Hypernatremia overview: Difference between revisions
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{{Hypernatremia}} | {{Hypernatremia}} | ||
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==Overview== | ==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]]. | ''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]]. | |||
== Classification == | |||
Hypernatremia can be classified based on the fluid status of the patients into hypovolemic, normovolemic, or hypervolemic hypernatremia. | |||
==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== | |||
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== | ==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. | ||
=== | === 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=== | ===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. | ||
=== 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== | ||
===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== | ||
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[[Category:Nephrology]] | [[Category:Nephrology]] | ||
[[Category:Electrolyte disturbance]] | [[Category:Electrolyte disturbance]] | ||
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{{WikiDoc Help Menu}} | {{WikiDoc Help Menu}} | ||
{{WikiDoc Sources}} | {{WikiDoc Sources}} | ||
Latest revision as of 15:13, 9 August 2018
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Hypernatremia overview On the Web |
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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.