The Lethal Electrolyte

Hyperkalemia

كراتينين 62مرد • و مزمن ي كليه نارسايي با اي ساله2.1 mg /dL باال رخون فشا دليل به نرمال پتاسيم و

. متوجه بعد هفته دو گيرد مي قرار نمك كم رژيم روي . مختصر فيزيكي ي معاينه در شود مي عضالني ضعف

پروگزيمال عضالت ضعف و پوست تورگور كاهششود . مي موج ECGيافته شدن Tبيمار پهن و بلند

كمپلكس Pموج . QRSو هاي آزمايش دهد مي رانشان: باشد مي زير بصورت وي

• Plasma Na = 130 meq /L• K= 9.8 meq /L• Cl= 98 meq /L• HCO3= 19meq /L• Cr= 2.7 mg/dL• Arterial pH= 7.32

هايپركالمي ي كننده ايجاد فاكتور محتملترينچيست؟ فرد ين درا

كليه. 1 اي زمينه نارساييحجم. 2 كمبودمتابوليك. 3 اسيدوزباال. 4 موارد ي همه

Causes and evaluation of hyperkalemia in adults

• Hyperkalemia is a common clinical problem.

• Potassium enters the body via oral intake or intravenous infusion, is largely stored in the cells, and is then excreted in the urine.

• The major causes of hyperkalemia are increased potassium release from the cells and, most often, reduced urinary potassium excretion

• Total body potassium stores are approximately 3000 meq or more (50 to 75 meq/kg body weight).

• In contrast to sodium, which is the major cation in the extracellular fluid and has a much lower concentration in the cells, potassium is primarily an intracellular cation, with the cells containing approximately 98 percent of body potassium.

• The intracellular potassium concentration is approximately 140 meq/L compared with 4 to 5 meq/L in the extracellular fluid.

• The difference in distribution of the two cations is maintained by the Na-K-ATPase pump in the cell membrane, which pumps sodium out of and potassium into the cell in a 3:2 ratio.

• The ratio of the potassium concentrations in the cells and the extracellular fluid is the major determinant of the resting membrane potential across the cell membrane, which sets the stage for the generation of the action potential that is essential for normal neural and muscle function.

• Thus, both hyperkalemia and hypokalemia can cause muscle paralysis and potentially fatal cardiac arrhythmias.

• The plasma potassium concentration is determined by the relationship among potassium intake, the distribution of potassium between the cells and the extracellular fluid, and urinary potassium excretion.

• In normal individuals, dietary potassium is absorbed in the intestines and then largely excreted in the urine, a process that is primarily determined by potassium secretion by the principal cells in the two segments that follow the distal tubule: the connecting segment and cortical collecting tubule

There are three major factors that stimulate principal cell potassium secretion:

●An increase in plasma potassium concentration and/or potassium intake

●An increase in aldosterone secretion●Enhanced delivery of sodium and water to the distal potassium

secretory site

• Ingestion of a potassium load leads initially to the uptake of most of the excess potassium by cells in muscle and the liver, a process that is facilitated by insulin and the beta-2-adrenergic receptors, both of which increase the activity of Na-K-ATPase pumps in the cell membrane

• Some of the ingested potassium remains in the extracellular fluid, producing a mild elevation in the plasma potassium concentration.

• The increase in plasma potassium stimulates the secretion of aldosterone, which enhances both sodium reabsorption and potassium secretion in the principal cells

• The net effect is that most of the potassium load is excreted within six to eight hours.

• Both cellular uptake and urinary excretion of an acute potassium load are impaired in patients with advanced acute or chronic kidney disease

• Potassium adaptation — Hyperkalemia is a rare occurrence in normal individuals because the cellular and urinary responses prevent significant potassium accumulation in the extracellular fluid.

• Furthermore, the efficiency of potassium excretion is enhanced if potassium intake is increased, thereby allowing what might otherwise be a fatal potassium load to be tolerated. This phenomenon, called potassium adaptation, is mostly due to the ability to more rapidly excrete potassium in the urine

●Increasing potassium intake alone is not a common cause of hyperkalemia unless it occurs acutely.

Acute hyperkalemia can rarely be induced (primarily in infants because of their small size) by the administration of potassium penicillin as an intravenous bolus, the accidental ingestion of a potassium-containing salt substitute, or the use of stored blood for exchange transfusions.

In addition, moderate increases in potassium intake can be an important contributor to the development of hyperkalemia in patients with impaired potassium excretion due, for example, to hypoaldosteronism and/or renal insufficiency

●Persistent hyperkalemia requires impaired urinary potassium excretion.

this is generally associated with a reduction in aldosterone secretion or responsiveness, acute or chronic kidney disease, and/or diminished delivery of sodium and water to the distal potassium secretory site.

Metabolic acidosis — In patients with metabolic acidosis other than organic acidosis due to lactic acidosis or ketoacidosis, buffering of excess hydrogen ions in the cells leads to potassium movement into the extracellular fluid, a transcellular shift that is obligated in part by the need to maintain electroneutrality

• Smaller effect in lactic acidosis or ketoacidosis — In contrast to the above finding, hyperkalemia due to an acidosis-induced shift of potassium from the cells into the extracellular fluid does not occur in the organic acidoses lactic acidosis and ketoacidosis

• A possible contributory factor in both disorders is the ability of the organic anion and the hydrogen ion to enter into the cell via a sodium-organic anion cotransporter.

• Smaller effect in respiratory acidosis :• Hyperkalemia due to respiratory acidosis is not a

common clinical problem.

• The effect of respiratory acidosis on the plasma potassium is greater with more severe acidosis and with a longer duration of acidosis

• The mechanisms responsible for the lesser increase in plasma potassium in respiratory acidosis compared with metabolic acidosis are not well defined

Insulin deficiency, hyperglycemia, hyperosmolality

Insulin promotes potassium entry into cells. Thus, the ingestion of glucose (which stimulates endogenous insulin secretion) minimizes the rise in the serum potassium concentration induced by concurrent potassium intake, while glucose ingestion alone in patients without diabetes modestly lowers the serum potassium

• The findings are different in uncontrolled diabetes mellitus. In this setting, the combination of insulin deficiency and hyperosmolality induced by hyperglycemia frequently leads to hyperkalemia

• In addition to hyperglycemia induced by insulin deficiency, hyperkalemia induced by hyperosmolality has also been described with hypernatremia /sucrose contained in intravenous immune globulin /radiocontrast media /and the administration of hypertonic mannitol

●Fasting is associated with an appropriate reduction in insulin levels that can lead to an increase in plasma potassium. This may be a particular problem in dialysis patients.

The risk of hyperkalemia during preoperative fasting can be minimized by the administration of insulin and glucose in patients with diabetes, or glucose alone in patients without diabetes

Increased tissue catabolism — Any cause of increased tissue breakdown leads to the release of intracellular potassium into the extracellular fluid. Hyperkalemia can occur in this setting, particularly if renal failure is also present.

• Clinical examples include trauma (including non-crush trauma), the administration of cytotoxic or radiation therapy to patients with lymphoma or leukemia (the tumor lysis syndrome), and severe accidental hypothermia

Beta blockers

• Beta blockers interfere with the beta-2-adrenergic facilitation of potassium uptake by the cells, particularly after a potassium load

• An increase in serum potassium is primarily seen with nonselective beta blockers (such as propranolol and labetalol). In contrast, beta-1-selective blockers such as atenolol have little effect on serum potassium since beta-2 receptor activity remains intact

• The rise in serum potassium with nonselective beta blocker therapy is usually less than 0.5 meq/L. True hyperkalemia is rare unless there is a large potassium load, marked exercise (or an additional defect in potassium handling that prevents excretion of the excess extracellular potassium, such as hypoaldosteronism or renal failure

Hyperkalemic periodic paralysis — Hyperkalemic periodic paralysis is an autosomal dominant disorder in which episodes of weakness or paralysis are usually precipitated by cold exposure, rest after exercise, fasting, or the ingestion of small amounts of potassium.

• The most common abnormality in hyperkalemic periodic paralysis is a point mutation in the gene for the alpha subunit of the skeletal muscle cell sodium channel

Other — Other rare causes of hyperkalemia due to translocation of potassium from the cells into the extracellular fluid include:

● Digitalis overdose; due to dose-dependent inhibition of the Na-K-ATPase pump .

● Red cell transfusion due to leakage of potassium out of the red cells during storage. Hyperkalemia primarily occurs in infants and with massive transfusions

● Use of drugs that activate ATP-dependent potassium channels in cell membranes, such as calcineurin inhibitors (eg, cyclosporine and tacrolimus), diazoxide, minoxidil, …

REDUCED URINARY POTASSIUM EXCRETION — Urinary potassium excretion is primarily mediated by potassium secretion in the principal cells in the two segments that follow the distal tubule: the CS and CCT

• Three major factors are required for adequate potassium secretion at these sites: adequate aldosterone secretion, adequate responsiveness to aldosterone, and adequate distal sodium and water delivery

• The widely used term, hypoaldosteronism, applies to both reduced aldosterone secretion and reduced response to aldosterone.

The four major causes of hyperkalemia due to reduced urinary potassium secretion are:

●Reduced aldosterone secretion●Reduced response to aldosterone (aldosterone

resistance)●Reduced distal sodium and water delivery as occurs in

effective arterial blood volume depletion●Acute and chronic kidney disease in which one or more of

the above factors are present

• EVALUATION — Evaluation of the patient with hyperkalemia usually begins with a careful history, evaluation for clinical manifestations of hyperkalemia such as muscle weakness and characteristic changes on the electrocardiogram, and laboratory testing for the causes of hyperkalemia

Exclude pseudohyperkalemia• Pseudohyperkalemia, refers to those conditions in which the

elevation in the measured serum potassium concentration is due to potassium movement out of the cells during or after the blood specimen has been drawn.

• It is usually related to the technique of blood drawing, but it can also occur in patients with marked elevations in platelet or white blood cell counts

• Pseudohyperkalemia should be suspected when there is no apparent cause for the hyperkalemia in an asymptomatic patient who has no clinical or electrocardiographic manifestations of hyperkalemia.

• One clue to the possible presence of pseudohyperkalemia is wide variability in repeated measurements of the serum potassium concentration (eg, from 5 to 6.5 meq/L, often including some normal values).

• Increasing potassium intake is not a major cause of hyperkalemia in individuals without another risk factor such as reduced aldosterone secretion or responsiveness or acute or chronic kidney disease.

• In healthy adults, raising potassium intake from a normal value of 100 meq/day to a much higher value of 400 meq/day only produces a modest elevation in serum potassium from 3.8 meq/L at baseline to 4.8 meq/L

• Urinary potassium excretion increases

• Clinical manifestations of hyperkalemia in adults

• CLINICAL MANIFESTATIONS — The most serious manifestations of hyperkalemia are muscle weakness or paralysis, cardiac conduction abnormalities, and cardiac arrhythmias.

• These manifestations usually occur when the serum potassium concentration is ≥7.0 meq/L with chronic hyperkalemia or possibly at lower levels with an acute rise in serum potassium

• Severe muscle weakness or paralysis — Hyperkalemia can cause ascending muscle weakness that begins with the legs and progresses to the trunk and arms

• This can progress to flaccid paralysis, mimicking Guillain-Barré syndrome .

• Sphincter tone and cranial nerve function are typically intact, and respiratory muscle weakness is rare

• These manifestations resolve with correction of the hyperkalemia.

• Cardiac manifestations — Hyperkalemia may be associated with electrocardiographic changes that, if present, may suggest the diagnosis before blood test results

• ECG changes — Tall peaked T waves with a shortened QT interval are usually the first findings

• As the hyperkalemia gets more severe, there is progressive lengthening of the PR interval and QRS duration, the P wave may disappear, and ultimately the QRS widens further to a sine wave pattern.

• Ventricular standstill with a flat line on the ECG ensues with complete absence of electrical activity.

ECG Changes

Hyperkalemia:

T wave in hyperkalemia is typically tall and narrow, but does not have to be tall(may be just narrow and peaked pulling ST segment).

Tall T means > 2 big boxes in the precordial leads or >1 small box in limb leads, or T wave taller than QRS.

• The progression and severity of ECG changes do not correlate well with the serum potassium concentration as illustrated by the following observations:

• Rare patients have a normal ECG despite a serum potassium above 9.0 meq/L

• ECG manifestations are more likely with rapid onset hyperkalemia, and the presence of concomitant hypocalcemia, acidemia, and/or hyponatremia

• Given the unreliable sensitivity, serial measurements of the serum potassium concentration should guide therapy in stable patients with hyperkalemia.

• The ECG cannot be reliably used to monitor the efficacy of hyperkalemia therapy

• In addition, peaked T waves alone are not specific for hyperkalemia, being seen in the early phase of acute myocardial infarction and with early repolarization, and some patients with left ventricular hypertrophy

• Conduction abnormalities and arrhythmias — Hyperkalemia can lead to a variety of conduction abnormalities and arrhythmias:

• Conduction abnormalities that may be seen include right bundle branch block, left bundle branch block, bifascicular block, and advanced atrioventricular block

• Cardiac arrhythmias associated with hyperkalemia include sinus bradycardia, sinus arrest, slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and asystole

• PATIENT ASSESSMENT — Careful monitoring of the ECG and muscle strength are indicated to assess the functional consequences of hyperkalemia.

• Severe muscle weakness and/or marked electrocardiographic changes, including conduction abnormalities and arrhythmias, are potentially life-threatening and require immediate treatment.

• These manifestations usually occur when the serum potassium concentration is ≥7.0 meq/L with chronic hyperkalemia or possibly at lower levels with an acute rise in serum potassium.

• Treatment and prevention of hyperkalemia in adults

. 60خانم نكته معاينه در كند مي مراجعه باال رخون فشا دليل به ديابتي ي سالهندارد مثبتي شده BP= 160/90ي انجام آزمايشات در و دارد

BUN:20 Cr:1.1 Na:137 K: 6.1

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هايپرتنسيو 1. آنتي ديگر داروي از استفاده و لوزارتان قطع

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كراتينين 62مرد • و مزمن ي كليه نارسايي با اي ساله2.1 mg /dL باال رخون فشا دليل به نرمال پتاسيم و

. متوجه بعد هفته دو گيرد مي قرار نمك كم رژيم روي . مختصر فيزيكي ي معاينه در شود مي عضالني ضعف

پروگزيمال عضالت ضعف و پوست تورگور كاهششود . مي موج ECGيافته شدن Tبيمار پهن و بلند

كمپلكس Pموج . QRSو هاي آزمايش دهد مي رانشان: باشد مي زير بصورت وي

• Plasma Na = 130 meq /L• K= 9.8 meq /L• Cl= 98 meq /L• HCO3= 19meq /L• Cr= 2.7 mg/dL• Arterial pH= 7.32

بيمارفوق براي شما درماني اقدام اوليناست؟ كدام

كلسيم. 1 گلوكونات انفوزيونانسولين. 2 و گلوكز انفوزيونسديم. 3 بيكربنات انفوزيوندياليز. 4 شروع

هايپر درمان در زير موارد از كداميكدارد؟ را تاثير كمترين بيمار اين كالمي

كلسيم. 1 گلوكونات انفوزيونانسولين. 2 و گلوكز انفوزيونسديم. 3 بيكربنات انفوزيوناگزاالت. 4 كي پودر از استفاده

Principles of Treatment

• Stabilise myocardium

• Move it into cells

• Increase elimination

• URGENCY OF THERAPY — The urgency of treatment of hyperkalemia varies with the cause and the presence or absence of the symptoms and signs associated with hyperkalemia.

• In addition, patients with marked tissue breakdown (eg, rhabdomyolysis, crush injury, tumor lysis syndrome) release large amounts of potassium from the cells, which can lead to rapid and substantial elevations in serum potassium. Thus, these patients should receive aggressive therapy to remove potassium even if there is only a mild degree of hyperkalemia

• The most serious manifestations of hyperkalemia are muscle weakness or paralysis, cardiac conduction abnormalities, and cardiac arrhythmia

• These manifestations usually occur when the serum potassium concentration is ≥7.0 meq/L with chronic hyperkalemia or possibly at lower levels with an acute rise in serum potassium.

• RAPIDLY ACTING TRANSIENT THERAPIES :

• Rapidly acting therapies include the administration of calcium, insulin with glucose, beta-2-adrenergic agonists, and, in selected patients, sodium bicarbonate.

Indications for use :

• Patients with hyperkalemia and electrocardiographic changes

• Patients with a serum potassium greater than 6.5 to 7 meq/L; some would not initiate such therapy until the serum potassium is ≥7.0 meq/L in patients who have no clinical or electrocardiographic signs of hyperkalemia.

• A lesser degree of hyperkalemia in patients with a serum potassium that is rapidly increasing

• Monitoring — Continuous cardiac monitoring and serial electrocardiograms are warranted in patients with hyperkalemia who require rapidly acting therapies.

• The serum potassium should be measured at one to two hours after the initiation of therapy.

• The timing of further measurements is determined by the serum potassium concentration and the response to therapy.

• Calcium — Calcium directly antagonizes the membrane actions of hyperkalemia, while hypocalcemia increases the cardiotoxicity of hyperkalemia.

• The effect of intravenous calcium administration begins within minutes but is relatively short-lived (30 to 60 minutes). As a result, calcium should not be administered as monotherapy for hyperkalemia but should rather be combined with therapies that drive extracellular potassium into cells.

• Calcium can be given as either calcium gluconate or calcium chloride.

• The usual dose of calcium gluconate is 1000 mg (10 mL of a 10 percent solution) infused over two to three minutes, with constant cardiac monitoring.

• The dose can be repeated after five minutes if the ECG changes persist or recur.

• Calcium gluconate can be given peripherally, ideally through a small needle or catheter in a large vein.

• Calcium should not be given in bicarbonate-containing solutions, which can lead to the precipitation of calcium

carbonate.

• When hyperkalemia occurs in patients treated with digitalis, calcium should be administered for the same indications as in patients not treated with digitalis (eg, widening of the QRS complex or loss of P waves) even though hypercalcemia potentiates the cardiotoxic effects of digitalis.

• In such patients, a dilute solution can be administered slowly, infusing 10 mL of 10 percent calcium gluconate in 100 mL of 5 percent dextrose in water over 20 to 30 minutes, to avoid acute hypercalcemia.

• In patients with hyperkalemia due to digitalis toxicity, the administration of digoxin-specific antibody fragments is the preferred therapy.

• Insulin with glucose — Insulin administration lowers the serum potassium concentration by driving potassium into the cells, primarily by enhancing the activity of the Na-K-ATPase pump in skeletal muscle

• Glucose is usually given with insulin to prevent the development of hypoglycemia.

• However, insulin should be given alone if the serum glucose is ≥250 mg/dL (13.9 mmol/L).

• The serum glucose should be measured one hour after the administration of insulin.

• One commonly used regimen for administering insulin and glucose is 10 units of regular insulin in 500 mL of 10 percent dextrose, given over 60 minutes.

• Another regimen consists of a bolus injection of 10 units of regular insulin, followed immediately by 50 mL of 50 percent dextrose (25 g of glucose). This regimen may provide a greater reduction in serum potassium since the potassium-lowering effect is greater at the higher insulin concentrations attained with bolus therapy.

• However, hypoglycemia occurs in up to 75 percent of patients treated with the bolus regimen, typically about one hour after the infusion

• To avoid this complication, we recommend subsequent infusion of 10 percent dextrose at 50 to 75 mL/hour and close monitoring of blood glucose levels

• The administration of glucose without insulin is not recommended since the release of endogenous insulin can be variable and the attained insulin levels are generally lower with a glucose infusion alone.

• Furthermore, in susceptible patients (primarily diabetic patients with hyporeninemic hypoaldosteronism), hypertonic glucose in the absence of insulin may acutely increase the serum potassium concentration by raising the plasma osmolality, which promotes water and potassium movement out of the cells

• The effect of insulin begins in 10 to 20 minutes, peaks at 30 to 60 minutes, and lasts for four to six hours

• In almost all patients, the serum potassium concentration drops by 0.5 to 1.2 meq/L .

• In particular, although patients with renal failure are resistant to the glucose-lowering effect of insulin, they are not resistant to the hypokalemic effect because Na-K-ATPase activity is still enhanced

• Beta-2 adrenergic agonists — Given the potential adverse effects, intravenous epinephrine should not be used in the treatment of hyperkalemia.

• Albuterol is not frequently used but can be considered as transient therapy in patients who have symptoms or serious ECG manifestations of hyperkalemia despite therapy with calcium and insulin with glucose.

• Like insulin, the beta-2 adrenergic agonists drive potassium into the cells by increasing the activity of the Na-K-ATPase pump in skeletal muscle .

• Beta-2-adrenergic agonists can be effective in the acute treatment of hyperkalemia, lowering the serum potassium concentration by 0.5 to 1.5 meq/L

• Albuterol, which is relatively selective for the beta-2 adrenergic receptors, can be given as 10 to 20 mg in 4 mL of saline by nebulization over 10 minutes (which is 4 to 8 times the dose used for bronchodilation).

• Alternatively and where available, albuterol 0.5 mg can be administered by intravenous infusion

• Albuterol and insulin with glucose have an additive effect, • reducing serum potassium concentration by approximately 1.2 to

1.5 meq/L

• Thus, although albuterol should not be used as monotherapy in hyperkalemic patients with ESRD.; it can be added to insulin plus glucose to maximize the reduction in serum potassium

• One problem in patients on maintenance hemodialysis is that lowering the serum potassium concentration by driving potassium into the cells can diminish subsequent potassium removal during the dialysis session (from 50 to 29 meq in one report), possibly leading to rebound hyperkalemia after dialysis

• Potential side effects of the beta-2 agonists include mild tachycardia and the possible induction of angina in susceptible subjects. Thus, these agents should probably be avoided in patients with active coronary disease.

• In addition, all patients with ESRD should be monitored carefully since they may have subclinical or overt coronary disease

• Sodium bicarbonate — Raising the systemic pH with sodium bicarbonate results in hydrogen ion release from the cells as part of the buffering reaction. This change is accompanied by potassium movement into the cells to maintain electroneutrality.

• The use of bicarbonate for the treatment of hyperkalemia was mainly based upon small uncontrolled clinical studies

• However, in a study that compared different potassium-lowering modalities in 10 patients undergoing HD, a bicarbonate infusion for up to 60 minutes had no effect on the serum potassium concentration .This lack of benefit was confirmed in several subsequent studies of hemodialysis patients

• Given the limited efficacy, we do not recommend the administration of sodium bicarbonate as the only therapy for the acute management of hyperkalemia, even in patients with mild to moderate metabolic acidosis

• However, prolonged bicarbonate therapy appears to be beneficial in patients with metabolic acidosis.

• TREATMENT OF REVERSIBLE CAUSES — A variety of factors can contribute to or cause hyperkalemia. These include reversible causes of impaired renal function, such as hypovolemia, nonsteroidal anti-inflammatory drugs, urinary tract obstruction, and inhibitors of the (RAAS), each of which can also directly cause hyperkalemia

• These abnormalities often cannot be corrected quickly, and their correction may not be sufficient to induce a large fall in serum potassium. Thus, when there is more than mild hyperkalemia, modalities directed at potassium removal should not be delayed

• POTASSIUM REMOVAL — The effective modalities described above only transiently lower the serum potassium concentration. Thus, additional therapy is typically required to remove excess potassium from the body.

• The three available modalities for potassium removal are diuretics, cation exchange resin, and dialysis.

• Loop or thiazide diuretics — Loop and thiazide diuretics increase potassium loss in the urine in patients with normal or mild to moderately impaired renal function, particularly when combined with saline hydration to maintain distal sodium delivery and flow.

• However, patients with persistent hyperkalemia typically have impaired renal potassium secretion, and there are no data demonstrating a clinically important short-term kaliuretic response to diuretic therapy.

• Cation exchange resins — The major available cation exchange resin is sodium polystyrene sulfonate.

• Cation exchange resins, which are effective in lowering the serum potassium after multiple doses, are usually not effective immediately and do not appear to be more effective in removing potassium from the body than laxative therapy.

• Although uncommon, cation exchange resins can produce severe side effects, particularly intestinal necrosis, which may be fatal.

• When to use cation exchange resins — Clinicians are often faced with a choice between using sodium sulfonate therapy and dialysis in patients with kidney disease and hyperkalemia.

• cation exchange resins are usually not effective after a single dose and may produce fatal side effects (particularly in postoperative patients or those with ileus or bowel obstruction and in patients who have received a kidney transplant).

• Given these concerns, dialysis is the preferred treatment in patients with severe kidney disease and potentially life-threatening hyperkalemia, particularly in patients who have a vascular access.

• In patients with less severe hyperkalemia, diuretic therapy, a low-potassium diet, and removal of potentially reversible causes (such as discontinuation of an angiotensin inhibitor) may be sufficient

• Thus, we suggest that sodium polystyrene sulfonate be used (in conjunction with the rapidly acting transient therapies mentioned above) only in a patient who meets all of the following criteria:

• Potentially life-threatening hyperkalemia • Dialysis is not readily available.• Other therapies to remove potassium (eg, diuretics, rapid

restoration of kidney function) have failed or are not possible.

• Sodium polystyrene sulfonate with or without sorbitol should not be given to the following patients because they may be at high risk for intestinal necrosis:

• Postoperative patients • Patients with an ileus or who are receiving opiates• Patients with a large or small bowel obstruction

• Even if restoration of renal function or dialysis are not possible or immediately available, sodium polystyrene sulfonate should not be given in these high-risk settings;

• such patients can be managed with repeated doses of insulin and glucose (or continuous infusions) until dialysis can be performed.

• Despite modest efficacy and the risk of catastrophic consequences, sodium polystyrene sulfonate remains the most widely used treatment for hyperkalemia

• Sodium polystyrene sulfonate is also frequently used as chronic therapy to control hyperkalemia in patients with CKD who do not have other indications for dialysis and whose hyperkalemia is not controlled adequately with a low-potassium diet, diuretic therapy, and removal of potentially reversible causes.

• Mechanism of action — In the gut, sodium polystyrene sulfonate takes up potassium (and calcium and magnesium to lesser degrees) and releases sodium.

• Each gram of resin may bind as much as 1 meq of potassium and release 1 to 2 meq of sodium.

• Thus, a potential side effect is exacerbation of edema due to sodium retention.

• Administration and dose — Sodium polystyrene sulfonate without or with sorbitol can be given orally and sodium polystyrene sulfonate without sorbitol can be given as a. retention enema .

• Oral dosing is probably more effective if intestinal motility is not impaired.

• The oral dose is usually 15 to 30 g, which can be repeated every four to six hours as necessary.

• Single doses are probably ineffective

• Sorbitol — the occurrence of intestinal necrosis in some patients treated with cation exchange resins led the FDA to issue a recommendation in September 2009 that sodium polystyrene sulfonate should no longer be administered in sorbitol

• Cation exchange resins do not appear to have superior efficacy as compared with laxatives alone.

• A major concern with sodium polystyrene sulfonate in sorbitol is the development of intestinal necrosis, usually involving the colon and ileum which is frequently a fatal complication

• In such cases, sodium polystyrene sulfonate crystals can often be detected in pathological specimens, adherent to the injured mucosa

• Sodium polystyrene sulfonate in sorbitol can also injure the esophagus and stomach when given orally, possibly resulting in manifestations such as bleeding and esophageal necrosis

• Other complications of sodium polystyrene sulfonate include hypocalcemia, volume overload and hypokalemia

• Intestinal necrosis in the absence of sorbitol — The association of sodium polystyrene sulfonate in sorbitol with intestinal necrosis may be coincidental since sorbitol is so widely used in conjunction with sodium polystyrene sulfonate.

• Multiple cases of intestinal necrosis with sodium polystyrene sulfonate and similar cation exchange resins without sorbitol have been reported

Thus, intestinal necrosis may be a complication of sodium polystyrene sulfonate independent of sorbitol.

• Dialysis — Dialysis is indicated if the measures listed above are insufficiently effective or the hyperkalemia is severe or is expected to increase rapidly as could occur with marked tissue breakdown, leading to the release of large amounts of potassium from injured cells

• Hemodialysis is preferred, since the rate of potassium removal is many times faster than with peritoneal dialysis

• Hemodialysis can remove 25 to 50 meq of potassium per hour, with variability based upon the initial serum potassium concentration, the type and surface area of the dialyzer used, the blood flow rate, the dialysate flow rate, the duration of dialysis, and the potassium concentration of the dialysate

• Postdialysis potassium rebound — A rebound increase in serum potassium concentration occurs after hemodialysis in all patients in whom potassium is removed, since the reduction in serum potassium during dialysis creates a gradient for potassium movement out of the cells.

• the serum potassium concentration should usually not be measured soon after the completion of hemodialysis, since the results are likely to be misleading.

• PREVENTION — There are several measures that can help to prevent hyperkalemia in patients with (CKD), particularly (ESRD):

• In addition to a low-potassium diet, the following modalities have been effective in stable maintenance hemodialysis patien

• Avoid episodes of fasting, which can increase potassium movement out of the cells due, at least in part, to reduced insulin secretion

• Avoid, if possible, drugs that raise the serum potassium concentration. These include inhibitors of the (RAAS), such as ACEI / ARB, aldosterone antagonists, and nonselective beta blockers

• Beta-1-selective blockers such as metoprolol and atenolol are much less likely to cause hyperkalemia

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