Electrolyte disorders can be some of the most complex and subtle clinical conditions facing the critical care or emergency medicine physician. A healthy degree of suspicion coupled with vigilant electrolyte monitoring is necessary in order to avoid missing these disorders. This is particularly true as many electrolyte disorders occur secondary to other severe disease states.
Sodium disorders are commonly encountered in clinical practice. Both hyponatremia and hypernatremia have multiple underlying causes and may develop acutely or chronically. Patients with acute or severe sodium disorders may be critically ill and require rapid, aggressive correction of their sodium abnormality, while aggressive treatment of the chronic, compensated hyponatremic or hypernatremic patient may cause dangerous fluid shifts. It is critical that the emergency physician understand how to identify, classify, and treat sodium disorders.
Hyponatremia is defined as a serum sodium less than 135 mEq/L. It is commonly found in both inpatients and outpatients.1 Hyponatremia is associated with increased morbidity and mortality in hospitalized patients admitted to both the medical ward and the intensive care unit.2 Even mild hyponatremia in outpatients is correlated with a poor outcome.3 Groups at particular risk for hyponatremia include hospitalized patients, elderly patients, and patients recently started on thiazide diuretics.4
The severity of symptoms due to hyponatremia depends on the rate of sodium decline as well as the absolute level. Mildly hyponatremic patients are often asymptomatic. Moderately hyponatremic patients (Na of 125–130 mEq/L) may experience nausea, headache, malaise, and myalgias, and have depressed tendon reflexes. Severe hyponatremia (Na <125 mEq/L) causes mental status changes; seizure, coma, and death occur at sodium levels of below 120 mEq/L. Acute hyponatremia occurs over less than 48 hours and is likely to cause neurologic manifestations secondary to cerebral edema. In chronic hyponatremia, neurologic effects are less likely, as there has been time for compensation and brain size remains normal. This compensatory response puts the patient at risk for a demyelinating syndrome if sodium is corrected too rapidly.
Evaluation of hyponatremia consists of a stepwise narrowing of the differential diagnosis based on history, physical exam, and laboratory testing1,5–8 (see Figure 28-1).
Etiologies of hyponatremia.
Hyperosmolar or Iso-Osmolar Hyponatremia
Hyponatremia in the absence of a hypoosmolar state is referred to as pseudohyponatremia. Hyperosmolar hyponatremia occurs when large amounts of an osmotically active substance (such as mannitol, glucose, or intravenous [IV] contrast dye) draw water into the vasculature and dilute sodium concentration. For pseudohyponatremia secondary to hyperglycemia, a correction factor of 1.6 mEq/L sodium decrease for every 100 mg/dL rise in glucose is often used; however, experimental evidence indicates that a correction factor of 2.4 mEq/L may be more accurate.9
Iso-osmolar hyponatremia may be due to severe hyperlipidemia or hyperproteinemia, which causes a lab artifact in which serum water content is overestimated. Large-volume irrigation with a sodium-free fluid such as sorbitol, which is frequently used in transurethral prostatic resection, can cause either an iso-osmolar or hypo-osmolar hyponatremia.8