Hyponatremia is a common finding in clinical practice and is estimated to occur in 15% of all hospital inpatients.   It is defined as a serum sodium <135 mEq/L; severe hyponatremia is defined as a serum sodium <120 mEq/L. Patients with hyponatremia have increased morbidity and mortality compared with patients without hyponatremia.  Mild hyponatremia is an independent risk factor of adverse outcome and mortality even in the general population. 
Sodium is a major osmotic solute in the extracellular fluid and is therefore an important determinant of the extracellular volume status, serum osmolality, and tonicity. The serum sodium concentration is a measure of water status rather than total body salt content. A low serum sodium concentration indicates dilute body fluids or an excess of water. The clinical manifestations of hyponatremia depend on the rate of decline of serum sodium. An acute fall in sodium over 24 to 48 hours produces severe cerebral edema, which can be fatal.  A gradual fall in sodium over several days or weeks can be compensated for by the brain, produces relatively modest morbidity and may be asymptomatic. 
Sodium homeostasis is maintained by thirst (which drives fluid intake), ADH (which increases renal water reabsorption), aldosterone (which increases renal sodium resorption), and the kidneys (which can control sodium resorption in the proximal tubule independent of external hormonal input).
Hyponatremia may result from an inappropriate hypotonic fluid intake, inappropriate fluid retention by excessive ADH, or inadequate renal reabsorption of sodium.
Hyponatremia can be classified into 5 main types.
Hypovolemic hyponatremia: total body water decreases, but total body sodium decreases to a greater extent. The extracellular fluid volume is also decreased.
Euvolemic hyponatremia: total body water increases, but total body sodium remains unchanged. There is a modest increase in extracellular fluid volume, but not enough to cause edema.
Hypervolemic hyponatremia: total body water and sodium both increase, but total body water increases to a greater extent. The extracellular fluid volume is markedly increased, causing edema.
Hypertonic (redistributive) hyponatremia: increased osmotic pressure in the extracellular compartment causes water to shift from the intracellular to the extracellular compartment diluting extracellular sodium. However, total body sodium and water are unchanged. This is commonly seen with hyperglycemia and mannitol administration. A simple formula to correct sodium level in the presence of hyperglycemia: serum sodium is decreased by 2.4 mEq/dL for every 100 mg/dL elevation of serum glucose over 100 mg/dL.
Pseudohyponatremia: excessive lipids or proteins dilute the aqueous phase of the extracellular compartment and the measured sodium levels are low. However, this decrease is an artifact and should be excluded before proceeding with further investigations. Total body sodium and water are unchanged, and there has not been a shift of fluid between compartments. The use of ion-specific electrodes has helped reduce the incidence of this artifact. 
Hyponatremia is significant when it is associated with a decline in extracellular osmolality, as it causes cellular edema. Most tissues can tolerate cellular edema, apart from the bony calvarium due to space limitations. Brain cells have long-term adaptive mechanisms that can compensate for low serum sodium and osmolality by giving up ions like potassium and synthesising organic osmolytes to preserve cell volume. If the sodium concentration falls slowly over several days or weeks, the brain is able to use such mechanisms to adapt. For this reason, patients with chronic hyponatremia have relatively modest cerebral edema and do not develop brainstem herniation. However, if the sodium concentration falls rapidly over 24 to 48 hours, the compensatory mechanisms of the brain are overwhelmed and severe cerebral edema occurs, leading to brainstem herniation, respiratory arrest, and death. This can occur even with a modest fall in sodium (125-130 mEq/L).
Associate Professor of Medicine
University of Florida
College of Medicine Jacksonville
GM declares that she has no competing interests.
University of Alberta Hospital
SMB declares that he has no competing interests.
Lancashire Teaching Hospitals
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Professor of Medicine
JWL declares that he has no competing interests.
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