- Clinical science
Sodium is the most important extracellular cation and plays an important role in maintaining the body's extracellular fluid volume. Sodium imbalances typically reflect a dilution or concentration of extracellular fluid rather than an actual loss or gain of sodium. These changes in extracellular fluid volume are mainly due to an increase or decrease in ADH serum levels (which causes the retention and loss of free water respectively). In certain cases, however, sodium imbalances may be the direct result of sodium loss (e.g., following diarrhea, vomiting, or the use of antidiuretics) or excessive sodium intake. Treating sodium imbalances involves careful correction of the sodium deficit/excess and treating the underlying cause. A rapid correction of sodium imbalance can have damaging osmotic effects such as central pontine myelinolysis.
Hypotonic hyponatremia (↓ serum osmolality)
- Hypovolemic hyponatremia
- Euvolemic hyponatremia
- Hypervolemic hyponatremia
Isotonic hyponatremia (↔︎ serum osmolality)
Hypertonic hyponatremia (↑ serum osmolality)
- Use of mannitol
- Effect: ADH causes water reabsorption and increases thirst.
- Release of ADH
- diarrhea) (e.g., due to poor oral fluid intake,
- Osmotic diuresis (e.g., hyperglycemia, uremia, high-protein tube feeding)
- Diabetes insipidus (central or renal)
- Lack of access to water
- Primary hyperaldosteronism
- Cushing's syndrome
- Iatrogenic: excessive infusion of NaCl or sodium bicarbonate solutions
- Drinking sea water
- Clinical features are primarily neurological and depend on the severity of the sodium imbalance.
- Symptoms also depend on the onset of sodium imbalance
- Acute onset (< 48 hours): usually symptomatic event even with mild sodium derangements
- Subacute or chronic onset (> 48 hours): usually asymptomatic unless severe derangements are present
- Serum sodium concentration
- Serum osmolality to assess volume status is always the first step in evaluation
Hyponatremia: urine sodium concentration
- > 20 mEq/L implies renal sodium loss
- < 20 mEq/L implies extrarenal sodium loss
Hypernatremia: urine osmolality
- > 800 mOsmol/kg implies extrarenal water loss
- < 800 mOsmol/kg implies renal water loss The kidneys continue to excrete water despite a water deficit.
- Hyponatremia: urine sodium concentration
- Treat underlying cause
- Patients with serum sodium values < 120 mEq/L or >160 mEq/L require intensive care.
Careful correction of sodium levels: maximum correction within 24 hours is 10 mEq/L (rate of correction: 0.5–1 mEq/L per hour)
Effects of rapid correction
- Rapid increase in sodium levels → risk of
- Rapid fall in serum sodium → risk of
- Effects of rapid correction
- Mild to moderate symptoms: normal saline
- Severe symptoms: hypertonic saline
- Mild to moderate symptoms: fluid restriction
- Severe symptoms: hypertonic saline
- Mild to moderate symptoms: fluid restriction ± loop diuretic
- Severe symptoms: isotonic saline
Correct free water deficit
- Mild hypernatremia in non-hospitalized patients: oral rehydration
- Moderate to severe hypernatremia, or hypernatremia in hospitalized patients: IV route
- Once adequately resuscitated: correct free water deficit
- Euvolemic hypernatremia: correct free water deficit
- Hypervolemic hypernatremia: loop diuretic + 5% dextrose
The cornerstone of the management of hypernatremia is correcting the free water deficit.
Slow correction to prevent osmotic cell damage!
- Definition: Damage to the myelin sheath of nerves in the CNS caused by a sudden rise in the osmolarity of blood.
- Rapid correction of chronic hyponatremia
- Clinical features
- Treatment: supportive care
We list the most important complications. The selection is not exhaustive.