Hypernatremia overview: Difference between revisions

Jump to navigation Jump to search
No edit summary
 
(23 intermediate revisions by 4 users not shown)
Line 1: Line 1:
<div style="-webkit-user-select: none;">
{| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;"
|-
| {{#ev:youtube|https://https://www.youtube.com/watch?v=xHA_GTWSDQk|350}}
|-
|}
__NOTOC__
{{Hypernatremia}}
{{Hypernatremia}}
{{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]]
{{CMG}};{{AE}}{{FT}}
==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]].
 
== Historical perspective ==
In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the [[central nervous system]] and renal excretion of osmotically active [[solutes]]. In 1913, Jungmann and Meyer in Germany induced [[polyuria]] and increased urinary salt excretion in animals through [[medullary]] lesion. In 1950, Peters, Welt, and co-workers described few patients with [[encephalitis]], hypertensive [[intracranial hemorrhage]], and bulbar [[poliomyelitis]] who presented with severe [[dehydration]] and [[hypernatremia]].


==Overview==
== Classification ==
'''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]].
Hypernatremia can be classified based on the fluid status of the patients into hypovolemic, normovolemic, or hypervolemic hypernatremia.


==Pathophysiology==
==Pathophysiology==
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.
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==
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 can be due to sodium salt ingestion or minaralocorticoid excess.
 
== Differentiating hypernatremia from Other Diseases ==
Hypernatremia must be differentiated among diseases that cause hypernatremia.
 
== Epidemiology and Demographics ==
The incidence of hypernatremia in hospitalized patients is approximately 3-5 per 100,000 individuals worldwide. The prevalence of hypernatremia in critically ill patients is approximately 9-26 per 100,000 individuals. Hypernatremia commonly affects older age.
 
==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]].


==Causes==
== Screening ==
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.
There is insufficient evidence to recommend routine screening for hypernatremia.  


==Differential diagnosis==
== Natural History, Complications, and Prognosis ==
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.


==Diagnosis==
==Diagnosis==
Diagnosis relies on a constellation of findings including:
===History and Symptoms===
===Symptoms===
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.
Usually nonspecific with lethargy and weakness being predominant. At higher levels of sodium concentrations, seizures and neurologic dysfunction become more evident.
 
===History===
=== Physical Examination ===
It should include any history of renal, GI or endocrine diseases. Moreover, drug and diet knowledge is essential for diagnosing the etiology.
Patients with hypernatremia appear lethargic, weak and confused. However, the physical examination findings are related to the amount of volume deificit in the body and neuronal shrinkage as a result of hypertonicity. For the physical exam findings to become apparent, acute elevation in the serum sodium concentration to above 158 mEq/L is required.
===Labs===
 
The urine osmolarity can help differentiate renal from extrarenal causes. The water deprivation test can help define the origin of diabetes insipidus (neurogenic vs nephrogenic)
===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.
 
=== Electrocardiogram ===
There are no ECG findings associated with hypernatremia.
 
=== CT scan ===
CT scan can be helpful in cases of hypernatremia due to diabetes insipidus in detecting head trauma.
 
=== MRI scan ===
There are no MRI findings associated with hypernatremia.
 
=== Other Diagnostic Findings ===
There are no other diagnostic studies associated with Hypernatremia.
 
=== Other Imaging Findings ===
There are no other imaging findings associated with hypernatremia.


==Treatment==
==Treatment==
It aims at correcting the free water deficit and removing the offending drug or osmotic agent. Specific etiologies such as DI can be treated accordingly.
===Medical Therapy===
The primary goals of treating hypernatremia are estimating the magnitude of water deficit, determining the proper rate of correction, addressing the concurrent electrolyte or volume deficits and calculating the fluid deficit regimen using the estimated water deficit and desired rate of correction. Correcting sodium level is vital in order to prevent any permanent brain damage.
 
=== Surgery ===
The mainstay of treatment for hypernatremia is medical therapy. Surgery is usually reserved for patients suffering severe central nervous system trauma and patients with central diabetes insipidus.
 
=== Primary prevention ===
Effective measures for the primary prevention of hypernatremia include an increase in water intake during increased insensible water losses. A low-sodium diet will reduce oral solute intake and therefore decrease renal water loss.
 
=== Secondary prevention ===
Patients who drink inadequately should be encouraged to drink at least 1-2 L of water each day. All nursing home patients, immobile patients, and in-patient patients should be encouraged to drink water regularly.


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


[[Category:Electrophysiology]]
[[Category:Inborn errors of metabolism]]
[[Category:Cardiology]]
[[Category:Blood tests]]
[[Category:Endocrinology]]
[[Category:Emergency medicine]]
[[Category:Emergency medicine]]
[[Category:Intensive care medicine]]
[[Category:Nephrology]]
[[Category:Nephrology]]
[[Category:Electrolyte disturbance]]
[[Category:Electrolyte disturbance]]
[[Category:Blood tests]]
[[Category:Needs overview]]
[[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 Help Menu}}
{{WikiDoc Sources}}
{{WikiDoc Sources}}

Latest revision as of 15:13, 9 August 2018

https://https://www.youtube.com/watch?v=xHA_GTWSDQk%7C350}}


Hypernatremia Microchapters

Home

Patient Information

Overview

Historical perspective

Classification

Pathophysiology

Causes

Differentiating Hypernatremia from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

CT

MRI

Other Diagnostic Studies

Other Imaging Findings

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Case Studies

Case #1

Hypernatremia overview On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hypernatremia overview

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hypernatremia overview

CDC on Hypernatremia overview

Hypernatremia overview in the news

Blogs on Hypernatremia overview

Directions to Hospitals Treating Hypernatremia

Risk calculators and risk factors for Hypernatremia overview

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

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.

Historical perspective

In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the central nervous system and renal excretion of osmotically active solutes. In 1913, Jungmann and Meyer in Germany induced polyuria and increased urinary salt excretion in animals through medullary lesion. In 1950, Peters, Welt, and co-workers described few patients with encephalitis, hypertensive intracranial hemorrhage, and bulbar poliomyelitis who presented with severe dehydration and hypernatremia.

Classification

Hypernatremia can be classified based on the fluid status of the patients into hypovolemic, normovolemic, or hypervolemic hypernatremia.

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 can be due to sodium salt ingestion or minaralocorticoid excess.

Differentiating hypernatremia from Other Diseases

Hypernatremia must be differentiated among diseases that cause hypernatremia.

Epidemiology and Demographics

The incidence of hypernatremia in hospitalized patients is approximately 3-5 per 100,000 individuals worldwide. The prevalence of hypernatremia in critically ill patients is approximately 9-26 per 100,000 individuals. Hypernatremia commonly affects older age.

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.

Screening

There is insufficient evidence to recommend routine screening for hypernatremia.

Natural History, Complications, and Prognosis

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.

Physical Examination

Patients with hypernatremia appear lethargic, weak and confused. However, the physical examination findings are related to the amount of volume deificit in the body and neuronal shrinkage as a result of hypertonicity. For the physical exam findings to become apparent, acute elevation in the serum sodium concentration to above 158 mEq/L is required.

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.

Electrocardiogram

There are no ECG findings associated with hypernatremia.

CT scan

CT scan can be helpful in cases of hypernatremia due to diabetes insipidus in detecting head trauma.

MRI scan

There are no MRI findings associated with hypernatremia.

Other Diagnostic Findings

There are no other diagnostic studies associated with Hypernatremia.

Other Imaging Findings

There are no other imaging findings associated with hypernatremia.

Treatment

Medical Therapy

The primary goals of treating hypernatremia are estimating the magnitude of water deficit, determining the proper rate of correction, addressing the concurrent electrolyte or volume deficits and calculating the fluid deficit regimen using the estimated water deficit and desired rate of correction. Correcting sodium level is vital in order to prevent any permanent brain damage.

Surgery

The mainstay of treatment for hypernatremia is medical therapy. Surgery is usually reserved for patients suffering severe central nervous system trauma and patients with central diabetes insipidus.

Primary prevention

Effective measures for the primary prevention of hypernatremia include an increase in water intake during increased insensible water losses. A low-sodium diet will reduce oral solute intake and therefore decrease renal water loss.

Secondary prevention

Patients who drink inadequately should be encouraged to drink at least 1-2 L of water each day. All nursing home patients, immobile patients, and in-patient patients should be encouraged to drink water regularly.

References

Template:WikiDoc Sources