HYPONATREMIA NEJM PDF

J Intensive Care Med. Epub Jan Hyponatremia: A Review. Buffington MA 1 , Abreo K 2.

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E-mail: moc. This article has been cited by other articles in PMC. Abstract Hyponatremia is an important and common clinical problem. The etiology is multifactorial.

Hyponatremia may be euvolemic, hypovolemic or hypervolemic. Proper interpretation of the various laboratory tests helps to differentiate the various types of hyponatremia.

Treatment varies with the nature of onset -acute or chronic, severity and symptoms. Hypervolemic hyponatremia responds well to fluid restriction and diuretics. There have been several recent advances in the last year with revision in the guidelines for treatment and availability of vaptans. Judicious use of vaptans may help in treatment of hyponatremia.

The varied etiologies of hyponatremia and the multiple formulae for its correction make it a nightmare for the students and physicians alike. The guidelines for management of hyponatremia have been revised recently and, in addition new agents vaptans have become available in market for treatment of hyponatremia.

The objective of this article is to apprise the clinician with the latest protocols for management of hyponatremia and current guidelines for the use of vaptans. Water intake depends upon thirst mechanism. Thirst is stimulated by increase in osmolality.

Thirst is sensed by osmoreceptors located in the hypothalamus and leads to the release of anti-diuretic hormone vasopressin from the posterior pituitary.

Antidiuretic hormone acts on the V2 receptors located at the basolateral aspect of the collecting duct cells and leads to increased aquaporin expression on the luminal aspect of the collecting duct cells which increases water absorption and abolishes thirst. Hyponatremia occurs if there is persistent ADH stimulation which is seen in following situations. Normal but persistent ADH secretion-In volume depletion the effect of decreased volume counteracts the effect of hypoosmolality and ADH stimulation continues to occur.

Effective arterial blood volume depletion occurs by two mechanisms: True volume depletion; and in edematous patients with heart failure or cirrhosis in whom tissue perfusion is reduced because of a low cardiac output or arterial vasodilation, respectively. The reduction in tissue perfusion is sensed by baroreceptors at three sites: i In the carotid sinus and aortic arch that regulate sympathetic activity and, with significant volume depletion, the release of antidiuretic hormone; ii In the glomerular afferent arterioles that regulate the activity of the renin-angiotensin system; and iii in the atria and ventricles that regulate the release of natriuretic peptides.

As a result there is water retention Abnormal ADH secretion e. Patients with acute hyponatremia develop neurologic symptoms resulting from cerebral edema induced by water movement into the brain. These may include seizures, impaired mental status or coma and death.

Brain adapts itself to hyponatremia by generation of idiogenic osmoles. This is a protective mechanism that reduces the degree of cerebral edema; it begins on the first day and is complete within several days. Hence in chronic hyponatremia patients may appear asymptomatic. Mild hyponatremia is characterized by gastrointestinal tract symptoms nausea, vomiting, loss of appetite.

Hyponatremia in the elderly may manifest with frequent falls and gait disturbances.

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Hyponatremia: A Review.

Nek NEJM — The Syndrome of Inappropriate Antidiuresis The Clinical Problem Hyponatremia, defined as an excess of water in relation to the sodium in the extracellular fluid, is the most common electrolyte disorder in hospitalized patients. Hyponatreia some patients, mutations of the aquaretic i. Ellison reports receiving research grants from Chemica Technologies, and Dr. Perioperative fluid therapy in children: Many limit correction to 8 mmol per liter over a period of 24 hours and 18 mmol per liter over a period of 48 hours; close monitoring hyponatremua the rate of correction every 2 to 3 hours 25 is recommended to avoid overcorrection. J Clin Pathol ; The rate of change in serum sodium levels must be monitored every 2 to 3 hours, and the infusion adjusted as needed. Oral intake of urea 30 g per day is effective but is nejmm tolerated.

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E-mail: moc. This article has been cited by other articles in PMC. Abstract Hyponatremia is an important and common clinical problem. The etiology is multifactorial. Hyponatremia may be euvolemic, hypovolemic or hypervolemic. Proper interpretation of the various laboratory tests helps to differentiate the various types of hyponatremia. Treatment varies with the nature of onset -acute or chronic, severity and symptoms.

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Hyponatremia: A practical approach

Therapy of dysnatremic disorders. Br J Anaesth ; In some patients, mutations of the aquaretic i. Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deficits. Disturbances of sodium in critically ill adult neurologic patients: This disorder, which includes both central pontine and extrapontine myelinolysis, begins with gyponatremia and affective changes generally after initial improvement of neurologic symptoms with treatmentfollowed by mutism or dysarthria, spastic quadriparesis, and pseudobulbar palsy. When diagnostic uncertainty remains, volume contraction of the extracellular fluid can be ruled out by infusing 2 liters of 0. The Clinical Problem Hyponatremia, defined as an excess hyopnatremia water in relation to the sodium in the extracellular fluid, is the most common electrolyte disorder in hospitalized patients.

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