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Table 2. Basic blood and urine tests for the diagnosis of the cause of hyponatremia
Blood test (serum) Urine test Gasometer
Protein
Glucose
Urea
Creatinine Creatinine
Osmolality Osmolality
Sodium Sodium Sodium
Potassium Potassium
Chlorine Chlorine
Cortisol
TSH
T4
TSH: thyroid stimulating hormone; T4: thyroxine

Table 3. Approach to diagnosis
Etiology approach for hyponatremia
The basic hyponatremia approach is based on clinical history, physical examination, full blood test (as described in Table 2), timing of
the onset of hyponatremia, symptoms, and type of hyponatremia [Table 4]
Urine sodium: essential for the With renal sodium loss (Urine sodium > 25 mmol/L): diuretics, bicarbonate intake, primary
differential diagnosis of hypovolemic adrenal insufficiency (Addison’s disease), isolated hypoaldosteronism, and salt wasting syndrome
hyponatremia. Without sodium renal loss (Urine sodium < 20 mmol/L): gastrointestinal losses (vomiting and
diarrhea), burns, hemorrhage, and pancreatitis
Urine osmolality: essential for the ≤ 100 mOsm/kg: secretion of the ADH is inhibited, polydipsia with or without low solute intake,
differential diagnosis of euvolemic water intoxication, and administration of hypotonic fluids
hyponatremia > 100 mOsm/kg: Secretion of ADH is not inhibited, ACTH deficit, severe hypothyroidism, pain,
postsurgical stress, nausea, vomiting, the syndrome of inappropriate antidiuretic hormone
secretion, use of thiazides, etc.
ADH: antidiuretic hormone; ACTH: adrenocorticotropic hormone

out true hyponatremia. Pseudohyponatremia, induced by high protein or lipid levels, can be excluded by
the determination of total blood sodium by gasometer.

The best and most direct way to ascertain whether the patient presents hypovolemic or euvolemic
[18]
eunatremia is by neck inspection of the highest point of the internal jugular vein pulse [Table 1] . The
evolution of serum creatinine together with SNa is also a good parameter. Serum creatinine usually
increases when natremia drops in the hypovolemic patient and usually decreases along with hyponatremia
in the euvolemic patient .
[14]

An appropriate intervention depends on determining the timing of hyponatremia onset, the severity of the
neurological symptoms, and the volemic classification [Table 4]. This information, together with clinical
history and blood and urine tests, is the basis for determining the etiology of hyponatremia [Table 3].

Note that a single patient could experience different volemic episodes (e.g., hypovolemic after having
[19]
been euvolemic) sequentially . That is why clinical examination remains necessary to assure correct
management of hyponatremia at any given point of time, and reevaluation of patients is essential.

[20]
Hyponatremia in oncology patients is often considered primarily euvolemic, secondary to SIADH .
However, some studies have found that hypovolemic or hypervolemic hyponatremia is more prevalent in
[3,6]
hospitalized cancer patients .

[21]
The clinician should remember that the diagnosis of SIADH is always a diagnosis of exclusion , in a
euvolemic patient with a urine osmolality higher than 100 mOSm/kg, in the absence of pain, nausea,
diuretics, adrenocorticotropic hormone (ACTH) deficit, diuretic use, or severe hypothyroidism. ACTH