A low serum uric acid can also be useful in differentiating hypovolemic and euvolemic hyponatremia, which is most commonly caused by SIADH. In SIADH, there is urinary wasting of uric acid, which leads to low serum uric acid. In a study of 105 patients with lung cancer, a serum uric acid of less than 4 mg/dL was 75% sensitive and 89% specific for SIADH.6
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Figure 1. Symptoms of euvolemic hyponatremia
Step 3: Urine osmolarity
After determining volume status, the physician should determine if there is excess ADH by measuring Uosm. Under normal conditions, hyponatremia should suppress ADH secretion and allow the kidney to excrete water by diluting the urine to less than 100 mosm/L. If Uosm is less than 100 mosm/L, then the kidneys are responding appropriately and can only persist in the following situations: The patient is drinking large volumes of water (e.g. primary polydipsia), there is insufficient solute to excrete free water (e.g. beer potomania, “tea and toast” diet), or the patient has a different set point for ADH suppression (i.e., reset osmostat). After determining volume status, UNa, and Uosm, the physician will have narrowed the cause of hyponatremia significantly (see Figure 2). Of note, when SIADH is diagnosed, it is important to look for and reverse causes (see Figure 3).
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Figure 2. Algorithmic approach to hyponatremia
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Figure 3. Causes of SIADH
Treatment
Severe symptomatic hyponatremia
In patients with severe neurologic symptoms, physicians must balance the need to reduce symptoms quickly with the dangers of overly rapid correction. After its use in marathon runners, several experts have endorsed the following regimen to reduce symptoms rapidly: an intravenous bolus of 100 mL of 3% saline is given and repeated if symptoms persist after 10 minutes.7,8 Once symptoms improve, the basal rate can be calculated using the equation below, but the rate of sodium correction in 24 hours with this regimen should not exceed 6 to 8 mEq/L in 24 hours or 12 to 14 mEq/L in 48 hours.9,10 This is based on several case studies showing that there were no cases of central pontine myelinolysis (CPM) if correction rates were less than 10 mEq/L over 24 hours.11,12
It is important to remember that this is only a rough guide, because the equation assumes the entire infusate is retained and there is no sodium or water output. The best way to avoid overly rapid correction is to check serum sodium every two hours and monitor urine output closely. If the patient is making large volumes of urine, serum sodium may be rising too quickly. If the patient corrects too rapidly, it may be possible to avoid CPM by re-lowering the sodium.13 This can be accomplished by giving desmopressin to slow urinary free water loss while simultaneously giving hypotonic fluids.
Asymptomatic or mildly symptomatic hyponatremia
Hypovolemic hyponatremia: Treatment of hypovolemic hyponatremia is aimed at correcting volume status, the underlying problem that drives ADH secretion. The body will always choose to preserve volume over osmolarity. In most cases, normal saline (NS) should be used to restore intravascular volume, and the rate of infusion can be calculated using the same equation as above. Once volume is replete, ADH release will cease. Patients will be in danger of overly rapid correction of serum sodium, so fluids should be switched to hypotonic solutions, such as ½ NS.