bananas, oranges, highprotein diets, tomatoes, salt substitutes). This alone is not likely
Ingestion of foods high in potassium (eg, to 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 antiinflammatory drugs (NSAIDs), beta-blockers, digoxin, succinylcholine, and digitalis glycoside 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, or bradycardia. Neurologic examination may reveal diminished deep tendon reflexes or decreased motor strength. 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
http://emedicine.medscape.com/article/766479-clinical#a0217

Causes

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 renal failure) 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

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 clinical setting. ECG changes have a sequential progression of effects, which roughly correlate with the potassium level. ECG findings may be observed as follows:

Early changes of hyperkalemia include peaked T waves, shortened QT interval, 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 QRS complexes 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 potassium level of 7.8 mEq/L and widened QRS complexes after receiving 1 ampule of calcium chloride. Notice narrowing of QRS complexes and reduction of T waves. Without treatment, the P wave eventually disappears and the QRS morphology widens to resemble a sine wave. Ventricular fibrillation or asystole follows.

ECG findings generally correlate with the potassium level, but potentially lifethreatening arrhythmias can occur without warning at almost any level of hyperkalemia.

Cortisol and aldosterone levels

To check for mineralocorticoid deficiency when other causes are eliminated

http://emedicine.medscape.com/article/766479-workup#a0721

Prehospital Care
A patient with known hyperkalemia or a patient with renal failure with suspected hyperkalemia should 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 in the face of digoxin-toxic cardiac arrhythmias.
http://emedicine.medscape.com/article/766479-treatment

Perform continuous ECG monitoring with frequent vital sign checks when hyperkalemia is suspected 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, begin treatment 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 only excretion 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

Class Summary

These agents are used to treat hyperkalemia and to reduce the risk of ventricular fibrillation caused 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 the ECG 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 of action 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, bringing potassium 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.
View full drug information Insulin (Humulin, Humalog, Novolin)

Stimulates cellular uptake of K+ within 20-30 min; administer glucose along with insulin to prevent hypoglycemia (monitor blood glucose levels closely).
http://emedicine.medscape.com/article/766479-medication#3

Alkalinizing agents

Class Summary

These agents increase the pH, which results in a temporary potassium shift from the extracellular to the intracellular environment. These agents enhance the effectiveness of insulin in patients with acidemia.
View full drug information 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 underlying acidosis 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 receptor cascade.
View full drug information 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 patients with 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.

View full drug information

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.
View full drug information 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.

View full drug information 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 approximately 0.5-1 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.
View full drug information Magnesium sulfate

Nutritional supplement in hyperalimentation; cofactor in enzyme systems involved in neurochemical transmission and muscular excitability. In adults, 60-180 mEq of potassium, 1030 mEq of magnesium, and 10-40 mmol of phosphate per day may be necessary for optimum metabolic 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 of electrolytes, and up to 8% of hospitalized patients 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 or greater). Sometimes people with hyperkalemia report nonspecific symptoms such as muscle weakness, tiredness, tingling sensations, or nausea. 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 rhythm and hyperkalemia can have potentially life-threatening effects. While mild hyperkalemia

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 neuromuscular activity of the heart), and severe hyperkalemia can cause the heart to stop beating. Hyperkalemic periodic paralysis 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 of potassium in the bloodstream. Potassium has several important 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 the smooth 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 per liter (mEq/L). Potassium levels between 5.1 mEq/L to 6.0 mEq/L are considered to be mild hyperkalemia. Potassium levels of 6.1 mEq/L to 7.0 mEq/L are moderate hyperkalemia, and levels 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, an emergency 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 destruction include:

trauma,

burns, surgical procedures, destruction of tumor cells or red blood cells, and rhabdomyolysis (a condition involving destruction of muscle cells that is sometimes 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 rid the body of excess potassium by excreting it in the urine. Examples of conditions that decrease kidney function are glomerulonephritis, acute or chronic 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 of sodium and fluid in the kidneys along with the excretion of potassium in the urine. Diseases of the adrenal gland (such as Addison's disease, that causes a decreased aldosterone secretion) lead to a decrease in kidney excretion of potassium resulting 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 to decrease potassium levels in the blood by increasing its movement back into cells. Cation-exchange resins are drugs that bind potassium and lead to its elimination via the gastrointestinal tract.

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 health status 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 the hospital, frequently in an intensive care unit.
http://www.emedicinehealth.com/hyperkalemia/page5_em.htm#treatment Prevention

It is not possible to prevent the majority of causes of hyperkalemia. However, maintaining a healthy 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

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 entirely absorbed 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 5.3 milliequivalents 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 needs to 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. In addition, hyperkalemia can result from drugs that inhibit potassium excretion (e.g., potassiumsparing 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).

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Symptoms of hyperkalemia stem from effects on skeletal muscles and the heart, including fatigue, 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 last resort, emergency dialysis.

Hypokalemia

Hypokalemia is when the serum potassium level is less than 3.5 mEq/L. Many causes of hypokalemia 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 of potassium 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 severe effects 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 blood pressure.

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 are impaired.

The normal potassium level is 3.5-5.0 mEq/L (mEq/L stand for milliequivalents per liter of blood and this is a measure used to evaluate the level). Low potassium is defined as a potassium level below 3.5 mEq/L. Almost one out of five people hospitalized in the United States has a low potassium level.

People with eating disorders such as anorexia nervosa and bulimia, patients with AIDS, alcoholics, and those who have had bariatric surgery have a higher incidence 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 sodium delivery 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 any ingested 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 than 15-20 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, even with 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 extracellular fluid 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

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 changes in hormone secretion and activity have still not been determined. Muscle contains the bulk of body potassium, and the notion that muscle could play a prominent role 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 ingestion increases 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 in muscle 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-term potassium homeostasis. High potassium states stimulate cellular uptake via insulin-mediated stimulation of sodium-pump activity in muscle and stimulate potassium secretion by the kidney via 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 extracellular space, 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 into cells, and (2) alpha-adrenergic stimuli impair potassium entry into cells. pH: (1) Alkalosis enhances potassium entry into cells, and (2) acidosis impairs potassium entry into cells.

An acute increase in osmolality causes potassium to exit from cells. An acute cell/tissue breakdown 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 patients receiving total parenteral nutrition (TPN), where potassium supplementation may be inadequate for a prolonged period of time.

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, as with 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 is complex. 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 secondary hyperaldosteronism, 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 for secretion in response to sodium reabsorption. The third is due to a shift from extracellular to intracellular space. This pathogenetic mechanism also 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 selflimited, 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 without exhibiting 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 to hypokalemic 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 in 20-50%. African Americans and females are more susceptible. Risk is enhanced by concomitant illness such as heart failure or nephrotic syndrome. Other groups with a high incidence of hypokalemia include individuals with eating disorders, published incidence ranging from 4.6%[6] to 19.7%[7] in an outpatient setting; patients with AIDS, of which 23.1% of hospitalized patients

are hypokalemic; and patients with alcoholism, where the incidence of hypokalemia in the inpatient setting is reportedly as high as 12.6%[8] and is likely due to a hypomagnesemia-induced decrease in tubular reabsorption of potassium. A relatively new and emerging group of individuals who are at high 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, an independent contribution of hypokalemia to increased morbidity/mortality has 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-induced hypokalemia in African Americans. The higher frequency of hypokalemia in this group may be due to the lower intake of potassium among African American 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-induced hypokalemia in women.

Age

With age, frequency increases, due to increased use of diuretics and poor diet, 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 pathophysiologic mechanisms. o Poor intake may result from the following:

Eating disorders Dental problems Poverty Increased excretion may be due to the following: Medications, including diuretics, AIDS therapy, or antibiotics Polyuria Vomiting or diarrhea 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 far more 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

o o

o o

Adrenocortical carcinoma Tumor that is producing adrenocorticotropic hormone Congenital disorders - Congenital adrenal hyperplasia (11-beta hydroxylase or 17-alpha hydroxylase deficiency) or glucocorticoidremediable hypertension Hyperreninism due to renal artery stenosis 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 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] They are the NaKCl (NKCC2) transporter; the ROMK1 potassium channel; the chloride channel CLCKa either alone or in combination with the chloride channel 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 volume depletion 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 Bartter syndrome, 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 caused by a defect in the thiazide-sensitive sodium chloride transporter in the distal 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 develop hypomagnesemia. 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 severe hypertension. Osmotic diuresis: Mannitol and hyperglycemia can cause osmotic diuresis. 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] Drugs

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 of antifungal 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. In most 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 in a 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 which hyperthyroidism 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 hypokalemia itself. 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

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 Hyperaldosteronism o 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 Steroids o 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 the pathophysiologic 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.

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 of potassium 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 urine osmolality 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 the low 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, in effect, 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 before urine 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 the serum osmolality. Urine potassium in 24 h: While more cumbersome to obtain, a 24-hour urine measurement of potassium excretion yields more precise data on exactly how much potassium 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 appropriate renal 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 depletion from gastrointestinal losses. o High serum sodium might suggest that nephrogenic diabetes insipidus has occurred secondary to hypokalemia. This could indicate that the hypokalemia is a long-standing problem. A high serum sodium level also might suggest the presence of primary hyperaldosteronism, especially if hypertension also is present. Serum bicarbonate level

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 consistent with 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 to prolonged 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 examination can 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 Fanconi syndrome (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.
o

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 on history, 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 prevent future 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 or underestimate 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 individuals develop 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

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 fluids to 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, potassiumsparing diuretics, ACE inhibitors, and angiotensin receptor blockers. The lowsodium diet and potassium-sparing diuretics limit the amount of sodium reabsorbed at the cortical collecting tubule, thus limiting the amount of potassium secreted. ACE inhibitors and angiotensin receptor blockers inhibit the release of aldosterone, 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 of alcohol abuse o Tailor the workup to the individual patient if the cause is not completely apparent. 4.2. Diagnosis Gangguan Keseimbangan Kalium 4.2.1. 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. Diukur dengan 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 menunjukkan adanya pembuangan kalium yang berlebihan pada saluran cerna seperti pada diare.

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 disertai hipotensi, merupakan pertanda Sindroma Bartter Hipokalemia dengan ekskresi kalium tinggi dengan alkalosis metabolik dan disertai tekanan darah tinggi merupakan pertanda hiperaldosteronisme primer Gejala 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 dengan manifestasi 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, psikosis Tanda Chovstek, yaitu Kontraksi otot wajah yang dirangsang dengan mengetuk ringan nervus fasialis pada lokasi lokasi tertentu Gbr. 7. Tanda Chovstek22 Tanda 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 pada keadaan 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

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 yang menunjang kehidupan sehari hari. Tubuh selalu berusaha agar segala sesuatu yang ada didalamnya 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 keseimbangan ini. 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 dan anion. 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 di dalam 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 menyebabkan ketidakseimbangan 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 sering dijumpai. 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 pada pasien pasien dengan penyakit kritis. Keadaan ini berhubungan dengan meningkatnya risiko mortalitas di rumah sakit. Insidensi gangguan elektrolit terbanyak adalah gangguan kalium dan natrium. 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 terkadang sering diabaikan oleh para klinisi. 6,7,8,9,10,11

Mengingat tingginya angka kejadian gangguan keseimbangan elektrolit dalam praktek klinik seharihari, terutama gangguan keseimbangan natrium, kalium, kalsium dan magnesium, maka perlu adanya suatu pemahaman yang lebih baik. Dengan pemahaman ini, akan memudahkan dalam hal penentuan diagnosis yang cepat dan akurat, sehingga terapi dan penatalaksanaan dapat diberikan dengan cepat dan akurat pula. Atas dasar inilah refrat ini ditulis. BAB II FISIOLOGI ELEKTROLIT 2.1. Keseimbangan Natrium dan Cairan Natrium adalah kation utama cairan ekstraseluler (CES). Dalam kondisi fisiologis, Natrium (Na) serum memiliki rentang nilai antara 138 142 mmol/L. Untuk menilai jumlah total partikel dalam darah, maka perlu diukur osmolalitas serum. Osmolalitas serum memiliki nilai berkisar antara 280 290 mOsm/kgH2O. Osmolalitas diukur dengan rumus3 : P_osm=2(Na)+(Nitrogen urea darah (mg/dl))/2,8+(glukosa(mg/dl))/18 Peningkatan osmolalitas akibat absorpsi Na atau kehilangan cairan yang berlebihan, menyebabkan cairan intraseluler keluar untuk menyeimbangkan tekanan osmotik. Untuk itu, perlu adanya suatu osmoregulator. Dalam hal ini, ada suatu sensor atau osmoreseptor yang ada di hipotalamus, dan Anti Diuretic Hormone (ADH), yang dikenal juga dengan antidiuretin atau vasopressin. Ginjal berperan sebagai organ target ADH. 12,13 Naik turunnya ekskresi natrium dalam urin diatur oleh filtrasi glomerulus dan reabsorpsi oleh tubulus ginjal. Kondisi hipervolemi dan peningkatan asupan Na akan meningkatkan Laju Filtrasi Glomerulus (LFG), begitupula sebaliknya. Perubahan pada LFG akan mempengaruhi reabsorpsi natrium di tubulus. Hampir 99 % Na yang sudah difiltrasi direabsorpsi kembali. Paling banyak direabsorpsi di tubulus proksimal 65 %, ansa henle 25 30 %, dan 5 % saja di tubulus distal dan 4 % di duktus koligentes.12,13 Setiap hari, sekitar 8 15 mg Natrium diabsorpsi setiap harinya. Ginjal harus mengekskresikan dalam jumlah yang sama setiap waktu, untuk mempertahankan homeostasis CES. Adapun faktor faktor yang mempengaruhi regulasi ini adalah 12: Sistem Renin Angiotensin / Renin Angiotensin System ( RAS ) Aktivasi sistem ini meningkatkan retensi natrium melalui angiotensin II, aldosteron dan ADH Atriopeptin / Atrial Natriuretic Peptide (ANP) Adalah hormon peptida yang disekresikan oleh sel spesifik dari atrium jantung sebagai respon terhadap peningkatan volume CES. Hormon ini meningkatkan ekskresi Na pada ginjal dengan meningkatkan fraksi filtrasi dan menginhibisi reasorpsi natrium dari duktus koligentes. ADH Sekresi hormon ini distimulasi oleh : Peningkatan osmolalitas plasma dan cairan serebrospinal Reflek Gauer-Henry, yang muncul ketika terjadi peregangan reseptor di atrium yang memberikan sinyal ke hipotalamus bahwa telah terjadi penurunan jumlah CES > 10 %. Angiotensin II Aldosteron Efek hormon ini adalah menstimulasi reabsorpsi natrium. Sekresi hormon ini distimulasi oleh angiotensin II

Gbr. 1. Regulasi Keseimbangan Air dan Garam12 2.2. Keseimbangan Kalium Kalium (K) adalah kation utama kompartemen cairan intraseluler ( CIS ). Sekitar 90 % asupan kalium diekskresikan di urin dan 10 % di feses. Konsentrasi normal kalium di plasma adalah 3,5 4,8 mmol/L, sedangkan konsentrasi intraseluler dapat 30 kali lebih tinggi, dan jumlahnya mencapai 98 % dari jumlah K keseluruhan. Walaupun kadar kalium di dalam CES hanya berkisar 2 % saja, akan tetapi memiliki peranan yang sangat penting dalam menjaga homeostasis. Perubahan sedikit saja pada kalium intraseluler, akan berdampak besar pada konsentrasi kalium plasma.2,14 Keseimbangan Kalium diatur dengan menyeimbangkan antara pemasukan dan ekskresi, serta distribusi antara intrasel dan ekstrasel. Regulasi akut kalium ekstraseluler dicapai dengan perpindahan kalium internal antara CES dan CIS. Ketika kadar kalium ekstrasel meningkat akibat asupan yang banyak, atau disebabkan oleh pembebasan kalium internal, maka regulasi akut ini akan terjadi. Regulasi ini merupakan kontrol hormonal, yaitu1,2,14 : Insulin disekresikan segera setelah makan, dan ini akan menstimulasi Na, K, ATPase dan mendistribusikan Kalium yang didapat dari selsel makhluk hidup yang dimakan ke intrasel. Epinefrin meningkatkan ambilan kalium sel, yang mana penting untuk kerja otot dan trauma. Kedua kondisi ini memicu terjadinya peningkatan kalium plasma. Aldosteron juga berperan dalam meningkatkan konsentrasi kalium intraseluler. Perubahan pH mempengaruhi distribusi kalium ekstra dan intraseluler. Pada asidosis, konsentrasi K ekstraseluler meningkat, sedangkan alkalosis cenderung membuat hipokalemia. Regulasi kronik untuk homeostasis K adalah oleh ginjal. 65 % dari K yang difiltrasi, direabsorpsi sebelum mencapai akhir dari tubulus proksimal ginjal, 20% di tubulus distal, dan 15 % lainnya di ansa henle. Jumlah ekskersi kalium ditentukan pada tubulus penghubung dan duktus koligentes Besarnya jumlah K yang direabsorpsi atau disekresi tergantung kepada kebutuhan. Pada keadaan dimana pemasukan berlebihan, maka ekskresi akan meningkat, begitupula sebaliknya.13,14 2.3. Keseimbangan Kalsium Ion kalsium (Ca) merupakan elektrolit yang banyak terdapat di ekstraseluler, dimana 99 % disimpan di tulang. Kadar normal kalsium plasma adalah 8,1 10,5 mmol/L. Ca berfungsi pada sistem neuromuskular, konduksi saraf, kontraksi otot, relaksasi otot, dan juga penting untuk mineralisasi tulang dan merupakan kofaktor penting untuk sekresi hormon pada organ endokrin. Pada tingkat sel, Ca merupakan regulator penting untuk transpor ion dan integritas membran. Tulang berperan ganda, dimana berperan sebagai yang mengambil kalsium untuk stabilitas dan sebagai depot untuk keadaan suplai kalsium yang rendah.2,9 Paratiroid Hormon (PTH), adalah suatu faktor yang penting dalam regulasi keseimbangan kalsium dengan menurunkan ekskresi dan meningkatkan absorpsi kalsium di ginjal dengan bantuan 1,25 COH2 Vitamin D3 (calcitrol), dan merangsang osteoklas melepaskan kalsium dari tulang. Efek PTH di tubulus adalah merangsang aktifitas 1 alfa hidroksilase yang akan memicu produksi calcitrol. PTH meningkatkan reabsorpsi Ca di TAL, dan begitu juga pada tubulus distal. Selain itu, calcitrol juga akan meningkatkan absorpsi kalsium di intestinal. PTH bergantung kepada Calsium Sensing Reseptor (CSR) untuk mendeteksi adanya kelebihan kalium serum, dan menghambat sekresi PTH. PTH disekresikan oleh chief cells pada kelenjar paratiroid yang akan meningkatkan kadar kalsium darah.2,9 Reasorbsi kalsium terjadi pada semua tubulus ginjal. 60 70 % terjadi di tubulus proksimal, 30 % di Thick Ascending Limb (TAL) dari ansa henle. Karena reasorpsi Ca pada TAL bergantung

kepada reabsorpsi NaCl, maka pada loop diuretic, kalsium diinhibisi untuk direabsorpsi. Asidosis menghambat reabsorpsi kalsium dengan mekanisme yang belum dapat dipahami.9,15,16 2.4. Keseimbangan Magnesium Magnesium (Mg) adalah kation keempat terbanyak di dalam tubuh dan kation ektraseluler kedua terbanyak. Konsentrasi magnesium plasma berkisar 0,7 1,2 mmol/L atau 1,5 1,9 mEq/L. Dan hampir 50 % terikat dengan protein. Magnesium berperan penting dalam ratusan reaksi enzim yang merupakan hal esensial bagi tubuh. Juga berperan dalam fungsi sel, termasuk transfer energi, penyimpanan dan penggunaan protein dan karbohidrat dan metabolisme lemak. Berperan juga dalam mempertahankan fungsi membran sel, dan regulasi sekresi hormon paratiroid. Sekitar 60 65 % dari magnesium tubuh disimpan di tulang dan selebihnya di dalam sel. Hanya 1 % saja yang terdapat di ekstraseluler. Tulang merupakan reservoir bagi Mg. Selebihnya dalam bentuk ion bebas di plasma. Keseimbangan Mg melibatkan ginjal, usus halus, dan tulang. 2,8 Hampir 80 % magnesium difiltrasi diglomerulus, dan direasorpsi disepanjang nefron. Mg direabsorpsi 15 % pada tubulus proximal. Sekitar 70 % terjadi reabsorpsi paraseluler di Thick Ascending Limb (TAL) dari ansa henle. Sebanyak 10 15 % lainnya dengan reabsorpsi transeluler di tubulus distal. Regulasi ekskresi Mg2+ distimulasi oleh hipermagnesemia, hiperkalsemia, hipervolemia dan loop diuretik. Dan mekanisme penghambat dipengaruhi oleh defisit magnesium, kalsium dan volume cairan. Dan juga dipengaruhi hormon paratiroid yang bekerja pada TAL. Seperti pada kalsium, Mg juga berperan dalam regulasi sekresi PTH. Keadaan dimana kadar Mg plasma meningkat, akan menekan pelepasan PTH, begitu juga sebaliknya.2,8

BAB III ETIOPATOGENESIS DAN PATOFISIOLOGI 3.1. Gangguan Keseimbangan Natrium 3.1.1. Hiponatremia Hiponatremia dapat terjadi pada keadaan tonisitas atau osmolalitas yang rendah, normal ataupun tinggi. Sebagian besar kejadian hiponatremia berkaitan dengan hipotonisitas, yang berarti bila jumlah asupan cairan melebihi kemampuan eskresi.1,17,18 Etiologi dari hiponatremia dapat dibagi atas1,17 : Hiponatremia dengan osmolalitas plasma normal pemberian cairan iso-osmotik yang tidak mengandung natrium ke cairan ekstra sel dapat menimbulkan hiponatremia dengan osmolalitas plasma normal. Termasuk dalam hal ini, keadaan hiperproteinemia dan hiperlipidemia Hiponatremia dengan osmolalitas plasma tinggi

Pada keadaan osmolalitas plasma yang tinggi, seperti pada keadaan hiperglikemia berat atau pemberian manitol intravena. Cairan intrasel akan keluar ke ekstrasel menyebabkan dilusi cairan ekstrasel, dan menyebabkan hiponatremia. Hiponatremia dengan osmolalitas plasma rendah Terjadi pada keadaan seperti gagal jantung, sirosis, insufisiensi renal, sindroma nefrotik. Keadaan-keadaan ini terjadi dengan volume CES yang meningkat. Pada SIADH, volume CES normal dan pada keadaan muntah atau pada pemakaian diuretik, volume CES menurun. Hiponatremia akut diartikan sebagai kejadian hiponatremia dalam jangka waktu kurang dari 48 jam. Pada keadaan ini tertjadi perpindahan cairan dari ekstrasel ke intrasel, termasuk ke sel otak. Hal ini akan menyebabkan terjadinya edema otak yang mana keadaan ini merupakan keadaan berat yang dapat menyebabkan kejang dan penurunan kesadaran. Edema otak yang terjadi, dibatasi oleh kranium disekitarnya, yang mengakibatkan terjadinya hipertensi intrakranial dengan resiko brain injury17,18 Hiponatremia kronik diartikan sebagai keadaan hiponatremia dalam jangka waktu yang lebih dari 48 jam. Gejala yang timbul tidak berat karena ada proses adaptasi. Pada keadaan ini, cairan akan keluar dari jaringan otak dalam beberapa jam. Gejala yang timbul hanya berupa lemas dan mengantuk, bahkan dapat tanpa gejala. Keadaan ini dikenal juga dengan hiponatremia asimtomatik. Namun perlu diperhatikan pada proses adaptasi ini dapat menjadi proses yang berlebihan yang berisiko terjadinya demyelinisasi osmotik.1,18 3.1.2 Hipernatremia Hipernatremia adalah suatu keadaan dengan defisit cairan relatif, dalam artian merupakan keadaan hipertonisitas, atau hiperosmolalitas. Etiologi dari hipernatremia adalah10,19 : Adanya defisit cairan tubuh akibat ekskresi air yang melebihi ekskresi natrium. Seperti pada pengeluaran keringat, insesible water loss, diare osmotik akibat pemberian laktulosa atau sorbitol Asupan air yang kurang, pada pasien dengan gangguan pusat rasa haus di hipotalamus akibat tumor dan gangguan vaskuler Penambahan natrium yang berlebihan, seperti pada koreksi asidosis dengan bikarbonat, atau pemberian natrium yang berlebihan Masuknya air tanpa elektrolit ke dalam sel, misalnya setelah latihan fisik berat. Keadaan hipernatremia akan membuat cairan intraseluler keluar ke ekstraseluler untuk menyeimbangkan osmolalitas cairan ekstrasel. Hal ini akan membuat terjadinya pengkerutan sel, dan bila terjadi pada sel saraf sistem saraf pusat, maka akan menimbulkan disfungsi kognitif, seperti lemah, bingung, sampai kejang.10,19 3.2. Gangguan Keseimbangan Kalium 3.2.1. Hipokalemia Penyebab hipokalemia antara lain1,7,13 : Asupan kalium yang kurang. Secara fisiologis, ekskresi kalium di ginjal sebanding dengan jumlah asupan. Hipokalemia jarang yang hanya disebabkan asupan kalium yang rendah saja. Pengeluaran Kalium yang berlebihan. Ekskresi kalium dapat melalui sistem pencernaan, keringat atau ginjal. Beberapa etiologi ekskresi kalium meningkat adalah muntah, pemakaian NGT, diare, pemakaian diuretik loop dan tiazid serta hiperaldosteronisme. Kalium berpindah dari ekstrasel ke intrasel (Redistribusi). Terjadi pada keadaan alkalosis, pemberian insulin, pemakaian beta 2 agonis, paralysis periodic hypokalemic, dan hipotermia. Konsentrasi ion kalium pada pada ekstrasel sangat keci dan keadaan ini tidak tercermin pada jumlah kalium serum. Pada hipokalemia kronik, penurunan kalium serum 1 mmol/L sebanding

dengan defisit 200 mmol/L kalium total tubuh, maka perlu dipertahankan kalium serum > 4 mEq/L. Defisiensi kalium dapat mempengaruhi berbagai sistem organ, seperti sistem kardiovaskuler, otot dan ginjal. Hipokalemia dapat menyebabkan hipertensi dan aritmia ventrikel. Mekanisme terjadinya hipertensi masih belum dapat dijelaskan dengan baik. Akan tetapi, keadaan ini dihubungkan dengan retensi garam di ginjal, selain akibat berbagai proses hormonal. Aritmia terjadi akibat membran potensial otot jantung yang terdepolarisasi sebagian, sehingga terjadi automatisasi, atau akan muncul gelombang u, dan pemanjangan QT. Gangguan jantung diperburuk oleh pengobatan digoksin dan pasien dengan iskemia. Keadaan hipokalemia dapat memeperburuk hiperglikemia pada pasien diabetes, akibat pengaruh terhadap pelepasan insulin dan sensitivitas organ terhadap insulin. Rabdomiolisis dapat terjadi sebagai akibat dari hiperpolarisasi sel otot rangka, selain adanya gejala kram, mialgia, dan mudah lelah. Hipokalemia dapat mempengaruhi keseimbangan asam basa sistemik, melalui efek terhadap berbagai komponen dari regulasi asam basa di ginjal. 20 3.2.2. Hiperkalemia Ada 2 mekanisme terjadinya hiperkalemia, yaitu1,20 : Kelebihan asupan kalium melalui makanan. Buahbuahan dan sayursayuran banyak mengandung kalium. Campuran garam dapat mengandung kalium, dan kelebihan asupan dapat terjadi pada pemberian makanan enteral. Keluarnya kalium dari intra sel ke ekstrasel. Keadaan asidosis metabolik, selain yang disebabkan oleh KAD atau asidosis laktat, defisisensi insulin, pemakaian beta blocker, dan pseudohiperkalemia akibat pengambilan sampel darah yang lisis. Kelainan klinik bergantung kepada kadar kalsium, dan keseimbangan asam-basa. Berkurangnya ekskresi melalui ginjal. Terjadi pada keadaan hiperaldosteronisme, gagal ginjal, deplesi volume sirkulasi efektif pada CHF dan pemakaian siklosporin. Dewasa ini diketahui pemakaian ACE inhibitor juga faktor resiko untuk hiperkalemia. Pada hiperkalemia, terjadi peningkatan kepekaan membran sel, sehingga dengan sedikit perubahan depolarisasi, potensial aksi dapat dengan mudah terjadi. Hal ini menimbulkan kelemahan otot sampai paralisis dan gagal nafas. Gejala yang paling buruk adalah penurunan kecepatan sistem konduksi miokard dan meningkatkan repolarisasi miokard. Gangguan konduksi akan menimbulkan pemanjangan PR interval, gelombang P yang mendatar atau QRS kompleks melebar pada EKG. Peningkatan repolarisasi akan menimbulkan gelombang T yang meninggi ( peaked T waves ), yang merupakan keadaan yang berisiko terjadinya aritmia.21
2.2. Keseimbangan Kalium Kalium (K) adalah kation utama kompartemen cairan intraseluler ( CIS ). Sekitar 90 % asupan kalium diekskresikan di urin dan 10 % di feses. Konsentrasi normal kalium di plasma adalah 3,5 4,8 mmol/L, sedangkan konsentrasi intraseluler dapat 30 kali lebih tinggi, dan jumlahnya mencapai 98 % dari jumlah K keseluruhan. Walaupun kadar kalium di dalam CES hanya berkisar 2 % saja, akan tetapi memiliki peranan yang sangat penting dalam menjaga homeostasis. Perubahan sedikit saja pada kalium intraseluler, akan berdampak besar pada konsentrasi kalium plasma.2,14 Keseimbangan Kalium diatur dengan menyeimbangkan antara pemasukan dan ekskresi, serta distribusi antara intrasel dan ekstrasel. Regulasi akut kalium ekstraseluler dicapai dengan perpindahan kalium internal antara CES dan CIS.

Ketika kadar kalium ekstrasel meningkat akibat asupan yang banyak, atau disebabkan oleh pembebasan kalium internal, maka regulasi akut ini akan terjadi. Regulasi ini merupakan kontrol hormonal, yaitu1,2,14 : Insulin disekresikan segera setelah makan, dan ini akan menstimulasi Na, K, ATPase dan mendistribusikan Kalium yang didapat dari selsel makhluk hidup yang dimakan ke intrasel. Epinefrin meningkatkan ambilan kalium sel, yang mana penting untuk kerja otot dan trauma. Kedua kondisi ini memicu terjadinya peningkatan kalium plasma. Aldosteron juga berperan dalam meningkatkan konsentrasi kalium intraseluler. Perubahan pH mempengaruhi distribusi kalium ekstra dan intraseluler. Pada asidosis, konsentrasi K ekstraseluler meningkat, sedangkan alkalosis cenderung membuat hipokalemia. Regulasi kronik untuk homeostasis K adalah oleh ginjal. 65 % dari K yang difiltrasi, direabsorpsi sebelum mencapai akhir dari tubulus proksimal ginjal, 20% di tubulus distal, dan 15 % lainnya di ansa henle. Jumlah ekskersi kalium ditentukan pada tubulus penghubung dan duktus koligentes Besarnya jumlah K yang direabsorpsi atau disekresi tergantung kepada kebutuhan. Pada keadaan dimana pemasukan berlebihan, maka ekskresi akan meningkat, begitupula sebaliknya.13,14 Hiperkalsemia terjadi pada lebih dari 70 % kasus keganasan. Hipomagnesemia muncul pada lebih dari 12% pasien, yang terkadang sering diabaikan oleh para klinisi. Perubahan pH mempengaruhi distribusi kalium ekstra dan intraseluler. Pada asidosis, konsentrasi K ekstraseluler meningkat, sedangkan alkalosis cenderung membuat hipokalemia.