Hypernatremia
Serum Na >145 mEq/L; almost always reflects free water deficit.
Also known as: hypernatremia, high sodium, diabetes insipidus, DI
Overview
Serum sodium concentration >145 mEq/L. Reflects relative free water deficit. Categorized by volume status: hypovolemic (water loss > sodium loss), euvolemic (pure water loss), and hypervolemic (sodium gain > water gain — uncommon).
Epidemiology
Less common than hyponatremia in outpatients but common in hospitalized patients, particularly elderly with impaired thirst, ICU patients, and those with limited water access. Hospital-acquired hypernatremia carries mortality 40-70%.
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Risk factors
- Impaired thirst or restricted access to water (elderly, infants, intubated, demented, bedridden)
- Excess water loss: insensible (fever, ventilator, burns), GI (diarrhea, especially osmotic), renal (diuretics, post-obstructive diuresis, recovery from ATN)
- Diabetes insipidus — central (CNS injury, surgery, idiopathic, infiltrative) or nephrogenic (lithium, hypercalcemia, hypokalemia, hereditary, sickle cell, demeclocycline)
- Osmotic diuresis: hyperglycemia, hypertonic feeding, mannitol
- Iatrogenic: hypertonic saline, sodium bicarbonate administration, hypertonic feedings without sufficient free water
Pathophysiology
Plasma sodium concentration is tightly regulated by thirst (primary defense) and ADH-mediated water reabsorption. Hypernatremia occurs only when thirst is impaired or water access restricted (otherwise patients drink to correct). Cellular dehydration in the brain causes neurologic symptoms; chronic hypernatremia leads to generation of intracellular 'idiogenic osmoles' that, if rapidly corrected, cause cerebral edema.
Clinical presentation
Symptoms
- Thirst (intact thirst mechanism) — if absent, suspect adipsic or impaired access
- Lethargy, weakness, restlessness
- Confusion, irritability
- Muscle twitching, hyperreflexia
- Seizures, coma (severe — Na >160)
- Polyuria, polydipsia (in DI)
Signs / physical exam
- Volume status — usually mildly hypovolemic in classic hypernatremia
- Hypovolemic: dry mucous membranes, decreased skin turgor, orthostatic hypotension, sunken eyes
- Tachycardia
- Altered mental status, focal neurologic deficits in severe or rapidly developing cases
- Hypervolemic (rare): edema, hypertension, signs of fluid overload
Classic findings
Elderly nursing home resident with poor oral intake presenting with confusion, dry mucous membranes, and Na >150 — classic hypovolemic hypernatremia from inadequate water intake.
Differential diagnosis
- Hypovolemic hypernatremia — Volume depletion + water loss; weight loss, dry membranes, orthostasis; urine concentrated if extrarenal loss
- Diabetes insipidus (central) — Polyuria with dilute urine (osm <300); responds to DDAVP (urine osm rises >50%)
- Diabetes insipidus (nephrogenic) — Polyuria with dilute urine; does NOT respond to DDAVP; lithium, hypercalcemia, hypokalemia
- Osmotic diuresis — Polyuria with urine osm 300-600 and high urine glucose or urea; hyperglycemia, tube feeds
- Adipsic hypernatremia — Hypothalamic lesion impairing thirst; chronic, often refractory; managed by scheduled water intake
- Hypervolemic hypernatremia — Iatrogenic salt loading (3% saline, NaHCO3); volume overload with elevated Na
Diagnostic workup
Diagnostic criteria
Serum Na >145 + clinical context (volume status, urine output, urine osm) determine etiology. DI confirmed by inability to concentrate urine despite hypertonic state; central DI shows >50% increase in urine osm after DDAVP, nephrogenic shows no response.
Labs
- BMP — serum Na, glucose, creatinine, urea
- Serum osmolality — confirms hypertonic state
- Urine osmolality — concentrated (>700) = appropriate ADH response; dilute (<300) = DI; intermediate = partial DI or osmotic diuresis
- Urine sodium and electrolytes
- Calcium, potassium (correct hypercalcemia/hypokalemia exacerbating nephrogenic DI)
- Water deprivation test ± DDAVP challenge to distinguish central vs nephrogenic DI
Imaging
- MRI pituitary/hypothalamus if central DI suspected (look for stalk lesion, tumor, infiltration; loss of posterior pituitary bright spot on T1)
Diagnostic algorithm
| Cause Category | Examples | Urine Osmolality | Treatment |
|---|---|---|---|
| Pure water loss | Insensible (fever), inadequate intake | High (>700) | Free water replacement |
| Hypotonic fluid loss | GI diarrhea, osmotic diuresis, sweating | Variable (300-700) | Isotonic resuscitation then free water |
| Central DI | Pituitary surgery, trauma, idiopathic | Low (<300); responds to DDAVP | DDAVP, water replacement |
| Nephrogenic DI | Lithium, hypercalcemia, hypokalemia, hereditary | Low (<300); no DDAVP response | Remove cause, thiazide, low Na diet |
| Sodium gain (rare) | Hypertonic saline, NaHCO3, salt poisoning | High | Loop diuretic + D5W |
Treatment
First-line
- Calculate free water deficit: TBW × ((current Na / 140) − 1), where TBW = 0.6 × kg (men) or 0.5 × kg (women)
- Restore volume first if hemodynamically unstable: isotonic saline (NS or LR) until perfusion adequate
- Then correct free water deficit with hypotonic fluid: oral water if alert, D5W IV, or 0.45% saline IV
- Maximum correction rate 10 mEq/L per 24 h (slower if chronic >48 h) to prevent cerebral edema
- Address ongoing losses (insensible, urinary, GI) plus deficit
- Treat underlying cause
Second-line / adjunct
- Central DI: desmopressin (DDAVP) — nasal, oral, or SC; dose-titrated to urine output and Na
- Nephrogenic DI: low-sodium diet, thiazide diuretic (paradoxically reduces urine output by inducing mild volume depletion), amiloride (for lithium-induced)
- Stop offending medication if drug-induced (lithium discontinuation may not reverse if long-term)
- Hypervolemic hypernatremia: loop diuretic + free water replacement (D5W)
- Monitor Na every 4-6 hours during acute correction
Complications
- Cerebral edema and seizures from rapid correction (especially chronic hypernatremia)
- Intracranial hemorrhage (cellular dehydration causes brain shrinkage and bridging vein tearing — especially infants)
- Subdural hematoma
- Renal failure (severe hypovolemia)
- Death — hospital-acquired hypernatremia has 40-70% mortality (often reflects severity of underlying illness)
- Permanent neurologic injury from acute severe hypernatremia
PANCE pearls
- Most hypernatremia reflects FREE WATER DEFICIT, not sodium excess. Treatment is water replacement, not sodium restriction.
- Thirst is a powerful defense against hypernatremia — its presence means the disease is mild; its absence (cognitive impairment, intubation, adipsia) is the setup for severe disease.
- Diabetes insipidus differentiation: central DI responds to DDAVP (urine osm rises >50%); nephrogenic does not.
- Correction rate <10 mEq/L per 24 h to avoid cerebral edema — analogous to the cautious approach in chronic hyponatremia.
- Lithium causes nephrogenic DI in ~20% of patients on chronic therapy; amiloride blocks lithium entry into collecting duct cells.
- Hospital-acquired hypernatremia is often iatrogenic from inadequate free water replacement in patients with ongoing losses — preventable with careful intake/output tracking.
References
- Adrogue Madias — Hypernatremia (Adrogué and Madias, NEJM 2000)
- Sterns 2015 — Disorders of Plasma Sodium — Causes, Consequences, and Correction (Sterns, NEJM 2015)
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