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    Hyperkalemia is one of the few potentially lethal electrolyte disturbances

    .Hyperkalemia is common in hospitalized patients, and may be associated withadverse clinical outcomes . Its prevalence and clinical impact in critically ill

    patients are unknown. Hyperkalaemia is rare in clients with normal kidney

    function but affects more than half of people with acute and chronic renal

    failure. Extremely high levels of potassium in the blood (severe hyperkalemia)

    can lead to cardiac arrest and death. When not recognized and treated properly,

    severe hyperkalemia results in mortality rate about 67%. Proper treatment of

    hyperkalemia depends on an understanding of the underlying physiology.

    What is hyperkalaemia

    Hyperkalemia means an abnormally elevated level of potassium in the

    blood. The normal potassium level in the blood is 3.5 -5.0 millie quivalents per

    liter (mEq/L). Potassium levels between 5.1 mEq/L to 6.0 mEq/L reflect mild

    hyperkalemia. Potassium levels of 6.1 mEq/L to 7.0 mEq/L are moderate

    hyperkalemia, and levels above 7 mEq/L are severe hyperkalemia.

    Potassium Regulation In The Body

    Potassium is the most abundant intracellular cation. It is critically

    important for many physiological processes, including maintenance of cellular

    membrane potential , homeostasis of cell volume, and transmission of action

    potentials in nerve cells. Its main dietary sources are vegetables (tomato and

    potato), fruits (orange and banana) and meat. Elimination is through the

    gastrointestinal tract and the kidney. At least 98% of the body's potassium is

    found inside cells, with the remainder in the blood. This concentration gradient

    is maintained principally by the Na+/K+ pump.

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    The serum potassium concentration is determined by the relationship

    between potassium intake, the distribution of potassium between the cells and

    the extracellular fluid, and urinary potassium excretion

    The renal elimination of potas sium is passive (through the glomeruli),

    and reabsorption is active in the proximal tubule and the ascending limb of the

    loop of Henle. There is active excretion of potassium in the distal tubule and the

    collecting duct; both are controlled by aldosterone.

    The ratio of extracellular to intracellular potassium (K) concentration

    largely determines the cell membrane resting electrical potential that, in turn,

    regulates the function of excitable tissues(cardiac and skeletal muscle, and

    nerve). Small absolute changes in the extracellular K concentration will have

    large effects on that ratio, and consequent ly on the function of excitable tissues.

    Thus, it is not surprising that the plasma K concentration (PK) normally is

    maintained within very narrow limits. This tight regulation is accomplished by

    two cooperative systems. One system defends against short -term changes in PK

    by regulating internal balance: the equilibrium of K across the cell membrane.

    This equilibrium is modulated by insulin, catecholamines and, to a lesser extent,

    by acid-base balance, plasma tonicity, and several other factors . The other

    system governs K homeostasis over the long-term by regulating external

    balance: the parity between K intake and elimination. In individuals with

    normal renal function, the kidneys are responsible for elimination of about 95%

    of the daily K load with the remainder exiting through the gut. External K

    balance is maintained largely by modulating renal K elimination.Almost all the

    K excreted by the kidney comes from K secreted in the distal nephron

    (connecting tubule and collecting duct) . Virtually all regulatio n of K excretion

    takes place at this site in the nephron, under the influence of two principle

    factors: the rate of flow and solute (sodium and chloride) delivery through that

    part of the nephron; and the effect of aldosterone . K secretion is directly

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    proportional to flow rate and sodium delivery through the lumen of the distal

    nephron, and to circulating aldosterone levels in the setting of an

    aldosteronesensitive epithelium. This explains, in part, why the use of diuretic

    drugs that work proximal to the K secretory site (loop and thiazide diuretics)

    often is accompanied by hypokalemia. K secretion is inversely proportional to

    the chloride concentration of the luminal fluid and is stimulated, for example,

    by luminal delivery of sodium bicarbonate . Convers ely, hyperkalemia

    commonly accompanies acute kidney injury, particularly in the setting of

    mineralocorticoid deficiency . Such mineralocorticoid deficiency is often

    induced by drugs that interfere with the renin-angiotensinaldosterone axis and

    commonly causes hyperkalemia in patients with chronic kidney disease, as well

    . Sustained hyperkalemia is always attributable to inadequate renal K


    Causes and risk factors ofhyperkalaemia

    Hyperkalemia occurs when the level of potassium in the bloodstream is

    higher than normal. This may be related to an increase in total body potassium

    or the excess release of potassium from the cells into the bloodstream

    1. Ineffectiveelimination

    y Renal insufficiencyy Medication that interferes with urinary excretion: ACE inhibitors and angiotensin receptor blockers Potassium-sparing diuretics (e.g. amiloride and spironolactone) NSAIDs such as ibuprofen, naproxen, orcelecoxib The calcineurin inhibitor immunosuppressants ciclosporin and


    The antibiotic trimethoprim The antiparasitic drugpentamidine

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    y Mineralocorticoid deficiency or resistance, such as: Addison's disease Aldosterone deficiency Some forms ofcongenital adrenal hyperplasia Type IV renal tubular acidosis (resistance of renal tubules to


    y Gordon's syndrome (familial hypertension with hyperkalemia), a raregenetic disorder caused by defective modulators of salt transporters,

    including the thiazide-sensitive Na-Cl cotransporter.

    2. Excessive release from cells

    y Rhabdomyolysis, burns,crush inuries,severe infections or any cause ofrapid tissue necrosis, including tumor lysis syndrome

    y Massiveblood transfusion or massive hemolysisy Shifts/transport out of cells caused by acidosis, low insulin levels, beta-

    blocker therapy, digoxin overdose, or the paralyzing agent


    3. Excessive intake

    y Excess intake with salt-substitute, potassium-containing dietarysupplements , (bananas,oranges,tomatoes,high protein diet,salt

    substitutes),potassium supplements orpotassium chloride (KCl) infusion.

    hyperkalemia by potassium intake would be seen only with large

    infusions of KCl or oral doses of several hundred milliequivalents of KCl.

    y Alcoholism or excessive consumption of aerated drinksy Stored bank blood transfusion(blood 10 days or older has an elevated

    serum potassium due to hemolysis of aging blood

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    4. Pseudohyperkalemia

    Pseudohyperkalemia is a rise in the amount of potassium that occurs due

    to excessive leakage of potassium from cells, during or after blood is drawn. It

    is a laboratory artifact rather than a biological abnormality and can be

    misleading to caregivers. pseudohyperkalemia is typically caused by hemolysis

    during venipuncture (by either excessive vacuum of the blood draw ,a collection

    needle that is of too fine a gauge,too tight application of tourniquets, multiple

    attempts to obtain blood samples from the same site); excessive tourniquet time

    or fist clenching during phlebotomy (which presumably leads to efflux of

    potassium from the muscle cells into the bloodstream);or by a delay in the

    processing of the blood specimen. It can also occur in specimens from patients

    with abnormally high numbers ofplatelets (>500,000/mm ), leukocytes (> 70

    000/mm ), or erythrocytes (hematocrit > 55%). People with "leakier" cell

    membranes have been found, whose blood must be separated immediately to

    avoid pseudohyperkalemia.

    Kidney dysfunction

    The kidneys normally remove excess potassium from the body. Because

    the kidneys are responsible for 80% to 90% of potassium excreation,m ost cases

    of hyperkalemia are caused by disorders that reduce the kidneys' abili ty to get

    rid of potassium.This may result from disorders such as:

    acute and chronic renal failure,

    glomerulonephritis, lupus nephritis, transplant rejection, and obstructive diseases of the urinary tract, such as urolithiasis (stones

    in the urinary tract).

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    With a decline in the GFR, the patient cannot excrete potassium

    normally. Patients with oliguria and anuria are at greater risk for hyperkalemia

    than those without oliguria. Protein catabolism results in the release of cellular

    potassium into the body fluids, causing severe hyperkalemia . People with as

    little as 5% glomular function can maintain normal potassium level if urine

    output is atleast 1L/day. In the presence of preserved GFR,the problem may be

    a failure of tubular potassium secretory mechanism. In CRF ,adaptation to a

    moderately elevated plasma potassium commonly develops, but a further rise

    can occure during intercurrent events which desta bilize the new steady state eg

    dietary load of potassium, hypovolaemia or drugs.

    Patients with kidney dysfunctions are especially sensitive to medications

    that can increase blood potassium levels. For example, patients with kidney

    dysfunctions can develop worsening hyperkalemia when given salt substitut es

    that contain potassium, when given potassium supplements (either orally or

    intravenously), or medications that can increase blood potassium levels.

    Diseases of theadrenalgland / hypoaldosteronism

    Adrenal glands are important in secreting hormones such as cortisol and

    aldosterone. Aldosterone causes the kidneys to retain sodium and fluid while

    excreting potassium in the urine. Therefore diseases of the adrenal gland, such

    as Addison's disease, that lead to decreased aldosterone secretion can decrease

    kidney excretion of potassium, resulting in body retention of potassium, and

    hence hyperkalemia.

    Potassium shifts

    Potassium can move out of and into cells. Our total body potassium stores

    are approximately 50 mEq/kg of body weight. At any given time, about 98% of

    the total potassium in the body is located inside of cells (intracellular), with only

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    2% located outside of cells (in the blood circulation and in the "extracellular"

    tissue). The blood tests for measurement of potassium levels measure only the

    potassium that is outside of the cells. Therefore, conditions that can cause

    potassium to move out of the cells into the blood circulation can increase the

    blood potassium levels even though the total amount of potassium in the body

    has not changed.

    In acidosis compensatory shifting of potassium occurs out of the cell in

    exchange for hydrogen which leads to hyperkalaemia. One example of

    potassium shift causing hyperkalemia is diabetic ketoacidosis. Insulin is vital to

    patients with type 1 diabetes. Without insulin, patients with type 1 diabetes can

    develop severely elevated blood glucose levels. Lack of insulin also causes the

    breakdown of fat cells, with the release of ketones into the blood, turning the

    blood acidic. The acidosis and high glucose levels in the blood work together to

    cause fluid and potassium to move out of the cells into the blood circulation. .

    Patients with diabetes often also have diminished kidney capacity to excret e

    potassium into urine. The combination of potassium shift out of cells and

    diminished urine potassium excretion cause hyperkalemia.

    People with fast growing cancers such as non Hodgkins Lymphoma,acute

    leukemia,small cell carcinomas and some metastatic ca ncer are at risk for tumor

    lysis syndrome(TLS).TLS is the consequence of rapid destruction of tumor

    cells, chemotherapy or irradiation,which results in hyperkalaemia


    Hyperkalemia develops when there is excessive production (oral intake,

    tissue breakdown) or ineffective elimination of potassium. Ineffective

    elimination can be hormonal (in aldosterone deficiency) or due to causes in the

    renal parenchyma that impair excretion.

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    Increased extracellular potassium levels result in depolarization of the

    membrane potentials of cells. This depolarization opens some voltage-gated

    sodium channels, but not enough to generate an action potential. After a short

    while, the open sodium channels inactivate and become refractory, increasing

    the threshold needed to generate an action potential. This leads to the

    impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of

    most concern is the impairment of cardiac conduction which can result in

    ventricular fibrillation or asystole


    Hyperkalaemia can be asymptomatic,sometimes mild hyperkalaemia can

    cause vague symptoms like nausea,vomiting,fatigue,muscleweaknessetc. The

    most important consequences of hyperkalaemia is its effect on the myocardium.

    Cardiac effects of an elevated serum potassium level are usually not significant

    below a concentration of 7 mEq/L,but they are almost always present when the

    level is 8 mEq/L or greater.

    Signs and symptoms associated with mild to moderate hyperkalaemia are the


    y Irritability, anxietyy Nausea,diarrhea,abdominal colic and crampsy Muscle weaknessy tachycardiay Paresthesias(numbness.tingling)

    As the plasma potassium level reaches 7 mEq/L sodium channels become

    progressively inactivated which causes disturbances in muscle and nerve

    functions which results in following signs and symptoms

    y Impaired cardiac conduction and ventricular contractiony Hypotensiony Cardiac arrest

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    y Convulsionsy Severe neuro muscular weakness progressing to flaccid paralysis

    and respiratory muscle paralysis

    Alterations in potassium have a variety of adverse clinical consequences,

    the expression of which may be magnified in the critically ill patient. The most

    serious of these manifestations are those involving excitab le tissues.

    Cardiac effects: More serious symptoms of hyperkalemia include slow

    heartbeat and weak pulse. Severe hyperkalemia can result in fatal cardiac

    standstill (heart stoppage). Hyperkalemia depolarizesthe cell membrane, slows

    ventricular conduction, and decreases the duration of the action potential. These

    changes produce the classic electrocardiographic(EKG) manifestations of

    hyperkalemia including peaked T waves, wideningof the QRS complex, loss of

    the Pwave, sine wave configuration, or ventricular fibrillation and asystole .

    Unless the rise in potassium has been very rapid, symptoms of

    hyperkalemia are usually not apparent until potassium levels are very high

    (typically 7.0 mEq/l or higher).

    Neuromuscular Effects. Hyperkalemia may result in paraesthesias and

    weakness progressing to a flaccid paralysis, which typically spares the

    diaphragm. Deep tendon reflexes are depressed or absent. Cranial nerves are

    rarely involved and sensory changes are minimal . Severe hyperkalemia causes

    skeletal muscle weakness and even paralysis, related to a depolarization block

    in muscle. Similarly, ventricular conduction is slowed. Although hyperkalemia

    has marked effects on the peripheral nervoussystem,it has little effect on the

    central nervous system. Rapidly ascending muscular weakness leading to

    flaccid quadriplegia has been reported in patients with very high serum

    potassium levels. Paralysis of respiratory and speech muscles can also occur.

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    Additionally, GI manifestations,such as nausea, intermittent intesti nal colic, and

    diarrhea, may occur in hyperkalemic patients.

    Diagnostic measures

    y Historyy Physical examinationy Blood test : serum electrolytes, RFT, blood sugar.creatin


    y Renal ultrasoundy Electrocardiogramy ABG analysis

    ECG findings

    With mild to moderate hyperkalemia, there is reduction of the size of the

    P wave and development of peaked T waves. Severe hyperkalemia results in a

    widening of the QRS complex and prolonged PR interval , The faster

    repolarization of the cardiac action potential causes the tenting of the T waves,

    and the inactivation of sodium channels causes a sluggish conduction of the

    electrical wave around the heart, which leads to smaller P waves and widening

    of the QRS complex.

    The serum K+

    concentration at which electrocardiographic changes

    develop is somewhat variable.

    Serum K5.5 - 6.5 mEq/L: peaked T waves; prolonged PRsegment

    Serum K 6.5 - 8.0 mEq/L: loss of P wave, prolonged QRS complex, ST-

    segment elevation, ectopic beats and escape rhythms

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    Serum K > 8.0 mEq/L: progressive widening of QRS complex, sine wave,

    ventricular fibrillation, asystole, axis deviations, bundle branch blocks,

    fascicular blocks.


    EKG changes may not accompany changes in PK. The sensitivity of the

    electrocardiogram to reveal changes of hyperkalemia is quite low . It does

    increase in proportion to the severity of the hyperkalemia , but normal

    electrocardiograms have been seen even with extreme hyperkalemia and the

    first cardiac manifestation of hyperkalemia may be ventricular fibrillation . The

    explanation for a normal electrocardiogram in the setting of extreme

    hyperkalemia is not entirely clear, but may relate to a slow rate of rise in thePK

    Given this insensitivity of the electrocardiogram, EKG changes should not be

    considered necessary for the emergency treatment of severe hyperkalemia.

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    Treatment of Hyperkalemia

    In general, the initial treatment of severe hyperkalemia is independent of

    the cause of the disturbance, whereas the rational therapy of chronic

    hyperkalemia depends on an understanding of its pathogenesis. In considering

    when hyperkalemia constitutes an emergency, several points should be kept in

    mind. First, the electrophysiologic effects of hyperkalemia are directly

    proportional to both the absolute plasma potassium level and its rate of rise .

    Second, concurrent metabolic disturbances may ameliorate (e.g.hypernatremia,

    hypercalcemia, alkalemia) or exacerbate (e.g.,hyponatremia, hypocalcemia,

    acidemia) the electrophysiologic consequences of hyperkalemia Third, although

    the EKG manifestations of hyperkalemia are generally progressive and

    proportional to thePK, ventricular fibrillation may be the first EKG disturbance

    of hyperkalemia; conversely, a normal EKG may be seen even with extreme

    hyperkalemia. With this in mind, it is apparent thatneither the EKG nor the PK

    alone is an adequate index of the urgency of hyperkalemia, and that the clinical

    context must be considered when assessing a hyperkalemic patient. Thus, any

    pronouncement on an absoluteP

    K value constituting an emergency must beseen as arbitrary.

    Because most patients manifest hyperkalemic EKG changes atPK greater

    than 6.7 mmol/L, hyperkalemia should be treated emergently for 1) PK _6.5

    mmol/L or 2) EKG manifestations of hyperkalemia regardless of the PK .

    Therapy of acute or severe hyperkalemia is directed at preventing or

    ameliorating its untoward electrophysiologic effects on the myocardium. The

    goals of therapy , are as follows:

    1. Antagonize the effect of K on excitable cell membranes.

    2. Redistribute extracellular K into cells.

    3. Enhance elimination of K from the body.

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    Redistribution of Potassium into Cells

    Insulin. Insulin reliably lowers PK in patients with end-stage renal disease,

    confirming its effect to shift K into cells. The effect of insulin on potassium is

    dose dependent from the physiolog ic through the pharmacologic range. It is

    mediated by activation of Na, K-ATPase, apparently by recruitment of

    intracellular pump components into the plasma membrane. An intravenous dose

    of ten units of regular insulin given as a bolus along with an intravenous bolus

    of dextrose (25 g as a 50% solution) to anephric adult patients lowers the PK by

    about 0.6 mmol/L . The onset of action is 15 mins and the effect is maximal

    between 30 and 60 mins aftera single bolus . After the initial bolus, a dextrose

    infusion should be started, since a single bolus of 25 g of dextrose has been

    shown to be inadequate to prevent hypoglycemia at 60 mins. It is interesting to

    note that when insulin was given by continuous intravenous infusion for 4 hrs to

    normal volunteers, PK fell over the first 90 mins and rose thereafter. Based on

    that observation,there seems to be no advantage of a continuous infusion over a

    bolus injection.Insulin should be used without dextrose in hyperglycemic

    patients; indeed,the cause of the hyperkalemia in those patients may be the

    hyperglycemia itself. The administration of hypertonic dextrose alone for

    hyperkalemia is not recommended for two reasons: first, endogenous insulin

    levels are unlikely to rise to the level necessary for a therapeutic effect; and

    second, there is a risk of exacerbating the hyperkalemia by inducing


    Beta Adrenoceptor Agonists.An appreciation for the effect of catecholamines

    on internal potassium balance recently has been applied to the clinic. Patients

    with renal failure given the selective beta adrenoceptor agonist, albuterol, by

    intravenous infusion (0.5 mg over 15 mins) show a significant decline in PK

    (about 1mmol/L) that is maximal between 30 and 60 mins . Nebulized albuterol

    in a high dose, administered to patients with ESRD, has a similar effect: PK

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    declines by 0.6 mmol/L after inhalation of 10 mg of albuterol, and by about 1.0

    mmol/L after20mg).The effective dose is at least four times higher than that

    typically used for bronchodilation , although a smaller decline in PK (about 0.4

    mmol/L after 60 mins) is seen even with a metered-dose inhaler . The effect of

    high-dose therapy is apparent at 30 mins and persists for at least 2 hrs . More

    recently, subcutaneous terbutaline (7 g/kg body weight) has been shown to

    reduce PK in selected dialysis patients by an average of 1.3 mmol/L within 60

    mins . Mild tachycardia is the most common reported side effect of high-dose

    nebulized albuterol or terbulatine.

    Bicarbonate.The putative benefits of a bolus injection of sodium bicarbonate in

    the emergency treatment of hyperkalemia pervaded the literature until the past

    decade. The administration of NaHCO3 decreases the concentration of H+


    the extracellular fluid (ECF) compartment. In theory, if the Na+/H


    (NHE) were in an active mode, and if the administration of NaHCO3 were to

    favour the movement of H+

    out of cells via the NHE, more Na+

    would enter the

    cell in an electroneutral manner. The subsequent electrogenic exit of Na+

    via the

    Na-K-ATPase would render the cell interior voltage more negative and allow a

    shift of K+

    into the cell It has now been clearly demonstrated that shortterm

    bicarbonate infusion does not reduce PK in patients with dialysis-dependent

    kidney failure, implying that it does not cause K shift into cells. Only after a 4-

    hr infusion was a small (0.6mmol/L) but significant decrease in PK is


    Elimination of Potassium from the Body

    Enhanced Renal Elimination. Improving urine output by forcing fluids.giving

    IV saline,or giving potassium wasting diuretic usually corrects mild

    hyperkalaemia.Hyperkalemia occurs most often in patients with renal

    insufficiency. However, renal K excretion may be enhanced even in patients

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    with significant renal impairment by increasing the delivery of solute to the

    distal nephron, the site of K secretion.Studies using acetazolamide show that

    bicarbonate delivery to this site in the nephron has a particular kaliuretic effect,

    even in patients with renal insufficiency (59). It would be unwise to administer

    acetazolamide alone to most patients with hyperkalemia, since they tend to

    present with a concomitant metabolic acidosis that would be exacerbated by the

    drug. But a sodium bicarbonate infusion administered during 46 hrs at a rate

    designed to alkalinize the urine may enhance urinary K excretion , and would be

    desirable especially in patients with metabolic acidosis. The risk of volume

    expansion with the bicarbonate infusion can be mitigated by the use of loop-

    acting diuretics, which would be likely to further enhance the kaliuretic effect.

    Loop-acting diuretics alone or in combination with a thiazide diuretic will

    induce a kaliuresis and will be beneficial in the volume expanded patient.

    Diuretic induced volume contraction must be avoided since this will lead to

    decreased distal nephron flow and reduced K excretion.

    Exchange Resin. Sodium polystyrene sulfonate (SPS, Kayexalate, Kionex) is a

    cation-exchange resin that is prepared in the sodium phase but has a higher

    affinityfor potassium than sodium . In the lumen of the intestine, it exchanges

    sodium for secreted potassium. Most of this exchange takes place in the colon,

    the site of most potassium secretion in the gut. Each gram of resin binds

    approximately 0.65 mmol of potassium. Kayexalate contains 4 mEq of Na+


    gram. This Na+

    is theoretically exchangeable for 4 mEq of K+. Thus, 30 g of

    Kayexalate could possibly remove 120 mEq of K+. However, this degree of

    exchange does not occur at the Na+

    and K+

    concentrations found in thegastrointestinal tract.

    The resin causes constipation and, hence, almost always is given with a

    cathartic. It may be given orally or by retention enema, although the oral route

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    is considered to be more effective because of the longer transit time through the

    gut lumen .

    There are two concerns with the use of SPS for the treatment of urgent

    hyperkalemia. The first is its slow effect. When given orally, the onset of action

    is at least 2 hrs and the maximum effect may not be seen for 6 hrs or more . The

    effect of SPS as a retention enema is more rapid but of lesser magnitude. One

    recent study in normokalemic hemodialysis patientsfailed to show any effect on

    PK during 12 hrs after an oral dose of 30 g of SPS with cathartic . The second

    concern with SPS is its possible toxicity. There are numerous case reports of

    patients who have developed intestinal necrosis after exposure to SPS in

    sorbitol as an enema and as an oral agent.A retrospective study estimated the

    prevalence of colonic necrosis to be 1.8% among postoperative patients

    receiving SPS . Thus, the slow onset of action and serious, albeit infrequent,

    toxicity make SPS a poor choice for the treatment of urgent hyperkalemia.

    Dialysis. Hemodialysis is the method of choice for removal of potassium from

    the body. Plasma potassium falls by over 1 mmol/L in the first 60 mins of

    hemodialysis and a total of 2 mmol/L by 180 mins, after which it reaches a

    plateau .Rebound always occurs after dialysis, with 35% of the reduction

    abolished after an hour andnearly 70% after 6 hr; the magnitude of the

    postrebound plasma potassium is proportional to the predialysis potassium

    level. There is controversy as to whether dialysis for severe hyperkalemia

    precipitates serious ventricular arrhythmias. Because of that possibility, patients

    dialyzed for severe hyperkalemia should have continuous EKG monitoring .

    The rate of potassium removal with peritoneal dialysis is much slower than with

    hemodialysis. Indeed, much of the decrement in PK with peritoneal dialysis

    seems to be due to translocation of potassium into cells as a result of the glucose

    load rather than extracorporeal disposal. This modality may be used forpatients

    on maintenance peritoneal dialysis who have modest hyperkalemia .

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    Treatment ofhyperkalemia

    Agent Dose Onset Duration Complication



    10 ml IV

    over 10


    Immediate 30-60




    3% sodium


    50 ml IV Immediate unknown Volume overlod

    Insulin regular

    with dextrose

    10 units IV 20 minutes 4-6 hrs hypoglycaemia

    Albuterol 20 mg in 4 ml

    NS nebulised

    over 10 mts

    30 mts 2hrs tachycardia

    Loop diuretic-


    40-80 mg IV 15 mts 2-3hrs Volume













    1530 g in

    1530 mL

    (70% sorbitol











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    Hyperkalemia Management protocol

    Step 1: Start evaluation ofHyperkalemia Confirm Hyperkalemia

    Step 2: Determine urgency of treatment Non-Emergent treatment:Go to Step 4

    Emergent treatment criteria not met below orSerum Potassium

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    Monitoring: Follow bedside Serum GlucoseNebulized Albuterol 5 mg/ml (typical neb is 2.5 mg/ml)

    Administer 10-20 mg over 10 minutes Onset: 15-30 minutes Duration: 2-3 hours Serum Potassium may increase briefly

    Bicarbonate (no longer used unless Metabolic Acidosis) Historically used as adjunct to Calcium above Consider in severe Metabolic Acidosis Sodium Bicarbonate 7.5% (44.6 meq)

    Give 1 ampule IV over 5 minutesMay repeat every 10-15 min if EKG changes persists

    Onset in 30 minutes Duration: 1-2 hours May also add to Glucose infusion below Avoid bicarbonate until Hypocalcemia corrected

    Risk ofTetany and SeizuresLowering of totalbodypotassium

    Sodium Polystyrene Sulfonate (Kayexalate) Cation-Exchange resin Dose: 50 grams

    Oral: Administer in 30 ml ofSorbitolRectal: Enema activity is faster than oral

    Onset: Up to 4-6 hours for oral route Precautions

    Avoid Sorbitol if bowel necrosis riskUse caution if risk ofCongestive Heart Failure

    1. Consider concurrent Furosemide (Lasix)

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    Furosemide (Lasix) Dose: 20-40 mg IV Coadminister normal saline if dehydrated Onset: 15-60 minutes Duration: 4 hours

    Dialysis (last resort) May experience significant Hyperkalemia on rebound

    2. Chronic Hyperkalemia Management Eliminate Medication Causes of Elevated Serum PotassiumNon-specific therapy

    Loop Diuretics (Lasix) Oral Kayexalate chronically

    Specific therapy Hyporeninemic Hypoaldosteronism

    Loop Diuretics (Lasix)Fludrocortisone 0.1 mg daily

    1. Taper gradually as an outpatient2. Restart ifHyperkalemia recurs

    Renal Failure (GFR< 10 ml/min)Restrict Dietary Potassium to 40-60 meq/day

    Renal Failure and ACE or ARB induced Hyperkalemia Indications: Metabolic AcidosisSodium Bicarbonate

    1. Dose A: 8 meq tabs, 2 tabs twice daily2. Dose B: 0.5 to 1 tsp baking soda daily

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    y Following these nutritional tips may help reduce symptoms:y Eliminate suspected food allergens, such as dairy (milk, cheese, and ice

    cream), wheat (gluten), soy, corn, preservatives, and chemical food

    additives. Your health care provider may want to test you for food


    y Avoid foods that contain high amounts of potassium, including bananas,lentils, nuts, peaches, potatoes, salmon, tomatoes, watermelon.

    y Avoid refined foods, such as white breads, pastas, and sugar.y Eat fewer red meats and more lean meats, cold water fish, or beans for

    protein. Limit the intake of processed meats, such as fast foods and lunch


    y Use healthy cooking oils, such as olive oil or vegetable oil.y Reduce or eliminate trans-fatty acids, found in commercially baked goods

    such as cookies, crackers, cakes, French fries, onion rings, donuts,

    processed foods, and margarine.

    y Avoid alcohol and tobacco. Talk to your doctor before using products thatcontain caffeine products, such as teas and soft drinks. Caffeine impacts

    several conditions and medications.

    y Drink more water. Dehydration can make hyperkalemia worse.y Exercise, if possible, 30 minutes daily, 5 days a week.y Avoid noni (Morinda citrifolia) juice, which is high in potassium.

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    Nursing Management


    Assessment focuses on identifying risk factors for hyperkalaemia through

    history taking and a thorough physical examination.Review laboratory results of

    potassium level.Report even borderline plasma potassium level to the phys ician.

    Patients at risk for potassium excess, for example those with renal failure,

    should be identified so they can be monitored closely for signs of hyperkalemia.

    The nurse observes for signs of muscle weakness and dysrhythmias. The

    presence of paresthesias is noted,as are GI symptoms such as nausea

    andintestinal colic. For patients at risk, serum potassium levels are measured periodically. Potassium supplements are extremely dangerous when patients

    have impaired renal function and thus decreased ability to excrete potassium.

    Even more dangerous is the IV administration of potassium to such patients, as

    serum levels can rise very quickly. Aged (stored) blood should not be

    administered to patients with impaired renal function because the serum

    potassium concentration of stored blood increases as the storage time increases,

    a result of red blood cell deterioration. It is possible to exceed the renal

    tolerance of any patient with rapid IV potassium administration, as well as wh en

    large amounts of oral potassium supplements are ingested.


    y Decreased cardiac output related to dysrhythmiasy Ineffective breathing pattern related to muscle hyperactivity

    progresses to respiratory muscle flaccidity and paralysis

    y Pain related to muscle crampy Diarrhea related to increased smooth muscle irritability

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    Nursing interventions


    Measures are taken to prevent hyperkalemia in patients at risk, when

    possible, by encouraging the patient to adhere to the prescribed potassium

    restriction. Potassium-rich foods to be avoided include coffee, cocoa, tea, dried

    fruits, dried beans, and wholegrain breads. Milk and eggs also contain

    substantial amounts of potassium. Conversely, foods with minimal potassium

    content include butter, margarine, cranberry juice or sauce, ginger ale,

    gumdrops or jellybeans, hard candy, root beer, sugar, and honey.


    High potassium level have the potential to induce life threatening

    arrhythmia.So treat according to protocols.,and report ECG changes that

    indicates worsening hyperkalaemia or over correction resulting in

    hypokalaemia.Set cardiac monitor alarms with narrow limits to ensure e arly

    detection of lethal dysrhythmias

    It is possible to exceed the tolerance for potassium in any person if it is

    administered rapidly by the IV route. Therefore, great care should be taken to

    monitor potassium solutions closely, paying close attention to the solutions

    concentration and rate of administration. When potassium is added to parenteral

    solutions, the potassium is mixed with the fluid by inverting the bottle several

    times. Potassium chloride should never be added to a hanging bottle because the

    potassium might be administered as a bolus (potassium chloride is heavy and

    settles to the bottom of the container). It is important to caution patients to use

    salt substitutes sparingly if they are taking other supplementary forms of

    potassium or potassium-conserving diuretics. Also, potassium-conserving

    diuretics, such as spironolactone (Aldactone), triamterene (Dyrenium), and

    amiloride (Midamor); potassium supplements; and salt substitutes should not

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    be administered to patients with renal dysfunction. Most salt substitutes contain

    approximately 5060 mEq of potassium per spoon

    Elevated serum potassium levels may be erroneous; thus, highly

    abnormal levels should always be verified. To avoid false reports of

    hyperkalemia, prolonged use of a tourniquet while drawing the blood sample is

    avoided, and the patient is cautioned not to exercise the extremity immediately

    before the blood sample is obtained. The blood sample is delivered to the

    laboratory as soon as possible, because hemolysis of the sample res ults in a

    falsely elevated serum potassium level.


    Hyperkalemia is one of the few potentially lethal electrolyte disorders. Its

    rational treatment has evolved as a result of our more complete understanding of

    the physiology of potassium homeostasis. Fortunately, most patients have mild

    hyperkalemia (which is usually well tolerated). However, any condition causing

    even mild hyperkalemia should be treated to prevent progression into more

    severe hyperkalemia. Evaluate the clients response to therapy every hour if

    severe hyperkalaemia is present or every 8 hrs if mild hyperkalaemia exist.

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    y Dona D Ignatavicius, Linda workman: Medical surgical nursing,Anursing process approach 2

    ndedition, Saunders publications,page


    y Brunner and Suddarths; Text book of medical surgical nursing, 11 thedition

    y Hawks and Black: medical surgical nursing, clinical management forpositive outcome,7

    thedition, Mosby publications,2004

    y Lewis etal medical surgical nursing 7 th edition(2005) mosbypublication

    y Harrisons principles of internal medicine 17 th edition (2008)Mc GrowHill publication pp-237-239

    y Davidsons principles and practice of Medicine 20 th edition.ChurchillLivingstone,Elsevier

    y www.wikipedia.comy www.nursing planet.comy www.medscape.com

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    Seminar on


    Submitted to : Submitted by:

    Mrs. SUMANGALA T.J Priyanka Jose

    Associate professor 1st

    year msc nursing

    Govt: college of nursing Govt: college of nursing

    Calicut Calicut

    Date of seminar: -4-2011

    Remarks :

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    Masterplan on hyperkalaemia


    Define hyperkalaemia Explain the types, causes and risk factors of hyperkalaemia Explain the pathophysiology of meningitis explain the signs and symptoms of hyperkalaemia List the diagnostic measures Explain the management

    y Introductiony Definitiony Typesy Etiology and risk factorsy Pathophysiologyy Signs and symptomsy Collaborative managementy Nursing managementy Conclusiony Bibliography