Hyperosmolality

Hyperosmolality is a state in which the serum osmolality is increased above the normal range, typically about 275–295 mOsm/kg. It results from an excess of osmotically active solutes or a relative water deficit, causing water to move from the intracellular to the extracellular space and producing cellular dehydration, notably in brain tissue.

Serum osmolality is primarily determined by sodium, glucose, and urea. A common calculation is Osm_calc = 2 × [Na+] + glucose/18 + BUN/2.8 (with glucose and BUN in mg/dL). The osmolal gap, the difference between measured and calculated osmolality, helps detect exogenous osmoles such as ethanol, methanol, ethylene glycol, or mannitol that raise osmolality without matching changes in sodium.

Causes include hypernatremia from water loss (diabetes insipidus, gastrointestinal losses, insensible losses) or inadequate water intake, and hyperglycemia with osmotic diuresis (diabetic ketoacidosis or hyperosmolar hyperglycemic state). Additional contributors are administration of osmotically active substances (mannitol, glycols), renal failure with reduced water excretion, and significant losses of water or ingestion of hypertonic fluids or saline.

Clinical features range from thirst and dry mucous membranes to confusion, lethargy, seizures, and coma, depending on the rapidity and degree of osmolality rise. Diagnosis rests on elevated serum osmolality with a high osmolal gap and assessment of sodium, glucose, BUN, ketones, and potential exogenous osmoles.

Management focuses on treating the underlying cause and correcting the hyperosmolality gradually to avoid neurologic complications. Initial fluid resuscitation may be with isotonic saline if volume depleted, followed by hypotonic fluids to restore free water. In hyperglycemic states, manage glucose and electrolytes with insulin as indicated. Monitor osmolality and electrolytes; the prognosis depends on the underlying cause and the safety of correction.