Hyponatremia

Pathophysiology

• Hyponatremia exerts its most prominent effects on the central nervous system. Low serum sodium causes water to move into brain cells through an osmotic gradient. The severity of the clinical syndromes depends on the magnitude as well as the rate of decline of the serum sodium.
• When hyponatremia occurs rapidly, there is less time for the brain to adapt, causing more marked cerebral edema and more marked symptoms, endocrine emergencies.

Diagnosis and Evaluation

• Patients are generally asymptomatic at levels >120.
• Symptoms of hyponatremia include nausea, vomiting, lethargy and confusion, with extreme manifestations such as seizure and coma, at levels < 115.
• Factitious hyponatremia occurs when the plasma osmolality is either normal or increased. In these cases, sodium is falsely decreased secondary to hyperosmolarity syndromes (such as extreme hyperglycemia, mannitol or glycerol therapy), severe hyperlipidemia or hyperproteinemia (e.g., multiple myeloma). In true hyponatremia, the plasma osmolality is decreased.
• True hyponatremia is classified according to the overall volume status of the patient; hypovolemic, euvolemic or hypervolemic. The treatment of hyponatremia will depend upon the clinical assessment of the patient’s volume status.
• Consider causes of hyponatremia that may require other critical actions:

  Causes	Actions
  Hypothermia	Warming measures
  Hypothyroidism	Administration of thyroid hormone
  Adrenal crisis	Intravenous corticosteroids
  Excessive fluid therapy	Turn off IV fluids
  Excessive water intake	Fluid restriction
  Head trauma or other insult	Consider CT Head

Laboratory/Studies

• Obtain serum electrolytes including STAT glucose; electrolytes should be followed during treatment every 1-2 h.
• Head CT is indicated for any alteration of mental status.
• In severely hyponatremic and critically ill patients, a Foley catheter is necessary to closely follow urine output and for urinary electrolytes.

ED Management

• A serum sodium >120 rarely requires emergent treatment. The urgency of treatment increases with lower levels and rapid decline in mental status.
• Decreased level of consciousness (LOC) may cause airway obstruction and may require airway adjuncts and/or intubation. If using RSI, caution must be used with succinylcholine (contraindicated if concomitant hyperkalemia present) and with barbiturates (if porphyria is cause of hyponatremia).
• If patient is hypovolemic or hypotensive, use normal saline (0.9%) boluses as the initial fluid of resuscitation. If patient is hypervolemic (e.g., signs of fluid overload are present), fluids may be restricted and loop diuretics administered intravenously (e.g., furosemide)
• Follow neurological status for decompensation, as change dictates more aggressive sodium repletion.
• Use normal saline (0.9%) at approx 50 ml/h (in adults),once euvolemic, for altered mental status. Keep 3% saline solution at bedside available for worsening neurological status.
• If seizures are present or there is rapid deterioration in LOC, give boluses of 50 ml of 3% normal saline until symptoms improve; watch for signs of fluid overload.
• If 3% saline is not available, a single ampule of sodium bicarbonate may be substituted for hypertonic saline solution (one ampule of 50 ml of 7.5% sodium bicarbonate is roughly equivalent to 100 ml of 3% saline)
• Important note: Focal weakness, hemiparesis, ataxia and abnormal plantar reflexes may be seen with hyponatremia itself or with central pontine myelinolysis from overaggressive correction. To avoid this complication, correction of hyponatremia should ideally not occur faster than 0.5 meq/L/h. More rapid correction appears to be safer when hyponatremia has developed more acutely and when diuretics are used during correction.