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Hypernatremia in Emergency Medicine Clinical Presentation

  • Author: Zina Semenovskaya, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
Updated: Jun 27, 2016


The history in the hypernatremic patient often points to the etiology of the syndrome. Search for any cause of extrarenal fluid losses (eg, burns, vomiting, diarrhea, fevers). Investigate the patient's perception of his or her fluid status and corrective measures he or she has taken. Does the patient complain of polyuria or polydipsia (ie, signs of DI or osmotic diuresis)? Does the patient have an intact thirst response? (This is often impaired in elderly persons.) A diminished thirst response is an indication to investigate the hypothalamus for a lesion in the thirst centers. For unclear reasons, patients with DI often crave ice-cold water (pagophagia).

In infants, seek sources of extra-renal losses, and investigate the patient's dietary habits. Hypernatremia in infants is often caused by improper preparation of formula or poor maternal milk production.[5]

In patients who are hospitalized, reviewing the medicines and the types of feedings that the patient has received is important to exclude iatrogenic excessive sodium load. Commonly identified sources include the administration of sodium bicarbonate during cardiac arrest, high-sodium tube feedings, or overaggressive infusion of 3% isotonic sodium chloride solution. Pharmaceutical causes of nephrogenic DI should also be considered (see Causes).

Symptoms of hypernatremia tend to be nonspecific. Anorexia, restlessness, nausea, and vomiting occur early. These symptoms are followed by altered mental status, lethargy or irritability, and, eventually, stupor or coma. Musculoskeletal symptoms may include twitching, hyperreflexia, ataxia, or tremor. Neurologic symptoms are generally nonfocal (eg, mental status changes, ataxia, seizure), but focal deficits such as hemiparesis have been reported.



Physical examination findings in hypernatremia are nonspecific.

Assessment of overall fluid status is important when determining the cause of the hypernatremia. Note signs of volume status, including mucous membranes, skin turgor, orthostatic vital signs, and neck veins.

Because neurologic deficits are common in hypernatremia, perform a thorough neurologic examination.

Significant hypovolemia can result when hypotonic fluid losses cause hypernatremia. The physical findings are those of dehydration or even hypovolemic shock, with tachycardia, orthostasis, and hypotension.



Hypernatremia is due to too little water, too much salt, or a combination thereof. The alteration can be in administration (too much salt or too little water) or output (too much dilute urine or extrarenal free water losses).[6, 7, 8]

The most common cause of hypernatremia in the elderly or institutionalized patients is lack of free water intake to meet losses adequately. Thirst is the body's main defense against increased serum tonicity. The thirst drive is activated through 2 pathways, one responsive to decreased intravascular volume and the other responsive to even slight increases in serum osmolarity. Most patients with an intact thirst mechanism and access to water can prevent the development of hypernatremia. Even patients with a defective renal concentrating mechanism (eg, patients with DI who may produce up to 20 L of urine a day) generally can keep up with water losses if they have free access to water.

Some patients, however, cannot respond to their thirst drive. Infants and elderly patients who are debilitated depend on caregivers to provide fluids. Similarly, institutionalized patients may have limited access to water secondary to either external or internal constraints (eg, no access to water in their room, they believe the water is poisoned and refuse to drink it). Intrinsic water losses cannot be avoided, and some urine must be produced, even if it is maximally concentrated. Without access to water, these patients encounter a free water deficit, and their serum sodium level increases.

In some instances, the difficulty stems from an inability of the kidneys to concentrate the urine. This is known as diabetes insipidus (DI). DI can be due to a lack of a central stimulus to concentrate the urine (ie, lack of antidiuretic hormone [ADH] production [central DI]) or to a lack of renal response to such stimulus (ie, nephrogenic DI). The kidneys can fail to respond secondary to resistance to vasopressin or due to loss of the medullary-concentrating gradient for urine.

The differential diagnosis is most easily managed if the physician considers the patient's volume status.

Hypovolemic hypernatremia (ie, water deficit >sodium deficit)

Adipsic hypernatremia is secondary to decreased thirst. This can be behavioral or, rarely, secondary to damage to the hypothalamic thirst centers.

  • Extrarenal losses - Diarrhea, vomiting, fistulas, significant burns
  • Renal losses - Osmotic diuretics, diuretics, postobstructive diuresis, intrinsic renal disease

Hypervolemic hypernatremia (ie, sodium gains >water gains)

See the list below:

  • Hypertonic saline
  • Sodium bicarbonate administration
  • Accidental salt ingestion (eg, error in preparation of infant formula)
  • Mineralocorticoid excess (Cushing syndrome)

Euvolemic hypernatremia

See the list below:

  • Extrarenal losses - Increased insensible loss (eg, hyperventilation)
  • Renal losses - Central DI, nephrogenic DI

These patients appear euvolemic because most of the free water loss is from intracellular and interstitial spaces, with less than 10% occurring from the intravascular space. Typically, symptoms result if serum sodium level is more than 160-170 mEq/L.

Central DI differential diagnosis

See the list below:

  • Head trauma
  • Suprasellar or intrasellar tumors
  • Granulomas (sarcoidosis, Wegener granulomatosis, tuberculosis, syphilis)
  • Histocytosis (eosinophilic granuloma)
  • Infectious (encephalitis, meningitis, Guillain-Barré syndrome)
  • Vascular (cerebral aneurysm, thrombosis, hemorrhage, Sheehan syndrome)
  • Congenital
  • Transient DI of pregnancy

Nephrogenic DI (deficient renal response to ADH) differential diagnosis

See the list below:

  • Advanced renal disease (interstitial disease)
  • Electrolyte disturbances - Hypokalemia, hypercalcemia
  • Systemic diseases - Sickle cell disease, Sjögren syndrome, amyloidosis, Fanconi syndrome, sarcoidosis, renal tubular acidosis, light-chain nephropathy
  • Dietary disturbances - Excessive water intake, decreased salt intake, decreased protein intake
  • Drugs - Lithium, demeclocycline, colchicine, vinblastine, amphotericin B, gentamicin, furosemide, angiographic dyes, osmotic diuretics
  • Miscellaneous - Postobstructive diuresis, diuretic phase of acute renal failure, osmotic diuresis, paroxysmal hypertension
Contributor Information and Disclosures

Zina Semenovskaya, MD Resident Physician, Department of Emergency Medicine, Kings County Hospital, State University of New York Downstate Medical Center College of Medicine

Disclosure: Nothing to disclose.


Richard H Sinert, DO Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Vice-Chair in Charge of Research, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven L Stephanides, MD Attending Physician, Department of Emergency Medicine, Eisenhower Medical Center

Steven L Stephanides, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

Joseph J Sachter, MD, FACEP Consulting Staff, Department of Emergency Medicine, Muhlenberg Regional Medical Center

Joseph J Sachter, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Association for Physician Leadership, American Medical Association, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Richard Sinert, DO, to the development and writing of this article.

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Figure A: Normal cell. Figure B: Cell initially responds to extracellular hypertonicity through passive osmosis of water extracellularly, resulting in cell shrinkage. Figure C: Cell actively responds to extracellular hypertonicity and cell shrinkage in order to limit water loss through transport of organic osmolytes across the cell membrane, as well as through intracellular production of these osmolytes. Figure D: Rapid correction of extracellular hypertonicity results in passive movement of water molecules into the relatively hypertonic intracellular space, causing cellular swelling, damage, and ultimately death.
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