Hyponatremia
Update August 19, 2019
The urgency of treatment is dictated by the severity of symptoms and how abruptly the hyponatremia is thought to have developed.
Correction of hyponatremia is controversial, but in acutely symptomatic patients even a 5% increase may be physiologically significant.
In the presence of severe hyponatremia (sodium <120 mEq/L) and seizures an infusion of 3% hypertonic saline solution (513 mEq/L) should be considered (see Appendix for formulas).
Electrolyte Replacement
Estimate total free water deficit or absolute sodium excess or deficiency. The use of the Adrogue-Madias equation offers a simple and reliable method for estimating the effect of infusion of 1 L of infusate on serum sodium.
Total body water may be estimated by multiplying the patient’s weight by the appropriate value in Table 44–19 to obtain a value in liters. Sodium concentrations of common infusate solutions are provided in Table 44–20.Table 44–19. Total body water in liters as fraction of body weight. Children 0.6 Adult male 0.6 Adult female 0.5 Elderly male 0.5 Elderly female 0.45
Table 44–20.Sodium concentrations of common IV solutions.
| Infusate | mEq/L |
|---|---|
| 5% dextrose in water | 0 |
| 0.2% NaCl in 5% dextrose in water | 34 |
| 0.45% NaCl in water | 77 |
| Ringer’s lactate | 130 |
| 0.9% NaCl in water | 154 |
| 3% NaCl in water | 513 |
| 5% NaCl in water | 855 |
The rate of rise of 1 mEq/L/h should be targeted for the first 3–4 hours or until symptoms resolve; otherwise, the rate of correction should not exceed 0.5 mEq/L/h. The use of 3% saline should be considered in the correction over the first 24 hours, so subsequent correction should be slowed. Simultaneous use of furosemide to limit expansion of the extracellular fluid volume may be required. A new class of AVP receptor antagonists (the “vaptans”) has been approved for the treatment of euvolemic and hypovolemic hyponatremia, but they are not commonly used in the emergency department (ED). Resolution of symptoms, particularly in the elderly, may lag correction of the serum sodium, and frequent monitoring is important to avoid overcorrection.
Concomitant endocrine disorder should be considered, with hypothyroidism and adrenal insufficiency causing hyponatremia in some cases. Replacement hormonal therapy should be started after appropriate laboratories are drawn. Most patients require only fluid restriction and observation. Profoundly hypovolemic patients may be treated initially with fluid resuscitation using isotonic saline to prevent cardiovascular compromise. Emergency dialysis should be considered for patients with renal failure, volume overload, and severe hyponatremia.
Osmotic demyelination, the most feared consequence of too rapid correction, is rare at a rate of correction below 10–12 mEq/L/d. Alcoholics, hypokalemic patients, burn victims, and women taking thiazide diuretics have an increased risk for this complication. Symptoms of osmotic demyelination include dysarthria, dysphagia, spastic paresis, coma, and occasionally seizures. These symptoms may be delayed for 2–6 days after correction of the serum sodium and imaging by computed tomography (CT) may be negative up to 4 weeks. Rapid reinduction of hyponatremia may be beneficial when this disorder is suspected.
All patients with clinically significant hyponatremia should be hospitalized. Intensive care unit (ICU) placement should be considered for those with severe symptoms or in whom 3% sodium has been used.
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In general, hyponatremia is treated with fluid restriction (in the setting of euvolemia), isotonic saline (in hypovolemia), and diuresis (in hypervolemia).
A combination of these therapies may be needed based on the presentation.
Hypertonic saline is used to treat severe symptomatic hyponatremia.
Medications such as vaptans may have a role in the treatment of euvolemic and hypervolemic hyponatremia.
The treatment of hypernatremia involves correcting the underlying cause and correcting the free water deficit.1
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SORT: KEY RECOMMENDATIONS FOR PRACTICE
| CLINICAL RECOMMENDATION | EVIDENCE RATING | REFERENCES | COMMENTS |
|---|---|---|---|
In patients with severe symptomatic hyponatremia, the rate of sodium correction should be 6 to 12 mEq per L in the first 24 hours and 18 mEq per L or less in 48 hours. (How do you order this????)2 |
C |
Consensus guidelines based on systematic reviews |
|
A bolus of 100 to 150 mL of hypertonic 3% saline can be given to correct severe hyponatremia. |
C |
Consensus guidelines based on small studies |
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Vaptans appear to be safe for the treatment of severe hypervolemic and euvolemic hyponatremia but should not be used routinely. |
C |
Consensus guidelines based on observational studies |
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Chronic hypernatremia should be corrected at a rate of 0.5 mEq per L per hour, with a maximum change of 8 to 10 mEq per L in a 24-hour period. |
C |
Expert opinion |
A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https://www.aafp.org/afpsort.
Inappropriate antidiuretic hormone (SIADH) can also occur as a paraneoplastic phenomenon, occurring most often in patients with small cell lung cancer. The result of ectopic ADH production is a retention of free water and consequent hyponatremia.
Severe hyponatremia can result in altered sensorium, coma, and death.
Hyponatremia results from:
1. An increase in circulating AVP and/or increased renal sensitivity to AVP
2. Low solute intake (such as “beer potomania”), wherein a markedly reduced urinary solute excretion is inadequate to support the excretion of sufficient free H2O.
Hyponatremia is primarily a disorder of H2O homeostasis.
Patients with hyponatremia are thus categorized diagnostically into three groups, depending on their clinical volume status:
hypovolemic,
euvolemic, and
hypervolemic
All three forms of hyponatremia share an exaggerated, “nonosmotic” increase in circulating AVP, in the setting of reduced serum osmolality.
Notably, hyponatremia is often multifactorial; clinically important nonosmotic stimuli that can cause a release of AVP and increase the risk of hyponatremia include drugs, pain, nausea, and strenuous exercise.
Hyponatremia cause neurological symptoms secondary to cell swelling and electrolyte imbalance; potentially fatal.