HYPERNATREMIA

Serum Na >145 mEq/L — always reflects free water deficit; most common in patients with impaired thirst or access to water (elderly, ICU, AMS)

SYMPTOMS / ASSOCIATED SX

  • Mild (Na 145–155): thirst, lethargy, weakness, irritability

  • Moderate-severe (Na >155): AMS, seizures, coma, intracerebral hemorrhage (brain shrinkage)

  • Polyuria with dilute urine = diabetes insipidus; polyuria with concentrated urine = osmotic diuresis

DENIES

  • Polyuria history (DI workup)

  • Recent neurosurgery or pituitary surgery (triphasic DI–SIADH–DI response)

  • Lithium or demeclocycline use (nephrogenic DI)

SOCIAL HISTORY

  • Elderly or cognitive impairment (impaired access to water)

  • NPO status without adequate IVF replacement; ICU admission

MAIN ETIOLOGY

  • Inadequate free water intake: impaired thirst (elderly, AMS, hypothalamic lesion), dependent patients, dementia

  • Free water loss — extrarenal: diarrhea, fever/sweating, burns, hyperventilation

  • Renal free water loss: DI (central or nephrogenic), osmotic diuresis (DKA, mannitol)

  • Na gain (rare): hypertonic saline, Conn's syndrome, salt ingestion

MOST COMMON DDX

  • Urine Osm >800 (appropriate): extrarenal losses or inadequate intake

  • Urine Osm 300–800 (partial): partial DI or osmotic diuresis

  • Urine Osm <150 (inappropriately dilute): DI

  • Central DI (no ADH): brain injury, neurosurgery, pituitary tumor — responds to DDAVP

  • Nephrogenic DI (ADH resistance): lithium, demeclocycline, CKD, hypercalcemia — does NOT respond to DDAVP

DATA

  • BMP, serum osmolality; urine Na, urine Osm, urine specific gravity

  • Urine output (polyuria >3 L/day = DI threshold)

  • Calcium, K (nephrogenic DI causes); lithium level; glucose/HbA1c (osmotic diuresis)

  • MRI brain/pituitary if central DI suspected

HOME MEDS

  • DDAVP — for central DI; monitor for water retention and hyponatremia

  • Thiazides — paradoxically treat nephrogenic DI (mild volume depletion → increased proximal reabsorption)

  • Amiloride 5–10 mg PO daily — preferred for lithium-induced nephrogenic DI

PLAN

  • Correction rate (avoid cerebral edema from rapid correction):

    • Chronic (>48h or unknown): no faster than 10–12 mEq/L per 24h (0.5 mEq/L/h)

    • Acute (<48h): can correct at 1–2 mEq/L/h

    • Free water deficit (L) = TBW × (current Na/140 − 1); account for ongoing losses

  • Fluid choice:

    • Mild depletion + hyperNa: D5W IV or 0.45% NaCl if some Na deficit also present

    • Severe hemodynamic instability: NS 0.9% FIRST to restore perfusion, then switch to hypotonic

    • Enteral route preferred when tolerated: free water via NGT or PO (200–300 mL q4–6h)

  • Central DI:

    • DDAVP 0.1–0.2 mg PO BID–TID or 1–4 mcg SC/IV BID

    • Monitor closely for water retention and hyponatremia with treatment

  • Nephrogenic DI:

    • Remove offending agent (lithium); amiloride 5–10 mg PO daily (preferred for lithium DI)

    • HCTZ 25 mg PO daily (paradoxical benefit — mild volume depletion → increased proximal reabsorption)

  • Trend: serum Na q2–4h during active correction; urine output hourly; strict I&Os

  • DISCHARGE:

    • Central DI: oral DDAVP; endocrinology follow-up; MRI pituitary if not done

    • Elderly: ensure adequate free water access at home; home health if dependent

RED FLAGS

  • Na >165 + AMS → ICU; careful correction to avoid cerebral edema from rapid overcorrection

  • Hemodynamic instability + hypernatremia → NS FIRST to restore perfusion; correct Na second

  • Overcorrection (>12 mEq/L/24h chronic) → cerebral edema: seizures, herniation

  • Polyuria >3 L/day + dilute urine + rising Na in ICU → central DI until proven otherwise

  • Post-neurosurgery/pituitary: triphasic response (DI → SIADH → DI) — monitor Na closely for days

SENIOR IM RESIDENT PEARLS

  • Hypernatremia in hospitalized patients almost always iatrogenic or from impaired free water access — most common: inadequate free water in IVF given to NPO patients

  • Brain generates idiogenic osmoles in chronic hypernatremia — rapid correction → cerebral edema → worse outcome; correct slowly

  • Thiazides PARADOXICALLY treat nephrogenic DI: mild volume depletion → increased proximal tubule reabsorption → less free water to collecting duct

  • Common mistake: correcting hypernatremia too rapidly — monitor Na q2–4h; titrate infusion rate down if correcting too fast

  • Common mistake: treating acute DI with hypotonic fluids alone — DDAVP required for central DI; fluids cannot keep up with output

  • Lithium DI: amiloride preferred over thiazides (blocks lithium entry into collecting duct cells)