Hypernatremia

Jump to navigation Jump to search

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 On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hypernatremia

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hypernatremia

CDC on Hypernatremia

Hypernatremia in the news

Blogs on Hypernatremia

Directions to Hospitals Treating Hypernatremia

Risk calculators and risk factors for Hypernatremia

Hypernatremia
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

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 loss: excessive sweating in the context of exercise or warm climate

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

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/L 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 the brain adapts rapidly to plasma hyperosmolarity due to intracellular accumulation of many osmolytes such as amino acids (eg, glutamate).

Treatment

The cornerstone of treatment is administration of free water to correct the relative water deficit. Water can be replaced orally or intravenously. However, overly rapid correction of hypernatremia is potentially very dangerous. 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. 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 per 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.

See also

Template:Endocrine, nutritional and metabolic pathology


Template:WikiDoc Sources