Hyponatremia

Defined as excess water in relation to sodium level in the extracellular fluid.

Defined as serum Na less than 137 mEq/L. 


Associated with increased morbidity and mortality.  

Mild hyponatremia with serum sodium <135 mmol per liter occurs in 15-22% of hospitalized patients with hyponatremia and in 7% of ambulatory patients.

Moderate hyponatremia with serum sodium <130 mmol per liter occurs in 1-7% of hospitalized patients.

Most common electrolyte abnormality in hospitalized patients.


The most common electrolyte disorder in clinical practice.

In acute hyponatremia, the rapid decrease of serum sodium with an hours induces life-threatening brain swelling, explaining the severe clinical signs of seizures and coma is often seen in these patients.

In chronic hyponatremia, hyponatremia develops over days or weeks  and is characterized by depletion of cerebral osmolytes rather than cerebral volume expansion.

Clinically chronic hyponatremia they vary from acute hyponatremia-like symptoms to almost asymptomatic states.

The neurocognitive and motor performance, and mood stability, are markedly impaired with more profound hyponatremia.

Misleading serum sodium levels-pseudohyponatremia, are most often caused by reduction in plasma water by serum lipids or proteins.

Common in heart failure and is present in approximately 20% of patients admitted with acute heart failure and develops during decongestive treatment in additional 15-25%.

Hyponatremia among patients admitted to the hospital with congestive heart failure is associated with an increased risk for readmission and death.

The inability to correct hyponatremia over the course of hospitalization in patients with congestive heart failure is frequent and independently associated with an increase of approximately 50% in the odds of having the 30 day unplanned readmission or death.

Most frequent cause of hyponatremia, although hyponatremia associated with volume depletion of the extracellular fluid is also common.

High incidence occurs in patients with heart failure, cirrhosis and ascites.

Differentiation of hyponatremia is triggered from decreased effective circulating volume leading to ADH release versus other nonosmotic stimuli leading to the ADH effectf is one of the two first questions in evaluating severe hyponatremia.

Hyponatremia with the serum sodium of 138 mEq per liter is associated with increased mortality.

Endogenous in this causes of hyponatremia include heart, renal, and liver failure.

The most important exogenous factor is pharmaceutical drugs such as thiazide diuretics and antidepressants.

Hyponatremia in congestive heart failure or is associated with worse outcomes and increased mortality.

It is an incompletely understood process because of the association with many underlying disease states, it’s causation by multiple etiologies with differing pathophysiology, and marked differences in symptomatology and clinical outcomes based on the acuteness of chronicity of hyponatremia.

Usually classified associated hypovolemic, euvolemic or hypervolemic.

Clinical spectrum ranges from asymptomatic to headache, nausea, confusion, seizures, ataxia, and coma.

Acute severe hyponatremia can cause morbidity and mortality.

Ingestion of excess water rarely causes hyponatremia, as normal kidney function can eliminate up to 20 to 30 L of free water daily.

Develops in the context of an underlying disruption of free water elimination, usually as a result of arginine vasopressin (AVP) release or renal failure.

AVP, also known as antidiuretic hormone, is a peptide hormone produced by the hypothalamus and transported via axons to the posterior pituitary, from which it is released.

AVP is primarily responsible for regulating osmotic homeostasis of body fluids.

AVP also plays a minor role in volume homeostasis, acting mostly through vasopressin type 1A and type 2 receptors.

AVP receptor activation causes a decrease in excretion of free water.

Most total body sodium is extracellular and thus is a primary determinant of plasma tonicity.

An increase in plasma tonicity stimulates the thirst center to increase fluid consumption and causes release of AVP.

Arginine vasopressin dysregulation can be caused by both osmotic and nonosmotic mechanisms.

Adverse outcomes, including mortality, higher in patients with hyponatremia with a wide range of underlying diseases.

High mortality rate occurs with acute hyponatremia due to osmotically induced brain edema.

Hyponatremia in patients with cirrhosis is a major predictor of the hepatorenal syndrome, hepatic encephalopathy and death.

Secretion of arginine vasopressin of central importance in decline of serum sodium concentrations.

Increases morbidity and mortality among patients with heart, liver and neurologic diseases.

Increased mortality in patients with heart failure, both hospitalized and in the outpatient setting.

Hyponatremia in patients with cirrhosis is a major predictor of the development of that hepatorenal syndrome, hepatic and cephalopathy, and death.

In severe hyperlipidemia a blood sample can contain up to 25% solids and only 75% water, and can cause pseudohyponatremia.

Most common causes of serious hyponatremia are thiazide use, postoperative status, SIADH, polydipsia in psychiatric patients and following transurethral prostatic resection.

Nearly 7% of healthy elderly persons, 15-18% of patients in chronic care facilities.

Incidence and prevalence higher among older persons.

May be present with low, normal or high serum osmolality.

The presence of high osmolality indicates the presence of excessive extracellular osmoles causing the entry of intracellular water into extracellular fluid diluting sodium concentration.

High glucose levels can cause hyponatremia.

May be seen in hypovolemia, liver disease, syndrome of inappropriate ADH secretion, low cardiac output, nephritic syndrome, hypoadrenalism, hypothyroidism and in these cases is associated with low serum osmolality.

Hyponatremia associated with negative prognostic factors in congestive heart failure, liver disease, chronic kidney disease, pneumonia and hospitalized patients.


Hyperosmolar hyponatremia which can be due to hyperglycemia or other iatrogenic causes such as administration of mannitol or intravenous immunoglobulin causing intracellular water to move into the extracellular space, resulting in cellular shrinkage and lowering the blood sodium level.

Pseudo hyponatremia results from high levels of proteins or lipids that interfere with blood sodium measurement.

Psychogenic polydipsia associated with low urine osmolality.

Mild chronic lowered sodium level can be associated with subtle neurologic defects, manifested as impaired balance and attention that can increase incidence of falls.

Severe levels with serum <125 mmol per liter can cause confusion, hallucinations, coma, seizures, respiratory arrest and decerebrate posturing.

Mild symptoms include impaired memory, impaired concentration, headache, muscle cramping, weakness and dysgeusia.

When chronic may be asymptomatic.

Threshold sodium levels at which neurological complications occur appear to be higher among women than man.

Associated with hepatorenal syndrome in cirrhosis, ascites and death from liver disease

Important predictor of mortality in patients waiting for 2242

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