2005 - emcna - disorders of potassium

Emerg Med Clin N Am 23 (2005) 723–747

Disorders of Potassium

Timothy J. Schaefer, MDa,b,*,Robert W. Wolford, MD, MMMc,d

aSection of Emergency Medicine, Department of Surgery, University of Illinois College

of Medicine at Peoria, Peoria, IL 61605, USAbDepartment of Emergency Medicine, OSF Saint Francis Medical Center,

530 Northeast Glen Oak Avenue, Peoria, IL 61637, USAcProgram in Emergency Medicine, Michigan State University College of Human Medicine,

Saginaw Campus, Saginaw MI 48601, USAdEmergency Care Center, Covenant Healthcare, 900 Cooper, Saginaw, MI 48602, USA

Of all the electrolytes, the serum potassium is probably the most testedfor, titrated, and treated. A potassium disorder is the most commonelectrolyte abnormality in hospitalized patients, and this is likely true ofemergency department (ED) patients as well [1–3]. Of the two conditions,hypokalemia is more common; affecting a broader range of patients, whilehyperkalemia is potentially more serious and occurs almost exclusively inpatients with some underlying renal abnormalities [4,5].

Physiology, total body balance, and pathophysiology of potassium

A brief review of the physiology and the body’s handling of potassiumwill help in understanding the pathophysiology, causes, and management ofhypo- and hyperkalemia. The total body potassium content is approxi-mately 50 mEq/kg, and is distributed asymmetrically in the body. (Note, forpotassium, 1 mEq ¼ 1 mmol ¼ 39.09 mg. The potassium concentration ofmilliequivalents per liter (mEq/L) and millimoles per liter (mmol/L) are usedinterchangeably throughout this article.) About 98% is intracellular, andapproximately 75% of the intracellular component is in muscle [6,7]. Only65 to 70 mEq, or 2%, is extracellular and of this extracellular component,about 15 mEq or 0.4% of the total body potassium is measurable in the

* Corresponding author.

E-mail address: [email protected] (T.J. Schaefer).

0733-8627/05/$ - see front matter � 2005 Elsevier Inc. All rights reserved.

doi:10.1016/j.emc.2005.03.016 emed.theclinics.com

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724 SCHAEFER & WOLFORD

plasma [6,7]. This tiny fraction of total body potassium is maintained ina fairly narrow serum concentration of 3.5 to 5.0 mmol/L. In comparison,the intracellular potassium concentration is about 150 mmol/L. Theintracellular to extracellular ratio (150 mmol/L/4 mmol/L) results ina voltage gradient across the cell membrane and plays a major role inestablishing the resting cell membrane potential, particularly in cardiac andneuromuscular cells [4]. It is apparent that changes in the large, intracellularconcentration would have little effect on this ratio, but even small changes inthe extracellular concentration will have significant effects on this ratio, thetransmembrane potential gradient, and thereby the function of neuromus-cular and cardiac tissues [4]. The sodium–potassium adenosinetriphosphate(Na-K-ATPase) enzyme pump, located in the cell membrane, maintains thepotassium concentration gradient by actively transporting potassium intoand sodium out of cells.

All disorders of potassium occur because of abnormal potassiumhandling in one of three ways: problems with potassium intake (relativelytoo much or too little), problems with distribution of potassium between theintracellular and extracellular spaces (ie, transcellular shifts and alterationsin the normal ratio), or problems with potassium excretion (relatively toomuch or too little excreted).

Intake disorders

Normally functioning kidneys protect against hyperkalemia by excretingexcess ingested potassium and handle large dietary intakes with littleproblem [3,8]. Although the kidney protects against hyperkalemia, it isunable to stop all urinary potassium losses. An inadequate intake, overa period of time, may lead to hypokalemia [8,9].

Transcellular shifting disorders

Transcellular potassium shifting is affected by a variety of factorsincluding; integrity of the cell membrane, Na-K-ATPase activity, and theinternal state of the body, that is, potassium concentration, acid-base status,and serum tonicity. For example, rhabdomyolysis may cause a massive leakof potassium to the extracellular space because approximately 70% to 75%of the total body potassium is stored in muscle cells [7]. Insulin or beta 2-adrenergic catecholamines increase the Na-K-ATPase activity and drivespotassium intracellularly leading to decreased serum potassium levels,whereas patients with impaired insulin production (eg, diabetes mellitus),are predisposed to the development of hyperkalemia [4]. Finally, the internalstate of the body may affect transcellular shifting. In acidosis, the highextracellular hydrogen ion concentration results in hydrogen ion movementinto and potassium movement out of cells to maintain electroneutrality [4].Conversely, alkalemia and hypertonicity (eg, hyperglycemia) will result inthe movement of potassium into cells.

725DISORDERS OF POTASSIUM

Excretion disorders

Last, potassium excretion may be relatively too much or too little, whichis primarily related to kidney function. The kidney accounts for 90% ofpotassium excretion with the remainder primarily from the gastrointestinaltract and generally negligible amounts in sweat [3,5]. About 85% to 90% offiltered potassium is reabsorbed before the distal cortical collecting tubules.It is the remaining 10% to15% that is either excreted or reabsorped [3,10].Normally functioning kidneys, with adequate perfusion, can compensate fora wide range of potassium intake by increasing or decreasing potassiumurinary output. The kidneys are able to lower urinary potassiumconcentration to as little as 5 mEq/L but cannot stop excretion completely [4].

The amount of potassium renally excreted is primarily influenced by threefactors: the plasma potassium concentration, plasma aldosterone, and thedelivery of sodium and water to the distal collecting tubules [3,11,12].Increased potassium concentration stimulates nephron Na-K-ATPaseactivity resulting in potassium movement into the tubular lumen andexertion. The renin–angiotensin–aldosterone system is also activated to in-crease potassium exertion (Fig. 1 gives a brief, simplied, schematic review ofthe renin–angiotensin–aldosterone system). Finally, increased sodium andwater delivery to the distal tubules stimulates the Na-K-ATPase (contrib-uting to potassium excretion) and increased tubular flow (eg, osmoticdiuresis) leading to potassium ‘‘washout’’ and elimination [3,4,11–13].

Hypokalemia

Hypokalemia (generally defined as a serum potassium less than 3.6 mEqper liter) is an exceptionally common electrolyte abnormality encountered inclinical practice. Over 20% of hospitalized patients have been reported to

Kidney

Renin

Angiotensinogen

Angiotensin-converting enzyme (ACE)

Angiotensin II

Angiotensin I

Adrenal Gland

Aldosterone

Renin release in response to; - perfusion - blood volume - NaCl ← ←

←←

- potassium

Aldosterone leads to; - sodium reabsorption - potassium exertion

Fig. 1. Renin–angiotensin–aldosterone system (simplified schematic).


have some degree of hypokalemia [14]. A significant fraction of thesepatients have serum potassiums less than 3 mEq per liter. Patients takingdiuretics, particularly thiazides, are at particular risk for hypokalemia.Hypokalemia is also frequently seen in trauma patients, with some centersreporting a 45% to 68% incidence on admission [15,16]. In these patients,hypokalemia is associated with higher injury severity scores and lowerglasgow coma scores [16,17].

Hypokalemia has shown to be associated with an increased risk ofessential hypertension, ischemic and hemorrhagic stroke, dysrhythmias, anddeaths and hospital admissions due to heart failure and cardiovascularevents [2,18,19]. Recently, it has been recommended that serum potassiumlevels be maintained at levels greater than 4.5 mEq per liter for patients withheart failure and patients experiencing an acute myocardial infarction [20].

Clinical manifestations of hypokalemia

The signs and symptoms of hypokalemia are primarily related to changesin the ratio of extracellular to intracellular potassium and its impact on theresting electrical potential across cell membranes. A greater decrease inextracellular potassium concentration compared with intracellular concen-tration, leads to hyperpolarization of cell membranes and prolongation ofaction potential and refractory periods. Increased automaticity andexcitability also occur in the cardiac system. The organ systems primarilyaffected by hypokalemia are: cardiac, skeletal muscle, gastrointestinal, andrenal [21] (Table 1).

Although very common, rarely is the diagnosis of hypokalemiaconsidered until the results of laboratory tests are known. The majority ofhypokalemic patients have serum potassium levels of 3.0 to 3.5 mEq per literand are asymptomatic. Occasionally, vague symptoms of tiredness andminimal muscle weakness may be reported [2,22]. Moderately hypokalemicpatients (serum potassium levels of 3.0 to 2.5 mEq per liter) maydemonstrate significant proximal muscle weakness [22]. Cranial musclesare typically spared, and the lower limbs are more affected than the upper

Table 1

Organ system effects of hypokalemia

Cardiac Dysrhythmias

Conduction defects

Increased likelihood of dysrhythmias due to digitalis

Skeletal muscle Weakness

Paralysis

Rhabdomyolysis

Fasiculations and tetany

Gastrointestinal Ileus

Renal Nephrogenic diabetes insipidus

Metabolic alkalosis


limbs [5,22]. Other vague symptoms including constipation may also bereported. Severely hypokalemic patients (serum potassium levels below 2.5mEq per liter) may develop rhabdomyolysis, myoglobinuria, an ascendingsymmetric paralysis with a clear sensorium, and even respiratory arrest [2].Central nervous system symptoms, although reported, are more likely theresult of acid-base changes or other coexisting abnormalities [22]. Symptomsare not only associated with the degree of hypokalemia found, but also therapidity with which it developed.

Electrocardiograph changes may be present and reflect hypokalemia’seffects on myocardial cell membranes (Table 2). The merging of a U-wavewith the T-wave may falsely appear to result in the appearance of QTinterval prolongation. Giant U-waves may occur, and may be mistaken forpeaked T-waves. These large U-waves, however, have a broader base thantrue for peaked T-waves [23]. Unfortunately, the presence or absence ofelectrocardiographic changes is not predictive of hypokalemia or of itsseverity.

Patients without heart disease rarely demonstrate any significant cardiacabnormalities due to hypokalemia. This is not the case for patients with leftventricular hypertrophy, cardiac ischemia, or heart failure [2,20,24].Numerous studies have demonstrated an increased incidence of ventriculardysrhythmias in patients with underlying heart disease, including acutemyocardial infarction, and even mild hypokalemia [2,20,24]. Hulting [25]studied patients with acute myocardial infarction and found the risk ofventricular fibrillation to be nearly five times greater for those with a serumpotassium of less than 3.9 mEq per liter. Hypokalemia also increases thepotential for digoxin toxicity and associated dysrhythmias.

Hypokalemia has a number of effects on renal function. Patients maypresent with symptoms of polyuria and polydypsia due to impaired abilityto concentrate the urine and a resulting picture of nephrogenic diabetesinsipidus [26]. Persistent metabolic alkalosis may occur as the result of thedecreased ability of the kidney to excrete bicarbonate and citrate, increasedammoniagenesis, and increased collecting duct proton secretion [26,27].Hypokalemia may also contribute to persistent metabolic alkalosis byincreasing urinary chloride excretion and causing serum hypochloremia [26].

Table 2

Electrocardiographic changes associated with hypokalemia

Increased P-wave amplitude

Prolonged PR interval

Apparent QT interval prolongation

Reduction in T-wave amplitude

T-wave inversion

ST segment depression

U-waves

From Webster A, Brady W, Morris F. Recognising signs of danger: ECG changes resulting

from an abnormal serum potassium concentration. Emerg Med J 2002;19:74–7.


Etiologies of hypokalemia

The etiology of hypokalemia, for a given patient, falls into three broadcategories: insufficient potassium intake, transcellular shift of potassiumfrom the extracellular to intracellular compartments, or excessive potassiumloss. The renal and gastrointestinal systems are the primary sites of excesspotassium loss from the body (Fig. 2).

Inadequate potassium intake

Inadequate intake of potassium is an exceedingly rare cause ofhypokalemia. The minimum daily dietary requirement for potassium isconsidered to be 1.6 g to 2 g (40 to 50 mEq) per day with the usual dietaryintake being 2.1 g to 3.4 g per day [8,24]. If potassium intake is less than40 mEq per day for a prolonged period, hypokalemia may develop. Theelderly, especially those living alone or with disabilities, are more likely tohave a potassium-poor diet and to develop hypokalemia on this basis [24].Hypokalemia is occasionally seen in those individuals who habitually eatclay. The clay binds potassium, making it unavailable for absorption.

Transcellular potassium shifts

The movement of potassium from the extracellular compartment intocells is a relatively uncommon cause of clinically significant hypokalemia.Importantly, although the serum potassium concentration may be low, theamount of total body potassium may be normal. Aggressive potassiumadministration may result in severe hyperkalemia once the underlying cause

Hypokalemia

Inadequate potassium

intake

Transcellular potassium shift

Excessivepotassium loss

Renal losses GI losses

Increased mineralocorticoidactivity

Non-druginduced

Drug-induced

Drug-induced

Non-druginduced

Increased urine flow or Nadelivery to distal nephron

Drug-induced

Non-drug induced

Non-druginduced

Drug induced

Other

Other

Fig. 2. Etiologies of hypokalemia.


is addressed. Transcellular shifts may be the result of medications or othernondrug causes.

Drug-induced potassium shifts

A large number of medications can cause transcellular potassium shifts[2]. The b2 sympathomimetic agonists are probably the most studied of thesedrugs. These drugs increase the movement of sodium into cells in exchangefor hydrogen protons and results in an increased intracellular sodiumconcentration. As a result, the Na-K-ATPase is driven to move sodium outand potassium into cells, resulting in a fall of extracellular potassium con-centrations [21]. The degree and duration of hypokalemia varies with theagent used. Interestingly, a study in primates has suggested that the tremorfrequently seen with the use of these agents is associated with hypokalemia[28]. Hypokalemia may also occur in patients with a high level of circulatingcatecholamines, probably via the same mechanism.

Other common medications causing transcellular shifts include phos-phodiesterase inhibitors (eg, theophylline and caffeine), insulin, bariumpoisoning, and verapamil overdose [2,26].

Nondrug-induced potassium shifts

A variety of disorders can cause movement of potassium into cells. Bothmetabolic and respiratory alkalosis can contribute to hypokalemia due tothe exchange of extracellular potassium for intracellular hydrogen ions. Theadministration of glucose or insulin may cause a decline in serum potassiumas insulin stimulates cellular uptake of potassium. Rare causes of severehypokalemia with paralysis include familial periodic paralysis (typicallycitizens of Western countries), thyrotoxic periodic paralysis (males of Asiandescent), sporadic periodic paralysis (Asian descent), and hypernatremichypokalemic paralysis. Hypokalemia and paralysis due to transcellular shiftshould be suspected when no evidence of a total body deficit of potassium isfound and there is no acid-base disorder present [29].

Excessive loss of potassium

The most common cause of hypokalemia is the excessive loss ofpotassium, either in the stool or via urine. Losses from the skin are rareexcept in the readily identifiable conditions of extensive burns or largevolumes of sweat production.

Gastrointestinal losses

Potassium losses via the gastrointestinal tract are likely the second mostcommon cause of hypokalemia in developed countries, and results primarilyfrom losses in the stool [2,4]. Normally, only about 10% of total potassium


excretion (w10 mEq) each day is via stool. Any cause of increased stoolvolumes will increase the amount of potassium lost and can result inhypokalemia if the intake of potassium is not increased.

Vomiting and nasogastric suctioning, by themselves, do not causesignificant potassium loss as the normal gastric fluid only contains 5 to 10mEq per liter. However, if aldosterone levels increase because of associatedvolume loss, an increase in potassium excretion in the urine will occur. Inaddition, an associated metabolic alkalosis will contribute to increasedurinary potassium loss and transcellular shifting of extracellular potassium,again contributing to the development of hypokalemia [4].

Renal losses

Hypokalemia due to increased potassium loss in the urine is probably themost common cause of hypokalemia in developed countries.

Potassium losses due to increased urinary flow or delivery of sodium todistal nephron

Diuretics are the most common drug-related cause of hypokalemia.Thiazide and loop diuretics both increase sodium and chloride delivery tothe distal collecting duct, which results in increased potassium secretion andchloride depletion. The incidence of hypokalemia for patients on diureticsmay be up to 56%, and the time to development of hypokalemia is quitevariable [30].

Osmotic diuresis from poorly controlled diabetes mellitus or the use ofmannitol or saline diuresis to treat hypercalcemia may also cause increasedrenal potassium loss due to increased urine flow and potassium secretion.Administration of high doses of some antibiotics, such as penicillin or itsderivatives, also increase the delivery of sodium to the distal nephron andincrease potassium secretion [2].

Rare causes of hypokalemia due to increased distal sodium deliveryinclude Type I and Type II renal tubular acidosis (RTA), Gitelman’ssyndrome, and Bartter’s syndrome [5]. In these disorders, although due todifferent mechanisms, increased delivery of sodium to the distal nephroncauses increased potassium secretion. RTA is one of the few disorders inwhich hypokalemia and metabolic acidosis occur [4].

Increased mineralocorticoid activity

Aldosterone is the primary hormonal regulator of renal potassiumsecretion. Increased aldosterone levels lead to an increased number of opensodium pores and increased Na-K-ATPase activity in the nephrons and, asa result, increased potassium secretion into the urine.

Primary hyperaldosteronism is the result of a unilateral adrenaladenoma, bilateral adrenal hyperplasia, or rarely an adrenocortical


carcinoma [2]. Secondary hyperaldosteronism is the outcome of the normalresponse to a variety of disease states causing decreased intravascularvolume and decreased renal perfusion or to increased renin production.Both result in increased potassium wasting by the kidneys. Other rare causesof aldosteronism include Cushing’s syndrome (adrenal, pituitary, or ectopictumor production of adrenocorticotropic hormone) and congenital adrenalhyperplasia [2].

Several drugs and dietary supplements may cause presentationssuggestive of hyperaldosteronism. Life-threatening hypokalemia has beenreported in a patient treated with high-dose hydrocortisone [31]. Gluco-corticoids with mineralocorticoid activity and in high doses may saturate 11b-hydoxysteroid dehydrogenase in the renal cortical collecting ducts. Excesssteroid then binds with the mineralocorticoid receptor and produces thesame effects as aldosterone [31]. Licorice containing glycyrrhizic acid,although no longer made in the United States, is still found in a variety ofherbal teas, chewing tobaccos, sweeteners, and other compounds producedinternationally. An active metabolite of licorice, glycyrrhetenic acid, bindsto the mineralocorticoid receptor [32]. It also inhibits 11 b-hydoxysteroiddehydrogenase, creating an apparent cortisol excess that also binds to themineralocorticoid receptor. The findings are similar to that of primaryhyperaldosteronism [32].

Other renal etiologies of potassium loss

Hypomagnesemia frequently occurs in many patients who are also at riskfor hypokalemia (eg, patients with congestive heart failure and on diuretics,alcoholics). One study of patients with congestive heart failure found 23%of the patients to be hypokalemic and 17% to be hypomagnesemic [33].Fifty percent of the hypokalemic patients were hypomagnesemic and67% of the hypomagnesemic patients also were hypokalemic [33]. Renalpotassium wasting is common in hypomagnesemic patients and thehypokalemia cannot be reversed until the magnesium deficit is corrected[2]. The mechanism by which a magnesium deficit causes renal potassiumwasting is unknown.

Treatment of hypokalemia

Hypokalemia rarely occurs as an isolated condition. In many cases,corrections of other abnormalities (eg, hypovolemia) must take precedenceover repletion of serum potassium. Underlying causes of the hypokalemia,such as hypomagnesemia, must also be addressed.

After the initial priorities of airway, breathing, and circulation areaddressed a search for the etiology of the hypokalemia should be made. Inmost cases, a thorough history and physical examination reveal the cause


(eg, severe diarrhea, use of diuretics without potassium supplementation). Ifthe etiology is still unclear, additional laboratory tests that will assist in thediagnosis include (1) serum sodium, chloride, bicarbonate, creatinine, andglucose; (2) arterial blood gas; and (3) spot urine measurements of sodium,potassium, chloride, and creatinine. Using the additional laboratory data,the etiology of the hypokalemia may be sorted into one of several categories(Table 3). To be complete, samples should also be sent for determination ofplasma renin and aldosterone levels, although they usually will not beavailable in the ED.

The decision to correct hypokalemia should be based on the clinical stateof the patient. Most patients who are asymptomatic and have mildhypokalemia (3.5 to 3.0 mEq per liter) do not require urgent correction,although they should be advised to eat a diet rich in potassium [27].Potassium supplementation may be required if the hypokalemia persists.However, patients with acute myocardial infarction are an exception, due tothe increased risk of ventricular dysrhythmias in the presence of even mildhypokalemia. It is recommended that the serum potassium be maintainedabove 4.5 mEq per liter in this population [20].

Patients with moderate to severe hypokalemia (!3.0 mEq/L) or thosewho are symptomatic with significant electrocardiogram changes, dysrhyth-mias, severe weakness, or paralysis require more urgent potassiumreplacement. The choice of route and formulation is dependent on theseverity of the symptoms and underlying conditions (Table 4).

Table 3

Diagnostic approach to etiology of hypokalemia

Laboratory abnormalities Etiology

Hypokalemia and normal acid-base

state and UK\Ucreat ! 2

Transcellular shift (eg, thyrotoxic periodic

paralysis, familial periodic paralysis)

Hypokalemia and normal gap

metabolic acidosis and

(UNa þ UK)-UCl R �10

Gastrointestinal losses of potassium (eg,

diarrhea or other gut fluid high in bicarbonate

Hypokalemia and normal gap metabolic

acidosis and (UNa þ UK)-UCl % �10

and UK\UcreatO 2

Renal-mediated potassium loss due to renal

tubular acidosis, drug induced RTA,

ureteral diversion

Hypokalemia and metabolic alkalosis

and UCl ! 20 mEq\L

Gastrointestinal loss of potassium due to

vomiting, NG suctioning

Diuretics (UCl measure after

diuretic effect resolved)

Hypokalemia and metabolic alkalosis

and UClO 20 mEq\L

Diuretics (UCl measured

during diuretic effect)

Increased mineralocorticoid effect

Abbreviations: UCl, chloride; UK, potassium; UNa, sodium; Ucreat, creatinine.

Adapted from Ref. [34]. Whittier WL, Rutecki GW. Primer on clinical acid-base problem

solving. Dis Mon 2004;50:117–62 and Lin SH, Chiu JS, Hsu CW, et al. A simple and rapid

approach to hypokalemic paralysis. Am J Emerg Med 2003;21:487–91.


Special care must be taken in the treatment of patients with low serumpotassium due to transcellular potassium shifts. These patients may nothave significant total body potassium deficits. Rebound hyperkalemia canoccur as the cause of the transcellular shift is corrected and if aggressivepotassium replacement has been given [29,35].

Hyperkalemia

Although hypokalemia is a more common clinical disorder, hyperkalemiais generally more serious and less well tolerated [2,6]. A total bodypotassium depletion of 200 to 400 mEq will reduce the serum concentrationby about 1 mEq/L, whereas an excess of only 100 to 200 mEq will increasethe serum potassium concentration by about 1 mEq/L [6]. With this in mind,it’s understandable that increases in the total body potassium content canresult in a rapid and potentially life-threatening hyperkalemia.

Case

A 40-year-old male presented to the ED with a chief complaint ofprofound weakness. He had noticed some mild weakness, generalizedmalaise, and mild nausea for 2 days but this marked weakness developedsuddenly on the morning of admission. He was unable to weight bear, andhad to slide himself along the floor to call a neighbor, and was brought in byambulance.

Until 3 weeks ago, the patient had been healthy with no known medicalproblems and had not seen a doctor ‘‘for years,’’ when he suffered a smallacute myocardial infarction. On that admission, hypertension (218/138 onarrival) and hypercholesterolemia were diagnosed and the patient wasstarted on enalapril (Vasotec) 20 mg twice a day, metolprolol (Lopressor) 50mg twice a day, pravastatin (Pravachol) 20 mg daily, aspirin 81 mg daily,and clopidogrel (Plavix) 75 mg daily.

Table 4

Treatment of hypokalemia

Formulation Dose and rate Indication

Oral potassium

chloride (multiple

formulations)

20–80 mEq/d in divided doses Nonurgent correction

and/or maintenance

Oral potassium liquid 40–60 mEq/dose: serum

potassium should be followed

to determine dosing interval

Rapid elevation for patients

requiring urgent, but not

emergent correction.

Intravenous

potassium chloride

20–40 mEq/h serum

potassium should be

reassessed after 60 mEq

Patients with severe symptoms

(eg, dysrhythmias, paralysis)

or unable to tolerate oral dosing

Adapted from Kim GH, Han JS. Therapeutic Approach to Hypokalemia. Nephron

2002;92(Supp. 1):28–32.


On arrival in the ED for the current visit, the patient complained ofsevere, bilateral weakness in the lower extremities greater than the upperextremities, lower extremity numbness and ‘‘tingling,’’ and nausea. Hedenied any chest pain or shortness of breath. His vital signs were; pulse 67,respirations 20, blood pressure 154/83, temperature 97.4 �F (36.3 �C).On physical examination, his head/neck, lung, and cardiac exam wasunremarkable. His abdominal exam revealed mild diffuse tenderness and theneurologic exam was remarkable for nonfocal generalized weakness greaterin the lower extremities, with normal sensation. When compared witha prior electrocardiogram, changes included ‘‘peaked’’ T-waves, PR intervalincrease from 126 millisecond to 172 millisecond and QRS durationincrease from 92 millisecond to 120 millisecond (Fig. 3). Laboratory resultsincluded serum potassium ¼ 9.1 mmol/L, sodium ¼ 127 mmol/L, CO2

venous ¼ 15 mmol/L, glucose ¼ 95 mg/dL, blood urea nitrogen (BUN) ¼31 mg/dL, and creatinine ¼ 1.5 mg/dL. (BUN and creatinine on the prioradmission were 11 mg/dL and 1.0 mg/dL, respectively).

The patient was treated with calcium gluconate 10 mL of a 10% solution(1 g) intravenously (IV), regular insulin 10 units IV, glucose 50 mL of 50%dextrose (25 g) IV, and sodium polystyrene sulfonate (Kayexalate) 30 gorally. After approximately 1 hour, the patient was feeling improved andrepeat labs included potassium ¼ 7.8 mmol/L and glucose ¼ 64 mg/dL. Anadditional 25 mL of 50% dextrose (12.5 g) IV was given.

Fig. 3. Electrocardiogram demonstrating the changes of hyperkalemia. ECG from Case #2

demonstrating peaked T-wave, QRS duration prolongation, and PR interval lengthening when

compared with an earlier ECG.


In this case, the patient’s impaired cardiac conduction and weakness aretypical symptoms of both hypo- and hyperkalemia; however, the ECGsuggests hyperkalemia.

Hyperkalemia is defined as a level O5.5 mmol/L [5,7]. Some furtherdivide hyperkalemia into: minimal, 5.5 to 6.5 mmol/L with only minorelectrocardiographic changes; moderate, 6.6 to 8.0 mmol/L with ECGchanges limited to peaking of T-waves; and severe, O8.0 mmol/L or anylevel with a widened QRS complex, atrioventricular (AV) block, orventricular dysrhythmia [36]. Readers are reminded that serious complica-tions do not strictly correlate with a given level, and are related more to therate of rise in the potassium level, the affect on cardiac conduction, and theunderlying cause than on the exact serum potassium concentration [5,7].

Clinical manifestations of hyperkalemia

As with hypokalemia, the organ systems affected are cardiac, neuromus-cular, and gastrointestinal. Patients often complain of only vague feelings ofnot feeling well, gastrointestinal symptoms, or generalized weakness [10].The most serious concern is impaired cardiac conduction with risk ofsudden death from asystole or ventricular fibrillation [4,6,7]. Neuromuscularsigns and symptoms include muscle cramps, weakness, paralysis, paresthe-sias, and decreased deep tendon reflexes [4,37].

Usually, severe symptoms do not occur until potassium levels reach 7.0mmol/L or above, but there are many individual patient variables, anda rapid rate of rise is more dangerous than a slowly rising level [8,36,38]. Inthe ED it may be impossible to know if the hyperkalemia is acute or morestable and chronic.

Physicians are unable to use the ECG alone to predict which patientsmight have hyperkalemia or how high the level might be [1,5,7,39,40].However, typical ECG changes in a patient with hyperkalemia, increasesthe urgency for treatment. The ‘‘classic’’ ECG changes associated withhyperkalemia are well described [3–7,40–42]. The earliest changes, oftenbeginning with levels above 6.5 mEq/L, are ‘‘peaked,’’ or ‘‘tented’’ T-waves,which are most prominent in the precordial leads. With further rise in serumlevels, there is diminished cardiac excitability manifested by flattening of theP-wave, PR interval lengthening, and the eventual disappearance of the P-wave. The QRS duration becomes prolonged, progressing to a ‘‘sine wave’’appearance, and finally ending in ventricular asystole or fibrillation withlevels 8 to 10 mmol/L [3–7,40–42].

Etiologies of hyperkalemia

As with hypokalemia, hyperkalemia results from an imbalance of normalpotassium handling. This imbalance can develop from increased potassiumload, transcellular shifting of potassium, or decreased potassium elimination


(Table 4). In addition to ‘‘real’’ disease, one other fairly common cause forelevated potassium readings is ‘‘pseudohyperkalemia,’’ which is discussedbelow.

Pseudohyperkalemia

This may be more common than true hyperkalemia, and occurs whenpotassium is unexpectedly released from cells either at the time ofphlebotomy or after collection [4,5]. Traumatic hemolysis during venipunc-ture or in vitro hemolysis is the most common cause of psyedohyperkalemiabeing reported in 20% of all blood samples with an elevated potassium level[6]. The laboratory will generally report a ‘‘slightly hemolyzed’’ specimen asa clue to explain the hyperkalemia [4]. Another cause is potassium releasedfrom muscle cells distal to a tourniquet with fist clenching duringphlebotomy. [3,6,12,43]. This can be avoided by not having the patientclench their fist, limiting tourniquet time, or releasing the tourniquet afterthe needle enters the vein. Finally, potassium can be released from whiteblood cells or platelets, after blood is drawn, in patients with severeleukocytosis (white blood cell countO50,000–100,000/mm3 or thrombocy-tosis (platelet counts O500,000–1 million/mm3). If this is suspected, recheckthe potassium from a tube of unclotted blood [5,12]. The possibility ofpseudohyperkalemia should always be considered if unexpected hyper-kalemia is found in an asymptomatic patient with otherwise normalelectrolytes and acid-base balance [5,6,12].

Decreased potassium excretion

The large majority of cases of hyperkalemia (over 80%) occur whenpotassium excretion is impaired by a medical condition or medications ina patient with some degree of underlying renal dysfunction [3,5,12,11]. Mostpatients with decreased ability to excrete potassium compensate and reacha steady state of normal serum potassium concentration until some secondevent tips the balance [5]. This second event could be decreased perfusion,infection, obstruction, or a new medication [3,11].

On a physiologic level, there are two possible problems. First isdiminished sodium and water delivery to the distal collecting system. Thismight occur with advanced renal failure or if there is real or effectivecirculating volume depletion as seen with hypovolemia, dehydration, orsevere heart failure. The second possibility is reduced effectiveness orconcentration of aldosterone [5,11,44]. We will discuss each of these twopossibilities.

Acute or chronic renal failure

Although all the possible causes of renal failure are beyond the scope ofthis article, any condition that leads to worsening renal insufficiency or renal


failure can result in hyperkalemia. There must be adequate blood flow forglomerular filtration and some amount of urinary tubular flow, to the distalcollecting tubule, for potassium secretion to occur. When the glomerularfiltration rate falls below about 10 mL/min or about 1 L/d, this can lead tohyperkalemia [6]. Patients with acute renal failure are at greater risk for life-threatening complications from hyperkalemia as the potassium level is risingmore rapidly, before the body has a chance to develop compensatorymechanisms.

Hypoaldosteronism

A more common renal cause for hyperkalemia than complete renal failureis renal insufficiency with development of hypoaldosteronism [4,7,10]. Thisis a condition of relatively well-preserved glomerular filtration rate butdecreased aldosterone levels. There are multiple medical causes andhypoaldosterone-inducing medications that play a role in the susceptiblepatient (see Box 1) [1–3,11]. Hypoaldosteronism can be subdivided by theaccompanying renin levels as low, normal, or high [10].

Hyporeninemic hypoaldosteronism results from impaired renin levelsultimately resulting in hypoaldosteronism. Several conditions are associatedwith defective renin production, including damage to the juxtaglomerularapparatus, dysfunction of sympathetic innervation, and inhibition ofprostaglandin synthesis [11]. The classic patient is an elderly diabeticpatient with mild to moderate renal insufficiency; however, any conditionthat damages or limits normal renal production of renin can result inhyporeninemia (see Box 1) [4,7]. The best examples of medicationsimplicated in causing hyporeninemic hypoaldosteronism associated hyper-kalemia are nonsteriodal anti-inflammatory drugs (NSAIDs). NSAIDs cancause hyperkalemia by decreasing glomerular filtration rate, increasingsodium retention, but primarily by suppressing renin output via inhibitionof prostaglandins [7,11]. Patients at increased risk for developing hyper-kalemia with NSAID use include the elderly, those with serum creatinineconcentration greater than 1.2 mg/dL, patients with congestive heart failure,or those using diuretics [11]. The selective cyclooxygenase-2 inhibitors havebeen reported to cause severe hyperkalemia by the same mechanism as thetraditional NSAIDs [45,46].

Hypereninemic hypoaldosteronism occurs when there is lack of aldoste-rone production. In adrenal insufficiency (Addison’s Disease), the adrenalglands do not produce enough aldosterone. Medications disrupting therenin–angiotensin–aldosterone system include angiotensin converting en-zyme inhibitors (eg, captopril, enalapril, lisinopril), angiotensin receptorblockers (eg, irbesartan, losartan, valsartan) and heparin. Identifyingpatients at risk for developing hyperkalemia before starting thesemedications is difficult. Hyperkalemia can occur in patients with onlymodest renal insufficiency, and may not be predicted by the pretreatment


Box 1. Causes of hyperkalemia

Pseudohyperkalemia

� Hemolysis

� Distal to tourniquet or with fist clenching

� Marked leukocystosis (white blood cell count >50,000 mm3)

� Marked thrombocystosis (platelets >1 million mm3)

Decreased potassium elimination

Acute or chronic decreased glomerular filtration rate (5–10 mL/min)

1. Acute or chronic renal failure

Hyopaldosteronism

1. With low renin levels (hyporeninemic hypoaldosteronism)

� Elderly

� Diabetic

� Interstitial nephritis

� Obstructive uropathy

� Systemic lupus erythematosus (SLE)

� Amyloidosis

� AIDS

� Nonsteroidal anti-inflammatory drugs

2. With high renin levels (hyperreninemic hypoaldosteronism)

� Addison’s Disease

� Angiotensin converting enzyme inhibitors

� Angiotension receptor blockers

� Heparin

End-organ resistance to aldosterone (normal or elevated aldosterone)

� SLE

� Sickle cell anemia

� Obstructive uropathy

� Transplantation

� Potassium-sparing diureticdspironolactone

Sodium channel blockade

� Potassium-sparing diureticsdamiloride, triamterene

� Trimethoprim (blocks sodium reabsorption)

� Pentamidine (blocks sodium reabsorption)

Increased potassium load

� Potassium supplements

� Dietary salt substitutes

� Potassium penicillin

� Massive blood transfusion

� Poisoning e.g. potassium chloride water softener pellet ingestion

Transcellular shifting

� Insulin deficiency

� Rhabdomyolysis/increased tissue catabolism

� Acidosis

� Hypertonicity

� Exercise

� Hyperkalemic periodic paralysis

� Drugs

1. Non-selective beta-blockers (inhibits Na-P-ATPase pump)

2. Digitalis toxicity (inhibits Na-P-ATPase pump)

3. Succinylcholine (membrane leak)

Modified from Zull DN. Disorders of potassium metabolism. Emerg Med Clin North Am 1989;7(4):771–94; with permission

and data from Gennari FJ. Disorders of potassium homeostasis: hypokalemia and hyperkalemia. Crit Care Clin 2002;18(2):273–88

and Linas SL. The patient with hypokalemia or hyperkalemia. In: Schrier RW, editor. Manual of Nephrology, 5th ed. Philadelphia:

Lippincott Williams & Wilkins; 2000.


serum creatinine level [11,47,48]. Heparin reduces aldosterone synthesis, andcan lead to hyperkalemia in about 7% of patients treated for 3 or more days[4,7,11,49].

End-organ resistance to aldosterone

In addition to hypoaldosterone states, normal or elevated aldosterone maybe seen when the kidneys develop end-organ resistance to aldosterone [5,10].Conditions such as obstructive uropathy, sickle cell anemia, systemic lupuserythematous, and renal transplantation predispose to hyperkalemia by thismechanism [10]. The classic medication example is the potassium-sparingdiuretic spironolactone (Aldactone), which competitively binds to thealdosterone receptor [11].

Sodium channel blockade

Finally, several medications cause hyperkalemia by inhibiting the sodiumchannels in the kidney, which leads to sodium excretion and potassiumretention. The potassium-sparing diuretics amiloride (Midamor) andtriamterene (Dyrenium) work by this mechanism [4,7,11]. An often over-looked possible cause of hyperkalemia by this mechanism are the antibioticstrimethoprim-sulfamethoxazole (Bactrim, Septra) (trimethoprim compo-nent) and pentamidine (Pentam), which also block sodium channels [7,11,50].

Use of potassium-sparing diuretics has increased since the results of the1999 randomized aldactone evaluation study (RALES), which demonstrateda 30% mortality reduction when low dose spironolactone (average dose was26 mg every day) was added to standard treatment for severe congestive heartfailure [51]. The incidence of serious hyperkalemia (Kþ O6.0 mmol/L) in thisstudy occurred in only 2% [51]. However, several reports of life-threateningand fatal hyperkalemia have subsequently been reported [48,52–54].

Increased potassium load

In patients with normal renal function, hyperkalemia from excesspotassium load is very uncommon. Possible causes include potassiumsupplement overdose, massive blood transfusions with hypoperfusion, oraccidental overdose ingestion of potassium chloride crystals used in watersofteners [6,55]. A more common scenario is gradual total body potassiumaccumulation in a patient with impaired kidney function. Dietary saltsubstitutes, potassium supplements, penicillin potassium therapy, anddrinking ‘‘potassium softened’’ water may cause hyperkalemia in the pre-disposed patient [6,55,56].

Transcellular shifting

Redistribution of potassium from the intracellular to the extracellularspace is another etiology of hyperkalemia. Insulin is a key hormone for


promoting potassium uptake into cells by stimulating the Na-K-ATPase asdescribed earlier. Insulin deficiency, in diabetes mellitus, can lead tohyperkalemia because of lack of transcellular uptake [3,12]. Cell breakdownand increased tissue catabolism can release large amounts of potassium intothe circulation. Examples include rhabdomyolysis, massive hemolysis (eg,transfusion reaction), resolving hematoma, catabolic states, or tumor lysissyndrome after chemotherapy initiation [4,6,10].

Although acidosis is frequently described as contributing to hyper-kalemia, clinically, there is an inconsistent response in respiratory acidosisand there is a limited response in organic acidosis (ie, lactic acidosis andketoacidosis) as these organic acids tend to move across membranes with thehydrogen ion [3,4,6,10,12]. Hypertonicity may lead to hyperkalemia by twomechanisms: loss of intracellular water, resulting in an increased in-tracellular potassium concentration, favoring a gradient for potassium tomove out of cells; and as water exits the cell, potassium is swept along with,‘‘solvent drag’’ [12]. The most common cause of hyperosmolarity ishyperglycemia in uncontrolled diabetes mellitus [3]. Other conditions withhypertonicity are hypernatremia and hypertonic mannitol. HyperkalemicPeriodic Paralysis [3,12] is a rare autosomal dominant disorder in whicha sudden rise in serum potassium levels results in transient weakness orparalysis. This often occurs during rest after strenuous exercise or aftera large potassium-containing meal. Treatment with insulin, glucose, anda beta-adrenergic agonist may be clinically indicated if the patient has severeweakness with respiratory compromise.

Finally, medications can disrupt the normal intracellular/extracellularpotassium ratio. Nonselective beta-blockers (eg, propranolol) can interferewith the Na-K-ATPase, inhibiting potassium uptake into cells [3,7,11].Generally, this effect is minimal and seems less likely to occur with selectivebeta-1 blockers such as atenolol or metoprolol [12]. Digoxin inhibits the Na-K-ATPase in a dose-dependent fashion and at toxic levels, potassiumtransport into cells is impaired, and can cause hyperkalemia [3,7,11].Succinylcholine may cause a rapid, transient hyperkalemia from intracel-lular leak. This occurs most commonly in patients with specific underlyingconditions, such as major burns, neuromuscular injury, or prolongedimmobilization [7].

Emergency department management of hyperkalemia

The risk of severe complications and the urgency for treatment ofhyperkalemia is determined by individual patient conditions includingpresenting symptoms, overall hemodynamic status, kidney function,underlying medical conditions, patient medications, rapidity of potassiumrise, serum potassium level, acid-base status, ECG findings, and so on[7,11,36]. Because of the wide variety of factors to consider, treatmentcannot be based on serum potassium levels alone, and there are no clear


guidelines for admission versus ED treatment versus outpatient treatment[7]. Some suggest that if patients have stable or slowly rising serumpotassium levels of 6.5 mmol/L or less and minimal or no ECG changes,then they could be treated as outpatients [36]. Another suggestion is thatpatients with moderate hyperkalmia (6.5–8.0 mmol/L), ECGs that arenormal or have changes limited to peaked T-waves only, and have anidentified and manageable cause of hyperkalemia, can be treated in the ED,observed for a short period of time, and sent home [36]. Finally, otherssuggest that because life-threatening arrhythmias are more likely withrapidly rising levels and the time course of the hyperkalemia is often notknown, then all patients with serum potassiums O6.0 mEq/L should beconsidered at risk for life-threatening arrhythmias and treated [3,11].

The following management suggestions are offered. Patients requireimmediate treatment and continuous cardiac monitoring with extendedobservation if levels are rising rapidly, if levels are 7.0 mmol/L or above, ifthey have severe muscle weakness, if they have marked electrocardiographicchanges (more that just peaked-T waves), if they have acute deterioration ofrenal function, or if they have significant coexisting medical problems[7,11,36]. Asymptomatic patients with stable or slowly rising levels between6.0 to 6.5 mmol/L, no ECG changes of hyperkalemia, and an identifiableand manageable etiology, can be treated in the ED with exchange resinalone, observed for a short time, and sent home. Last, asymptomaticpatients with stable levels below 6.0 mmol/L and an identifiable/manageableetiology can be treated with diet or medication changes as an outpatient[2,4,7,38].

There is a four-pronged approached to the acute management of severehyperkalemia; cardiac membrane stabilization, reducing plasma potassiumconcentrations by moving potassium from the extracellular to theintracellular space, removing potassium from the body, and determiningcause and preventing recurrence [7,11,57] (Table 5).

Membrane stabilization

Calcium is used to temporarily antagonize and stabilize the cardiacmembrane from the effects of hyperkalemia. It is indicated in patients withsignificant ECG abnormalities (ie, loss of P-waves and prolonged QRSduration) and when it is potentially dangerous to wait 30 to 60 minutes forother therapies to take affect [6,38]. Calcium gluconate is generally used, andTable 5 gives dosing. The calcium dose can be repeated in 10 minutes [4,5,7].Calcium chloride can also be used with 10 mL of a 10% solution providingthree times the elemental calcium than that of 10 mL of 10% calciumgluconate. This higher dose of calcium, theoretically, may be beneficial inpatients with marked cardiovascular compromise and instability [6].

There are several cautions with calcium use. First, calcium can potentiatedigitalis toxicity [4,5,7,40]. If it is necessary to give calcium to a patient


taking digitalis, it is recommended that the calcium be added to 100 mL ofD5W and infused over 20 to 30 minutes [7,9,11]. Second, it cannot be giventhrough the same IV line as sodium bicarbonate, as it can precipitate out asa calcium salt. Third, calcium is irritating to tissue, and can cause phlebitisand tissue necrosis if it extravagates. Fourth, repeated doses can lead tohypercalcemia. Finally, calcium is a temporary measure that does notdecrease serum potassium levels and must be used with other therapies.

Intracellular shifting

InsulinThe next step in acute management is to shift potassium from the

extracellular to the intracellular space. Insulin is the most consistent andreliable treatment (even in patients with end-stage renal disease), and isindicated in all cases of hyperkalemia requiring emergency treatment [7,40]

Table 5

Treatment of hyperkalemia

Medication Dose and route Onset Duration

Membrane stabilizing

Calcium Gluconate

(caution: digoxin

toxic pt.)

10 mL of 10% solution,

may repeat once in 5–10 min

(children, 0.5 mL/kg

IV)

1–3 min 20–60 min

Transcellular potassium

shifting

Insulin, regular AND

Glucose (if serum glucose

!250 mg/dL) (caution:

monitor glucose)

10 units IV with 50 mL

of 50% solution

(consider following

with D10W infusion at

50 mL/h) OR

10 units in 500 mL

of D10W over 1 h (children,

insulin 0.1 units/kg with

D25W infusion 2 mL/kg

(0.5 g/kg over 30 min)

10–20 min 2–4 h

Albuterol (nebulized)

(caution: pts with severe

coronary artery disease)

10–20 mg in 4 mL saline

nebulized over 20 min

(children, 2.5 mg if !25

kg or 5 mg if O25 kg)

20–30 min 2–4 h

NaHCO3 (Only in

metabolic acidosis)

50–100 mEq IV over 5 min

(children, 1–2 mEq/kg IV)

!30 min 1–2 h

Elimination of potassium

Sodium polystyrene

sulfonate (caution:

give with laxative)

30 g PO, 50 g PR

(children, 1–2 g/kg

PO or PR)

w2 h (PO)

w1 h (PR)

d

Furosemide 20–40 mg IV (children,

1–2 mg/kg IV)

30–60 min d

Hemodialysis minutes d

Created from data from Refs. [58,59,60].


(see Table 5 for different dosing options). Treatment should lower thepotassium level by about 0.5 to 1.2 mmol/L in 1 hour [6,7,40]. If glucoselevels are below about 250 to 300, then glucose should also be administerdwith the insulin to prevent hypoglycemia (typical 50 mL of 50% glucose; 1ampule or 25 g). Hypoglycemia occurs in 11% to 75% of normoglycemicpatients, in 30 to 60 minutes, if they are given less than 25 g of glucose [7,40].In all patients treated with insulin, close glucose monitoring and ifnecessary, infusion of 10% dextrose at 50 mL/h or repeat dextrose bolusesshould be given as needed [7,40].

Beta-2 agonistAnother possible treatment to shift potassium intracellularly is IV or

nebulized beta-2 agonists. The nebulized dose is 10 to 20 mg in 4 mL ofsaline, which is higher that the typical 2.5 to 10 mg every 1 to 4 hoursrecommended for acute bronchospasm (see Table 5). Side effects may includetachycardia or possible development of angina in susceptible patients [7,38].

Bicarbonate

Another historically suggested treatment is sodium bicarbonate. How-ever, the routine use of sodium bicarbonate is controversial, and has fallenout of favor for several reasons [3,6,7,11,40,61]. First, bicarbonate is mosteffective in the clinically uncommon condition of nonanion gap metabolicacidosis [6]. Bicarbonate is less effective in organic metabolic acidosis (ie,lactic and ketoacidosis) and in patients with renal failure (which is one of themost common causes of hyperkalemia) [6]. Second, bicarbonate willprecipitate with calcium if given in the same line. Finally, patients couldreceive a large amount of sodium, a concern in heart failure and renal failurepatients [7]. In Ahee and Crowe’s [42] review of the efficacy of varioustreatments for hyperkalemia, they cited four studies showing no reduction inserum potassium within 60 minutes after sodium bicarbonate treatment. Soit seems, in the most ‘‘clinically common’’ cases of hyperkalemia, thereappears to be little or no value in routinely adding sodium bicarbonate, andthis treatment should be reserved for selective cases of nonanion gapmetabolic acidosis [2,7,11,40,61].

It must be remembered that these steps to shift potassium to theintracellular space are also only temporary measures. Most cases ofhyperkalemia are caused by a total body potassium excess and this excesspotassium must be removed.

Enhancing clearance

Sodium polystyrene sulfonate (Kayexalate)Sodium polystyrene sulfonate (Kayexalate) is an exchange resin that

works across the gastrointestinal mucosa [7,38]. Each gram of resin will


remove about 1 mEq of potassium by exchanging it with about 2 mEq ofsodium [3,4,7,38,62]. This can be give orally or as a retention enema (seeTable 5 for dosing). The oral dose can be repeated every 2 to 4 hours and therectal dose every 1 to 2 hours [4,7,38,62]. This treatment may cause sodiumretention, edema, and exacerbation of congestive heart failure in patientswith severe cardiac dysfunction.

DiureticsLoop (eg, furosemide [Lasix] and bumetanide [Bumex]) and thiazide

diuretics can be used to increase renal tubular flow and potassiumelimination. However, the patient must have an adequately functioningkidney, and this is obviously a limiting factor for patients with chronic renalfailure. In other patients (particularly those with hyporeninemic hypo-aldosteronism) this is an effective additional treatment [7].

HemodialysisFinally, the most definitive and effective method of rapidly lowering the

serum potassium is hemodialysis, which can lower levels by as much as1.2 to 1.5 mEq/h [5,7,38,40]. This is indicated in patients when the abovetreatments are ineffective or in cases of severe rapidly rising serumpotassium levels. Because hemodialysis only affects the extracellularcomponent, small amounts of the total body potassium content may beremoved and rebound hyperkalemia may occur in 1 to 2 hours [4,7].

Addressing underlying cause

Finally, treating the underlying conditions, changing medications oraltering diets may be indicated. If the cause is not apparent, furtherevaluation for worsening renal function, determining renin and aldosteronelevels, checking cortisol levels, calculating the transtubular potassiumgradient, and so on, are indicated [57].

Summary

Regarding hyperkalemia, several closing comments are offered. First, inthe area of causation, the majority of patients that develop hyperkalemiahave some underlying renal dysfunction. Medications are frequentlyassociated with the development of acute hyperkalemia, especially inpatients predisposed by age, medical condition, other medication use, orkidney disorders.

Next in the area of diagnosis, the ‘‘classic’’ ECG changes in a patient withhyperkalemia indicate need for emergent treatment but the ECG by itself isnot a consistent predictor of the presence or severity of hyperkalemia.

Finally, in the area of treatment, rapidly rising levels are more seriousthan slowing rising levels, and the most consistent response to treatment, in


all types of patients, is with insulin and glucose. Remember to monitor forhypoglycemia. Routine bicarbonate therapy is not indicated, and should bereserved for patients with nonanion metabolic acidosis. Finally, inhaledalbuterol is perhaps an underused treatment.

Hypokalemia and hyperkalemia are frequently encountered in the EDand are the result of disturbances in potassium intake, potassium secretion,and transcellular shifts. An understanding of these disturbances ishelpful, and guides appropriate management and prevention of significantmorbidity and even death. Presenting symptoms tend to be vague, andgenerally affect the cardiac, neuromuscular, and gastrointestinal systems.

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