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%.
🔒 Free preview limit reached
Keep reading — start your free trial
You've read your 2 free diagnosis previews. Create your free account to unlock the full Hypernatremia outline — plus all 514 diagnoses, 3,500+ board-style questions, flashcards, and an AI tutor. Your 7-day free trial includes everything, and there's no credit card required.
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)
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
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
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)
Practice Renal/Urology questions on FirstPassPA
Turn this outline into retention. 3,500+ board-style questions with an AI tutor that explains every answer — free to start, no card required.
Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants.