Differential Diagnosis of Hyponatremia

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Hyponatremia, one of the more common fluid and electrolyte disturbances, can be the result of multiple causes and is highly prevalent in critically ill patients.2,3 It is defined as a serum sodium concentration of less than 135 mmol/L. Conceptually, hyponatremia can be classified into dilutional and depletional causes. Dilutional hyponatremia is the result of increased extracellular fluid (ECF) in the presence of normal or an increased total body sodium (Na+) that is less than the increase in ECF volume. Depletional hyponatremia is found when Na+ is lost in the presence of normal ECF volume or when there is a greater decrease in total body Na+ than a decrease in ECF volume.

Clinically, hyponatremia is often classified into three basic types depending on the ECF status of the patient (Table 11.1). Thus, a careful physical exam to assess the patient's volume status is critical. The exam should note signs of either excess volume (recent weight gain, edema, swelling) or decreased ECF (dry skin and mucous membranes, lack of skin targor, and flat jugular veins). Appropriate laboratory tests to help differentiate the hyponatremia include serum and urine electrolytes, serum and urine osmolality, and thyroid and adrenal hormones.

Hyponatremic plasma can be either hyperosmotic, isotonic, or hypoosmotic, making the measurement of plasma osmolality an important initial step in the assessment of hyponatremia. Of these, the most common is hypoosmotic hyponatremia since Na+ is the primary determinant of plasma osmolality. When hyponatremia occurs in the presence of increased plasma osmolality, this can only be due to an increased amount of other

Table 11.1 Clinical Classification of Hyponatremia

Volume status





Loss of both water

Total body water increased,

Excess of both total

and Na+ Na

normal to mild

body water and Na+

loss > water loss

decrease in Na+; prevention of free water excretion

Water retention > renal Na+ loss


Gastrointestinal fluid loss


Heart failure



Nephrotic syndrome


Psychogenic polydipsia,


beer-drinker's potomania

Addison's disease


Renal failure

solutes in the ECF that causes an extracellular shift of water or an intracellular shift of Na+ to maintain osmotic balance between the extra- and intracellular. The most common cause of this type of hyponatremia is severe hyperglycemia. In fact, "true" plasma Na+ in the setting of hyperglycemia can be calculated by adding 1.6 mmol/L of Na+ for every 100 mg/dL increase of glucose above 100 mg/dL.

If the measured Na+ concentration in plasma is decreased, but measured plasma osmolality, glucose, and urea are normal, the only explanation is pseudohyponatremia caused by the electrolyte exclusion effect. This can occur in patients with severe hyperli-pidemia or hyperproteinemia (e.g., paraprotein, multiple myeloma) when Na+ is measured by either flame emission spectrophotometry or by an indirect ion-selective electrode (see discussion below).

Most often when hyponatremia is present the plasma osmolality will also be low. As stated above, this type of hyponatremia can be due to either excess loss of Na+ (deple-tional hyponatremia) or increased extracellular volume (dilutional hyponatremia). Differentiating causes of this type of hyponatremia initially requires a clinical assessment of volume status. This is best accomplished by a history and physical examination.

Depletional hyponatremia (excess loss of Na+) is almost always accompanied by a loss of water but to a lesser extent than the loss of Na+. Hypovolemia is apparent in the physical examination (orthostatic hypotension, tachycardia, decreased skin turgor, flat jugular veins). Loss of fluid is the cause of the hyponatremia, and this can occur through either renal or extrarenal losses. If urine Na+ is low (generally <10 mmol/L), the loss will be extrarenal most typically from the gastrointestinal tract or the skin. If, on the other hand, urine Na+ is elevated in this setting (generally >20 mmol/L), renal loss of Na+ is occuring. Renal loss of Na+ can occur with osmotic diuresis, thiazide diuretics, adrenal insufficiency (the absence of aldosterone and cortisone prevents distal tubule reabsorption of Na+), or "potassium-sparing" diuretics, such as spironolactone, which block aldosterone-mediated distal reabsorption of Na+. Renal loss of Na+ in excess of H2O will also occur in metabolic alkalosis as a result of prolonged vomiting, because the increased renal HCO2 excretion that occurs with alkalosis is accompanied by Na+ ions.

Dilutional hyponatremia is a result of excess H2O retention and can sometimes be detected during the physical examination. When total body water (TBW) is increased, but the central intravascular volume is decreased, as in congestive heart failure, hepatic cirrhosis, or the nephrotic syndrome, and a vicious cycle is established. The decreased blood volume is sensed by peripheral baroreceptors and results in increased aldosterone and antidiarectic hormone (ADH) even though TBW is excessive. The kidneys properly reabsorb Na+ and H2O in response to the increased aldosterone and ADH to restore the blood volume, but this simply results in further increases in TBW and further dilution of Na+. In this setting urine Na+ will be low.

In hypoosmotic hyponatremia with normal volume status, the most common etiologies are the syndrome of inappropriate ADH (SIADH), primary polydypsia, hypothyroidism, or adrenal insufficiency. SIADH is usually a result of ectopic or otherwise "inappropriate" ADH production arising from a variety of conditions and results in excessive H2O retention. SIADH often is diagnosed by a urine osmolality that is greater than plasma osmolality in the setting of hyponatremia, but only when renal, adrenal, and thyroid functions are normal.

In this patient the clinical findings indicate a relatively normovolemic hyponatremia in the presence of a hypoosmolar plasma and an inappropriately high excretion of Na+ in the urine. Her history of recurrent oat cell carcinoma and chronic refractory hyponatremia, together with normal thyroid and adrenal function, would place SIADH high on the differential diagnosis for this patient.

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    How to differentiate siadh from addisons?
    2 months ago

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