Management of hypokalemia

Introduction

Hypokalemia – defined by a serum potassium level of < 3.5 mEq/liter – is one of the most commonly encountered electrolyte abnormalities in clinical medicine.^1-4Weiner ID, Wingo CS. Hypokalemia–consequences, causes, and correction. J Am Soc Nephrol. 1997 Jul;8(7):1179-88.
Vavruk AM, Martins C, Nascimento MM, et al. Association between hypokalemia, malnutrition and mortality in peritoneal dialysis patients. J Bras Nefrol. 2012;34(4):349-54.
Lam MH, Chau SW, Wing YK. High prevalence of hypokalemia in acute psychiatric inpatients. Gen Hosp Psychiatry. 2009 May-Jun;31(3):262-5.
Andrew ME, Jones DW, Wofford MR, Wyatt SB, Schreiner PJ, Brown CA, Young DB, Taylor HA. Ethnicity and unprovoked hypokalemia in the Atherosclerosis Risk in Communities Study. Am J Hypertens. 2002 Jul;15(7 Pt 1):594-9.   The disorder may be present as a chronic condition, or may manifest acutely. Chronic hypokalemia is generally attributable to decreased potassium intake and/or increased loss (gastrointestinal or renal). In contrast, acute hypokalemia results from rapid loss of extracellular K+, either because of transcellular shift of K+ into the cells, or from rapid extracorporeal losses, which occur through gastrointestinal or renal routes.⁵Hypokalemia. Clinical key, Elsevier. Available at: https://www.clinicalkey.com/topics/%20nephrology/hypokalemia.html. [Accessed on 14 /08/2013].  

Causes of hypokalemia

Hypokalemia in clinical practice can be an asymptomatic finding identified only on routine electrolyte screening, or can be a manifestation of multiple clinical conditions. Figure 1 depicts number of possible etiologies of hypokalemia.^5-9Hypokalemia. Clinical key, Elsevier. Available at: https://www.clinicalkey.com/topics/%20nephrology/hypokalemia.html. [Accessed on 14 /08/2013].
Hypokalemia. Available at: http://umm.edu/Health/Medical/Ency/Articles/Hypokalemia [Accessed on 5/08/2013].
Ben Salem C, Hmouda H, Bouraoui K. Drug-induced hypokalemia. Curr Drug Saf. 2009 Jan;4(1):55-61.
Ng JL, Morgan DJ, Loh NK, et al. Life-threatening hypokalemia associated with ibuprofen-induced renal tubular acidosis. Med J Aust. 2011 Mar 21;194(6):313-6.
Siau K. Hypokalemia and cardiac arrest complicating vancomycin and furosemide therapy: a case report. Cases J. 2009;2:8244.   Diarrhea and/or vomiting, diuretic therapy, nutritional causes constitute most of the cases of hypokalemia.¹⁰Reid A, Jones G, Isles C. Hypokalemia: common things occur commonly – a retrospective survey. JRSM Short Rep. 2012 Nov;3(11):80.  

Consequences of hypokalemia

Hypokalemia can alter the function of several organs, ultimately determining the associated morbidity and mortality that is related to both the potassium deficiency and the underlying disease state. The

organ systems affected most prominently include the cardiovascular system, neurologic system, muscles, and kidneys (Table 1).¹Weiner ID, Wingo CS. Hypokalemia–consequences, causes, and correction. J Am Soc Nephrol. 1997 Jul;8(7):1179-88.   Clinical manifestations are thus dependent on the extent of hypokalemia, and include generalized muscle weakness, paralytic ileus, and cardiac arrhythmias (atrial tachycardia with or without block, atrioventricular dissociation, ventricular tachycardia, and ventricular fibrillation). Typical electrocardiographic (ECG) changes include flat or inverted T waves, ST-segment depression, and prominent U waves.¹¹Cohn JN, Kowey PR, Whelton PK, Prisant LM. New Guidelines for Potassium Replacement in Clinical Practice. A Contemporary Review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000;160:2429-2436.   In cases of severe untreated hypokalemia, myopathy may progress to rhabdomyolysis, myoglobinuria, and acute renal failure (ARF), and life-threatening paralysis. Particularly, elderly patients are at a higher risk of severe consequences.

Prevalence and classification of hypokalemia

The reported prevalence of hypokalemia varies from 3.5% to 23%, which may be dependent on not only the patents characteristics but also clinical settings. Generally, hypokalemia is more common in hospitalized patients (∼15%) than in outpatients (∼3%). Elderly patients are particularly at risk because of poor dietary intake of potassium and/or use of diuretics.⁵Hypokalemia. Clinical key, Elsevier. Available at: https://www.clinicalkey.com/topics/%20nephrology/hypokalemia.html. [Accessed on 14 /08/2013].   As well, hypertensive patients taking thiazide diuretic have been found to have low serum potassium concentration, showing higher prevalence of hypokalemia.¹²Toner JM, Ramsay LE. Thiazide-induced hypokalemia; prevalence higher in women. Br J Clin Pharmacol. 1984;18(3):449-52.  

Clinical hypokalemia

Hypokalemia is clinically defined as a plasma potassium concentration <3.5 mEq/L.7 However, as serum potassium concentration does not always reflect total body potassium, hypokalemia can coexist with both normal and low total body potassium

(Table 2).¹³Rastegar A. EditorsIn: Walker HK, Hall WD, Hurst JW, editors. Serum potassium. Clinical methods: The history, physical, and laboratory examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 195. http://www.ncbi.nlm.nih.gov/pubmed/21250149   Dependent on the origin; hypokalemia associated with low total body potassium can either be due to poor dietary K⁺ intake or increased potassium loss, the latter being more common.14 The broad groups of etiologies for hypokalemia include: redistribution, extra-renal potassium loss, and renal potassium loss (Figure 1).

Redistribution

As more than 98% of total body potassium is present within the cells, mainly the skeletal muscle cells, small changes in potassium distribution can produce marked alteration in the extracellular concentration. Normal levels of serum potassium levels span over a narrow range (3.5 to 5.5 mEq/L); therefore, a minor absolute deviation in this narrow range can result in significant changes in the ratio of intra and extracellular potassium. Certain hormones, particularly insulin, aldosterone, and sympathomimetics, are the most common cause of redistribution-induced hypokalemia. In addition, hypokalemia because of potassium redistribution can also occur from acute anabolic states.¹Weiner ID, Wingo CS. Hypokalemia–consequences, causes, and correction. J Am Soc Nephrol. 1997 Jul;8(7):1179-88.  

Non-renal potassium loss

In normal conditions, net fluid and potassium loss from skin and the gastrointestinal tract is small. However, conditions such as prolonged exertion in hot and dry environments or chronic diarrhea can result in severe potassium loss, leading to hypokalemia. Most of these cases also present with intravascular volume depletion, leading to secondary hyperaldosteronism, stimulation of renal potassium excretion, and further worsening of the potassium deficit.¹Weiner ID, Wingo CS. Hypokalemia–consequences, causes, and correction. J Am Soc Nephrol. 1997 Jul;8(7):1179-88.  

Prolonged loss of gastric contents from vomiting can also lead to hypokalemia. Herein, besides direct potassium depletion due to fluid loss, the concomitant metabolic alkalosis increases renal potassium excretion by increasing potassium secretion and probably by direct suppression of potassium reabsorption. As well, there is worsening of intravascular volume depletion. Similarly, diarrhea, whether secretory or because of laxative abuse, can also cause profound gastrointestinal potassium loss.

Renal potassium loss

The most common cause of hypokalemia is excess loss of potassium through renal route. This can occur because of a number of conditions, both intrinsic and extrinsic to the kidneys (Figure 1).

Drug induced hypokalemia

Drug induced hypokalemia may be asymptomatic or symptomatic, which may be life threatening.⁷Ben Salem C, Hmouda H, Bouraoui K. Drug-induced hypokalemia. Curr Drug Saf. 2009 Jan;4(1):55-61.  ^–9Siau K. Hypokalemia and cardiac arrest complicating vancomycin and furosemide therapy: a case report. Cases J. 2009;2:8244.   Diuretic medications increase sodium delivery to the collecting ducts, where it is reabsorbed, and therefore create a favourable gradient for potassium secretion via potassium channels. Medications such as sympathomimetics (brochodilators such as salbuterol) or phosphodiesterase inhibitors (theophylline and caffeine), exogenous insulin, and rarely calcium channel blockers, can also cause hypokalemia.¹⁴Rastegar A, Soleimani M. Hypokalemia and hyperkalaemia. Postgrad Med J. 2001 Dec;77(914):759-64.   Taking large doses of laxatives can also cause hypokalemia because of increased loss of K⁺ in the stool.

In effect, metabolic implications of potassium homeostasis identify drug-induced hypokalemia as an important problem particularly in the elderly and in patients with cardiovascular, renal or hepatic disease. These conditions qualify patients as vulnerable population to hypokalemia as the therapeutic index of most drugs is narrowed.

Understanding potassium homeostasis

Serum potassium is normally maintained within a narrow defined range through an exquisite balance between cellular K⁺ influx and efflux, and between the intake and excretion of potassium from the body (Figure 2).¹⁰Reid A, Jones G, Isles C. Hypokalemia: common things occur commonly – a retrospective survey. JRSM Short Rep. 2012 Nov;3(11):80.   Such balances are determined by cell membrane molecules, which affect K⁺ transfer from one milieu to another.¹⁵ Antes LM, Kujubu DA, Fernandez PC. Hypokalemia and the pathology of ion transport molecules. Seminars in Nephrology 1998;18(1):31-45.   The high concentration difference is maintained by Na-K-ATPase enzyme that actively pumps potassium into the cell while moving sodium out of the cell.

A number of factors may affect the internal regulation of potassium through changes in transcellular distribution of potassium (Figure 2; Table 3).¹⁰Reid A, Jones G, Isles C. Hypokalemia: common things occur commonly – a retrospective survey. JRSM Short Rep. 2012 Nov;3(11):80.   ¹³Rastegar A. EditorsIn: Walker HK, Hall WD, Hurst JW, editors. Serum potassium. Clinical methods: The history, physical, and laboratory examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 195. http://www.ncbi.nlm.nih.gov/pubmed/21250149   ¹⁴Rastegar A, Soleimani M. Hypokalemia and hyperkalaemia. Postgrad Med J. 2001 Dec;77(914):759-64.   The ratio of intracellular to extracellular potassium is the major determinant of the resting membrane potential and plays a crucial role in the normal functioning of all cells, especially those with inherent excitability, such as cardiac and neural cells. This also justifies the clinical consequences of hypokalemia.

Renal function in potassium excretion

Long-term potassium homeostasis and serum potassium is dependent on the renal function. Potassium is freely filtered, and then 90% reabsorbed in the nephron segments proximal to the distal convoluted tubule (DCT). The majority of the K+ excreted is secreted by specialized cells in the DCT and/or cortical and outer medullary collecting ducts. Collecting duct can reabsorb potassium under severe potassium deprivation; however, urinary potassium never approaches zero, and hence there is an obligatory potassium loss of 10 to 15 mEq/day.

The factors influencing potassium secretion (and therefore excretion) include: potassium intake; intracellular potassium concentration; urine flow rate; distal delivery of sodium; mineralocorticoid activity; and tubular responsiveness to mineralocorticoids. In addition, acid–base balance affects serum potassium by the exchange of hydrogen ions for potassium across the cell membrane.¹³Rastegar A. EditorsIn: Walker HK, Hall WD, Hurst JW, editors. Serum potassium. Clinical methods: The history, physical, and laboratory examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 195. http://www.ncbi.nlm.nih.gov/pubmed/21250149  

The aldosterone impact

Aldosterone plays an important role in regulation of potassium homeostasis. Renal potassium loss is most commonly associated with a high aldosterone level. Use of diuretics, the most common cause of renal potassium wastage, induces kaliuresis (excess potassium in the urine) through several mechanisms, including rise in aldosterone level. Other putative mechanisms include increased urine volume, increased delivery of sodium to exchange sites, hypochloremia and metabolic alkalosis.¹³Rastegar A. EditorsIn: Walker HK, Hall WD, Hurst JW, editors. Serum potassium. Clinical methods: The history, physical, and laboratory examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 195. http://www.ncbi.nlm.nih.gov/pubmed/21250149  

Diagnosis of hypokalemic states

Symptomatic diagnosis

The symptomatic profile of hypokalemia can span from being asymptomatic at one end to being life threatening at the other end – usually, a small drop in potassium levels does not cause symptoms of hypokalemia; however, it can be life threatening if K⁺ levels drop extremely.¹⁶Glover P. Hypokalemia. Crit Care Resusc. 1999 Sep;1(3):239-51.   Clinical features associated with hypokalemia include abnormalities of cardiovascular, neurological and metabolic function.⁶Hypokalemia. Available at: http://umm.edu/Health/Medical/Ency/Articles/Hypokalemia [Accessed on 5/08/2013].   Table 4 summarizes clinical findings in hypokalemia that should alert the clinician to the possible existence of a significant derangement in serum potassium.¹³Rastegar A. EditorsIn: Walker HK, Hall WD, Hurst JW, editors. Serum potassium. Clinical methods: The history, physical, and laboratory examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 195. http://www.ncbi.nlm.nih.gov/pubmed/21250149   The neuromuscular and cardiac signs and symptoms can overlap, and can include nonspecific minor complaints (such as weakness, tiredness and palpitation), as well as major symptoms (paralysis and sudden death).

However, the clinical picture may at times not be directly obvious. It is therefore important that the clinician utilizes all historical and physical information available to transform a gross approximation of low body potassium to a more definite diagnosis of hypokalemia. As drug induced hypokalemia may often be overlooked in practice, because of the numerous etiologies of hypokalemia, physicians should pay close attention to this common side effect through a careful review of medications history while evaluating and managing a hypokalemic patient. In addition, further more sophisticated laboratory testing might often be needed to reach a specific diagnosis in either etiologic category.

Definitive diagnosis

Definitive diagnosis involves the recognition of true hypokalemia and pseudohypokalemia. The latter is a laboratory identification that manifests as an artifact of the storage procedure, and could account for false-positive cases of clinical hypokalemia, possibly resulting in inappropriate treatment. Abnormal white blood cells (WBCs), if present in large enough numbers such as in acute myelogenous leukemia, can take up extracellular K⁺ when stored for prolonged periods at room temperature, thereby resulting in a low level of measured plasma potassium. Rapid separation of the plasma or storing the sample at 4ºC avoids this artifact and confirms the diagnosis. Overt hypokalemia may be diagnosed when the serum potassium level is less than 3.5 mmol/L.

The levels of potassium excreted in urine may vary dependent on whether the cause of origin of hypokalemia is gastrointestinal or renal. While urine potassium is usually < 20 mEq/L in the former, it is > 20 mEq/L in the latter. However, high urinary potassium is also seen secondary to increased aldosterone in patients with vomiting or diarrhea, and is therefore not very helpful. Nevertheless, proper medical history (e.g., history of vomiting, diarrhea, or diuretic use) and physical data (such as blood pressure and pulse) in such instances gives most critical data to differentiate these two large groups.¹³Rastegar A. EditorsIn: Walker HK, Hall WD, Hurst JW, editors. Serum potassium. Clinical methods: The history, physical, and laboratory examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 195. http://www.ncbi.nlm.nih.gov/pubmed/21250149  

The etiologies should therefore be considered first before exhaustive work-up is initiated. As well, an important initial step is to identify if hypokalemia is in association with systemic hypertension or not (Figure 3).

While estimating the levels of serum potassium is fundamental to the diagnosis of hypokalemia, some other tests, such as arterial blood gas analysis, basic or comprehensive metabolic panel, electrocardiogram (ECG; such as presence of a U wave), and blood tests to check glucose, magnesium, calcium,

sodium, phosphorous, thyroxine, and aldosterone levels may help in identifying the cause and effect of hypokalemia.⁶ Hypokalemia. Available at: http://umm.edu/Health/Medical/Ency/Articles/Hypokalemia [Accessed on 5/08/2013].   Serum bicarbonate is perhaps the single most useful additional test. The urinary chloride levels are also helpful in distinguishing the causes of hypokalemia. Under appropriate conditions, measurement of the renin, aldosterone, and cortisol concentrations would help in differentiating among the etiologies.

Management of hypokalemia

In most cases, hypokalemia is because of an obvious underlying cause. However, the anomaly can rarely be the sole presentation of a more threatening disorder. As such, a high index of suspicion and a systematic approach are required to avoid delays in the management.¹⁷ Mahmood MM, John K. Hypokalemia: common but not always benign. Severe, persistent hypokalemia secondary to ectopic ACTH from a carcinoid tumour. BMJ Case Rep. 2012;2012. pii: bcr-2012-007193.   Management is often dependent on the acute or chronic nature of hypokalemia.

The four important goals of treatment in hypokalemia are:

• To minimize the potassium losses
• To replenish the potassium stores
• To evaluate potential toxicities
• To determine the underlying cause to prevent recurrences.

It may be prudent to discontinue using diuretics – the common causative agents for hypokalemia or, if deemed necessary, switch over to potassium sparing diuretics like triamterene, amiloride, spironolactone, etc.⁵Hypokalemia. Clinical key, Elsevier. Available at: https://www.clinicalkey.com/topics/%20nephrology/hypokalemia.html. [Accessed on 14 /08/2013].  ^,6 Hypokalemia. Available at: http://umm.edu/Health/Medical/Ency/Articles/Hypokalemia [Accessed on 5/08/2013].   Potassium-sparing diuretics are, however, generally used only in patients with normal renal function who are prone to significant hypokalemia.¹⁸Lederer E, Alsauskas ZC, Mackelaite L, et al. Hypokalemia Treatment & Management. Available at: http://emedicine.medscape.com/article/242008-treatment [Accessed on 8/8/2013].  

Potassium supplementation

The treatment of hypokalemia invariably involves replenishing the potassium levels. Increasing potassium intake should therefore be considered when serum potassium levels are between 3.5 and 4.0 mmol. Potassium supplementation may however be warranted even in asymptomatic patients with mild-to-moderate hypertension if serum potassium level is below 3.5 mmol.¹¹Cohn JN, Kowey PR, Whelton PK, Prisant LM. New Guidelines for Potassium Replacement in Clinical Practice. A Contemporary Review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000;160:2429-2436.  

Dietary potassium: Increasing dietary potassium appears to be the most straightforward means of enhancing potassium intake. Patients with excessive potassium losses (for instance, diuretic or laxative use) or patients with hypokalemia who are at increased risk, such as those receiving digoxin, may benefit from such dietary modifications. In addition, avoidance of specific foods (such as licorice) may also be crucial for high-risk individuals. However, the lack of measures to know if the required level of potassium is being supplemented or not is a potential limitation to dietary potassium supplementation. In addition, some potassium-rich foods may have inappropriately high potassium content.¹¹Cohn JN, Kowey PR, Whelton PK, Prisant LM. New Guidelines for Potassium Replacement in Clinical Practice. A Contemporary Review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000;160:2429-2436.   As such, these natural sources may not supplant the potassium supplements.

It is therefore better to take a potassium supplement rather than being dependent on dietary potassium since amount of potassium present in diet cannot be quantified. Moreover, dietary potassium is almost entirely coupled with phosphate, rather than with chloride; therefore, it is not effective in correcting the potassium loss associated with chloride depletion, such as in diuretic therapy, vomiting, and nasogastric drainage.¹¹Cohn JN, Kowey PR, Whelton PK, Prisant LM. New Guidelines for Potassium Replacement in Clinical Practice. A Contemporary Review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000;160:2429-2436.  

Route of administration for potassium supplements

Both oral and intravenous potassium supplements can be used to replenish the potassium levels in the body. However, the amount and route of administration usually depends on the severity of hypokalemia. Generally, clinical features associated with mild hypokalemia may be successfully treated with oral potassium salts, though life threatening conditions, such as cardiac arrhythmias, require rapid intravenous correction. Close follow-up care, with continuous ECG monitoring, and serial estimation of potassium levels, is required mainly in acute cases.

An estimate of the potassium deficit may help in calculating the amount of potassium supplement.¹⁴Rastegar A, Soleimani M. Hypokalemia and hyperkalaemia. Postgrad Med J. 2001 Dec;77(914):759-64.   While a reduction of serum potassium by 0.3 mmol/l would generally correspond to a total body deficit of 100 mmol, broadly, for every 1 mEq/L decrease in serum potassium, the potassium deficit may be considered as in between 200-400 mEq. The deficit may however not depict absolute reduction as potassium balance is affected by various factors. The calculation could, hence, either overestimate or underestimate the true potassium deficit. Therefore, while attempting to calculate the total body potassium deficit, it is prudent to consider factors that can independently affect serum potassium levels, for instance the blood pH.

Intravenous supplements

As compared to oral potassium, intravenous potassium is not well tolerated, and can be highly irritating to veins.¹⁸Lederer E, Alsauskas ZC, Mackelaite L, et al. Hypokalemia Treatment & Management. Available at: http://emedicine.medscape.com/article/242008-treatment [Accessed on 8/8/2013].   In most cases, it is therefore advised that the rate of intravenous potassium administration should not exceed 20 mmol per hour, though it may be dependent on upon the salt used. As such, intravenous route is reserved for those with severe hypokalemia. When indicated, intravenous potassium solutions should never be given as an intravenous push, and should be administered as a dilute solution.

Oral supplements

As oral potassium is absorbed readily, is easy to administer, and relatively large doses can be given safely, oral route is generally preferred in most clinical settings of hypokalemia, more so seeing the safety concerns for administering intravenous potassium particularly in fluid restricted patients.¹⁹Sladdin C, Lee G. Safely treating hypokalemia in high dependency cardiac surgical patients. Nurs Crit Care. 2006;11(6):267-72.   Oral replacement is normally sufficient for most patients with mild hypokalemia and minimal symptoms. Subpopulation of patients with chronic hypokalemia may in fact require long-term oral substitution of potassium.²⁰Ehren K, Marx A, Wasmuth JC. Unexplained chronic hypokalemia in a young woman. Dtsch Med Wochenschr. 2010 Oct;135(41):2021-3.   Furthermore, as potassium can shift in and out of cells under multiple influences; it is, therefore, important, after potassium has been replenished, to check again for several days to determine whether potassium has stabilized or has started falling again.¹⁸Lederer E, Alsauskas ZC, Mackelaite L, et al. Hypokalemia Treatment & Management. Available at: http://emedicine.medscape.com/article/242008-treatment [Accessed on 8/8/2013].  

Potassium chloride

Potassium salts include potassium chloride, potassium phosphate, and potassium bicarbonate. However, potassium chloride is the preferred potassium supplement in treating mild or moderate hypokalemia. Potassium phosphate is found primarily in food, and potassium bicarbonate is typically recommended when potassium depletion occurs in the setting of metabolic acidosis (pH<7.4). In all other settings, potassium chloride should be used because of its unique effectiveness against the most common causes of potassium depletion. Moreover, hypochloremia may develop if citrate, gluconate, bicarbonate or another alkalinizing salt is administered, particularly in patients adhering to diets that restrict the chloride intake.¹¹Cohn JN, Kowey PR, Whelton PK, Prisant LM. New Guidelines for Potassium Replacement in Clinical Practice. A Contemporary Review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000;160:2429-2436.  

Potassium chloride is therefore the usual choice for replenishment of potassium levels and for maintenance of potassium levels in patients with ongoing potassium loss. Dose of 50 to 100 mmol of potassium chloride is generally required per day in order to maintain serum potassium concentration within the normal range in patients with increased potassium loss (such as those receiving a diuretic).

Potassium chloride may also be used in preoperative setting as a prophylactic measure for hypokalemia. It has been observed that oral potassium chloride with oral rehydration solution supplement for sodium phosphate bowel preparation regimen can prevent hypokalemia prior to surgery.²¹Kamolpornwijit W, Phupong V. Oral potassium chloride and oral rehydration solution supplement to prevent hypokalemia in sodium phosphate regimen for bowel preparation prior to gynecological laparoscopic surgery. J Med Assoc Thai. 2008 May;91(5):615-8.  

Potassium chloride is available in liquid or tablet formulations¹¹Cohn JN, Kowey PR, Whelton PK, Prisant LM. New Guidelines for Potassium Replacement in Clinical Practice. A Contemporary Review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000;160:2429-2436.  ; however, while tablets have a number of attributes, such as the size of medication, ease of swallowing, and rate of disintegration, which might limit their use, liquid formulation has immediate effect with few erosions.

Conclusion

Potassium is a cation that is generally ignored despite the known benefits of dietary intake and effect on multiple organ systems. Particularly, it maintains acid-base balance, and plays a critical role in the excitability of skeletal, cardiac, smooth muscle and nerves. The normal potassium levels, which span over a narrow range, are therefore essential for proper functioning of these organs and maintain the homeostatic milieu.

Hypokalemia is a commonly encountered fluid and electrolyte abnormality in clinical medicine. A number of possible etiologies may result in the clinical presentation of hypokalemia, though the most common cause is increased loss of potassium through renal or gastroenterologic route. Hypokalemia is often mild; however, when severe, it may lead to a life-threatening condition.

Potassium supplements are commonly used to replenish potassium levels in patients with hypokalemia. While oral route is preferred in most cases, more severe cases of hypokalemia require intravenous administration in addition to oral route. Oral supplementation is also safer than intravenous route, which require more cautious administration. Potassium chloride is the usual choice for supplementation in most cases of mild hypokalemia because of its unique effectiveness against the most common causes of potassium depletion. A dosage of 20 mmol/d of potassium in oral form would be generally sufficient for the prevention of hypokalemia, and 40 to 100 mmol/d sufficient for its treatment. However, dosage must be tailored to the individual needs of each patient. It is prudent that dosage be divided if > 20 mEq per day is required to be given, such that no more than 20 mEq is given in a single dose.

Regular follow-up, with regular renal function test and serial serum potassium checks, would help in optimizing the outcome in long-term by optimally replenishing the potassium levels. This is also important seeing the dependence of potassium homeostasis on several factors.

References

1. Weiner ID, Wingo CS. Hypokalemia–consequences, causes, and correction. J Am Soc Nephrol. 1997 Jul;8(7):1179-88.
2. Vavruk AM, Martins C, Nascimento MM, et al. Association between hypokalemia, malnutrition and mortality in peritoneal dialysis patients. J Bras Nefrol. 2012;34(4):349-54.
3. Lam MH, Chau SW, Wing YK. High prevalence of hypokalemia in acute psychiatric inpatients. Gen Hosp Psychiatry. 2009 May-Jun;31(3):262-5.
4. Andrew ME, Jones DW, Wofford MR, Wyatt SB, Schreiner PJ, Brown CA, Young DB, Taylor HA. Ethnicity and unprovoked hypokalemia in the Atherosclerosis Risk in Communities Study. Am J Hypertens. 2002 Jul;15(7 Pt 1):594-9.
5. Hypokalemia. Clinical key, Elsevier. Available at: https://www.clinicalkey.com/topics/%20nephrology/hypokalemia.html. [Accessed on 14 /08/2013].
6. Hypokalemia. Available at: http://umm.edu/Health/Medical/Ency/Articles/Hypokalemia [Accessed on 5/08/2013].
7. Ben Salem C, Hmouda H, Bouraoui K. Drug-induced hypokalemia. Curr Drug Saf. 2009 Jan;4(1):55-61.
8. Ng JL, Morgan DJ, Loh NK, et al. Life-threatening hypokalemia associated with ibuprofen-induced renal tubular acidosis. Med J Aust. 2011 Mar 21;194(6):313-6.
9. Siau K. Hypokalemia and cardiac arrest complicating vancomycin and furosemide therapy: a case report. Cases J. 2009;2:8244.
10. Reid A, Jones G, Isles C. Hypokalemia: common things occur commonly – a retrospective survey. JRSM Short Rep. 2012 Nov;3(11):80.
11. Cohn JN, Kowey PR, Whelton PK, Prisant LM. New Guidelines for Potassium Replacement in Clinical Practice. A Contemporary Review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000;160:2429-2436.
12. Toner JM, Ramsay LE. Thiazide-induced hypokalemia; prevalence higher in women. Br J Clin Pharmacol. 1984;18(3):449-52.
13. Rastegar A. EditorsIn: Walker HK, Hall WD, Hurst JW, editors. Serum potassium. Clinical methods: The history, physical, and laboratory examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 195. http://www.ncbi.nlm.nih.gov/pubmed/21250149
14. Rastegar A, Soleimani M. Hypokalemia and hyperkalaemia. Postgrad Med J. 2001 Dec;77(914):759-64.
15. Antes LM, Kujubu DA, Fernandez PC. Hypokalemia and the pathology of ion transport molecules. Seminars in Nephrology 1998;18(1):31-45.
16. Glover P. Hypokalemia. Crit Care Resusc. 1999 Sep;1(3):239-51.
17. Mahmood MM, John K. Hypokalemia: common but not always benign. Severe, persistent hypokalemia secondary to ectopic ACTH from a carcinoid tumour. BMJ Case Rep. 2012;2012. pii: bcr-2012-007193.
18. Lederer E, Alsauskas ZC, Mackelaite L, et al. Hypokalemia Treatment & Management. Available at: http://emedicine.medscape.com/article/242008-treatment [Accessed on 8/8/2013].
19. Sladdin C, Lee G. Safely treating hypokalemia in high dependency cardiac surgical patients. Nurs Crit Care. 2006;11(6):267-72.
20. Ehren K, Marx A, Wasmuth JC. Unexplained chronic hypokalemia in a young woman. Dtsch Med Wochenschr. 2010 Oct;135(41):2021-3.
21. Kamolpornwijit W, Phupong V. Oral potassium chloride and oral rehydration solution supplement to prevent hypokalemia in sodium phosphate regimen for bowel preparation prior to gynecological laparoscopic surgery. J Med Assoc Thai. 2008 May;91(5):615-8.