Hypokalemia - ClinicalKey

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CLINICAL OVERVIEW
Hypokalemia
Elsevier Point of Care (see details)
Updated October 1, 2021. Copyright Elsevier BV. All rights reserved.
Synopsis
Key Points Urgent Action

Hypokalemia is associated with many different Severe hypokalemia with
conditions, including renal dysfunction and severe or life-threatening
gastrointestinal disease manifestations requires
hospitalization and
Diagnosis is based on medical history and laboratory
immediate correction
tests to detect and determine the underlying etiology
with IV potassium
of hypokalemia
replacement
Determining the cause of hypokalemia is essential to
In patients with
prescribe the appropriate initial treatment and
significant dysrhythmias
ongoing prevention
(eg, ventricular
Causes of potassium loss may include diuresis from tachycardia) as a
potassium-wasting drugs, abnormal renal losses presenting symptom, 20
induced by metabolic alkalosis, or loss in the stool mEq IV potassium
secondary to diarrhea chloride can be pushed
over 3 to 10 minutes to
Chronic, mild hypokalemia is often asymptomatic, prevent deterioration into
whereas acute, severe hypokalemia is associated with cardiac arrest 1
a wide range of clinical manifestations
Treatment includes both potassium and magnesium repletion, as well as addressing
https://www.clinicalkey.com/#!/content/clinical_overview/67-s2.0-f493c228-fe54-486c-8bb1-a49f1fc99f48 Page 1 of 20
the underlying cause
In the setting of hypomagnesemia, hypokalemia can be refractory to potassium

replacement alone, and coexisting magnesium deficiency should always be addressed
with oral or parenteral repletion
Complications can include depressed neuromuscular excitability, cardiovascular

complications, renal dysfunction, glucose intolerance, and hepatic encephalopathy
Hypokalemia is associated with increased morbidity and mortality in patients with

cardiovascular or chronic renal disease
Pitfalls 2 3
In patients with severe hypokalemia, repletion of both potassium and magnesium
may be required, even when the serum magnesium level is within the reference
range, to ensure maintenance of intracellular potassium levels 1
IV potassium chloride causes burning and discomfort at the IV site and can cause
phlebitis; a central line is recommended for rates greater than 10 mEq/h
Chronic hypokalemia results in hypokalemic nephropathy, a tubulointerstitial

disease that is characterized by nephrogenic diabetes insipidus, alkalosis, and
progressive decline in GFR 4
Terminology
Clinical Clarification 2
Hypokalemia occurs when serum potassium level is less than 3.5 mEq/L
Classification
By severity: 5
Mild
Potassium level of 3.0 to 3.5 mEq/L
Severe
Potassium level less than 3.0 mEq/L
By duration: 6
Acute
Rapid rate of potassium depletion that develops over a short period
Suspect intracellular shift of potassium from extracellular space
Chronic
Slow rate of potassium depletion that develops over a long period
Suspect gastrointestinal loss (diarrhea) or a defect that causes renal potassium

wasting
Diagnosis
Clinical Presentation
History
Usually asymptomatic in mild and chronic hypokalemia
With acute and/or severe hypokalemia and potassium levels below 3.0 mEq/L,
symptoms may include the following:
Muscle weakness, originating in lower extremities and progressing to upper

extremities
Myalgias, originating in lower extremities and progressing to upper extremities
Ascending paralysis
Constipation
Nausea, vomiting
Palpitations
Syncope
Polyuria, owing to decreased concentrating ability
Physical examination 5
No pathognomonic sign or specific potassium level is associated with the onset of
physical signs
Hypertension
Depressed deep muscle reflexes due to delayed peripheral nerve conduction
Muscle weakness; decreased strength typically more pronounced in proximal

muscles and lower extremities
Irregular cardiac rhythm
Abdominal distention (with ileus)
Causes and Risk Factors
Causes
Potassium loss; routes include:
Gastrointestinal 5
Diarrhea
Infectious
Malabsorptive
Fistula or ileostomy (potassium lost in drainage of liquid stool)
Drugs
Laxative abuse
Sodium polystyrene sulfonate
Renal 2 5
Hypomagnesemia
Hyperglycemia resulting in osmotic diuresis
Salt-wasting nephropathies (eg, Bartter syndrome)
Mineralocorticoid excess (primary aldosteronism)
Can be induced by prolonged ingestion of licorice
Proximal or distal renal tubular acidosis
Interstitial renal disease with concentrating defects
Diabetic ketoacidosis
Drugs
Diuretics (eg, thiazide, loop)
Amphotericin B
Mineralocorticoids (eg, fludrocortisone)
High-dose glucocorticoids
High doses of penicillin and penicillin derivatives
Cisplatin
Aminoglycosides
Toluene (if abused)
5
Cutaneous 5
Diaphoresis
Extensive burns
Dialysis 5
Plasmapheresis 5
Inadequate potassium intake
Prolonged and extremely low dietary intake (eg, anorexia, starvation) 5
Total parenteral nutrition with inadequate potassium supplementation
Intracellular shift of potassium from extracellular space 5
Metabolic alkalosis
Total parenteral nutrition
Hypokalemic periodic paralysis
Hypothermia
Barium toxicity
Drugs
Insulin; typically with larger doses of immediate acting preparations
β₂-adrenergic agonists, such as those used with nebulized albuterol (acute 0.2-
0.4 mmol/L reduction in potassium with each nebulizer dose) 2 5
Risk factors and/or associations
Genetics
Associated with rare genetic disorders including: 7
Liddle syndrome
Autosomal dominant disorder characterized by early-onset salt-sensitive

hypertension, hypokalemia, and metabolic alkalosis
Caused by mutations in genes encoding the renal epithelial sodium channel (ie,
SCNN1B, SCNN1G)
Gitelman syndrome
Autosomal recessive renal tubular salt-wasting disorder characterized by

hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalciuria
Caused by mutation in the thiazide-sensitive NaCl cotransporter (ie, SLC12A3)
Bartter syndrome
Autosomal recessive disorder of impaired salt reabsorption characterized by

pronounced salt wasting, hypokalemic metabolic alkalosis, and hypercalciuria
Caused by mutation in the kidney chloride channel B gene (ie, CLCNKB)
Diagnostic Procedures
Primary diagnostic tools

Diagnosed based on serum potassium level 8
If cause is not obvious from clinical

presentation, initial tests include: 9
Electrocardiographic changes in
Serum chemistry panel and magnesium level hypokalemia.
24-hour urine potassium collection to

distinguish renal potassium losses from other
causes of hypokalemia 10
Spot urine potassium concentration
Additional tests may be performed under

selected conditions to determine cause,
including:
The clinical approach to
hypokalemia. - AME, Apparent
mineralocorticoid excess; BP,

Arterial blood gas to assess acid-base status if blood pressure; CCD, cortical
collecting duct; DKA, diabetic
urine potassium excretion is high (above 20
ketoacidosis; FHPP, familial
mEq/d) 6 hypokalemic periodic paralysis;
GI, gastrointestinal; GRA,
Spot urine chloride measurement to further glucocorticoid-remediable
define the cause of hypokalemia if metabolic aldosteronism; HTN,
alkalosis is present 8 hypertension; PA, primary
aldosteronism; RAS, renal artery
stenosis; RST, renin-secreting
Imaging of the adrenal glands if suspect tumor; RTA, renal tubular
mineralocorticoid, glucocorticoid, or acidosis; TTKG, transtubular
catecholamine excess, the pituitary gland to potassium gradient
exclude Cushing disease, or the abdomen if
suspect VIPoma 10
If hypokalemia is severe (less than 3.0 mEq/L),

obtain ECG to detect any potential heart block or
arrhythmias 1
Laboratory
Functional testing
Differential Diagnosis
Most common
Hypokalemia is a
laboratory diagnosis
that does not require
distinction from other
entities once laboratory
error has been excluded
Treatment
Goals
Replace potassium deficit
Treat underlying cause to prevent further episodes
Prevent or treat life-threatening manifestations and

complications of hypokalemia
General principles of hypokalemia
management. - These steps should
be helpful in most cases of
Disposition hypokalemia; however, clinical
judgment should be exercised
when applying it to individual
patients. Serum potassium (K+)
Admission criteria concentration generally should
Severe hypokalemia (less than 3.0 mEq/L) accompanied not be checked until 1 hour after
an IV dose is given (2 hours after
by complications such as cardiac arrhythmias, paralysis, an oral dose). Parenteral
or rhabdomyolysis potassium should be avoided
except in the urgent conditions
listed and transitioned to oral
preparations as soon as possible.
Criteria for ICU admission Serum potassium levels should be
Life-threatening complications such as cardiac monitored carefully, especially in
patients with kidney or cardiac
arrhythmias or respiratory failure
disease. Abbreviation: KCl,
potassium chloride.
Recommendations for specialist referral

Refer to nephrologist to manage renal causes of hypokalemia and any coexisting
hypertension or kidney disease
Refer to cardiologist to manage cardiac arrhythmias
Refer to endocrinologist to treat mineralocorticoid excess due to aldosteronism
Treatment Options
Potassium replacement 2
Oral dietary or pharmacologic potassium supplements are used for mild

hypokalemia
Potassium chloride: default and preferred salt choice 14
Potassium bicarbonate: indicated for patients with hypokalemia and metabolic

acidosis (pH less than 7.4)
Potassium phosphate: indicated for patients with phosphate deficits (as in diabetic
ketoacidosis)
IV potassium chloride saline solution is used for severe (less than 3.0 mEq/L)
symptomatic hypokalemia or for hypokalemia associated with life-threatening ECG
changes
In patients with significant dysrhythmias (eg, ventricular tachycardia) as a

presenting symptom, 20 mEq IV potassium chloride can be pushed over 3 to 10
minutes to prevent deterioration into cardiac arrest 1
Monitor potassium levels periodically during and after repletion to prevent

overcorrection 15
Magnesium replacement 2
Magnesium levels must be restored if concomitant hypomagnesemia coexists
In patients with severe hypokalemia, repletion of both potassium and magnesium

may be required, even when the serum magnesium level is within the reference
range, to ensure maintenance of intracellular potassium levels 1
Treat or correct underlying cause of hypokalemia
Drug therapy
Potassium supplements 2
Recommended for mild hypokalemia (3.0-3.5 mEq/L)
Potassium Oral tablet; Children: 1—2 mEq/kg/day PO in 1—2 divided doses.
Potassium Oral tablet; Adults: 20 mEq/day PO, given in 1—2 divided doses, is
recommended for the prevention of hypokalemia. Max single dose is 20 mEq.
The dose should be taken after a meal. Adjust dosage according to clinical need
and tolerance.
Potassium chloride
Preferred potassium replacement therapy; recommended for the most common

causes of hypokalemia
Oral
Potassium Chloride Oral solution; Children: 2—5 mEq/kg/day PO in divided

doses.
Potassium Chloride Effervescent tablet; Adults: 40—100 mEq/day PO, given

in 2—4 divided doses, is used for the treatment of potassium depletion.
Adjust dosage according to clinical need and tolerance. Max single dose is 20
mEq. The dose should be taken after a meal. Max 100 mEq/day.
Potassium Chloride Effervescent tablet; Geriatric: See adult dosage. Because

elderly patients are more likely to have renal dysfunction, the dose should be
individualized based on the degree of renal impairment and clinical goals.
IV 2
May be required to correct severe hypokalemia (less than 3.0 mEq/L)
ECG and potassium levels must be closely monitored
IV potassium chloride causes burning and discomfort at the IV site and can
cause phlebitis; a central line is recommended for rates greater than 10
mEq/h
Potassium Chloride Solution for injection; Infants†, Children†, and

Adolescents†: 0.25 to 0.5 mEq/kg/dose IV; up to 1 mEq/kg/dose (usual Max:
40 mEq/dose) IV in critical situations with appropriate monitoring. Usual
infusion rates are 0.25 to 0.5 mEq/kg/hour; usual Max infusion rate: 1
mEq/kg/hour (Max: 40 mEq/hour), which should be done via a central
catheter. Higher infusion rates (up to 2 mEq/kg/hour) have been reported
in cases of life-threatening hypokalemia. Continuous ECG recommended
for higher doses (i.e., greater than 0.5 mEq/kg/dose) and faster infusion
rates (i.e., greater than 0.3 mEq/kg/hour).
Potassium Chloride Solution for injection; Adults with a serum potassium

concentration more than 2.5 mEq/L: Administer at a rate not to exceed 10
mEq/hour IV with a 24-hour dose not to exceed 200 mEq. An initial dose
of 20 to 40 mEq IV has been recommended. If an infusion rate exceeding
10 mEq/hour is needed, infuse via a central vein in the presence of

continuous cardiac monitoring. Multiple doses may be required to
normalize serum potassium. Check serum potassium concentration after
administration of 60 to 80 mEq (within 1 to 4 hours after administration)
before further potassium is administered.
Potassium Chloride Solution for injection; Adults with a serum potassium

concentration less than 2 mEq/L and ECG changes and/or muscle
paralysis: In critical situations and under continuous cardiac monitoring,
potassium may be cautiously administered via a central vein at a rate up to
40 mEq/hour IV not to exceed 400 mEq IV in 24 hours. Initial doses of up
to 40 to 80 mEq have been recommended. Multiple doses may be required
to normalize serum potassium. Check serum potassium concentration
after administration of 60 to 80 mEq (within 1 to 4 hours after
administration) before further potassium is administered. Infusion rates
exceeding 20 mEq/hour are rarely needed.
Potassium bicarbonate
Recommended for hypokalemia in the setting of metabolic acidosis (pH less

than 7.4)
Potassium Bicarbonate Effervescent tablet; Children: 1—2 mEq/kg/day PO in

1—2 divided doses.
Potassium Bicarbonate Effervescent tablet; Adults: 40—100 mEq/day PO,

given in 2—4 divided doses, is used for the treatment of potassium
depletion. Adjust dosage according to clinical need and tolerance. Max single
dose is 20 mEq. The dose should be taken after a meal. Max 100 mEq/day.
Potassium Bicarbonate Effervescent tablet; Geriatric: See adult dosage.

Because elderly patients are more likely to have renal dysfunction, the dose
should be individualized based on the degree of renal impairment and
clinical goals.
Potassium phosphate
Recommended for hypokalemia in the setting of phosphate deficits
For the treatment of mild hypophosphatemia (i.e., phosphorus serum

concentration 2 to 2.5 mg/dL)
Potassium Phosphate, Dibasic, Potassium Phosphate, Monobasic Solution
for injection; Infants, Children, and Adolescents: 0.16 to 0.31

mmol/kg/dose (Max: 45 mmol/dose) IV over 2 to 6 hours; repeat doses may
be necessary; specific infusion rate dependent on dose and route of
administration (peripheral or central venous catheter).

for injection; Adults: 0.16 to 0.31 mmol/kg/dose (Max: 45 mmol/dose) IV
over 2 to 6 hours; repeat doses may be necessary; specific infusion rate
dependent on dose and route of administration (peripheral or central
venous catheter).
For the treatment of moderate hypophosphatemia (i.e., phosphorus serum

concentration 1 to 2 mg/dL)

mmol/kg/dose (Max: 45 mmol/dose) IV over 2 to 6 hours; repeat doses may
be necessary; specific infusion rate dependent on dose and route of

over 2 to 6 hours is FDA-approved dosage; however, higher doses have
been used (0.64 mmol/kg/dose [Usual Max: 50 mmol/dose]); repeat doses
may be necessary. Specific infusion rate dependent on dose and route of
For the treatment of severe hypophosphatemia (i.e., phosphorus serum

concentration less than 1 mg/dL)

mmol/kg/dose (Max: 45 mmol/dose) IV over 2 to 6 hours is FDA-approved
dosage; however, higher doses have been used (1 mmol/kg/dose [Usual
Adult Max: 50 mmol/dose]); repeat doses may be necessary. Specific
infusion rate dependent on dose and route of administration (peripheral
or central venous catheter).

over 2 to 6 hours is FDA-approved dosage; however, higher doses have
been used (1 mmol/kg/dose [Usual Max: 50 mmol/dose]); repeat doses may
be necessary. Specific infusion rate dependent on dose and route of

Magnesium replacement
Magnesium is an important cofactor for potassium uptake and maintenance of

intracellular potassium levels
Patients with hypokalemia may be refractory to treatment if coexisting

hypomagnesemia is not corrected first 16
IV or intramuscular magnesium sulfate
Magnesium Sulfate Solution for injection; Neonates, Infants, Children, and

Adolescents: 25 to 50 mg/kg/dose IV over 30 to 60 minutes (Max: 2 g/dose);
repeat as necessary based on serum magnesium concentrations.
Magnesium Sulfate Solution for injection; Adults: 1 to 2 g IV (or 15 to 30 mg/kg

lean body weight) every 6 hours for 24 hours. After the first 24 hours,
approximately 60 mg/kg/day may be given in divided doses or via IV drip for
the next 2 to 5 days.
Oral magnesium
Magnesium Oral solution; Infants, Children, and Adolescents: 10 to 40 mg

elemental magnesium/kg/day PO in 2 to 4 divided doses; higher doses (100 mg
elemental magnesium/kg/day PO) have been reported; however, the use of
higher doses may be limited by the occurrence of diarrhea. Titrate dose based
on serum magnesium concentrations.
Magnesium Oral tablet; Adults: 360 to 672 mg elemental mag PO in divided

doses for severe hypomagnesemia or 120 to 336 mg elemental mag PO in
divided doses for mild has been recommended; another source suggests 20 to
50 mmol (480 to 1200 mg) PO daily in divided doses.
Comorbidities
Cardiac disease
Mild to moderate hypokalemia increases the likelihood of cardiac arrhythmias in

patients who have ischemic heart disease, heart failure, or left ventricular
hypertrophy 17 18
28
Maintain potassium concentration at 4.0 mEq/L or higher 2 8
Potassium supplementation may be beneficial in patients with initial potassium

levels within the reference range 2
Hypertension
Maintain potassium concentration at 4.0 mEq/L or higher in patients with mild to

moderate hypertension 2
Severe hepatic disease
Hypokalemia can exacerbate hepatic encephalopathy by increasing systemic

ammonia levels 19
Maintain potassium concentration at 4.0 mEq/L or higher
Monitoring
Monitor potassium levels periodically during and after repletion to prevent
overcorrection
Monitor ECG when potassium is administered intravenously for severe hypokalemia
Complications and Prognosis
Complications 5
Depressed neuromuscular excitability
Muscle weakness
Myalgias
Paralysis
Hypoventilation and respiratory paralysis
Ileus
Rhabdomyolysis
Cardiovascular complications
Arrhythmias 17
Premature atrial and ventricular beats
Sinus bradycardia
Atrial tachycardia
Atrioventricular block
Ventricular tachycardia or fibrillation
Ventricular arrhythmias associated with:
Myocardial ischemia
Heart failure
Left ventricular hypertrophy
Digoxin toxicity
Hypertension
Renal dysfunction
Metabolic alkalosis due to increased ammonia production and increased

bicarbonate resorption
Impairment in urinary concentrating ability
Hypokalemia nephropathy (tubulointerstitial disease that is characterized by

nephrogenic diabetes insipidus, alkalosis, and progressive decline in GFR) 4
Glucose intolerance
Impaired insulin secretion
Peripheral insulin resistance
Hepatic encephalopathy
Increased ammonia production predisposes patients with cirrhosis to develop

hepatic encephalopathy
Prognosis
Prognosis depends upon the underlying disorder and associated comorbidities
Hypokalemia is associated with increased morbidity and mortality in patients with

cardiovascular or chronic renal disease 20 21 22
Patients with hypokalemia and congestive heart failure are at greater risk of
dysrhythmias, syncope, cardiac arrest, and death 2
Patients with hypokalemia who are younger than 65 years are more prone to adverse
outcomes than older patients 2
In a study of hospitalized medical patients, serum potassium levels less than 2.9
mEq/L were associated with increased 8- and 30-day mortality; a separate study
among hospitalized patients showed levels below 3.9 mEq/L were associated with
increased 1-year mortality 21 23
Screening and Prevention
Prevention 2 3
Ensure adequate dietary intake of potassium
Potassium-rich foods (eg, dried figs, nuts, avocados) are the most direct way to
enhance potassium intake
Dietary sources of potassium are not effective in correcting hypokalemia

associated with chloride depletion (eg, diuretic therapy, vomiting, nasogastric
drainage), as dietary potassium is coupled with phosphate rather than chloride
24
WHO daily intake recommendations 24
Adults: at least 3.5 mg/d (90 mmol/d), to reduce blood pressure and risk of
cardiovascular disease, stroke, and coronary heart disease
Children: at least 3.5 mg/d (90 mmol/d), adjusted downward in proportion to

the energy requirements of children relative to those of adults
Reduce sodium salt intake
A high-sodium diet can result in excessive urinary potassium loss
Provide potassium supplementation when prescribing drugs that cause hypokalemia
Minimize the dosage of non–potassium-sparing diuretics
REFERENCES
1: Pepin J et al: Advances in diagnosis and management of hypokalemic and hyperkalemic
emergencies. Emerg Med Pract. 14(2):1-17; quiz 17-8, 2012
View In Article | Cross Reference (https://pubmed.ncbi.nlm.nih.gov/22413702)
2: Cohn JN et al: New guidelines for potassium replacement in clinical practice: a

contemporary review by the National Council on Potassium in Clinical Practice. Arch Intern
Med. 160(16):2429-36, 2000
3: Weir MR et al: Clinical perspectives on the rationale for potassium supplementation.

Postgrad Med. 127(5):539-48, 2015
4: Weiner ID et al: Hypokalemia--consequences, causes, and correction. J Am Soc Nephrol.

8(7):1179-88, 1997
5: Theisen-Toupal J: Hypokalemia and hyperkalemia. Hosp Med Clin. 4(1):34-50, 2015

View In Article
6: Halperin ML et al: Hypokalemia. In: Halperin ML et al, eds. Fluid, Electrolyte, and Acid-
Base Physiology: A Problem-Based Approach. 4th ed. Saunders; 2010:460-511
View In Article
7: Jain G et al: Genetic disorders of potassium homeostasis. Semin Nephrol. 33(3):300-9,

2013
8: Mount DB et al: Disorders of potassium balance. In: Taal MB et al, eds. Brenner and
Rector's The Kidney. 9th ed. Saunders; 2012:640-88
View In Article
9: Linas SL et al: Hypokalemia and hyperkalemia. In: Parsons PE et al, eds. Critical Care
Secrets. 5th ed. Mosby; 2013:315-21
View In Article
10: Kardalas E et al: Hypokalemia: a clinical update. Endocr Connect. 7(4):R135-R146, 2018
11: Elin RJ: Reference intervals and laboratory values. In: Goldman L et al, eds. Goldman-
Cecil Medicine. 25th ed. Saunders; 2016:2712-22
View In Article
12: Levis JT: ECG diagnosis: hypokalemia. Perm J. 16(2):57, 2012

13: Helfant RH: Hypokalemia and arrhythmias. Am J Med. 80(4A):13-22, 1986

14: Asmar A et al: A physiologic-based approach to the treatment of a patient with

hypokalemia. Am J Kidney Dis. 60(3):492-7, 2012
15: Medford-Davis L et al: Derangements of potassium. Emerg Med Clin North Am.
32(2):329-47, 2014
16: Lewis JL: Hypomagnesemia. Merck Manual Professional Version website. Updated April
2020. Accessed March 8, 2021. https://www.merckmanuals.com/professional/endocrine-and-
metabolic-disorders/electrolyte-disorders/hypomagnesemia
View In Article | Cross Reference
(https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/electrolyte-
disorders/hypomagnesemia)
17: Skogestad J et al: Hypokalemia-induced arrhythmias and heart failure: new insights and
implications for therapy. Front Physiol. 9:1500, 2018
18: Schulman M et al: Hypokalemia and cardiovascular disease. Am J Cardiol. 65(10):4E-9E;

discussion 22E-23E, 1990
19: Ahya SN et al: Acid-base and potassium disorders in liver disease. Semin Nephrol.
26(6):466-70, 2006
20: Basnet S et al: Influence of abnormal potassium levels on mortality among hospitalized
heart failure patients in the US: data from National Inpatient Sample. J Community Hosp
Intern Med Perspect. 9(2):103-7, 2019
21: Jensen HK et al: Hypokalemia in acute medical patients: risk factors and prognosis. Am
J Med. 128(1):60-7.e1, 2015
22: Collins AJ et al: Association of serum potassium with all-cause mortality in patients with
and without heart failure, chronic kidney disease, and/or diabetes. Am J Nephrol. 46(3):213-
21, 2017
23: Thongprayoon C et al: Admission serum potassium levels in hospitalized patients and
one-year mortality. Medicines (Basel). 7(1):2, 2019
24: World Health Organization: Guideline: potassium intake for adults and children. World
Health Organization; 2012
Copyright © 2021 Elsevier, Inc. All rights reserved.

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Hypokalemia - ClinicalKey 12/10/2021, 19:01

All Types Type your search Search

Key Points Urgent Action

Treatment includes both potassium and magnesium repletion, as well as addressing

the underlying cause

In the setting of hypomagnesemia, hypokalemia can be refractory to potassium

Complications can include depressed neuromuscular excitability, cardiovascular

Hypokalemia is associated with increased morbidity and mortality in patients with

Chronic hypokalemia results in hypokalemic nephropathy, a tubulointerstitial

Potassium level of 3.0 to 3.5 mEq/L

Potassium level less than 3.0 mEq/L

Rapid rate of potassium depletion that develops over a short period

Suspect intracellular shift of potassium from extracellular space

Slow rate of potassium depletion that develops over a long period

Suspect gastrointestinal loss (diarrhea) or a defect that causes renal potassium

Muscle weakness, originating in lower extremities and progressing to upper

Myalgias, originating in lower extremities and progressing to upper extremities

Polyuria, owing to decreased concentrating ability

Depressed deep muscle reflexes due to delayed peripheral nerve conduction

Muscle weakness; decreased strength typically more pronounced in proximal

Irregular cardiac rhythm

Abdominal distention (with ileus)

Causes and Risk Factors

Fistula or ileostomy (potassium lost in drainage of liquid stool)

Sodium polystyrene sulfonate

Hyperglycemia resulting in osmotic diuresis

Salt-wasting nephropathies (eg, Bartter syndrome)

Mineralocorticoid excess (primary aldosteronism)

Can be induced by prolonged ingestion of licorice

Proximal or distal renal tubular acidosis

Interstitial renal disease with concentrating defects

Diuretics (eg, thiazide, loop)

Mineralocorticoids (eg, fludrocortisone)

High doses of penicillin and penicillin derivatives

Toluene (if abused)

Inadequate potassium intake

Prolonged and extremely low dietary intake (eg, anorexia, starvation) 5

Total parenteral nutrition with inadequate potassium supplementation

Intracellular shift of potassium from extracellular space 5

Total parenteral nutrition

Hypokalemic periodic paralysis

Insulin; typically with larger doses of immediate acting preparations

Risk factors and/or associations

Autosomal dominant disorder characterized by early-onset salt-sensitive

Autosomal recessive renal tubular salt-wasting disorder characterized by

Caused by mutation in the thiazide-sensitive NaCl cotransporter (ie, SLC12A3)

Autosomal recessive disorder of impaired salt reabsorption characterized by

Caused by mutation in the kidney chloride channel B gene (ie, CLCNKB)

Primary diagnostic tools

If cause is not obvious from clinical

24-hour urine potassium collection to

Spot urine potassium concentration

Additional tests may be performed under

mineralocorticoid excess; BP,

If hypokalemia is severe (less than 3.0 mEq/L),

Treat underlying cause to prevent further episodes

Prevent or treat life-threatening manifestations and

Recommendations for specialist referral

Refer to cardiologist to manage cardiac arrhythmias

Refer to endocrinologist to treat mineralocorticoid excess due to aldosteronism

Oral dietary or pharmacologic potassium supplements are used for mild

Potassium chloride: default and preferred salt choice 14

Potassium bicarbonate: indicated for patients with hypokalemia and metabolic

In patients with significant dysrhythmias (eg, ventricular tachycardia) as a