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Severe hyponatremia (often defined as a serum sodium < 120 mEq/L) occurs most often in people with pituitary or lung tumors, those taking antipsychotic or other neuroleptic drugs, heavy beer drinkers, or the elderly. Usually sodium levels decline slowly over weeks or months prior to detection, allowing time for the brain to compensate, with only minor neurologic symptoms.
Sodium levels will often return to normal just as slowly, with minimal intervention by physicians (change in drug therapy, fluid restriction, etc). But new evidence shows that when patients with hyponatremia get admitted to the hospital, their impatient treatment teams often correct sodium levels too quickly, increasing the risk for dangerous complications.
Too-rapid correction of sodium can cause osmotic demyelination syndrome (ODS), a form of brain damage. Symptoms may not manifest for several days after a sodium overcorrection, and can include impaired speech or swallowing, limb weakness, seizures, confusion or depressed consciousness -- or in the most severe cases of pontine myolysis, locked-in syndrome. The damage and dysfunction can be permanent.
The diagnosis of ODS is made by MRI, but brain changes may not be fully visible on imaging for weeks after the insult. CT scanning is suboptimal. Follow-up studies with cognitive testing in large cohorts of patients with rapidly corrected hyponatremia have never been performed, so it's possible that minor iatrogenic neurologic injury could persist in patients with "reversible" ODS.
In one of the few published studies on real-world treatment of hyponatremia and incidence of ODS, authors looked back at almost 1,500 patients 2001-2017 with severe hyponatremia at seven hospitals associated with a single health care system.
Over half of patients had their sodium corrected faster than experts recommend (>6 mEq/L in 24 hours). In more than 40%, the rate of correction was above what is considered dangerous (>8 mEq/L in 24 hours).
Eight patients (0.5% of the entire cohort) developed new osmotic demyelination, as diagnosed by MRI. Only 1 in 5 patients underwent MRI, so the incidence of ODS could have been higher.
The new neurologic symptoms attributed to osmotic demyelination were persistent in three of the eight patients with identified ODS, and resolved in the other five patients. Almost all of the patients with ODS had their sodium corrected too quickly.
What's the reason behind our rush to correct sodium levels?
Part of the problem is published expert guidance on correction of hyponatremia. Clinicians have been advised (in expert-produced topic reviews) to give boluses of 3% hypertonic saline for patients with only moderate hyponatremia (Na = 120 to 130 mEq/L) causing only minimal symptoms. For patients with severe hyponatremia -- even if present for weeks or months -- clinicians have been advised to provide continuous 3% NaCl infusions. With such a low threshold to use powerful osmotic agents for relatively non-threatening hyponatremia, it's unsurprising that over-correction of serum sodium is so common.
The increasing pressure inside hospital systems to discharge patients sooner, along with our general impatience, likely also contribute. A patient's sodium increase of 2 mEq/L, or none, after 24 hours of fluid restriction or a single dose of saline provokes the urge to be more "aggressive." Unfortunately, patients' metabolic responses may be nonlinear or influenced by other factors, with the frequent result that sodium levels jump by 10 or 12 mEq/L after what seemed like an incremental intensification of therapy. A complex process like sodium homeostasis doesn't respond consistently to simplistic total body water calculations taught in training programs.
Acute, severe hyponatremia can rapidly shift fluid into brain cells, causing cerebral edema with symptoms of seizures or brain herniation. A true neurologic emergency, symptomatic acute hyponatremia can be corrected with sequential boluses of 100-300 mL of 3% saline to rapidly increase the sodium level by a goal of 4 to 6 mEq/L, a change experts say will forestall osmotic shifts and prevent the most dangerous immediate neurologic effects of a low serum sodium.
Few patients who are admitted with hyponatremia present this way, or require such dramatic and potentially dangerous interventions. Rather, the large majority (who have subacute or chronic hyponatremia) may be as much at risk from overly rapid correction of their sodium levels as they are for serious neurologic sequelae from the hyponatremia itself.
Source: Clin J Am Soc Nephrol.