Pediatric Hyponatremia Workup

Updated: Dec 21, 2020
  • Author: Muthukumar Vellaichamy, MD, FAAP; Chief Editor: Timothy E Corden, MD  more...
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Laboratory Studies

Verify the accuracy of laboratory results in patients with hyponatremia.

Measurement of fractional excretion of urate (FEurate) appears to have the potential for use to differentiate causes of hyponatremia such as inappropriate antidiuretic hormone secretion (SIADH) versus cerebral or renal salt wasting (RSW) versus reset osmostat (RO). [13, 14] The following is based on a proposed algorithm using levels of FEurate in patients with hyponatremia [14] :

  • FEurate level below 4%: Volume depletion, Addison disease, edematous states (congestive heart failure, cirrhosis, nephrosis, preeclampsia)
  • FE urate level of 4-11%: Psychogenic polydipsia, reset osmostat
  • FE urate level above 11%, with correction to normonatremia: If FEurate level falls below 11%, then SIADH or hydrochlorothiazide; if FEurate level remains over 11%, then RSW.

The investigators also suggest that it is possible some patients with RSW may bypass hyponatremia because of very little water intake and thus have normonatremia but a hight FEurate level (ie, >11%). [14]

Exclude pseudohyponatremia

Findings on flame emission spectrophotometry

  • If Na measurement is performed by using flame emission spectrophotometry, hyponatremia is falsely low in patients with hyperproteinemia and hypertriglyceridemia.
  • Raised proteins and lipid levels increase the nonaqueous portion of plasma, which normally forms 7% of the plasma.
  • However, new ion-specific Na electrodes measure Na from only the aqueous phase, enabling accurate estimation of serum Na concentrations.

Correction factors for raised proteins and lipids

  • Triglycerides (in milligrams per deciliter) X 0.002 = decrease in plasma Na level (in milliequivalents per liter)
  • (Plasma protein level [in grams per deciliter] - 8) X 0.25 = decrease in plasma Na (in milliequivalents per liter)

Exclude distributive hyponatremia

Distributive hyponatremia occurs when the plasma glucose concentration exceeds 100 mg/dL.

Each 100-mg/dL increase in the glucose level above 100 mg/dL leads to a 1.6-mEq/L decrease in the Na concentration.

Obtain routine laboratory tests

Obtain routine laboratory studies to assess the following:

  • Serum Na level

  • Serum osmolality

  • Blood urea nitrogen (BUN) and creatinine levels

  • Urine osmolality

  • Urine Na level

Evaluate urine Na

Urine Na level changes according to the type of hyponatremia.

Hypovolemic hyponatremia

  • Renal losses caused by diuretic excess, osmotic diuresis, salt-wasting nephropathy, adrenal insufficiency, proximal renal tubular acidosis, metabolic alkalosis, or pseudohypoaldosteronism result in a urine Na concentration of more than 20 mEq/L.
  • Extrarenal losses caused by vomiting, diarrhea, sweat, or third spacing result in a urine Na concentration of less than 20 mEq/L secondary to increased tubular reabsorption of Na.

Normovolemic hyponatremia

When hyponatremia is caused by syndrome of SIADH, reset osmostat, glucocorticoid deficiency, hypothyroidism, or water intoxication, the urine Na concentration is more than 20 mEq/L.

Hypervolemic hyponatremia

  • If hyponatremia is caused by an edema-forming state (eg, congestive heart failure, hepatic failure), the urine Na concentration is less than 20 mEq/L because effective arterial perfusion is low despite an increase in total body water. Use of diuretics affects urine Na concentration.
  • If hyponatremia is caused by acute or chronic renal failure, the urine Na concentration is more than 20 mEq/L.


  • Urine sodium concentration is more than 40mEq/L with normal dietary salt intake.

Cerebral salt-wasting syndrome (CSWS)

  • Urine loss is significantly higher and frequently exceeds 80 mEq/L.

Other laboratory tests

Special laboratory studies include tests of the following:

  • Aldosterone level

  • Cortisol level

  • Free T4 and thyroid-stimulating hormone (TSH) levels

  • Adrenocorticotropic hormone (ACTH) level

  • Antidiuretic hormone (ADH) level


Imaging Studies

Neuroimaging (only if clinically indicated, not routinely performed)

Computed tomography (CT) scanning is useful for evaluating causative intracranial pathologies, such as tumors, hydrocephalus, and hemorrhage. It is also useful for detecting cerebral edema and demyelinating lesions that occur during treatment. CT scanning is superior to magnetic resonance imaging (MRI) in delineating hemorrhage and calcifications.

MRI is sensitive for detecting tumors and demyelination.

Abdominal imaging (only if clinically indicated, not routinely performed)

Ultrasonography may be performed to detect abdominal masses, such as those due to bilateral adrenal hyperplasia, and adrenal tumors.

CT scanning and MRI may help in further delineating the tumor.