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

Hyponatremia is the sodium level of less than 135 mmol per liter and is the most common electrolyte abnormality, affecting approximately 5% of adults, and 35% of hospitalized patients.

Defined as serum Na less than 135 mEq/L.

It is characterized as mild (130-1 34 mmol per liter), moderate (125–129 mmol per liter), or severe (less than 125 mmol per liter).

About 70% of hyponatremia cases are mild.

Even mild hyponatremia is associated with adverse outcomes: increased rates of hospitalization, readmission, resource use, and death.

Serum sodium levels approximate the ratio of osmotically active sodium and potassium content to total body water.

Hyponatremia typically reflects water, excess relative to these body cations, most commonly from disorders impairing electrolyte free water excretion by the kidneys (aquaresis).

Impaired aquaresis largely depends on increased secretion of arginine vasopressin (AVP), the antidiuretic hormone, which activates the vasopressin 2 receptor in the collecting duct of the nephron, thus promoting water retention.

Arginine vasopressin is triggered by osmotic and hemodynamic, stimuli (hypertonicity and reduced defective arterial blood volume, respectively.

Typically, hyponatremia is due to water retention that dilutes the serum sodium level and osmolality of less than 275 mOsm/kg.

Effective osmolality, tonicity, refers to the contribution of osmolality by solutes with low cell membrane permeability (sodium, its anions, and glucose), causing transcellular water shifts.

Tonicity is calculated from sodium and glucose, and for patients without hypoglycemia, tonicity is approximated by serum sodium level.

Normal tonicity is 270 mOsm per kilogram to 285 mOsm/kilogram.

In contrast to sodium and glucose, urea increases osmolality, but not tonicity, because it has a high cell membrane permeability: Alcohol acts similarly.

Hyponatremia may be associated with normal or high tonicity.

Hyperglycemia translocates water from cells into extracellular fluid and causes hyponatremia simultaneously with hypertonicity; each 100 g milligram per deciliter increase in the glucose level decreases serum sodium level by approximately 2 mEq per liter.

Pseudo hyponatremia is a laboratory artifact that occurs with severe hyperproteinemia or extreme hyperlipidemia, in which hyponatremia is associated with normal tonicity.

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.

Affects approximately 5% of adults.

Approximately 20% of people who are older than 65 years of age have hyponatremia as well as 35% of patients who are hospitalized, 30% of patients with heart failure, and 50% of patients with cancer or cirrhosis.

Most common electrolyte abnormality in hospitalized patients.

The most common electrolyte disorder in clinical practice.

Approximately sodium of potassium and 85% of potassium are osmotically active, and hyponatremia represents excess water relative to the exchangeable sodium and potassium levels; Hyponatremia may develop with normal, decreased, or increased sodium content.

Primary polydipsia is characterized by increase total body water.

Hypovolemic hyponatremia occurs with diarrhea is characterized by reduced exchangeable sodium and potassium levels, with a smaller decrease in total body water.

Hypervolemic hyponatremia as with heart failure is characterized by increased exchangeable sodium level with a larger increase in total body water.

The syndrome of inappropriate ADH is characterized by mildly reduced exchangeable sodium and potassium levels combined with increase total body water.

Clinical manifestations of hyponatremia depend on the rapidity of development, duration, and severity of hyponatremia.

Symptoms are more common in patients with acute hyponatremia in those with chronic hyponatremia because of brain adaptation which corrects hypotonicity induced brain swelling

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.

Because of the skull rigidity, brain swelling from hypotonicity induced water entry into brain cells causes intracranial hypertension, which may reduce cerebral blood flow.

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.

Symptoms of hyponatremia range from mild and nonspecific complaints of weakness, nausea, headache, to severe and life-threatening symptoms of vomiting, somnolence, seizures, and cardiorespiratory distress.

Acute severe hyponatremia can be associated with brain herniation, respiratory arrest, permanent brain damage, and death.

Menstruating women are at higher risk of having severe symptoms when they develop acute hyponatremia.

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

Hypotonic hyponatremia can result in cerebral edema.

Hyponatremia is associated with neurologic symptoms that range from fatigue, cognitive impairment to seizures, coma, and death.

Mild chronic hyponatremia in older individuals is associated with cognitive deficits, gait disturbances, increased rates of falls and fractures.

Noncardiac pulmonary edema can occur in patients with hyponatremia due to water intoxication during endurance sports or intoxication with ecstasy, with hypoxemia worsening brain edema.

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.

Osmotic demyelinization syndrome can complicate hyponatremia with symptoms including seizures, paralysis, and Parkinson like neuropathologic features.

Endogenous 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.

The correction of serum sodium level by 4 to 6 mEq per liter within one to two hours is recommended and can reverse hyponatremic encephalopathy.

Intravenous bolus containing 100 mL or 150 mL dose of 3% sodium chloride administered over 10to 20 minutes and repeated 2 to 3 times until the desired sodium level is achieved.

Serum sodium should not be increased by more than 10 mEq per liter within the first 24 hours and by 18 hours within the first 48 hours.

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.

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.

Hyponatremia is a secondary cause of osteoporosis and bone fractures with the risk increasing with severity of hyponatremia.

Brain volume adaptation to hyponatremia increases the risk of osmotic demyelination.

Osmotic demyelination results from overly rapid correction of chronic hyponatremia whose daily correction of serum sodium level by greater than 12 mEq per liter.

In patients with high risk osmotic demyelinization, the serum sodium level should not be increased by more than 8 mEq per liter within any 24 hour period.

Osmotic demyelination involves the central pons and other areas of the brain.

Depletion of organic osmolytes predisposes individuals to astrocyte injury, disruption of the blood brain barrier, and myelinosis after the osmotic stress of overly rapid correction of chronic hyponatremia.

Bolus infusion of 3% sodium chloride attained a target change in serum sodium level faster than a continuous infusion of 3% sodium chloride, but is associated with higher rates of overly rapid correction, and need for relowering therapy for serum sodium level.

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