Hypernatremia: Difference between revisions
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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. | 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 | '''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=== | ===History=== | ||
Revision as of 17:01, 9 December 2011
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Hypernatremia Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Hypernatremia On the Web |
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American Roentgen Ray Society Images of Hypernatremia |
| Hypernatremia | |
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| Sodium | |
| ICD-10 | E87.0 |
| ICD-9 | 276.0 |
| DiseasesDB | 6266 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor(s)-In-Chief: 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 free water in the body. For this reason, hypernatremia is often synonymous with the less precise term dehydration.
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.
Causes
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.
Differential diagnosis
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 relies on a constellation of findings including:
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 infants, those with impaired 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 diuretics 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
| Cardiovascular | No underlying causes |
| Chemical / poisoning | No underlying causes |
| Dermatologic | Burns, Excessive sweating |
| Drug Side Effect | diuretics |
| Ear Nose Throat | No underlying causes |
| Endocrine | Adrenal, Diabetes Insipidus, Congenital Adrenal Hyperplasia, Conn's Syndrome,Cushing's Syndrome, Ectopic adrenocorticotropic hormone (ACTH) production, Hyperaldosteronism, Hyperglycemia, Hyperlipidemia, Thyrotoxicosis |
| Environmental | No underlying causes |
| Gastroenterologic | Gastrointestinal losses (diarrhea, vomiting), inability to swallow water (physical limitation) |
| Genetic | No underlying causes |
| Hematologic | No underlying causes |
| Iatrogenic | Inappropriate IV fluids |
| Infectious Disease | Fever |
| Musculoskeletal / Ortho | No underlying causes |
| Neurologic | Essential hypernatremia, Dementia, Coma, hypothalamic lesion, inability to recognize thirst for water |
| Nutritional / Metabolic | ingestion of large quantities of sodium (seawater), decreased protein intake |
| Obstetric/Gynecologic | No underlying causes |
| Oncologic | Multiple Myeloma |
| Opthalmologic | No underlying causes |
| Overdose / Toxicity | Alcoholism |
| Psychiatric | No underlying causes |
| Pulmonary | Sarcoidosis, Hyperventilation |
| Renal / Electrolyte | High urea levels with renal failure, Hypercalcemia, Hypokalemia, Osmotic diuresis, Peritoneal dialysis,Diuresis phase of acute renal failure |
| Rheum / Immune / Allergy | Sjogren's Syndrome |
| Sexual | No underlying causes |
| Trauma | No underlying causes |
| Urologic | No underlying causes |
| Miscellaneous | 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, seizures 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 intravenously.
- 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 imbalances.
- 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.