Hypernatremia overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The | Sodium regulation is key to maintain normal cellular function. The kidney is a major organ involved in sodium and water balance. Once water loss is excessive or sodium intake is high, sodium levels go up. However, [[osmoreceptor]]s in our [[hypothalamus]] detect alterations in plasma [[osmolarity]] and stimulate the thirst response and the secretion of [[vasopressin]] (the [[antidiuretic hormone]] (ADH) in order to restore the body's fluid balance. As a result, hypernatremia is seen when our body's defense against hyperosmolarity is overwhelmed or defective. | ||
==Causes== | ==Causes== | ||
Hypernatremia can be caused by many disease processes and drugs. Free water loss is the most important mechanism leading to sodium excess. [[Diarrhea]], [[diabetes insipidus]], [[diuretics]], [[osmotic agents]], [[insensible losses]] or [[impaired thirst]] response due to any disease process affecting the hypothalamus are common causes. Primary sodium excess is a rare cause of hypernatremia and ca be due to sodium salt ingestion or [[minaralocorticoid excess]]. | |||
==Risk Factors== | |||
== | Patients at risk of hypernatremia include those patients who have impaired thirst (such as those in coma or those with a neurologic deficit) and those with a high rate of [[insensible losses]] of free water such as [[burn]] victims and patients with [[diarrhea]]. | ||
==Diagnosis== | ==Diagnosis== | ||
===History and Symptoms=== | |||
===History | The symptoms of hypernatremia are subtle and include [[weakness]] or [[lethargy]]. With more severe elevations of the sodium level, [[seizure]]s and [[coma]] may occur. | ||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
The urine osmolarity | The diagnostic work-up of hypernatremia includes many lab studies including urine [[osmolarity]] which tells whether the kidney's function is altered or not. The water deprivation test aims at diagnosing the cause of [[diabetes insipidus]] (DI). In response to water deprivation, fluid homeostatic mechanisms work to retain water by stimulating the secretion of a hormone called [[vasopressin]] (antidiuretic hormone (ADH) from the posterior pituitary gland. Vasopressin exerts its effects on the medullary collecting ducts of the kidney where it increases water retention and thus maintaining normal osmolar balance. In patients with DI, this mechanism is impaired, either due to decreased ADH secretion (central DI) or renal resistance to ADH urine concentrating effects (nephrogenic DI) (see below for a more detailed discussion of this test). Other lab studies can be done to investigate about adrenal or thyroid disease. Brain imagery can identify any cerebral process causing hypothalamic dysfunction. | ||
==Treatment== | ==Treatment== | ||
===Medical Therapy=== | |||
Correcting sodium level is vital in order to prevent any permanent brain damage. Free water replacement is required and the amount is calculated using a formula mentioned below. The management of any other condition causing hypernatremia should be adressed as well. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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[[Category:Nephrology]] | [[Category:Nephrology]] | ||
[[Category:Electrolyte disturbance]] | [[Category:Electrolyte disturbance]] | ||
[[Category:Needs overview]] | |||
{{WikiDoc Help Menu}} | {{WikiDoc Help Menu}} | ||
{{WikiDoc Sources}} | {{WikiDoc Sources}} | ||
Revision as of 20:56, 7 February 2013
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Assistant Editor(s)-In-Chief: Jack Khouri
Overview
Hypernatremia is an electrolyte disturbance consisting of an elevated sodium level in the blood (compare to hyponatremia, meaning a low sodium level). It is defined as a serum sodium concentration exceeding 145 mEq/L. The most common cause of hypernatremia is not an excess of sodium, but a relative deficit of free water in the body. For this reason, hypernatremia is often synonymous with the less precise term dehydration.
Pathophysiology
Sodium regulation is key to maintain normal cellular function. The kidney is a major organ involved in sodium and water balance. Once water loss is excessive or sodium intake is high, sodium levels go up. However, osmoreceptors in our hypothalamus detect alterations in plasma osmolarity and stimulate the thirst response and the secretion of vasopressin (the antidiuretic hormone (ADH) in order to restore the body's fluid balance. As a result, hypernatremia is seen when our body's defense against hyperosmolarity is overwhelmed or defective.
Causes
Hypernatremia can be caused by many disease processes and drugs. Free water loss is the most important mechanism leading to sodium excess. Diarrhea, diabetes insipidus, diuretics, osmotic agents, insensible losses or impaired thirst response due to any disease process affecting the hypothalamus are common causes. Primary sodium excess is a rare cause of hypernatremia and ca be due to sodium salt ingestion or minaralocorticoid excess.
Risk Factors
Patients at risk of hypernatremia include those patients who have impaired thirst (such as those in coma or those with a neurologic deficit) and those with a high rate of insensible losses of free water such as burn victims and patients with diarrhea.
Diagnosis
History and Symptoms
The symptoms of hypernatremia are subtle and include weakness or lethargy. With more severe elevations of the sodium level, seizures and coma may occur.
Laboratory Findings
The diagnostic work-up of hypernatremia includes many lab studies including urine osmolarity which tells whether the kidney's function is altered or not. The water deprivation test aims at diagnosing the cause of diabetes insipidus (DI). In response to water deprivation, fluid homeostatic mechanisms work to retain water by stimulating the secretion of a hormone called vasopressin (antidiuretic hormone (ADH) from the posterior pituitary gland. Vasopressin exerts its effects on the medullary collecting ducts of the kidney where it increases water retention and thus maintaining normal osmolar balance. In patients with DI, this mechanism is impaired, either due to decreased ADH secretion (central DI) or renal resistance to ADH urine concentrating effects (nephrogenic DI) (see below for a more detailed discussion of this test). Other lab studies can be done to investigate about adrenal or thyroid disease. Brain imagery can identify any cerebral process causing hypothalamic dysfunction.
Treatment
Medical Therapy
Correcting sodium level is vital in order to prevent any permanent brain damage. Free water replacement is required and the amount is calculated using a formula mentioned below. The management of any other condition causing hypernatremia should be adressed as well.