Electrolyte imbalance

Electrolyte imbalance, or water-electrolyte imbalance, is an abnormality in the concentration of electrolytes in the body. Electrolytes play a vital role in maintaining homeostasis within the body. They help to regulate heart and neurological function, fluid balance, oxygen delivery, acid–base balance and much more. Electrolyte imbalances can develop by consuming too little or too much electrolyte as well as excreting too little or too much electrolyte.

Water–electrolyte imbalance

Electrolyte disturbances are involved in many disease processes, and are an important part of patient management in medicine.[1] The causes, severity, treatment, and outcomes of these disturbances can vastly differ depending on the implicated electrolyte.[2] The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium or calcium. Other electrolyte imbalances are less common and often occur in conjunction with major electrolyte changes. The kidney is the most important organ in maintaining appropriate fluid and electrolyte balance, but other factors such as hormonal changes and physiological stress play a role.[1] Chronic laxative abuse or severe diarrhea or vomiting (gastroenteritis) can lead to electrolyte disturbances along with dehydration. People suffering from bulimia or anorexia nervosa are at especially high risk for an electrolyte imbalance. At worst, electrolyte imbalance can lead to death by cardiac failure if not treated appropriately and rapidly enough,[3][4][5] as may be observed with the refeeding syndrome.

General function

Electrolytes are important because they are what cells (especially nerve, heart and muscle cells) use to maintain voltages across their cell membranes and to carry electrical impulses (nerve impulses, muscle contractions) across themselves and to other cells. Kidneys work to keep the electrolyte concentrations in blood constant despite changes in the body.[3][5] For example, during heavy exercise, electrolytes are lost in sweat, particularly in the form of sodium and potassium.[5] The kidneys can also generate dilute urine to balance sodium levels.[5] These electrolytes must be replaced to keep the electrolyte concentrations of the body fluids constant. Hyponatremia, or low sodium, is the most commonly seen type of electrolyte imbalance.[6][7]

Treatment of electrolyte imbalance depends on the specific electrolyte involved and whether the levels are too high or too low.[2] The level of aggressiveness of treatment and choice of treatment may change depending on the severity of the disturbance.[2] If the levels of an electrolyte are too low, a common response to electrolyte imbalance may be to prescribe supplementation. However, if the electrolyte involved is sodium, the issue is not a deficiency of sodium, but rather a water excess, causing the imbalance. Supplementation for these people may correct the electrolyte imbalance but at the expense of volume overload, which can be dangerous particularly for neonates.[3] Because each individual electrolyte affects physiological function differently, they must be considered separately when discussing causes, treatment, and complications.


Sodium and its homeostasis in the human body is highly dependent on fluids. The human body is approximately 60% water, a percentage which is also known as total body water. The total body water can be divided into two compartments called extracellular fluid (ECF) and intracellular fluid (ICF). The majority of the sodium in the body stays in the extracellular fluid compartment.[8] This compartment consists of the fluid surrounding the cells and the fluid inside the blood vessels. ECF has a sodium concentration of approximately 140 mEq/L.[8] Because cells membranes are permeable to water and not sodium, the movement of water across membranes impacts the concentration of sodium in the blood. Sodium acts as a force that pulls water across membranes, and water moves from places with lower sodium concentration to places with higher sodium concentration. This happens through a process called Osmosis.[8] When evaluating sodium imbalances, both total body water and total body sodium must be considered.[2]


Hypernatremia means that the concentration of sodium in the blood is too high. An individual is considered to be have high sodium at levels above 145 mEq/L of sodium. Hypernatremia is not common in individuals with no other health concerns.[2] Most individuals with this disorder have either experienced loss of water from diarrhea, altered sense of thirst, inability to consume water, inability of kidneys to make concentrated urine, or increased salt intake.[2][8]


There are three types of hypernatremia each with different causes.[2] The first is dehydration along with low total body sodium. This is most commonly caused by heatstroke, burns, extreme sweating, vomiting, and diarrhea.[2] The second is low total body water with normal body sodium. This can be caused by Diabetes insipidus, renal disease, Hypothalamic dysfunction, Sickle cell disease, and certain drugs.[2] The third is increased total body sodium which is caused by increased ingestion, Conn's Disease, or Cushing's syndrome.[2]


Symptoms of hypernatremia may vary depending on type and how quickly the electrolyte disturbance developed.[8] Common symptoms are dehydration, nausea, vomiting, fatigue, weakness, increased thirst, excess urination. Patients may be on medications that caused the imbalance such as Diuretics or Nonsteroidal anti-inflammatory drugs.[8] Some patients may have no obvious symptoms at all.[8]


It is crucial to first assess the stability of the patient. If there are any signs of shock such as Tachycardia or Hypotension, these must be treated immediately with IV saline infusion.[2][8]  Once the patient is stable, it is important to identify the underlying cause of hypernatremia as that may affect the treatment plan.[2][8] The final step in treatment is to calculate the patients free water deficit, and to replace it at a steady rate using a combination of oral or IV fluids.[2][8]  The rate of replacement of fluids varies depending on how long the patient has been hypernatremic. Lowering the sodium level too quickly can cause cerebral edema.[8]


Hyponatremia means that the concentration of sodium in the blood is too low. It is generally defined as a concentration lower than 135 mEq/L.[9] This relatively common electrolyte disorder can indicate the presence of a disease process, but in the hospital setting is more often due to administration of Hypotonic fluids.[10][9] The majority of hospitalized patients only experience mild hyponatremia, with levels above 130 mEq/L. Only 1-4% of patients experience levels lower than 130 mEq/L.[10]


Hyponatremia has many causes including Heart failure, Chronic kidney disease, Liver disease, treatment with Thiazide diurectics, Psychogenic polydipsia, Syndrome of inappropriate antidiuretic hormone secretion.[9] It can also be found in the postoperative state, and in the setting of accidental water intoxication as can be seen with intense exercise. [9] Common causes in pediatric patients may be diarrheal illness, frequent feedings with dilute formula, water intoxication via excessive consumption, and Enemas.[9] Pseudohyponatremia is a false low sodium reading that can be caused by high levels of fats or proteins in the blood.[10][9] Dilutional hyponatremia can happen in diabetics as high glucose levels pull water into the blood stream causing the sodium concentration to be lower.[10][9] Diagnosis of the cause of hyponatremia relies on three factors: volume status, Plasma osmolality, urine sodium levels and Urine osmolality.[10][9]


Many individuals with mild hyponatremia will not experience symptoms. Severity of symptoms is directly correlated with severity of hyponatremia and rapidness of onset.[9] General symptoms include loss of appetite, nausea, vomiting, confusion, agitation, and weakness.[10][9] More concerning symptoms involve the Central nervous system and include seizures, coma, and death due to Brain herniation.[10][9] These usually do not occur until sodium levels fall below 120 mEq/L.[9]


Severity of symptoms, time to onset, volume status, and sodium concentration all dictate appropriate treatment.[10] The patient is immediately treated with Hypertonic saline where the sodium level is <120 mEq/L, the patient is experiencing severe neurological symptoms, or the onset was rapid.[10] In non-emergent situations, it is important to correct the sodium slowly to minimize risk of Osmotic demyelination syndrome.[10][9] Method of correction depends on the underlying cause of the imbalance. If a patient has low total body water and low sodium they are typically given an IV fluid called Normal saline.[9] If a patient has high total body water due to heart failure or kidney disease, they may be placed on fluid and salt restriction or treated with a Loop diuretic.[9] If a patient has a normal volume of total body water, they are placed on fluid restriction alone.[9]


Potassium resides mainly inside the cells of the body, so its concentration in the blood can range anywhere from 3.5 mEq/L to 5 mEq/L.[10] The kidneys are responsible for excreting the majority of potassium from the body.[10] This means their function is crucial for maintaining a proper balance of potassium in the blood stream.


Hyperkalemia means the concentration of potassium in the blood is too high. This occurs when the concentration of potassium is >5 mEq/L.[9][10] It can lead to cardiac Arrhythmias and even death.[9] As such it is considered to be the most dangerous electrolyte disturbance.[9]


Hyperkalemia is typically caused by decreased excretion by the kidneys, shift of potassium to the extracellular space, or increased consumption of potassium rich foods in patients with kidney failure.[9] The most common cause of hyperkalemia is lab error due to potassium released as blood cells from the sample break down.[10] Other common causes are kidney disease, cell death, Acidosis, and drugs that affect kidney function.[9]


Part of the danger of hyperkalemia is that it is often asymptomatic, and only detected during normal lab work done by primary care physicians.[9] As potassium levels get higher, individuals may begin to experience nausea, vomiting, and diarrhea.[9] Patients with severe hyperkalemia, defined by levels above 7 mEq/L, may experience muscle cramps, numbness, tingling, absence of reflexes, and paralysis.[9][10] Patients may experience arrhythmias that can result in death.[9][10]


There are three mainstays of treatment of hyperkalemia. These are stabilization of cardiac cells, shift of potassium into the cells, and removal of potassium from the body.[9][10] Stabilization of cardiac muscle cells is done by administering calcium intravenously.[9] Shift of potassium into the cells is done using both insulin and albuterol inhalers.[9] Excretion of potassium from the body is done using either hemodialysis, loop diuretics, or a resin that causes potassium to be excreted in the fecal matter.[9]


The most common electrolyte disturbance, hypokalemia means that the concentration of potassium is <3.5 mEq/L.[9] It often occurs concurrently with low magnesium levels.[9]


Low potassium is caused by increased excretion of potassium, decreased consumption of potassium rich foods, movement of potassium into the cells, or certain endocrine diseases.[9] Excretion is the most common cause of hypokalemia and can be caused by diuretic use, metabolic acidosis, diabetic ketoacidosis, hyperaldosteronism, and renal tubular acidosis.[9] Potassium can also be lost through vomiting and diarrhea.[10]


Hypokalemia is often asymptomatic, and symptoms may not appear until potassium concentration is <2.5 mEq/L.[10] Typical symptoms consist of muscle weakness and cramping. Low potassium can also cause cardiac arrythmias.[9][10]


Hypokalemia is treated by replacing the body's potassium. This can occur either orally or intravenously.[9][10] Because low potassium is usually accompanied by low magnesium, patients are often given magnesium alongside potassium.[10]


Though calcium is the most plentiful electrolyte in the body, a large percentage of it is used to form the bones.[10] It is mainly absorbed and excreted through the GI system.[10] The majority of calcium resides extracellularly, and it is crucial for the function of neurons, muscle cells, function of enzymes, and coagulation.[10]


Hypercalcemia is when the concentration of calcium in the blood is too high. This occurs above 10.5 mEq/dL.[9] Very high levels of calcium in the blood can cause severe issues.[9]


The most common causes of hypercalcemia are certain types of cancer, hyperparathyroidism, hyperthyroidism, pheochromocytoma, excessive ingestion of vitamin D, sarcoidosis, and tuberculosis.[9] Hyperparathyroidism and malignancy are the predominate causes.[10] It can also be caused by muscle cell breakdown, prolonged immobilization, dehydration.[9]


The predominate symptoms of hypercalcemia are abdominal pain, constipation, kidney stones, extreme thirst, excessive urination, nausea and vomiting.[9][10] In severe cases where the calcium concentration is >14 mEq/dL, individuals may experience confusion, altered mental status, coma, and seizure.[9][10]


Primary treatment of hypercalcemia consists of administering IV fluids.[9] If the hypercalcemia is severe and/or associated with cancer, it may be treated with bisphosphonates.[9][10] For very severe cases, hemodialysis may be considered for rapid removal of calcium from the blood.[9][10]



Hypoparathyroidism and vitamin D deficiency are common causes of hypocalcemia.[9] It can also be caused by malnutrition, blood transfusion, ethylene glycol intoxication, and pancreatitis.[9]


Neurological and cardiovascular symptoms are the most common manifestations of hypocalcemia.[9][10] Patients may experience muscle cramping or twitching, and numbness around the mouth and fingers. They may also have shortness of breath, low blood pressure, and cardiac arrhythmias.[9]


Patients with hypocalcemia may be treated with either oral or IV calcium.[9] Typically, IV calcium is reserved for patients with severe hypocalcemia.[9][10] It is also important to check magnesium levels in patients with hypocalcemia and to replace magnesium if it is low.[10]

See also


  1. Balcı, Arif Kadri; Koksal, Ozlem; Kose, Ataman; Armagan, Erol; Ozdemir, Fatma; Inal, Taylan; Oner, Nuran (2013). "General characteristics of patients with electrolyte imbalance admitted to emergency department". World Journal of Emergency Medicine. 4 (2): 113–116. doi:10.5847/wjem.j.issn.1920-8642.2013.02.005. ISSN 1920-8642. PMC 4129840. PMID 25215103.
  2. Walls, Ron M.; Hockberger, Robert S.; Gausche-Hill, Marianne (2018). Rosen's Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Elsevier. pp. 1516–1532. ISBN 978-0-323-35479-0.
  3. Bockenhauer, D; Zieg, J (September 2014). "Electrolyte disorders". Clinics in Perinatology. 41 (3): 575–90. doi:10.1016/j.clp.2014.05.007. PMID 25155728.
  4. Tisdall, M; Crocker, M; Watkiss, J; Smith, M (January 2006). "Disturbances of sodium in critically ill adult neurologic patients: a clinical review". Journal of Neurosurgical Anesthesiology. 18 (1): 57–63. doi:10.1097/01.ana.0000191280.05170.0f. PMC 1513666. PMID 16369141.
  5. Moritz, ML; Ayus, JC (November 2002). "Disorders of water metabolism in children: hyponatremia and hypernatremia". Pediatrics in Review. 23 (11): 371–80. doi:10.1542/pir.23-11-371. PMID 12415016.
  6. Dineen, R; Thompson, CJ; Sherlock, M (June 2017). "Hyponatraemia – presentations and management". Clinical Medicine. 17 (3): 263–69. doi:10.7861/clinmedicine.17-3-263. PMC 6297575. PMID 28572229.
  7. Ályarez L, E; González C, E (June 2014). "[Pathophysiology of sodium disorders in children]". Revista chilena de pediatria (Review). 85 (3): 269–80. doi:10.4067/S0370-41062014000300002. PMID 25697243.
  8. Tintinalli, Judith E.; Stapczynski, J. Stephan; Ma, O. John; Yealy, Donald M.; Meckler, Garth D.; Cline, David M. (2016). Tintinalli's Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill. ISBN 978-0-07-179476-3.
  9. Walls, Ron M.; Hockberger, Robert S.; Gausche-Hill, Marianne (2018). Rosen's Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Elsevier. pp. 1516–1532. ISBN 978-0-323-35479-0.
  10. Tintinalli, JE; Stapczynski, J; Ma, O; Yealy, DM; Meckler, GD; Cline, DM (2016). Tintinalli's Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill. ISBN 978-0-07-179476-3.
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