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| | __NOTOC__ |
| | {| class="infobox" style="float:right;" |
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| | | [[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}} | | {{Hypernatremia}} |
| {{Infobox_Disease | | | {{CMG}}; {{AE}}{{FT}} |
| Name = {{PAGENAME}} |
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| Image = Na-TableImage.png |
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| Caption = [[Sodium]] |
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| DiseasesDB = 6266 |
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| ICD10 = {{ICD10|E|87|0|e|70}} |
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| ICD9 = {{ICD9|276.0}} |
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| ICDO = |
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| OMIM = |
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| MedlinePlus = |
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| }} | |
| {{CMG}}'''; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]] | |
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| ==Overview==
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| '''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]].
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| ==Pathophysiology==
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| The main cause of hypernatremia is water loss with the inability to replace the losses either because of a defective thirst mechanism or inability to access water. Sosium retention is an uncommon cause.
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| ==Causes==
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| As mentioned before, water loss and sodium retention are the main culprits. water loss can be due to wasting of a significant amount of '''free''' water through the excretion of dilute urine (eg, diabetes insipidus), the GI tract (diarrhea), perspiration or any hypothalamic disease that can alter the thirst response to water deficit.
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| ==Differential diagnosis==
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| The differential diagnosis of the etiology of hypernatremia is wide but mainly involves the kidney, the hypothalamus, the skin, the endocrine system (diabetes mellitus, adrenals and thyroid diseases) and the GI tract.
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| ==Pathophysiology==
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| 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.
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| 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).
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| 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.
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| 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.
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| ==Causes==
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| Hypernatremia can result from water loss (most common) or sodium retention (rare).
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| ===Causes of water loss===
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| * 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. [[Hypothalamus|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))
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| * 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)
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| * GI loss: [[osmotic]] [[diarrhea]] (infectious, malabsorptive, [[lactulose]] intake)
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| * Insensible losses: excessive [[perspiration|sweating]] in the context of exercise or warm climate
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| * Water loss into cells: [[seizure]], severe exercise, [[rhabdomyolysis]]
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| ===Causes of increased sodium retention===
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| * 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.
| | {{SK}} Hyperosmolarity; hypernatraemia |
| * [[Mineralcorticoid]] excess due to a disease state such as [[Conn's syndrome]] or [[Cushing's Syndrome]].
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| ==Differential Diagnosis of Associated Disorders and Causes of Hypernatremia== | | ==[[Hypernatremia overview|Overview]]== |
| | ==[[Hypernatremia historical perspective|Historical perspective]]== |
| | ==[[Hypernatremia pathophysiology|Pathophysiology]]== |
| | ==[[Hypernatremia causes|Causes]]== |
| | ==[[Differentiating etiologies of Hypernatremia|Differentiating Hypernatremia from other Diseases]]== |
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| | | ==[[Hypernatremia epidemiology and demographics|Epidemiology and Demographics]]== |
| {|style="width:75%; height:100px" border="1"
| | ==[[Hypernatremia risk factors|Risk Factors]]== |
| |style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
| | ==[[Hypernatremia natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| |style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Chemical / poisoning'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Dermatologic'''
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| |bgcolor="Beige"| [[Burns]], Excessive [[sweating]]
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| |-bgcolor="LightSteelBlue" | |
| | '''Drug Side Effect'''
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| |bgcolor="Beige"| [[diuretics]]
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| |-bgcolor="LightSteelBlue"
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| | '''Ear Nose Throat'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Endocrine'''
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| |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]]
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| |-bgcolor="LightSteelBlue"
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| | '''Environmental'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Gastroenterologic'''
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| |bgcolor="Beige"| Gastrointestinal losses (diarrhea, vomiting), inability to swallow water (physical limitation)
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| |-bgcolor="LightSteelBlue"
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| | '''Genetic'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Hematologic'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Iatrogenic'''
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| |bgcolor="Beige"| Inappropriate IV fluids
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| |-bgcolor="LightSteelBlue"
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| | '''Infectious Disease'''
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| |bgcolor="Beige"| [[Fever]]
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| |-bgcolor="LightSteelBlue"
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| | '''Musculoskeletal / Ortho'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Neurologic'''
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| |bgcolor="Beige"| Essential hypernatremia, [[Dementia]], [[Coma]], hypothalamic lesion, inability to recognize thirst for water
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| |- | |
| |-bgcolor="LightSteelBlue"
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| | '''Nutritional / Metabolic'''
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| |bgcolor="Beige"| ingestion of large quantities of sodium (seawater), decreased protein intake
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| |-bgcolor="LightSteelBlue"
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| | '''Obstetric/Gynecologic'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Oncologic'''
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| |bgcolor="Beige"| [[Multiple Myeloma]]
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| |-bgcolor="LightSteelBlue"
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| | '''Opthalmologic'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Overdose / Toxicity'''
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| |bgcolor="Beige"| [[Alcoholism]]
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| |-bgcolor="LightSteelBlue"
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| | '''Psychiatric'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Pulmonary'''
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| |bgcolor="Beige"| [[Sarcoidosis]], [[Hyperventilation]]
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| |-bgcolor="LightSteelBlue"
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| | '''Renal / Electrolyte'''
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| |bgcolor="Beige"| High urea levels with renal failure, [[Hypercalcemia]], [[Hypokalemia]], [[Osmotic diuresis]], Peritoneal dialysis,[[Diuresis]] phase of [[acute renal failure]]
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| |-bgcolor="LightSteelBlue"
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| | '''Rheum / Immune / Allergy'''
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| |bgcolor="Beige"| [[Sjogren's Syndrome]]
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| |-bgcolor="LightSteelBlue"
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| | '''Sexual'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Trauma'''
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| |bgcolor="Beige"| No underlying causes
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| |-
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| |-bgcolor="LightSteelBlue"
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| | '''Urologic'''
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| |bgcolor="Beige"| No underlying causes
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| |-bgcolor="LightSteelBlue"
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| | '''Miscellaneous'''
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| |bgcolor="Beige"| Amyloidosis
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| |-
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| |}
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| ==Diagnosis== | | ==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]] |
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| ==History and Symptoms==
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| ===Symptoms===
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| 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.
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| 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.
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| '''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)'''.
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| ===History===
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| 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).
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| ==Labs and Procedures==
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| * 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.
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| ** Urine osmolarity <300 mosm/kg is consistent with renal water losses due to diabetes insipidus (neurogenic vs nephrogenic).
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| ** Urine osmolarity between 300 and 800 mosm/kg indicates partial diabetes insipidus or osmotic diuresis.
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| ** Urine osmolarity >800 mosm/kg points out to insensible or GI losses, increased sodium ingestion or primary hypodypsia.
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| * The water deprivation test
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| ** The objective of this test is to distinguish the origin of diabetes insipidus (DI).
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| ** Desmopressin (AVP), a synthetic analogue of vasopressin, is effective in patients with central DI.
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| ** Upon AVP adminstration, patients will have different urine osmolarities depending on their DI etiology.
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| ** 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.
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| ** Patients with nephrogenic DI have little or no increase in urine osmolarity in response to AVP.
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| ** Patients with partial central DI show an increase in urine osmolarity of >10%.
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| ==Treatment== | | ==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]] |
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| * ''Free Water deficit (L)= 0.6 x (body weight(kg)) x ((plasma[Sodium]/140)-1)''
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| * Central DI should be treated with desmopressin and drugs that increase vasopressin release eg Clofibrate.
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| * Nephrogenic DI can be treated with Thiazide diuretics, low salt and low protein diet.
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| ==See also== | | ==Related Chapters== |
| * [[Dehydration]] | | * [[Dehydration]] |
| * [[Hyponatremia]] | | * [[Hyponatremia]] |
| * [[Cerebral edema]] | | * [[Cerebral edema|Cerebral Edema]] |
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| {{Endocrine, nutritional and metabolic pathology}} | | {{Endocrine, nutritional and metabolic pathology}} |
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| [[ja:高ナトリウム血症]] | | [[ja:高ナトリウム血症]] |
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| [[Category: electrolyte disturbance|Hypernatremia]]
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| [[Category:Inborn errors of metabolism]] | | [[Category:Inborn errors of metabolism]] |
| [[Category:Blood tests]] | | [[Category:Blood tests]] |
| [[Category:Emergency medicine]] | | [[Category:Emergency medicine]] |
| [[Category:Intensive care medicine]] | | [[Category:Intensive care medicine]] |
| | [[Category:Nephrology]] |
| | [[Category:Electrolyte disturbance]] |
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| {{WikiDoc Help Menu}} | | {{WikiDoc Help Menu}} |
| {{WikiDoc Sources}} | | {{WikiDoc Sources}} |
