Hyponatremia in Emergency Medicine Workup

  • Author: Sandy Craig, MD; Chief Editor: Erik D Schraga, MD   more...
 
Updated: Apr 13, 2010
 

Laboratory Studies

The diagnosis of hyponatremia depends entirely on the ability to properly obtain a sample of the patient's serum and to accurately measure its concentration of sodium.

When interpreting serum sodium levels, always consider the possibility of sampling error, especially when the reported value does not seem consistent with the history or physical findings.

  • Was the patient's blood sample properly labeled?
  • Was it obtained from a venous site proximal to an infusion of hypotonic saline or dextrose in water?
  • Is laboratory measurement or reporting in error?
  • If an error is suspected, a second sample should be submitted for testing before therapeutic measures are initiated.

In addition to sampling and analysis errors, several physiologic states exist in which correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hyposmolar state.

The most common example is serum hyperglycemia. Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space. Serum sodium concentration is diluted by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration. Systemic osmolarity is normal or even increased, not decreased, as in true (ie, hyposmolar) hyponatremia. This hypertonic hyponatremia has no physiologic significance, and serum sodium concentration corrects as normoglycemia is reestablished.

A similar phenomenon is observed in patients treated with glycerol or mannitol in an effort to control acute glaucoma or intracranial hypertension. This phenomenon is also seen in patients with advanced renal disease who receive radiocontrast agents for diagnostic testing.

Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid. In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved. Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range. This phenomenon, known as pseudohyponatremia, occurs when flame emission spectrophotometry or indirect potentiometry is used to assay serum sodium levels rather than direct potentiometry techniques. This occurs in approximately 60% of US laboratories.

Serum osmolarity remains undisturbed, and attempts at correcting serum sodium level are not indicated. Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample. Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.

Serum osmolarity is helpful in establishing the diagnosis of true hyposmolar hyponatremia. Serum osmolarity is abnormally low in patients with hyposmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.

Urine sodium levels are helpful in distinguishing renal causes of hyponatremia from nonrenal causes.

Patients with hypovolemic hyponatremia due to nonrenal causes (eg, vomiting, diarrhea, fistulas, GI drainage, third spacing of fluids) have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L, whereas those with hypovolemic hyponatremia due to renal causes (eg, diuretics, salt-losing nephropathy, aldosterone deficiency) have inappropriately elevated urine sodium levels in excess of 20 mEq/L.

Patients with hypervolemic hyponatremia due to decreases in effective circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L, whereas those with renal causes of hypervolemic hyponatremia or with SIADH have urine sodium levels in excess of 20 mEq/L.

Urine osmolarity may be helpful in establishing the diagnosis of SIADH. Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L. Patients with other forms of hyponatremia and appropriately depressed levels of ADH have urine osmolarities below 100 mOsm/L.

Serum thyroid-stimulating hormone (TSH) and free thyroxine levels should be checked if the clinical presentation is consistent with hypothyroidism.

Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.

Serum ADH levels are not routinely used in the evaluation of hyponatremia because the assay is technically difficult and not widely available on a stat basis. Recently, a serum peptide known as copeptin has been studied in the evaluation of hyponatremia. Copeptin is the C terminal portion of provasopressin and is released in equimolar amounts with vasopressin (ADH). One prospective observational study of 106 patients being evaluated for hyponatremia suggests that copeptin may prove to be a useful marker in the differential diagnosis of hyponatremia.[11]

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Imaging Studies

Imaging studies may be indicated depending on the underlying etiology of the hyponatremia (eg, chest radiograph in a patient with congestive heart failure).

Usually, a head CT scan is indicated in the patient with altered mental status to ensure that no other underlying cause for the mental status is present.

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Contributor Information and Disclosures
Author

Sandy Craig, MD  Residency Program Director, Carolinas Medical Center; Associate Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill School of Medicine

Sandy Craig, MD is a member of the following medical societies: Alpha Omega Alpha and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Erik D Schraga, MD  Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD  Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

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