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Last Update: August 24, 2023.

Continuing Education Activity

The human body maintains sodium and water homeostasis by concentrating the urine secondary to the action of antidiuretic hormone (ADH) and increased fluid intake by a powerful thirst response. These mechanisms to protect against developing hypernatremia are impaired in certain vulnerable populations and conditions with vasopressin deficiency or unresponsiveness at the renal tubular level. Hypernatremia is defined as a serum sodium concentration of greater than 145 meq/l. This activity reviews the causes and presentation and highlights the role of the interprofessional team in its management


  • Review the causes of hypernatremia.
  • Describe the evaluation of a patient with hypernatremia.
  • Summarize the treatment of hypernatremia.
  • Explain the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by hypernatremia.
Access free multiple choice questions on this topic.


Sodium is a dominant cation in extracellular fluid and is necessary for the maintenance of intravascular volume. The human body maintains sodium and water homeostasis by concentrating the urine secondary to the action of antidiuretic hormone (ADH) and increased fluid intake by a powerful thirst response. These mechanisms to protect against developing hypernatremia are impaired in certain vulnerable populations, vasopressin deficiency, or unresponsiveness at the renal tubular level. Hypernatremia is defined as a serum sodium concentration of greater than 145 meq/L.[1][2][3][4]


The basic mechanisms of hypernatremia are water deficit and excess solute. Total body water loss relative to solute loss is the most common reason for developing hypernatremia. Hypernatremia is usually associated with hypovolemia, which can occur in conditions that cause combined water and solute loss, where water loss is greater than sodium loss or free water loss. Combined loss can be seen in extra-renal conditions such as gastroenteritis, vomiting, prolonged nasogastric drainage, burns, and excessive sweating. Excessive sweating can occur due to exercise, fever, or high heat exposure. Renal losses can be seen in intrinsic renal disease, post-obstructive diuresis, and with the use of osmotic or loop diuretics. Hyperglycemia and mannitol are common causes of osmotic diuresis. Free water loss is seen with central or nephrogenic diabetes insipidus (DI) and also in conditions with increased insensible loss. Central DI can occur due to inadequate production of ADH. Common causes of central DI are idiopathic, head trauma, cranial neoplasm, and pituitary infiltrative diseases, such as sarcoidosis and histiocytosis. Nephrogenic DI occurs due to tubular unresponsiveness to the action of ADH and can be inherited in an X-linked pattern or secondary to certain medications, including lithium, foscarnet, and demeclocycline. Rarely, hypernatremia with inadequate fluid intake can be seen in breastfed babies, child or elder abuse, and patients with an impaired thirst response. Excess sodium usually is iatrogenic and seen in the hospital setting but can be associated with improper formula mixing, excess sodium bicarbonate ingestion, salt tablet poisoning, hyperaldosteronism, and seawater drowning.[5][6][7][8]


Hypernatremia is primarily seen in infants and the elderly population. Infants receiving inadequate water replacement in the setting of gastroenteritis or ineffective breastfeeding are common scenarios. Premature infants are at higher risk due to their relatively small mass to surface area and their dependency on the caretaker to administer fluids. Patients with neurologic impairment also are at risk due to impaired thirst mechanism and lack of water availability. Hypernatremia can occur in the hospital setting due to hypertonic fluid infusions, especially when combined with the patient's inability for adequate water intake.[9]


Sodium is important to maintain extracellular fluid (ECF) volume. Changes in the ECF volume provide feedback to maintain total sodium content by increasing or decreasing sodium excretion in the urine. Sodium excretion also involves regulatory mechanisms such as the renin-angiotensin-aldosterone systems. When serum sodium increases, the plasma osmolality increases, which triggers the thirst response and ADH secretion, leading to renal water conservation and concentrated urine.[10]

History and Physical

Most patients present with symptoms suggestive of fluid loss and clinical signs of dehydration. Symptoms and signs of hypernatremia are secondary to central nervous system dysfunction and are seen when serum sodium rises rapidly or is greater than 160 meq/L. Infants and Children present with irritability and agitation, which can progress to lethargy, somnolence, and coma. Other symptoms include increased thirst response in alert patients and high-pitched cries in infants. Patients with diabetes insipidus present with polyuria and polydipsia. The skin can feel doughy or velvety due to intracellular water loss. Orthostatic hypotension and tachycardia are usually present in hypovolemic hypernatremia. The patient may have increased tone with brisk reflexes and myoclonus. It is important to remember that the degree of dehydration can be underestimated in children with hypernatremia due to a shift of water from the intracellular space to the extravascular space. Polyuria is one of the common symptoms of diabetes insipidus.[11][12]


The etiology of hypernatremia usually is evident based on history and physical examination. Plasma volume, plasma osmolality, urine volume, concentrating ability, and osmolality can help to further differentiate between renal and extrarenal causes. In DI, the urine is inappropriately diluted with normal urine volume and urine osmolality less than the serum osmolality. When DI is suspected, a water deprivation test may be performed with the administration of desmopressin. In central DI, desmopressin administration demonstrates an increase in urine osmolality, while in the nephrogenic variety, there is no response to desmopressin. In extrarenal causes, the body tries to conserve fluids with appropriately low urine volume, high specific gravity, and urine osmolality greater than serum osmolality.[13]

Treatment / Management

Proper management of hypernatremia involves identifying the underlying condition and correcting the hypertonicity. The goal of therapy is to correct both the serum sodium and the intravascular volume. Fluids should be administered orally or via a feeding tube whenever possible. In patients with severe dehydration or shock, the initial step is fluid resuscitation with isotonic fluids before free water correction. Hypernatremia is corrected by calculating the free water deficit using one of the following formulas.[14][15]

  • Total Body Water[0.6 in men and 0.5 in women x body weight(kg)] x [(plasma sodium/140) -1]
  • 4ml x bodyweight x (desired change in serum sodium meq/L)

It is important to remember that rapid correction of hypernatremia can lead to cerebral edema because water moves from the serum into the brain cells. The goal is to decrease serum sodium by not more than 12 meq in 24 hours. Close serial monitoring of serum sodium every 2 to 4 hours is essential during the acute phase of correction. Seizures occurring during the correction of hypernatremia are a sign of cerebral edema due to rapid shifts in osmolality, and the administration of hypotonic fluids should be halted. The estimated free water deficit should be corrected over 48 to 72 hours with a decrease in serum sodium not exceeding 0.5 meq per hour. Patients should be carefully monitored for the rate of correction, urine output, and ongoing losses. In cases of sodium intoxication, the free water requirement may be too large and cause volume overload, requiring the use of loop diuretics and, at times, peritoneal dialysis to remove excess sodium. There are no published reports of seizures or cerebral edema complicating rapid correction of hypernatremia in adults. Older children and adults with central DI may need desmopressin, which is available in intranasal and oral forms. Water intoxication and hyponatremia are adverse effects seen with the use of desmopressin.

Differential Diagnosis

  • Cirrhosis
  • Central diabetes insipidus
  • Diarrhea
  • Hypocalcemia
  • Hyponatremia
  • Nephrogenic diabetes insipidus
  • Thirst defect
  • Type 1 diabetes mellitus


The most serious complication of hypernatremia is subarachnoid or subdural hemorrhage due to the rupture of bridging veins and dural sinus thrombosis. It can lead to permanent brain damage or death. Rapid correction of chronic hypernatremia causes cerebral edema, seizure, and permanent brain damage.[16]

Pearls and Other Issues

  • Hypernatremia occurs due to net water loss or excess sodium intake. 
  • It is more common in infants or older populations with neurological or physical impairment.
  • It is crucial to identify acute versus chronic onset hypernatremia before correcting the free water deficit. 
  • It is important to remember that hypernatremia should be corrected over 48 hours. Rapid correction can lead to cerebral edema and seizures.

Enhancing Healthcare Team Outcomes

Hypernatremia is best managed by an interprofessional team that includes an internist, endocrinologist, emergency department physician, nurse practitioner, and the primary care provider. The key is to identify the cause and correct the hypertonicity. The goal of therapy is to correct both the serum sodium and the intravascular volume. In patients with severe dehydration or shock, the initial step is fluid resuscitation with isotonic fluids before free water correction.

Healthcare providers should be cognizant of the fact that rapid correction of hypernatremia can lead to cerebral edema because water moves from the serum into the brain cells. The goal is to decrease the serum sodium by not more than 10 to 12 meq/L in 24 hours. The acute phase of sodium correction requires monitoring of serum sodium levels every 2 to 4 hours. Frequent communication between the attending physician, the nursing staff, and the pharmacist is crucial to avoid the rapid correction of sodium levels. Rapid correction of sodium levels can lead to a seizure, cerebral edema, or permanent neurological deficit. Special attention should be given to high-risk nursing home patients with neurological or physical impairments who are prone to develop recurrent hypernatremia. Discharge care coordination among discharging physicians, primary care physicians, and nursing home staff can prevent readmission due to hypernatremia. Serum sodium and drug levels should be periodically monitored in patients who are taking medications known to cause nephrogenic diabetes insipidus.[17][18] [Level 5]

Review Questions


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Qian Q. Hypernatremia. Clin J Am Soc Nephrol. 2019 Mar 07;14(3):432-434. [PMC free article: PMC6419289] [PubMed: 30728169]
Slaughter RJ, Watts M, Vale JA, Grieve JR, Schep LJ. The clinical toxicology of sodium hypochlorite. Clin Toxicol (Phila). 2019 May;57(5):303-311. [PubMed: 30689457]
Rubin AN, Espiridion ED, Kattan M, Desmarais EC. Serotonin Syndrome with Atypical Hypernatremia. Cureus. 2018 Nov 19;10(11):e3616. [PMC free article: PMC6340410] [PubMed: 30680272]
Yano T, Uchimura S, Nagahama M, Yonaha T, Taniguchi M, Tsuneyoshi I. Continuous hemodiafiltration for hypernatremia and a simple formula for stepwise regulation of the sodium concentration in a dialysate. J Clin Anesth. 2019 Aug;55:144-145. [PubMed: 30660092]
Iraqi B, Abilkassem R, Dini N, Agadr A. A three-year-old boy with hypodipsic hypernatremia syndrome. Pan Afr Med J. 2018;30:250. [PMC free article: PMC6307918] [PubMed: 30627311]
Das MK, Ali MA, Latif T, Islam MN, Hossain MA, Moniruzzaman MM, Oliullah M, Haque SA, Gosh AK. Comparison of Serum Electrolytes Abnormality and Renal Function Status in Asphyxiated and Normal Baby in a Tertiary Level Hospital. Mymensingh Med J. 2018 Oct;27(4):723-729. [PubMed: 30487486]
Imai N, Shibagaki Y. The prevalence of dysnatremia in the elderly patients without CKD. Am J Emerg Med. 2019 Mar;37(3):499-501. [PubMed: 30595426]
Braun MM, Barstow CH, Pyzocha NJ. Diagnosis and management of sodium disorders: hyponatremia and hypernatremia. Am Fam Physician. 2015 Mar 01;91(5):299-307. [PubMed: 25822386]
Muhsin SA, Mount DB. Diagnosis and treatment of hypernatremia. Best Pract Res Clin Endocrinol Metab. 2016 Mar;30(2):189-203. [PubMed: 27156758]
McManus ML, Churchwell KB, Strange K. Regulation of cell volume in health and disease. N Engl J Med. 1995 Nov 09;333(19):1260-6. [PubMed: 7566004]
Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med. 2000 May 18;342(20):1493-9. [PubMed: 10816188]
Nigro N, Grossmann M, Chiang C, Inder WJ. Polyuria-polydipsia syndrome: a diagnostic challenge. Intern Med J. 2018 Mar;48(3):244-253. [PubMed: 28967192]
Baldeweg SE, Ball S, Brooke A, Gleeson HK, Levy MJ, Prentice M, Wass J., Society for Endocrinology Clinical Committee. SOCIETY FOR ENDOCRINOLOGY CLINICAL GUIDANCE: Inpatient management of cranial diabetes insipidus. Endocr Connect. 2018 Jul;7(7):G8-G11. [PMC free article: PMC6013691] [PubMed: 29930026]
Koch CA, Fulop T. Clinical aspects of changes in water and sodium homeostasis in the elderly. Rev Endocr Metab Disord. 2017 Mar;18(1):49-66. [PubMed: 28303369]
Kim SW. Hypernatemia : successful treatment. Electrolyte Blood Press. 2006 Nov;4(2):66-71. [PMC free article: PMC3894528] [PubMed: 24459489]
Hoffman H, Verhave B, Chin LS. Hypernatremia is associated with poorer outcomes following aneurysmal subarachnoid hemorrhage: a nationwide inpatient sample analysis. J Neurosurg Sci. 2021 Oct;65(5):486-493. [PubMed: 30514071]
Ramburuth M, Moodley Y, Gopalan PD. Preoperative serum sodium measurements and postoperative inpatient mortality: A case-control analysis of data from the South African Surgical Outcomes Study. S Afr Med J. 2018 Oct 02;108(10):847-851. [PubMed: 30421713]

Disclosure: Bhavin Sonani declares no relevant financial relationships with ineligible companies.

Disclosure: Srividya Naganathan declares no relevant financial relationships with ineligible companies.

Disclosure: Mohammed Al-Dhahir declares no relevant financial relationships with ineligible companies.

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Bookshelf ID: NBK441960PMID: 28722989


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