Table 129-6 outlines disease states associated with disruption in serum sodium levels and total body water (volume).
TABLE 129-6Conditions Altering Serum Sodium and Total Body Water Balance ||Download (.pdf) TABLE 129-6 Conditions Altering Serum Sodium and Total Body Water Balance
|Total Body Water (volume) ||Hypernatremia ||Hyponatremia |
|Increased ||Excessive saline infusion || |
Congestive heart failure
Advanced renal failure
|Normal || |
Hypertonic saline infusion
Low solute intake
|Decreased || |
Improperly prepared formula
Osmotic stool softeners
Burns, heat illnesses (exhaustion/stroke)
Renal free water losses
Increased osmoles (diabetes mellitus, mannitol)
Chronic kidney disease
ATN (if polyuric)
Hyponatremia is a serum sodium level <135 mEq/L. First determine if a low sodium value is a true value by relating the sodium value to the osmolarity. If hyponatremia occurs in a hyperosmolar state (i.e., >290 mOsm/kg), this suggests an osmotically active solute in the plasma such as excess glucose or alcohol. If hyponatremia occurs in the presence of normal osmolarity (275 to 290 mOsm/kg), this is likely due to hyperlipidemia or hyperproteinemia.19 In such cases, correct the underlying disorder rather than the serum sodium level. When hyponatremia occurs in a hypo-osmolar state (<275 mOsm/kg), this is likely due to gain of free water or loss of sodium. The most common causes of hyponatremia seen in the ED are GI losses and water intoxication caused by ingestion of hypotonic replacement fluids, especially during infancy.
Signs and symptoms of hyponatremia depend on the serum sodium level and the speed at which sodium level falls. Symptoms primarily involve the CNS, as free water moves from the extracellular to intracellular space, and the musculoskeletal system. Neurologic symptoms include nausea, vomiting, headache, mental status changes, altered consciousness, diminished reflexes, hypothermia, pseudobulbar palsy, and seizures. Musculoskeletal symptoms include weakness, muscle cramps, and lethargy.
Although patients may be only mildly symptomatic with sodium levels as low as 120 mEq/L, if the low level is chronic (>48 hours), symptoms usually occur with an acute drop in serum sodium level below 120 mEq/L. Without appropriate treatment, complications include respiratory failure, seizures, and death.
Treatment depends on the stability of the patient and associated symptoms. General guidelines are presented in Table 129-7. Take special care to avoid rapid shifts in sodium levels. Although hyponatremia itself can have dire consequences, rapid correction can cause severe demyelination of brainstem neurons.20 Therefore, correct hyponatremia slowly and in a controlled manner (Table 129-7). The exception to this is in the setting of severe neurologic symptoms, such as confusion, altered level of consciousness, or seizures, typically with sodium level <120 mmol/L. When this occurs, a rapid, controlled increase in sodium level is required until neurologic symptoms resolve or a sodium level of 120 mmol/L is achieved.21
TABLE 129-7Treatment of Hyponatremia ||Download (.pdf) TABLE 129-7 Treatment of Hyponatremia
|Symptoms ||Treatment* |
|If hypovolemic and hemodynamically unstable ||Correct instability with NS boluses (20 mL/kg over 5 min followed by reassessment after each bolus) |
|Asymptomatic || |
Correct deficit to normal over 48 h
mEq Na required = [(Na+ desired) – (measured Na+)] × (0.6 × weight in kg)
|Neurologic symptoms (altered mental status, seizures) ||1–2 mL/kg/h of 3% sodium chloride until asymptomatic or Na level >120 mEq/mL, then increase Na level 0.5 mEq/mL/h (not to exceed increase of 12 mEq/mL in first 24 h or 18 mEq/mL in first 48 h) |
For euvolemic hyponatremia, after correction of serum sodium level, institute water restriction and treat the underlying disorder. For hypervolemic hyponatremia (edema), institute sodium and water restriction, and administer diuretics if needed to treat the clinical condition (e.g., congestive heart failure).
Hypernatremia is a serum sodium level >145 mEq/L. Hypernatremia generally indicates a lack of total body water in relation to total body solute and often occurs as a result of dehydration (loss of water through the GI tract, kidney, or insensible losses), but may also occur secondary to excessive sodium intake (e.g., inadequate water intake or hypertonic solution intake) (Table 129-8).22 Diarrhea is the most common cause in children. Other diseases to consider include renal disease and diabetes insipidus. Children are at risk for hypernatremia if free water is limited or if formula is mixed improperly. Mild hypernatremia is commonly found in ill children, particularly infants with gastroenteritis. If mild, it is usually asymptomatic and corrects with treatment of the underlying cause. Serum sodium levels of >160 mEq/L require immediate attention due to the potential for serious complications and permanent neurologic sequelae, including intellectual deficits, seizure disorder, or other neurologic impairments. Conversely, patients who have a sodium level of <160 mEq/L and receive treatment typically have symptoms that are relatively mild and self-limited.
TABLE 129-8Treatment of Hypovolemic or Euvolemic Hypernatremia ||Download (.pdf) TABLE 129-8 Treatment of Hypovolemic or Euvolemic Hypernatremia
|Condition ||Treatment* |
|If hypovolemic and hemodynamically unstable ||Correct instability with NS boluses (20 mL/kg boluses followed by reassessment after each bolus) |
|Once hemodynamically stable and hypovolemic or euvolemic hypernatremia || |
Correct deficit to normal over 24 h
Free water deficit (mL) = 4 mL × body weight (kg) × [desired change in serum sodium mEq/L (mmol/L)]
Subtract bolus fluids given from deficit; correct remaining deficit giving half of deficit over first 8 h and remainder over the next 16 h (see text for monitoring criteria)†
Signs and symptoms of hypernatremia result from cellular dehydration as free water moves from the intracellular to extracellular space and include mental status changes, muscular weakness, ataxia, tremors, hyperreflexia, seizures, unresponsiveness, intracerebral hemorrhage, permanent neurologic dysfunction, and death. In addition, when extracellular fluid hypertonicity develops, brain intracellular osmolar contents increase to prevent or minimize cell shrinkage. In severe hypernatremic dehydration, neurologic findings may include any of the following: increased peripheral tone with brisk reflexes, muscle weakness, high-pitched cry, nuchal rigidity, myoclonus, asterixis, chorea, altered level of consciousness, or seizures.22,23
Treatment is the restoration of intravascular volume while decreasing the serum sodium level. Correct serum sodium gradually to avoid cerebral edema and associated central pontine myelinolysis (Table 129-8). Closely monitor serum sodium levels every hour initially to ensure that the level is reduced no faster than 1 mEq/L/h and no more than 15 mEq/L in the first 24 hours. This may require more than 48 hours for complete correction. Monitor urine output given the risk of acute tubular necrosis.22 Correct underlying causes. Hypervolemic hypernatremia may require dialysis if sodium levels cannot be decreased without volume overload. Dialysis may also be required for hypernatremia of any type if the initial serum sodium is >180 mmol/L.