{{Hypernatremia}}
{{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]]

==Overview==
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.

==Treatment==

* Three factors should be considered when treating hypernatremia: the volume status, the severity of the patient's symptoms and the time over which hypernatremia has occured.

* The cornerstone of treatment is administration of free water to correct the relative water deficit.

* Water can be replaced orally or [[intravenous]]ly (IV).

* Patients with hypovolemic hypernatremia (ie, patients with GI losses (diarrhea, vomiting), skin losses (burn patients) or renal losses (loop diuretics or osmotic diuresis)): water and sodium deficit should be replaced with isotonic normal saline (0.9%) solutions because there is concomitant loss of both sodium and water. when the patient is hemodynamically stable, 0.45% saline solutions should be used to replace the remainder of the sodium and water deficit.

* Patients with euvolemic hypernatremia (ie, patients with renal losses due to diabetes insipidus (both neurogenic and nephrogenic) or extrarenal losses (sweating, fever, mechanical ventilation, defective thirst mechanism) with no replacement of the water deficit): water losses can be calculated by the following formula:

''Free Water deficit (L)= 0.6 x (body weight(kg)) x ((plasma[Sodium]/140)-1)''.

Oral intake of water or IV 5% dextrose solutions can be used to replace water loss in euvolemic hypernatremia.
** Acute hypernatremia should be treated by rapid replacement of water losses. The remainder of the deficit could be administered over 24 to 48hours after the neurologic manifestations resolve.
** '''Overly rapid correction of chronic hypernatremia is potentially very dangerous'''. As we mentioned before, The body (in particular the [[brain]]) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, once this adaptation has occurred especially in patients with chronic hypernatremia, causes water to flow into brain cells and causes them to swell (cerebral edema). This can lead to [[cerebral edema]], potentially resulting in seizures, permanent [[brain damage]], or death. The rate of chronic hypernatremia correction should be '''0.5 meq/l/hour''' and no more than 1 meq per hour. Significant hypernatremia should be treated carefully by a [[physician]] or other medical professional with experience in treatment of [[electrolyte imbalance]]s.
** Central DI should be treated with desmopressin and drugs that increase vasopressin release eg Clofibrate.
** Nephrogenic DI can be treated with Thiazide diuretics, low salt and low protein diet.

* Patients with hypervolemic hypernatremia: These patients have excess sodium with an increased total body volume; diuretics should be administered to remove the excess sodium.

==References==
{{Reflist|2}}

[[Category:Electrophysiology]]
[[Category:Cardiology]]
[[Category:Endocrinology]]
[[Category:Emergency medicine]]
[[Category:Nephrology]]
[[Category:Electrolyte disturbance]]
[[Category:Blood tests]]
[[Category:Intensive care medicine]]

[[fr:Hypokaliémie]]
[[pl:Hipokaliemia]]
[[pt:Hipocaliémia]]
[[ru:Гипокалиемия]]
[[vi:Hạ kali máu]]
[[Category:Inborn errors of metabolism]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Hypernatremia treatment

2011-12-12T14:33:13Z

Jack Khouri: /* Treatment */

{{Hypernatremia}}
{{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]]

==Overview==
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.

==Treatment==

* Three factors should be considered when treating hypernatremia: the volume status, the severity of the patient's symptoms and the time over which hypernatremia has occured.

* The cornerstone of treatment is administration of free water to correct the relative water deficit.

* Water can be replaced orally or [[intravenous]]ly (IV).

* Patients with hypovolemic hypernatremia (ie, patients with GI losses (diarrhea, vomiting), skin losses (burn patients) or renal losses (loop diuretics or osmotic diuresis)): water and sodium deficit should be replaced with isotonic normal saline (0.9%) solutions because there is concomitant loss of both sodium and water. when the patient is hemodynamically stable, 0.45% saline solutions should be used to replace the remainder of the sodium and water deficit.

* Patients with euvolemic hypernatremia (ie, patients with renal losses due to diabetes insipidus (both neurogenic and nephrogenic) or extrarenal losses (sweating, fever, mechanical ventilation, defective thirst mechanism) with no replacement of the water deficit): water losses can be calculated by the following formula:

''Free Water deficit (L)= 0.6 x (body weight(kg)) x ((plasma[Sodium]/140)-1)''.

Oral intake of water or IV 5% dextrose solutions can be used to replace water loss in euvolemic hypernatremia.

** Acute hypernatremia should be treated by rapid replacement of water losses. The remainder of the deficit could be administered over 24 to 48hours after the neurologic manifestations resolve.

** '''Overly rapid correction of chronic hypernatremia is potentially very dangerous'''. As we mentioned before, The body (in particular the [[brain]]) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, once this adaptation has occurred especially in patients with chronic hypernatremia, causes water to flow into brain cells and causes them to swell (cerebral edema). This can lead to [[cerebral edema]], potentially resulting in seizures, permanent [[brain damage]], or death. The rate of chronic hypernatremia correction should be '''0.5 meq/l/hour''' and no more than 1 meq per hour. Significant hypernatremia should be treated carefully by a [[physician]] or other medical professional with experience in treatment of [[electrolyte imbalance]]s.

** Central DI should be treated with desmopressin and drugs that increase vasopressin release eg Clofibrate.

** Nephrogenic DI can be treated with Thiazide diuretics, low salt and low protein diet.

* Patients with hypervolemic hypernatremia: These patients have excess sodium with an increased total body volume; diuretics should be administered to remove the excess sodium.

==References==
{{Reflist|2}}

[[Category:Electrophysiology]]
[[Category:Cardiology]]
[[Category:Endocrinology]]
[[Category:Emergency medicine]]
[[Category:Nephrology]]
[[Category:Electrolyte disturbance]]
[[Category:Blood tests]]
[[Category:Intensive care medicine]]

[[fr:Hypokaliémie]]
[[pl:Hipokaliemia]]
[[pt:Hipocaliémia]]
[[ru:Гипокалиемия]]
[[vi:Hạ kali máu]]
[[Category:Inborn errors of metabolism]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

2011-12-09T19:48:17Z

Jack Khouri:

Hypernatremia

2011-12-09T19:45:44Z

Jack Khouri: /* Differential Diagnosis of Associated Disorders and Causes of Hypernatremia */

2011-12-08T21:19:23Z

Jack Khouri: /* Treatment */

{{Hypernatremia}}
{{Infobox_Disease |
Name = {{PAGENAME}} |
Image = Na-TableImage.png |
Caption = [[Sodium]] |
DiseasesDB = 6266 |
ICD10 = {{ICD10|E|87|0|e|70}} |
ICD9 = {{ICD9|276.0}} |
ICDO = |
OMIM = |
MedlinePlus = |
}}
{{CMG}}'''; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|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 [[water|free water]] in the body. For this reason, hypernatremia is often synonymous with the less precise term [[dehydration]].

==Pathophysiology==
Water is lost from the body in a variety of ways, including [[perspiration]], insensible losses from breathing, and in the [[feces]] and [[urine]]. If the amount of water ingested consistently falls below the amount of water lost, the serum sodium level will begin to rise, leading to hypernatremia. Rarely, hypernatremia can result from massive [[salt]] ingestion, such as may occur from drinking seawater.

The kidney has concentrating mechanisms that prevent hypernatremia. Once the kidney's function is impaired due to any cause, thirst becomes the main defense mechanism that prevents hypenatremia unless it is dysfunctional or access to water is limited (most often occurs in people such as [[infant|infants]], those with impaired [[cognition|mental status]], or the elderly, who may have an intact thirst mechanism but are unable to ask for or obtain water).

The hyperosmolarity caused by the high serum sodium concentrations drives water out of the cells. The most sensitive organ to this water shift is the brain where the neurons and other cells become dehydrated and are responsible for the neurologic symptoms associated with hypernatremia.

As discussed before, thirst is an essential process that impedes hypernatremia. Consequently, hypernatremia above 150 mEq/l is very rare in alert patients and those who have access to free water who increase their water intake to match water loss.

==Causes==
Hypernatremia can result from water loss (most common) or sodium retention (rare).

===Causes of water loss===

* Inadequate intake of water: typically in elderly or otherwise disabled patients who are unable to take in water as their thirst dictates. This is the most common cause of hypernatremia. Hypothalamic disorders can lead to impairement of the thirst mechanism (primary hypodipsia, '''essential hypernatremia''' caused by the loss of the hypothalamic osmoreceptor function (the plasma osmolarity sensor that stimulates thirst once the plasma is hyperosmolar))
* Renal loss: Inappropriate excretion of water, often in the urine, which can be due to medications like [[diuretic]]s or [[lithium]] or can be due to a medical condition called [[diabetes insipidus]]. Osmotic diuresis can occur when osmotically active substances are present in large amounts in the plasma (glucose, urea, mannitol, etc)
* GI loss: osmotic diarrhea (infectious, malabsorptive, lactulose intake)
* Insensible losses: excessive sweating in the context of exercise or warm climate
* Water loss into cells: seizure, severe exercise, rhabdomyolysis

===Causes of increased sodium retention===

* Intake of a [[hypertonic]] fluid (a fluid with a higher concentration of solutes than the remainder of the body). This is relatively uncommon, though it can occur after a vigorous resuscitation where a patient receives a large volume of a concentrated [[sodium bicarbonate]] solution. Ingesting seawater also causes hypernatremia because seawater is hypertonic.
* [[Mineralcorticoid]] excess due to a disease state such as [[Conn's syndrome]] or [[Cushing's Syndrome]].

==Differential Diagnosis of Associated Disorders and Causes of Hypernatremia==

{|style="width:75%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Chemical / poisoning'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Dermatologic'''
|bgcolor="Beige"| [[Burns]], Excessive [[sweating]]
|-
|-bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
|bgcolor="Beige"| [[diuretics]]
|-
|-bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Endocrine'''
|bgcolor="Beige"| [[Adrenal insufficiency|Adrenal]], [[Diabetes Insipidus]], [[Congenital Adrenal Hyperplasia]], [[Conn's Syndrome]],[[Cushing's Syndrome]], Ectopic adrenocorticotropic hormone ([[ACTH]]) production, [[Hyperaldosteronism]], [[Hyperglycemia]], [[Hyperlipidemia]], [[Thyrotoxicosis]]
|-
|-bgcolor="LightSteelBlue"
| '''Environmental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
|bgcolor="Beige"| Gastrointestinal losses (diarrhea, vomiting), inability to swallow water (physical limitation)
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Iatrogenic'''
|bgcolor="Beige"| Inappropriate IV fluids
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"| [[Fever]]
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| Essential hypernatremia, [[Dementia]], [[Coma]], hypothalamic lesion, inability to recognize thirst for water
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional / Metabolic'''
|bgcolor="Beige"| ingestion of large quantities of sodium (seawater), decreased protein intake
|-
|-bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| [[Multiple Myeloma]]
|-bgcolor="LightSteelBlue"
| '''Opthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose / Toxicity'''
|bgcolor="Beige"| [[Alcoholism]]
|-
|-bgcolor="LightSteelBlue"
| '''Psychiatric'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"| [[Sarcoidosis]], [[Hyperventilation]]
|-
|-bgcolor="LightSteelBlue"
| '''Renal / Electrolyte'''
|bgcolor="Beige"| High urea levels with renal failure, [[Hypercalcemia]], [[Hypokalemia]], [[Osmotic diuresis]], Peritoneal dialysis,[[Diuresis]] phase of [[acute renal failure]]
|-
|-bgcolor="LightSteelBlue"
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| [[Sjogren's Syndrome]]
|-
|-bgcolor="LightSteelBlue"
| '''Sexual'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| Amyloidosis
|-
|}

==Diagnosis==
Diagnosing the etiology of hypernatremia is essential. Symptoms, urine osmolarity and water deprivation studies are all helpful.

==History and Symptoms==
===Symptoms===
Clinical manifestations of hypernatremia can be subtle, consisting of [[lethargy]], weakness, irritability, and [[edema]]. With more severe elevations of the sodium level, [[seizure]]s and [[coma]] may occur.

Severe symptoms are usually due to acute elevation of the plasma sodium concentration to above 158 mEq/L, which corresponds to an osmolar gradient of 30-35 mEq/kg between plasma and brain. Beyond that level, the rapid reduction of brain volume can cause rupture of cerebral veins leading to intracerebral and subarachnoid hemorrhage. Values above 180 mEq/L are associated with a high mortality rate, particularly in adults. However such high levels of sodium rarely occur without severe coexisting medical conditions.

'''To note that if hypernatremia progresses over more than 24 hours, the brain adapts rapidly to plasma hyperosmolarity due to intracellular accumulation of many osmolytes such as amino acids (eg, glutamate)'''.

===History===
A detailed history is important for the diagnosis of the etiology of hypernatremia. It should mention any history of diabetes insipidus, hyperaldosteronism, Cushing's disease, neurologic disease, seizure disorder, malabsorptive disease and ingestion of osmotic agents (eg, mannitol, lactulose) or excess sodium salts. Current diarrhea, burns, exercise (increased sweating), polyuria and polydypsia should be emphasized.

==Approach==
* Urine osmolarity is essential to differentiate renal from extrarenal water loss. A normal kidney would respond to hypernatremia by excreting a highly concentrated urinewith a urine osmolality >800 mosmol/kg.
** Urine osmolarity <300 mosm/kg is consistent with renal water losses due to diabetes insipidus (neurogenic vs nephrogenic).
** Urine osmolarity between 300 and 800 mosm/kg indicates partial diabetes insipidus or osmotic diuresis.
** Urine osmolarity >800 mosm/kg points out to insensible or GI losses, increased sodium ingestion or primary hypodypsia.

* The water deprivation test
** The objective of this test is to distinguish the origin of diabetes insipidus (DI).
** Desmopressin (AVP), a synthetic analogue of vasopressin, is effective in patients with central DI.
** Upon AVP adminstration, patients will have different urine osmolarities depending on their DI etiology.
** Patients with central DI have intact kidney response to vasopressin and will have a substantial increase in urine osmolarity in response to water deprivation and desmopressin administrarion.
** Patients with nephrogenic DI have little or no increase in urine osmolarity in response to AVP.
** Patients with partial central DI show an increase in urine osmolarity of >10%.

==Treatment==
* The cornerstone of treatment is administration of free water to correct the relative water deficit. Water can be replaced orally or [[intravenous]]ly.

* '''Overly rapid correction of hypernatremia is potentially very dangerous'''. As we mentioned before, The body (in particular the [[brain]]) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, once this adaptation has occurred, causes water to flow into brain cells and causes them to swell (cerebral edema). This can lead to [[cerebral edema]], potentially resulting in seizures, permanent [[brain damage]], or death. [[Central pontine myelinolysis]] can also occur with over rapid correction of the sodium which should be about '''0.5 meq/l/hour''' and no more than 1 meq per hour. Significant hypernatremia should be treated carefully by a [[physician]] or other medical professional with experience in treatment of [[electrolyte imbalance]]s.

* ''Free Water deficit (L)= 0.6 x �(body weight(kg)) x �((Sodium/140)-1)''

* Central DI should be treated with desmopressin and drugs that increase vasopressin release eg Clofibrate.

* Nephrogenic DI can be treated with Thiazide diuretics, low salt and low protein diet.

==See also==
* [[Dehydration]]
* [[Hyponatremia]]
* [[Cerebral edema]]

{{Endocrine, nutritional and metabolic pathology}}

[[es:Hipernatremia]]
[[ja:高ナトリウム血症]]

[[Category: electrolyte disturbance|Hypernatremia]]
[[Category:Inborn errors of metabolism]]
[[Category:Blood tests]]
[[Category:Emergency medicine]]
[[Category:Intensive care medicine]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Hypernatremia

2011-12-08T21:02:16Z

Jack Khouri: /* History */

{{Hypernatremia}}
{{Infobox_Disease |
Name = {{PAGENAME}} |
Image = Na-TableImage.png |
Caption = [[Sodium]] |
DiseasesDB = 6266 |
ICD10 = {{ICD10|E|87|0|e|70}} |
ICD9 = {{ICD9|276.0}} |
ICDO = |
OMIM = |
MedlinePlus = |
}}
{{CMG}}'''; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|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 [[water|free water]] in the body. For this reason, hypernatremia is often synonymous with the less precise term [[dehydration]].

==Pathophysiology==
Water is lost from the body in a variety of ways, including [[perspiration]], insensible losses from breathing, and in the [[feces]] and [[urine]]. If the amount of water ingested consistently falls below the amount of water lost, the serum sodium level will begin to rise, leading to hypernatremia. Rarely, hypernatremia can result from massive [[salt]] ingestion, such as may occur from drinking seawater.

The kidney has concentrating mechanisms that prevent hypernatremia. Once the kidney's function is impaired due to any cause, thirst becomes the main defense mechanism that prevents hypenatremia unless it is dysfunctional or access to water is limited (most often occurs in people such as [[infant|infants]], those with impaired [[cognition|mental status]], or the elderly, who may have an intact thirst mechanism but are unable to ask for or obtain water).

The hyperosmolarity caused by the high serum sodium concentrations drives water out of the cells. The most sensitive organ to this water shift is the brain where the neurons and other cells become dehydrated and are responsible for the neurologic symptoms associated with hypernatremia.

As discussed before, thirst is an essential process that impedes hypernatremia. Consequently, hypernatremia above 150 mEq/l is very rare in alert patients and those who have access to free water who increase their water intake to match water loss.

==Causes==
Hypernatremia can result from water loss (most common) or sodium retention (rare).

===Causes of water loss===

* Inadequate intake of water: typically in elderly or otherwise disabled patients who are unable to take in water as their thirst dictates. This is the most common cause of hypernatremia. Hypothalamic disorders can lead to impairement of the thirst mechanism (primary hypodipsia, '''essential hypernatremia''' caused by the loss of the hypothalamic osmoreceptor function (the plasma osmolarity sensor that stimulates thirst once the plasma is hyperosmolar))
* Renal loss: Inappropriate excretion of water, often in the urine, which can be due to medications like [[diuretic]]s or [[lithium]] or can be due to a medical condition called [[diabetes insipidus]]. Osmotic diuresis can occur when osmotically active substances are present in large amounts in the plasma (glucose, urea, mannitol, etc)
* GI loss: osmotic diarrhea (infectious, malabsorptive, lactulose intake)
* Insensible losses: excessive sweating in the context of exercise or warm climate
* Water loss into cells: seizure, severe exercise, rhabdomyolysis

===Causes of increased sodium retention===

* Intake of a [[hypertonic]] fluid (a fluid with a higher concentration of solutes than the remainder of the body). This is relatively uncommon, though it can occur after a vigorous resuscitation where a patient receives a large volume of a concentrated [[sodium bicarbonate]] solution. Ingesting seawater also causes hypernatremia because seawater is hypertonic.
* [[Mineralcorticoid]] excess due to a disease state such as [[Conn's syndrome]] or [[Cushing's Syndrome]].

==Differential Diagnosis of Associated Disorders and Causes of Hypernatremia==

{|style="width:75%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Chemical / poisoning'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Dermatologic'''
|bgcolor="Beige"| [[Burns]], Excessive [[sweating]]
|-
|-bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
|bgcolor="Beige"| [[diuretics]]
|-
|-bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Endocrine'''
|bgcolor="Beige"| [[Adrenal insufficiency|Adrenal]], [[Diabetes Insipidus]], [[Congenital Adrenal Hyperplasia]], [[Conn's Syndrome]],[[Cushing's Syndrome]], Ectopic adrenocorticotropic hormone ([[ACTH]]) production, [[Hyperaldosteronism]], [[Hyperglycemia]], [[Hyperlipidemia]], [[Thyrotoxicosis]]
|-
|-bgcolor="LightSteelBlue"
| '''Environmental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
|bgcolor="Beige"| Gastrointestinal losses (diarrhea, vomiting), inability to swallow water (physical limitation)
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Iatrogenic'''
|bgcolor="Beige"| Inappropriate IV fluids
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"| [[Fever]]
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| Essential hypernatremia, [[Dementia]], [[Coma]], hypothalamic lesion, inability to recognize thirst for water
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional / Metabolic'''
|bgcolor="Beige"| ingestion of large quantities of sodium (seawater), decreased protein intake
|-
|-bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| [[Multiple Myeloma]]
|-bgcolor="LightSteelBlue"
| '''Opthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose / Toxicity'''
|bgcolor="Beige"| [[Alcoholism]]
|-
|-bgcolor="LightSteelBlue"
| '''Psychiatric'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"| [[Sarcoidosis]], [[Hyperventilation]]
|-
|-bgcolor="LightSteelBlue"
| '''Renal / Electrolyte'''
|bgcolor="Beige"| High urea levels with renal failure, [[Hypercalcemia]], [[Hypokalemia]], [[Osmotic diuresis]], Peritoneal dialysis,[[Diuresis]] phase of [[acute renal failure]]
|-
|-bgcolor="LightSteelBlue"
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| [[Sjogren's Syndrome]]
|-
|-bgcolor="LightSteelBlue"
| '''Sexual'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| Amyloidosis
|-
|}

==Diagnosis==
Diagnosing the etiology of hypernatremia is essential. Symptoms, urine osmolarity and water deprivation studies are all helpful.

==History and Symptoms==
===Symptoms===
Clinical manifestations of hypernatremia can be subtle, consisting of [[lethargy]], weakness, irritability, and [[edema]]. With more severe elevations of the sodium level, [[seizure]]s and [[coma]] may occur.

Severe symptoms are usually due to acute elevation of the plasma sodium concentration to above 158 mEq/L, which corresponds to an osmolar gradient of 30-35 mEq/kg between plasma and brain. Beyond that level, the rapid reduction of brain volume can cause rupture of cerebral veins leading to intracerebral and subarachnoid hemorrhage. Values above 180 mEq/L are associated with a high mortality rate, particularly in adults. However such high levels of sodium rarely occur without severe coexisting medical conditions.

'''To note that if hypernatremia progresses over more than 24 hours, the brain adapts rapidly to plasma hyperosmolarity due to intracellular accumulation of many osmolytes such as amino acids (eg, glutamate)'''.

===History===
A detailed history is important for the diagnosis of the etiology of hypernatremia. It should mention any history of diabetes insipidus, hyperaldosteronism, Cushing's disease, neurologic disease, seizure disorder, malabsorptive disease and ingestion of osmotic agents (eg, mannitol, lactulose) or excess sodium salts. Current diarrhea, burns, exercise (increased sweating), polyuria and polydypsia should be emphasized.

==Approach==
* Urine osmolarity is essential to differentiate renal from extrarenal water loss. A normal kidney would respond to hypernatremia by excreting a highly concentrated urinewith a urine osmolality >800 mosmol/kg.
** Urine osmolarity <300 mosm/kg is consistent with renal water losses due to diabetes insipidus (neurogenic vs nephrogenic).
** Urine osmolarity between 300 and 800 mosm/kg indicates partial diabetes insipidus or osmotic diuresis.
** Urine osmolarity >800 mosm/kg points out to insensible or GI losses, increased sodium ingestion or primary hypodypsia.

* The water deprivation test
** The objective of this test is to distinguish the origin of diabetes insipidus (DI).
** Desmopressin (AVP), a synthetic analogue of vasopressin, is effective in patients with central DI.
** Upon AVP adminstration, patients will have different urine osmolarities depending on their DI etiology.
** Patients with central DI have intact kidney response to vasopressin and will have a substantial increase in urine osmolarity in response to water deprivation and desmopressin administrarion.
** Patients with nephrogenic DI have little or no increase in urine osmolarity in response to AVP.
** Patients with partial central DI show an increase in urine osmolarity of >10%.

==Treatment==
The cornerstone of treatment is administration of free water to correct the relative water deficit. Water can be replaced orally or [[intravenous]]ly. However, overly rapid correction of hypernatremia is potentially very dangerous. The body (in particular the [[brain]]) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, once this adaptation has occurred, causes water to flow into brain cells and causes them to swell. This can lead to [[cerebral edema]], potentially resulting in seizures, permanent [[brain damage]], or death. [[Central pontine myelinolysis]] can also occur with over rapid correction of the sodium which should be about 0.5 meq per hour and no more than 1 meq per hour. Significant hypernatremia should be treated carefully by a [[physician]] or other medical professional with experience in treatment of [[electrolyte imbalance]]s.

==See also==
* [[Dehydration]]
* [[Hyponatremia]]
* [[Cerebral edema]]

{{Endocrine, nutritional and metabolic pathology}}

[[es:Hipernatremia]]
[[ja:高ナトリウム血症]]

[[Category: electrolyte disturbance|Hypernatremia]]
[[Category:Inborn errors of metabolism]]
[[Category:Blood tests]]
[[Category:Emergency medicine]]
[[Category:Intensive care medicine]]

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{{WikiDoc Sources}}

Hypernatremia

2011-12-08T21:01:35Z

Jack Khouri: /* Causes of water loss */

{{Hypernatremia}}
{{Infobox_Disease |
Name = {{PAGENAME}} |
Image = Na-TableImage.png |
Caption = [[Sodium]] |
DiseasesDB = 6266 |
ICD10 = {{ICD10|E|87|0|e|70}} |
ICD9 = {{ICD9|276.0}} |
ICDO = |
OMIM = |
MedlinePlus = |
}}
{{CMG}}'''; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|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 [[water|free water]] in the body. For this reason, hypernatremia is often synonymous with the less precise term [[dehydration]].

==Pathophysiology==
Water is lost from the body in a variety of ways, including [[perspiration]], insensible losses from breathing, and in the [[feces]] and [[urine]]. If the amount of water ingested consistently falls below the amount of water lost, the serum sodium level will begin to rise, leading to hypernatremia. Rarely, hypernatremia can result from massive [[salt]] ingestion, such as may occur from drinking seawater.

The kidney has concentrating mechanisms that prevent hypernatremia. Once the kidney's function is impaired due to any cause, thirst becomes the main defense mechanism that prevents hypenatremia unless it is dysfunctional or access to water is limited (most often occurs in people such as [[infant|infants]], those with impaired [[cognition|mental status]], or the elderly, who may have an intact thirst mechanism but are unable to ask for or obtain water).

The hyperosmolarity caused by the high serum sodium concentrations drives water out of the cells. The most sensitive organ to this water shift is the brain where the neurons and other cells become dehydrated and are responsible for the neurologic symptoms associated with hypernatremia.

As discussed before, thirst is an essential process that impedes hypernatremia. Consequently, hypernatremia above 150 mEq/l is very rare in alert patients and those who have access to free water who increase their water intake to match water loss.

==Causes==
Hypernatremia can result from water loss (most common) or sodium retention (rare).

===Causes of water loss===

* Inadequate intake of water: typically in elderly or otherwise disabled patients who are unable to take in water as their thirst dictates. This is the most common cause of hypernatremia. Hypothalamic disorders can lead to impairement of the thirst mechanism (primary hypodipsia, '''essential hypernatremia''' caused by the loss of the hypothalamic osmoreceptor function (the plasma osmolarity sensor that stimulates thirst once the plasma is hyperosmolar))
* Renal loss: Inappropriate excretion of water, often in the urine, which can be due to medications like [[diuretic]]s or [[lithium]] or can be due to a medical condition called [[diabetes insipidus]]. Osmotic diuresis can occur when osmotically active substances are present in large amounts in the plasma (glucose, urea, mannitol, etc)
* GI loss: osmotic diarrhea (infectious, malabsorptive, lactulose intake)
* Insensible losses: excessive sweating in the context of exercise or warm climate
* Water loss into cells: seizure, severe exercise, rhabdomyolysis

===Causes of increased sodium retention===

* Intake of a [[hypertonic]] fluid (a fluid with a higher concentration of solutes than the remainder of the body). This is relatively uncommon, though it can occur after a vigorous resuscitation where a patient receives a large volume of a concentrated [[sodium bicarbonate]] solution. Ingesting seawater also causes hypernatremia because seawater is hypertonic.
* [[Mineralcorticoid]] excess due to a disease state such as [[Conn's syndrome]] or [[Cushing's Syndrome]].

==Differential Diagnosis of Associated Disorders and Causes of Hypernatremia==

{|style="width:75%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Chemical / poisoning'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Dermatologic'''
|bgcolor="Beige"| [[Burns]], Excessive [[sweating]]
|-
|-bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
|bgcolor="Beige"| [[diuretics]]
|-
|-bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Endocrine'''
|bgcolor="Beige"| [[Adrenal insufficiency|Adrenal]], [[Diabetes Insipidus]], [[Congenital Adrenal Hyperplasia]], [[Conn's Syndrome]],[[Cushing's Syndrome]], Ectopic adrenocorticotropic hormone ([[ACTH]]) production, [[Hyperaldosteronism]], [[Hyperglycemia]], [[Hyperlipidemia]], [[Thyrotoxicosis]]
|-
|-bgcolor="LightSteelBlue"
| '''Environmental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
|bgcolor="Beige"| Gastrointestinal losses (diarrhea, vomiting), inability to swallow water (physical limitation)
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Iatrogenic'''
|bgcolor="Beige"| Inappropriate IV fluids
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"| [[Fever]]
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| Essential hypernatremia, [[Dementia]], [[Coma]], hypothalamic lesion, inability to recognize thirst for water
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional / Metabolic'''
|bgcolor="Beige"| ingestion of large quantities of sodium (seawater), decreased protein intake
|-
|-bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| [[Multiple Myeloma]]
|-bgcolor="LightSteelBlue"
| '''Opthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose / Toxicity'''
|bgcolor="Beige"| [[Alcoholism]]
|-
|-bgcolor="LightSteelBlue"
| '''Psychiatric'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"| [[Sarcoidosis]], [[Hyperventilation]]
|-
|-bgcolor="LightSteelBlue"
| '''Renal / Electrolyte'''
|bgcolor="Beige"| High urea levels with renal failure, [[Hypercalcemia]], [[Hypokalemia]], [[Osmotic diuresis]], Peritoneal dialysis,[[Diuresis]] phase of [[acute renal failure]]
|-
|-bgcolor="LightSteelBlue"
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| [[Sjogren's Syndrome]]
|-
|-bgcolor="LightSteelBlue"
| '''Sexual'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| Amyloidosis
|-
|}

==Diagnosis==
Diagnosing the etiology of hypernatremia is essential. Symptoms, urine osmolarity and water deprivation studies are all helpful.

==History and Symptoms==
===Symptoms===
Clinical manifestations of hypernatremia can be subtle, consisting of [[lethargy]], weakness, irritability, and [[edema]]. With more severe elevations of the sodium level, [[seizure]]s and [[coma]] may occur.

Severe symptoms are usually due to acute elevation of the plasma sodium concentration to above 158 mEq/L, which corresponds to an osmolar gradient of 30-35 mEq/kg between plasma and brain. Beyond that level, the rapid reduction of brain volume can cause rupture of cerebral veins leading to intracerebral and subarachnoid hemorrhage. Values above 180 mEq/L are associated with a high mortality rate, particularly in adults. However such high levels of sodium rarely occur without severe coexisting medical conditions.

'''To note that if hypernatremia progresses over more than 24 hours, the brain adapts rapidly to plasma hyperosmolarity due to intracellular accumulation of many osmolytes such as amino acids (eg, glutamate)'''.

===History===
A detailed history is important for the diagnosis of the etiology of hypernatremia. It should mention any history of diabetes insipidus, hyperaldosteronism, Cushing's disease, neurologic disease, seizure disorder and ingestion of osmotic agents (eg, mannitol, lactulose) or excess sodium salts. Current diarrhea, burns, exercise (increased sweating), polyuria and polydypsia should be emphasized.

==Approach==
* Urine osmolarity is essential to differentiate renal from extrarenal water loss. A normal kidney would respond to hypernatremia by excreting a highly concentrated urinewith a urine osmolality >800 mosmol/kg.
** Urine osmolarity <300 mosm/kg is consistent with renal water losses due to diabetes insipidus (neurogenic vs nephrogenic).
** Urine osmolarity between 300 and 800 mosm/kg indicates partial diabetes insipidus or osmotic diuresis.
** Urine osmolarity >800 mosm/kg points out to insensible or GI losses, increased sodium ingestion or primary hypodypsia.

* The water deprivation test
** The objective of this test is to distinguish the origin of diabetes insipidus (DI).
** Desmopressin (AVP), a synthetic analogue of vasopressin, is effective in patients with central DI.
** Upon AVP adminstration, patients will have different urine osmolarities depending on their DI etiology.
** Patients with central DI have intact kidney response to vasopressin and will have a substantial increase in urine osmolarity in response to water deprivation and desmopressin administrarion.
** Patients with nephrogenic DI have little or no increase in urine osmolarity in response to AVP.
** Patients with partial central DI show an increase in urine osmolarity of >10%.

==Treatment==
The cornerstone of treatment is administration of free water to correct the relative water deficit. Water can be replaced orally or [[intravenous]]ly. However, overly rapid correction of hypernatremia is potentially very dangerous. The body (in particular the [[brain]]) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, once this adaptation has occurred, causes water to flow into brain cells and causes them to swell. This can lead to [[cerebral edema]], potentially resulting in seizures, permanent [[brain damage]], or death. [[Central pontine myelinolysis]] can also occur with over rapid correction of the sodium which should be about 0.5 meq per hour and no more than 1 meq per hour. Significant hypernatremia should be treated carefully by a [[physician]] or other medical professional with experience in treatment of [[electrolyte imbalance]]s.

==See also==
* [[Dehydration]]
* [[Hyponatremia]]
* [[Cerebral edema]]

{{Endocrine, nutritional and metabolic pathology}}

[[es:Hipernatremia]]
[[ja:高ナトリウム血症]]

[[Category: electrolyte disturbance|Hypernatremia]]
[[Category:Inborn errors of metabolism]]
[[Category:Blood tests]]
[[Category:Emergency medicine]]
[[Category:Intensive care medicine]]

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{{WikiDoc Sources}}