Hypernatremia: Difference between revisions

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Latest revision as of 00:09, 12 August 2020

For patient information, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

Synonyms and keywords: Hyperosmolarity; hypernatraemia

Overview

Historical perspective

Pathophysiology

Causes

Differentiating Hypernatremia from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention

Case Studies

Case #1

Related Chapters

Template:Endocrine, nutritional and metabolic pathology

Template:WikiDoc Sources

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+__NOTOC__
+{| class="infobox" style="float:right;"
+|-
+| [[File:Siren.gif|link=Hypernatremia resident survival guide|41x41px]]|| <br> || <br>
+| [[Hypernatremia resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']]
+|}
+'''For patient information, click [[Hypernatremia (patient information)|here]]'''
 {{Hypernatremia}}
-{{Infobox_Disease |
+{{CMG}}; {{AE}}{{FT}}
-  Name           = {{PAGENAME}} |
-  Image          = Na-TableImage.png  |
+{{SK}} Hyperosmolarity; hypernatraemia
-  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]]
 ==[[Hypernatremia overview|Overview]]==
+==[[Hypernatremia historical perspective|Historical perspective]]==
 ==[[Hypernatremia pathophysiology|Pathophysiology]]==
 ==[[Hypernatremia causes|Causes]]==
+==[[Differentiating etiologies of Hypernatremia|Differentiating Hypernatremia from other Diseases]]==
-==[[Hypernatremia differential diagnosis|Differential Diagnosis]]==
+==[[Hypernatremia epidemiology and demographics|Epidemiology and Demographics]]==
+==[[Hypernatremia risk factors|Risk Factors]]==
+==[[Hypernatremia natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
 ==Diagnosis==
-Diagnosing the etiology of hypernatremia is essential. Symptoms, urine osmolarity and water deprivation studies are all helpful.
+[[Hypernatremia history and symptoms|History and Symptoms]] | [[Hypernatremia physical examination|Physical Examination]] | [[Hypernatremia laboratory findings|Laboratory Findings]] | [[Hypernatremia electrocardiogram|Electrocardiogram]] | [[Hypernatremia CT|CT]] | [[Hypernatremia MRI|MRI]] | [[Hypernatremia other diagnostic studies|Other Diagnostic Studies]]
-==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 by the 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 excess sodium salts. Current diarrhea, burns, exercise (increased sweating), polyuria and polydypsia should be emphasized. Drug history should include diuretic use or ingestion of osmotic agents (eg, mannitol, lactulose).
-==Labs and Procedures==
-* 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.
+[[Hypernatremia medical therapy|Medical Therapy]] | [[Hypernatremia surgery|Surgery]] | [[Hypernatremia primary prevention|Primary Prevention]] | [[Hypernatremia secondary prevention|Secondary Prevention]]
+==Case Studies==
-* '''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.
+[[Hypernatremia case study one|Case #1]]
-* ''Free Water deficit (L)= 0.6 x (body weight(kg)) x ((plasma[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==
+==Related Chapters==
 * [[Dehydration]]
 * [[Hyponatremia]]
-* [[Cerebral edema]]
+* [[Cerebral edema|Cerebral Edema]]
 {{Endocrine, nutritional and metabolic pathology}}
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 [[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]]
+[[Category:Nephrology]]
+[[Category:Electrolyte disturbance]]
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