Diseases of Potassium
Does this patient have potassium disorder?
What tests to perform?
- How should patients with hyper- or hypokalemia be managed?
- What happens to patients with hyper- or hypokalemia?
- How to utilize team care?
Are there clinical practice guidelines to inform decision making?
- Other considerations
What is the evidence?
Does this patient have potassium disorder?
Disorders of potassium balance are classically identified by abnormalities in the serum or plasma potassium concentration. The normal range for the plasma potassium concentration is typically from low levels of ~3.5 mEq/L to upper levels of ~5.5 mEq/L.
It is important when evaluating a plasma potassium measurement to ensure that artifacts that alter the measurement of the serum or plasma potassium have not developed.
The most common artifact is hemolysis, which results in an artificially elevated measurement. The potassium concentration inside erythrocytes is substantially greater, and damage to even a small percentage of erythrocytes can release sufficient intracellular potassium to significantly alter and increase extracellular potassium. If this is not recognized, then inappropriate and potentially dangerous treatments may be instituted incorrectly.
Less common artifacts are related to either leukocytosis, particularly when associated with leukemia, or severe thrombocytosis, particularly if the platelet concentration is greater than 500,000.
What tests to perform?
The first test to perform in evaluating for a potassium disorder is to measure the extracellular potassium concentration. These typically done using either a serum or plasma specimen. With rare exceptions, the result should be interchangeable.
If the resultant concentration is elevated, then evaluating whether this is an artifact is important. Artifact-induced elevations in the potassium concentration are termed pseudo-hyperkalemia. Because pseudo-hyperkalemia is only an artifact, the patient does not need to be treated. Instead, avoiding inappropriate treatment becomes the "appropriate treatment."
Hemolysis is the most common cause of artifact-induced etiologies of apparent hyperkalemia. The laboratory report should he specifically evaluated for report of hemolysis.
If any hemolysis is present, then the sample is essentially uninterpretable with regards to the serum potassium concentration. A new sample should be obtained for measurement of the potassium concentration.
Severe thrombocytosis, particularly if the platelet count is greater than 500 x 109/L, can cause pseudohyperkalemia. This occurs as a result of potassium release from platelets during the clotting process. Consequently, it is only observed in serum potassium measurements. In the patient with thrombocytosis and hyperkalemia, the use only of plasma potassium measurements avoids this cause of pseudo-hyperkalemia.
We recommend routine assessment of the plasma, rather than serum, potassium concentration in patients with a platelet count greater than 500 x 109/L. Unfortunately, inter-patient variations in the correlation between platelet count and severity of pseudo-hyperkalemia make derivations of formula to "correct" for the severity of thrombocytosis sufficiently inaccurate to preclude their clinical use.
Severe leukocytosis, typically with white cell count greater than 100 x 109/L, and typically found in association with either acute or chronic leukemia, can lead to pseudo-hyperkalemia. This may occur either during the clotting process, with the release of potassium from the abnormal white blood cells It may also result from leakage of potassium from the white blood cells if there is a prolonged period of storage of this sample prior to the laboratory's measurement of the potassium concentration. This may occur particularly in plasma samples. Rapidly measuring the plasma potassium concentration after this sample is obtained may be essential to avoiding pseudo-hyperkalemia in this condition.
Another etiology that has been identified is mechanical trauma to leukemic white blood cells from pneumatic tube transport of the specimen. Because of the increased fragility of white blood cells in patients with acute leukemia, specific care of the handling of the specimen may be necessary to avoid this.
If the patient clinches their fist during the time when the blood is being drawn, local release of potassium from the contracting skeletal muscle cells may result in inappropriate elevation of the potassium concentration in the specimen. Patients and phlebotomists should be counseled to avoid fist clinching during the phlebotomy procedure.
The most critical side effect of hyperkalemia is the development of cardiac arrhythmias, which may include ventricular fibrillation and subsequent sudden cardiac death. The electrocardiogram (ECG) can be very helpful in identifying cardiac effects of hyperkalemia. These effects include development of peaked T waves, widening of the QRS complex, prolongation of the PR interval, development of a junctional rhythm, development of a "sine wave" electrocardiogram pattern and development of ventricular fibrillation.
Progression of the cardiac effects from peaked T waves to ventricular fibrillation may be unpredictable. Patients with any of these cardiac manifestations, if confirmed to be new and not present on previous electrocardiograms, may need emergent treatment.
Acute changes in the potassium concentration may result from transcellular shifts; ie,, changes in the distribution of intracellular and extracellular potassium. Under normal circumstances, more than 98% of total body potassium is present in intracellular compartment. Changes in the transcellular distribution can result in substantial changes in extracellular potassium concentration.
Medications associated with stimulation of cellular potassium uptake, and thus in the development of acute hypokalemia, include ß-adrenergic agonists and the aminophylline and theophylline. Medications that decrease cellular potassium uptake and can result in redistribution-induced hyperkalemia include digoxin and ß-adrenergic antagonists.
Hyperosmolarity, if due to osmotically active solutes, such as mannitol or glucose in a patient with diabetes mellitus, result in transcellular potassium shifts from the intracellular to the extracellular fluid compartments and the development of hyperkalemia. Recognizing that transcellular potassium shifts are responsible for the abnormal potassium concentration is critical for appropriate management. Discontinuing the responsible medication or correcting the underlying condition will result in normalization of the potassium concentration.
How should patients with hyper- or hypokalemia be managed?
Management of the patient with hyperkalemia
The first step in the management of a patient with hyperkalemia is to exclude hemolysis as the etiology of. If the specimen is hemolyzed, then a fresh specimen should be obtained for repeat potassium concentration measurement. Clinical decisions should, in general, not be made based upon potassium concentration measurements from hemolyzed specimens.
Next, it is important to determine whether there are potentially life-threatening clinical manifestations. This refers to cardiac effects, which are evaluated in the ECG. Typically they are observed only in patients with potassium concentrations greater than 6.0 mmol per liter. These patients may require an emergency ECG.
If any of these electrocardiographic manifestations of severe hyperkalemia are present, the patient should undergo emergency treatment in either an emergency department or an intensive care unit and should have continuous electrocardiographic monitoring. The medications used for treatment of hyperkalemia, their time of onset and duration of action are detailed below.
At the same time, one should evaluate the possibility of pseudo-hyperkalemia. The possibility of pseudo-hyperkalemia resulting from either thrombocytosis or leukocytosis is discussed above. Another cause of pseudo-hyperkalemia is abnormally fragile red blood cell membranes, resulting in potassium leakage during the clotting process in serum samples. This can be identified by measuring the potassium concentration in simultaneous serum and plasma samples. Normally these values should be within 0.3 mmol per liter of each other. If the serum sample is substantially greater than the plasma sample, then pseudo-hyperkalemia can be diagnosed, and future clinical decisions should be based solely upon a plasma potassium concentration measurement.
Clinically significant chronic hyperkalemia is almost always associated with the presence of either chronic kidney disease or the use of medications that impair renal potassium excretion. In the absence of either chronic kidney disease or the use of these medications, the diagnosis of chronic hyperkalemia may need to be questioned, and specific testing for pseudo-hyperkalemia undertaken.
Medications that can cause hyperkalemia and their mechanism by which they do so are listed below:
Ace inhibitor: Inhibition of angiotensin II and aldosterone formation
Angiotensin receptor blocker (ARB): Inhibition of angiotensin II action, which decreases aldosterone formation
Beta-adrenergic receptor antagonist : Inhibition of renin release, which decreases angiotensin II and aldosterone formation
Heparin: Inhibition of aldosterone formation)
Mineralocorticoid receptor antagonists: Inhibition of aldosterone-stimulated renal potassium excretion
Digoxin and other digitalis glycosides: Inhibition of renal potassium excretion; inhibition of cellular potassium uptake, which results in the transcellular potassium shift from intracellular to extracellular fluids
Potassium sparing diuretics (amiloride and triamterene): Inhibition of renal potassium excretion
Trimethoprim :Inhibition of renal potassium excretion (has analogous functions as amiloride in the kidney)
Calcineurin inhibitors (cyclosporine and tacrolimus): Inhibition of renal potassium excretion
Nonsteroidal anti-inflammatory drugs and Cox-2 inhibitors: Inhibition of renal potassium excretion
Long-term therapy in the patient with hyperkalemia may require reconsideration of the necessity for any medication which the patient is taking which can cause hyperkalemia. However, because of the important benefits of ace inhibitors, ARBs and beta blockers on cardiovascular mortality, identification of treatment regimens for hyperkalemia which avoid discontinuing these medications is important.
Treatments for hyperkalemia include immediate, short-term, intermediate and long-term treatment approaches. Different treatment options, including their time of onset, duration of action and mechanism are listed below.
Calcium gluconate, intravenous
Time of onset: seconds
Duration of action: 20-60 minutes
Mechanism of action: inhibition of cardiac effects of hyperkalemia
Insulin (10 units intravenous), with intravenous glucose
Time of onset:10-30 minutes
Duration of action: 4-6 hours
Mechanism of action: insulin-stimulated increase in cellular potassium uptake
Comment: temporizing measure only, because does not result in potassium removal from the body, and cellular potassium leak will result in recurrence of hyperkalemia after insulin bolus is cleared by normal metabolic pathways
Inhaled beta-2-adrenergic agonist (nebulized albuterol, 10 mg)
Time of onset: 10-30 minutes
Duration of action: 2-4 hours
Mechanism of action: beta-2-adrenergic receptor activation stimulates cellular potassium uptake
Comment: similar to insulin, this is only a temporary scene measure. It does not result in potassium removal from the body. Accordingly, cellular potassium leak will result in recurrence of hyperkalemia after the agonist is cleared by normal metabolic mechanisms
Sodium bicarbonate administration
Comment: not routinely recommended for the short-term management patient with hyperkalemia because the changes in serum potassium with intravenous bicarbonate administration are small and inconsistent.
In patients with hyperkalemia, metabolic acidosis and intravenous volume depletion, rehydration with 5% dextrose solutions with the addition of 150 millimolar per liter sodium bicarbonate (3 ampules of sodium bicarbonate in 1 L D5W ) may be a preferable solution for rehydration rather than normal saline solutions.
Sodium polystyrene sulfonate (Kayexalate, 30-60 gram, in 20% sorbitol given orally or 60 g without sorbitol given as a retention enema)
Time of onset: 1-2 hours (longer if an ileus is is present, because therapeutic action requires presence in the colon for its effect)
Time to maximal action: 4-6 hours
Comment: results in potassium removal. Accordingly, a repent increase in the serum potassium following administration should not be expected.
Comment: several case reports have suggested an association of intestinal necrosis with use of this medication, but the actual incidence is unknown. If given as an enema, sorbitol administration should be avoided as sorbitol administration increases the risk of intestinal necrosis in experimental models.
Diuretics (both "loop" and thiazide diuretics)
Time of onset: 1-2 hours
Time to maximal action: 4-12 hours
Comment: effectiveness use is proportional to the extent of renal function that is present. Since most patients with hyperkalemia have chronic kidney disease, they are are generally not a component of the short-term management of patients with clinically significant acute hyperkalemia.
In long-term management, diuretics can be effective in patients with chronic kidney disease and hyperkalemia because of direct stimulation of renal potassium excretion. Thiazide diuretics, when dosed to equivalent effects on sodium excretion, have a greater ability to increase renal potassium excretion and the loop diuretics.
Time of onset: dependent on time to initiation of dialysis
Time to maximal action: maximal effect typically present at termination of dialysis procedure
Comment: delay in the ability to initiate the hemodialysis procedure is often significant, and relates to the necessity placement of a hemodialysis catheter, vascular access is not already present, and time to prepare hemodialysis machine for the procedure.
Dietary potassium restriction
Chronic hyperkalemia is often associated with both chronic kidney disease and with excessive dietary potassium intake. Consultation with a trained dietitian to identify the food products which the patient is ingesting with high potassium content and to identify substitute foods is often helpful.
Both "loop" (eg, furosemide and bumetanide) and thiazide diuretics increase renal potassium excretion. These medications are often useful in the patient with chronic kidney disease and hyperkalemia is hypertension because that they are benefits on both volume, hypertension and potassium management. When dosed for equivalent effects on sodium excretion, thiazide diuretics stimulate a greater increase in renal potassium excretion than do loop diuretics. Metolazone is a thiazide diuretic with persistent effects on renal sodium and potassium excretion even when GFR is less than 30 mL per minute per 1.73 m².
Medications which can induce hyperkalemia are listed above. Approximately 85% of patients with hyperkalemia or receiving one or more medications associated with the development of hyperkalemia. Appropriate reevaluation of the necessity of each medication is appropriate. However, given the important effects of ace inhibitor, ARB's and beta blockers and cardiovascular mortality, these medications should, in general, not be routinely discontinued, and other approaches to controlling hyperkalemia should be pursued.
How should the patient with hypokalemia be managed?
A critical issue in the management of the patient hypokalemia is to recognize that there is a substantial difference in me a cute risk between intravenous and oral potassium replacement. With `intravenous potassium replacement, there is a significant risk of excessively fast replacement, resulting in acute hyperkalemia with subsequent acute cardiac toxicity. With oral replacement, cellular uptake of potassium is more rapid, and there is almost no risk of excessively rapid replacement. Accordingly, oral replacement is preferred if the patient can take oral medications and there is intact intestinal absorption. In patients with an ileus or intestinal obstruction, inconsistent and/or unreliable intestinal absorption may preclude oral treatment and necessitate intravenous potassium replacement.
The major short-term risk of hypokalemia is increased cardiac susceptibility to arrhythmias. The presence of sustained ventricular arrhythmias, in particular, indicates a need for rapid potassium replacement. In patients with hypokalemic periodic paralysis, potassium replacement may be necessary to avoid respiratory compromise. Otherwise, although hypokalemia can cause muscular weakness, it generally does not cause respiratory failure.
When evaluating a patient with hypokalemia, it is important to identify whether the hypokalemia represents true total body potassium depletion or whether this is a result of transcellular shifts of potassium from the extracellular to the intracellular fluid compartments. The latter typically results with correction of the cause initiating the transcellular shifts, often catecholamine excess, whether exogenous or endogenous, intravenous insulin administration in the treatment of hyperglycemia, and administration of either aminophylline or theophylline in the treatment of asthma and reactive airway disease.
The total body deficit of potassium is often substantially greater than appreciated. Because of concentration of potassium inside cells, the effective "volume of distribution" for potassium is greater than plasma water volume, total extracellular fluid volume and even total body water volume. A serum potassium of 3.0 mmol/liter often indicates a total body potassium deficit of 100 mmol, 2.5 mmol per liter potassium indicates often they deficit of 200-300 mmol, and a serum potassium of 2.0 mmol/liter or less may indicate a potassium deficit of 500 mmol or more.
Potassium replacement should be given typically as potassium chloride. It may be given either through the intravenous or oral administration routes.
Intravenous potassium chloride is most commonly given at a rate of 10 mmol per hour. Under rare conditions, it can be given safely at a rate of 20 mmol per hour. In emergency conditions, where there are either ongoing ventricular arrhythmias or there is severe hypokalemia, typically less than 2.5 mmol per liter, and there is a need for emergency surgery, where the risk for ventricular arrhythmias is increased, potassium chloride may be administered at a rate of as high as 40 mmol per hour. Under these conditions, the patient should be in an intensive care unit and have continuous electrocardiographic monitoring in order to assess for hyperkalemic-cardiac toxicity.
Intravenous potassium chloride should not be given in dextrose containing solutions. The dextrose in the solution can stimulate insulin release, which can then stimulate insulin-mediated cellular potassium uptake, and results in paradoxical worsening of the hypokalemia.
Oral potassium chloride may be typically administered at doses of 40 mmol per dose, with doses repeated every 2 to 4 hours. With acute release potassium chloride, there is a risk of gastric irritation with repeated high doses.
Depending on the severity of the hypokalemia and the significance of clinical side effects associated with it, repeat measurement of the serum or plasma potassium should occur as often as every 4-12 hours, as needed.
Chronic hypokalemia is typically associated with some combination of poor dietary potassium intake, diuretic administration and either primary or secondary hyperaldosteronism. Under rare circumstances, hypokalemia is associated with genetic etiologies, and in these occasions is typically associated with either low or refractory high blood pressure.
Diets low in potassium typically have a high sodium content. The high sodium content worsens the hypokalemia by worsening renal potassium losses. Either restriction of dietary sodium or increasing potassium can improve the hypokalemia.
Both "loop" and thiazide diuretics significantly increase renal potassium excretion. Hypokalemia is common with both classes have diuretics. Management may involve either instructions in dietary changes to increase potassium intake or addition of a potassium-sparing diuretic, commonly either amiloride or triamterene, two the diuretic regimen. Combination diuretics including a potassium-sparing diuretic in the single pill are widely available.
Hyperaldosteronism, whether primary or secondary, is often present in patients with hypokalemia. In the patient with hypokalemia and hypertension, particularly if the hypokalemia is present in the absence of diuretics or is severe, consideration and evaluation of the possibility of either primary hyperaldosteronism or renovascular hypertension may assist in the management of the patient.
Refractory or difficult to treat hypokalemia in either children or young adults should suggest the possibility of a genetic defect in proteins involved in renal ion transport. These are often associated either with significant hypotension, particularly if occurring in children, relatively low blood pressure, when occurring in young adults, or refractory and difficult to control hypertension in adults.
Bartter syndrome is a condition due to genetic defects in proteins involved in ion transport in the thick ascending limb of the loop of Henle. This typically present with refractory hypokalemia in a child, teenager or young adult, low blood pressure and, if measured, increased urinary calcium excretion.
Gittleman syndrome results from genetic defects in ion transport proteins expressed in the distal convoluted tubule. It is associated with similar manifestations as Bartter syndrome, with the exception that they are typically milder and present a little bit later in life, and urinary calcium excretion is suppressed, rather than elevated.
Both Bartter and Gittleman syndrome have similar clinical manifestations as loop diuretic and thiazide diuretic administration, respectively. When managing patients with suspected Bartter or Gittleman syndrome, it is critical to exclude surreptitious diuretic usage by evaluating urine samples for the presence of diuretics.
Hypokalemia associated with hypertension, particularly if the hypertension is refractory or difficult to control, can result from either Liddle syndrome or primary hyperaldosteronism. These two conditions can be differentiated by measurement of the plasma aldosterone and plasma renin activity. With Liddle syndrome, both measurements are suppressed both normal level of the assay used. With primary hyperaldosteronism, plasma renin activity is suppressed, but the plasma aldosterone level is either elevated or in the middle portion of the "normal" range.
Liddle syndrome is treated with specific antagonists of the epithelial sodium channel is regulation is abnormal due to genetic abnormalities. The most commonly used medication is amiloride, and triamterene is generally reserved for patients unable to tolerate amiloride because of side effects.
Primary hyperaldosteronism is treated with either mineralocorticoid receptor antagonists or adrenalectomy, depending on whether the patient has bilateral adrenal hyperplasia or an aldosterone producing adenoma. Evaluation and management of primary hyperaldosteronism is discussed in detail in other chapters.
What happens to patients with hyper- or hypokalemia?
Complications associated with hyperkalemia
The most important side effect associated with hyperkalemia is cardiac toxicity and development of ventricular arrhythmias. These have been discussed in detail above. Chronic hyperkalemia can impair renal acid excretion and resulted in mild metabolic acidosis. This is particularly common in patients with chronic kidney disease.
The coexistence of diabetes mellitus with chronic kidney disease increases the likelihood of hyperkalemia and secondary metabolic acidosis. This combination of hyperkalemia and secondary metabolic acidosis is often termed "Type IV renal tubular acidosis" or "hyperkalemic renal tubular acidosis." In most cases, treating the hyperkalemia causes resolution of the metabolic acidosis.
Hyperkalernia also affects other cells throughout the body. Skeletal muscles are sensitive to hyperkalemia, resulting in increased weakness and fatigue. Smooth muscles are also sensitive to hyperkalernia. Hyperkalemia has been reported to cause severe respiratory depression.
Complications resulting from hypokalemia
Increased myocardial susceptibility to arrhythmias, both atrial and ventricular.
Impaired glucose tolerance, which may result in either new onset or worsening of previously existing diabetes mellitus.
Either the development of new hypertension or the worsening of control of existing hypertension.
Increased urine volume, particularly of dilute urine.
Muscle weakness, particularly of skeletal muscles.
How to utilize team care?
Chronic hyperkalemia and hypokalemia almost always involve abnormalities in renal potassium handling. Involvement of a nephrologist in the evaluation may be helpful, particularly appears the coexistence of either abnormal blood pressure control or the presence of chronic kidney disease.
Nurses have an important role in the management and care of the patient with hyper and hypokalemia. It is important to ensure that replacement doses of potassium given to the patient with hypokalemia and are not given at excessive rates. Medications used for the treatment of hyperkalemia may have only transient effects. It is important that the nurses involved in the management of these patients are aware of of these medications, and know the time of onset and duration of action of these medications.
Pharmacists may be very helpful in the management of patients with hypokalemia and hyperkalemia because of the very frequent association of medications with the generation of both hypokalemia and hyperkalemia. In the patient with hyperkalemia, careful consideration must be given to the risks and benefits of each of the medications used that can be associated with hyperkalemia. In particular, because of the important effects of ACE inhibitors, angiotensin receptor blockers (ARBs), and beta blockers in decreasing cardiovascular mortality. In general, these medications should not be routinely discontinued, but other measures to control the potassium concentration should be utilized.
Dieticians play an important role in the management of patients with chronic potassium disorders. Patients with hypokalemia need instruction in foods higher in potassium content, and often in foods lower in sodium content. Patients with hyperkalemia need careful consultation and recommendations regarding how to avoid foods high in potassium.
Are there clinical practice guidelines to inform decision making?
Typical lengths of stay
Isolated hypokalemia and hyperkalemia can often be treated effectively within 24 hours. Severe hypokalemia may require 48-72 hours if the total body potassium deficit is very high.
What is the evidence?
Lehnhardt, A, Kemper, MJ. "Pathogenesis, diagnosis and management of hyperkalemia". Pediatr Nephrol. vol. 26. 2011. pp. 377-384.
Elliott, MJ, Ronksley, PE, Clase, CM, Ahmed, SB, Hemmelgarn, BR. "Management of patients with acute hyperkalemia". CMAJ. vol. 182. 2010. pp. 1631-1635.
Desai, AS. "Hyperkalemia in patients with heart failure: incidence, prevalence, and management". Curr Heart Fail Rep. vol. 6. 2009. pp. 272-280.
Nyirenda, MJ, Tang, JI, Padfield, PL, Seckl, JR. "Hyperkalaemia". Br Med Jour. vol. 339. 2009. pp. b4114.
Khanna, A, White, WB. "The management of hyperkalemia in patients with cardiovascular disease". Am J Med. vol. 122. 2009. pp. 215-221.
Weisberg, LS. "Management of severe hyperkalemia". Crit Care Med. vol. 36. 2008. pp. 3246-3251.
Unwin, RJ, Luft, FC, Shirley, DG. "Pathophysiology and management of hypokalemia: a clinical perspective". Nat Rev Nephrol. vol. 7. 2011. pp. 75-84.
Ben, SC, Hmouda, H, Bouraoui, K. "Drug-induced hypokalaemia". Curr Drug Saf. vol. 4. 2009. pp. 55-61.
Lin, SH, Halperin, ML. "Hypokalemia: a practical approach to diagnosis and its genetic basis". Curr Med Chem. vol. 14. 2007. pp. 1551-1565.
Weiner, ID, Linus, S, Wingo, CS, Johnson, RJ, Fluege, J, Feehally, J. "Disorders of potassium metabolism". Comprehensive Clinical Nephrology. Saunders. 2010. pp. 118-129.
Weiner, ID, Wingo, CS, DuBose, TD, Hamm, LL. "Hyperkalemia". Acid-base and electrolyte disorders: A companion to Brenner & Rector's The Kidney. Saunders. 2002. pp. 395-412.
Wingo, CS, Weiner, ID, Brenner, BM. "Disorders of potassium balance". The Kidney. W.B. Sauders Co.. 2002. pp. 998-1036.
Weiner, ID, Wingo, CS. "Hyperkalemia: a potential silent killer". J Am Soc Nephrol. vol. 9. 1998. pp. 1535-1543.
Weiner, ID, Wingo, CS. "Hypokalemia - consequences, causes and correction". J Am Soc Nephrol. vol. 8. 1997. pp. 1179-1188.
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