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Sodium[edit]

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.[1] This compartment is comprised of the fluid surrounding the cells and the fluid inside the blood vessels. ECF has a sodium concentration of approximately 140 mEq/L.[1] 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.[1] When evaluating sodium imbalances, both total body water and total body sodium must be considered.[2]

Hypernatremia[edit]

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.[1][2]

Causes[edit]

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[edit]

Symptoms of hypernatremia may vary depending on type and how quickly the electrolyte disturbance developed.[1] 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.[1] Some patients may have no obvious symptoms at all.[1]

Treatment[edit]

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. [1][2] Once the patient is stable, it is important to identify the underlying cause of hypernatremia as that may affect the treatment plan.[1][2] 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. [1][2] 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.[1]

Hyponatremia[edit]

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.[2] 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.[1][2] 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.[1]

Causes[edit]

Hyponatremia has many causes including Heart failure, Chronic kidney disease, Liver disease, treatment with Thiazide diurectics, Psychogenic polydipsia, Syndrome of inappropriate antidiuretic hormone secretion.[2] It can also be found in the postoperative state, and in the setting of accidental water intoxication as can be seen with intense exercise. [2] Common causes in pediatric patients may be diarrheal illness, frequent feedings with dilute formula, water intoxication via excessive consumption, and Enemas.[2] Pseudohyponatremia is a false low sodium reading that can be caused by high levels of fats or proteins in the blood.[1][2] Dilutional hyponatremia can happen in diabetics as high glucose levels pull water into the blood stream causing the sodium concentration to be lower.[1][2] Diagnosis of the cause of hyponatremia relies on three factors: volume status, Plasma osmolality, urine sodium levels and Urine osmolality.[1][2]

Symptoms[edit]

Many individuals with mild hyponatremia will not experience symptoms. Severity of symptoms is directly correlated with severity of hyponatremia and rapidness of onset.[2] General symptoms include loss of appetite, nausea, vomiting, confusion, agitation, and weakness.[1][2] More concerning symptoms involve the Central nervous system and include seizures, coma, and death due to Brain herniation.[1][2] These usually do not occur until sodium levels fall below 120 mEq/L.[2]

Treatment[edit]

Severity of symptoms, time to onset, volume status, and sodium concentration all dictate appropriate treatment.[1] 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.[1] In non-emergent situations, it is important to correct the sodium slowly to minimize risk of Osmotic demyelination syndrome.[1][2] Method of correction depends on the underlying cause. If a patient has low total body water and low sodium

References[edit]

  1. ^ a b c d e f g h i j k l m n o p q r s t u 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.
  2. ^ a b c d e f g h i j k l m n o p q r s t u v w 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.