Hypernatremia is defined as a serum sodium concentration exceeding 145 mEq/L. Sodium is the most important osmotically active particle in the extracellular space and closely linked to the body's fluid balance. An increase in the serum sodium concentration is most often due to a free water deficit caused by excessive fluid loss (e.g., diarrhea/vomiting, sweating, increased diuresis) or insufficient water intake (e.g., altered mental status, impaired thirst mechanism). In some cases, hypernatremia is due to a real sodium overload caused by high sodium intake (e.g., hypertonic infusion, drinking sea water) or inadequately high sodium reabsorption by the kidneys (e.g., primary hyperaldosteronism, Cushing syndrome). Symptoms are predominantly neurological and nonspecific (e.g., lethargy, confusion, focal neurological deficits, seizures, coma), and they are often accompanied by signs of cellular dehydration (e.g., dry mucous membranes, decreased salivation). Assessing the patient's volume status (during physical examination) and their renal ability to reabsorb free water (urine osmolality) can help determine the etiology of hypernatremia. Acuity of onset, volume status, and etiology should all be considered in order to determine the appropriate therapeutic approach and avoid complications. In children, a rapid decrease in the serum sodium concentration can cause cerebral edema, which carries the risk of brain herniation. In adults, a relationship between rapid correction and cerebral edema has not been observed; however, guidelines still recommend cautious correction.
In hypernatremia, serum osmolality is always increased, resulting in a hypertonic state. This is either due to a free water deficit (due to low intake or loss) or increased sodium (due to high intake or retention).
- Description: high serum Na+ levels with decreased extracellular volume as a result of hypotonic fluid loss
- Extrarenal cause (manifests with oliguria due to dehydration)
- Renal cause (leads to dehydration due to polyuria)
- Description: high serum Na+ levels with normal or minimal changes in extracellular volume as a result of pure water deficit
- Extrarenal causes (manifests with oliguria due to decreased water intake)
- Renal cause (causes increased thirst due to polyuria)
- Description: high serum Na+ levels with increased extracellular volume as a result of intake of hypertonic water or retention of sodium in excess of water
- Extrarenal causes (initially manifests with polyuria due to fluid overload, followed by dehydration due to polyuria)
- Renal causes (causes hypertension and hypokalemia with normal urine output and no fluid overload)
Overview of fluid compartment changes
|Volume status||Fluid compartment changes|
|Total body water||Total body sodium|
Hypernatremia is always a hyperosmolar state!
Acute hypernatremia (onset < 48 hours) 
Symptoms are primarily neurological and depend on the severity of hypernatremia.
- Mild symptoms: signs of dehydration
- Moderate symptoms
- Severe symptoms: typically occur only with severe hypernatremia (serum concentration > 160 mEq/L) 
Chronic hypernatremia (onset > 48 hours ago)
- Confirm hypernatremia (repeat BMP).
- Determine the etiology through clinical evaluation, and, if unclear, perform diagnostic studies.
- Patient history (e.g., low fluid intake, diarrhea)
- Clinical assessment of volume status (i.e., hypovolemia, euvolemia, versus hypervolemia) and fluid balance monitoring
- Urine osmolality and urine sodium concentration help differentiate renal causes from extrarenal causes.
- Additional studies as needed (e.g., water deprivation test for diabetes insipidus)
- CBC: Hematocrit level depends on volume status.
- Increased serum osmolality (SOsm) 
Urine osmolality; (UOsm) 
- High UOsm (> 600 mOsmol/kg) supports an extrarenal mechanism.
- Low UOsm (< 600 mOsmol/kg) supports an intrarenal mechanism.
- Urine sodium concentration (UNa)
- Water deprivation test and exogenous ADH challenge, if indicated (see “Diagnostics” in “Diabetes insipidus”)
Hypernatremia is always a hypertonic state!
|Evaluation of hypernatremia |
|Etiology||History and clinical features||Supportive diagnostic findings|
|Urine osmolality > 600 mOsm/kg |
|Insufficient access to water|
|Excessive salt intake|| || |
|Urine osmolality < 600 mOsm/kg |
|Nephrogenic diabetes insipidus|
|Central diabetes insipidus |
Treatment of hypernatremia requires replacing the free water deficit with sterile water enterally (oral, nasogastric tube, PEG tube) or 5% dextrose in water (D5W) intravenously. All patients should be carefully monitored with serial labs and some may need additional therapies to restore volume status.
- Hypovolemic patients: volume resuscitation
- Identify and treat underlying causes
- Hypernatremia correction
The cornerstone of hypernatremia management is replacing the free water deficit.
Calculation of free water deficit in hypernatremia 
Calculations of the free water deficit and ongoing water losses are more accurate than rough estimates. Electrolytes must be carefully monitored during treatment and regimens should be individually tailored.
- Combine free water deficit (FWD) and ongoing losses.
- Timeframe of volume replacement
- Acute hypernatremia: over 24 hours
- Chronic hypernatremia: over 48– 72 hours 
Correction of free water deficit 
- Acute hypernatremia (onset within < 48 hours)
Chronic hypernatremia (onset within > 48 hours)
- Gradually restore a normal Na+ level by decreasing Na+ concentration by 0.5 mEq/L/hour (max. 10–12 mEq/L per 24 hours). 
- Oral rehydration with free access to water may be sufficient in stable and alert patients.
- Estimated fluid replacement regimen: 1.35 mL/kg/hour of IV D5W or enteral water 
Adjustment of infusion rate
- Fluids other than D5W or sterile water require a different flow rate to provide the same amount of free water.
- Depending on serial Na+ concentration
Additional fluid management strategies
- Hypervolemic hypernatremia: Consider loop diuretics (e.g., furosemide oral or IV bolus ) alongside free water replacement. 
- Severe renal impairment or refractory fluid overload: Consider nephrology referral for hemodialysis. 
- Sodium restriction to < 2 grams per day 
Alleviate Acute hypernatremia Aggressively and Correct Chronic hypernatremia Carefully!
Monitoring and disposition
- Serial BMPs every 1–2 hours for acute hypernatremia; every 4–6 hours for chronic hypernatremia
- Adjust free water infusion rate according to target Na+ correction rates.
- Monitor for hyperglycemia. 
- Replace electrolyte deficiencies (see “Electrolyte repletion").
- Consider ICU admission for patients with severe hypernatremia (Na+ > 160 mEq/L) and high-risk symptoms (e.g., seizures).
- Confirm hypernatremia (repeat BMP).
- Assess volume status.
- If the patient is hypovolemic, volume resuscitate first with isotonic fluids (e.g., normal saline).
- Determine whether hypernatremia is acute or chronic in nature.
- Free water replacement (enterally or D5W IV): Correct aggressively for acute hypernatremia and gradually for chronic hypernatremia.
- Order serial BMPs, monitor closely, and adjust fluid rate as needed.
- Treat the underlying cause and prevent further fluid losses.
- Consider ICU admission in patients with severe hypernatremia (i.e., > 160 mEq/L).
Complications of hypernatremia
- Cell dehydration and shrinkage of brain tissue can cause intracranial vessels to rupture.
- Hemorrhages may lead to irreversible neurological deficits.
- the cell membranes of muscle cells. : Severe hypernatremia can damage
Complications of hypernatremia treatment
- Cerebral edema: may develop from rapid correction of chronic hypernatremia 
- Hypervolemia complications: secondary to hypernatremia correction with large-volume IV fluid administration (e.g., noncardiogenic pulmonary edema)
We list the most important complications. The selection is not exhaustive.