How hyponatremia is tested on Step 1

A vignette gives sodium, osmolality, urine studies, and a clinical setting, and asks for the cause, the mechanism, or the complication of treatment.

Serum osmLow = truehypotonicUrine osm< 100: ADHoff> 100ADH activeVolumestatusHypo, eu,hyperUrine NaRenal vsextrarenal
Approach. Each step narrows the differential.

Classifying hypotonic hyponatremia

Volume status and urine sodium separate the causes when ADH is active.

Volume statusCausesUrine Na⁺
HypovolemicVomiting, diarrhea, burns< 20 mEq/L (kidneys conserve)
HypovolemicThiazides, adrenal insufficiency (mineralocorticoid deficiency), cerebral salt wasting> 20 mEq/L (renal loss)
EuvolemicSIADH, hypothyroidism, glucocorticoid deficiency> 20–40 mEq/L
Euvolemic, urine osm < 100Primary polydipsia, beer potomania, "tea and toast"Low
HypervolemicHeart failure, cirrhosis, nephrotic syndrome< 20 mEq/L (low effective arterial volume)
HypervolemicAdvanced kidney failure> 20 mEq/L

In heart failure and cirrhosis, low effective arterial volume triggers ADH even though total body water is high.

SIADHADH inappropriately highUrine concentrated (> 100)Urine Na > 30–40 mEq/LLow uric acid and BUNFluid restriction helpsPrimary polydipsiaADH suppressedUrine very dilute (< 100)Intake exceeds excretionPsychiatric illness commonReduce water intakevs
SIADH vs polydipsia. Urine osmolality is the key difference.

SIADH

ADH acts on V2 receptors to insert aquaporin-2 in the collecting duct, so free water is retained.

SIADH causesCancerSmall cell lungcancerCNSStroke, hemorrhage,infection, traumaLungPneumonia, TBDrugsSSRIs,carbamazepine,cyclophosphamide
Causes of SIADH. Pain, nausea, and surgery are common stimuli in hospitalized patients.
  • Volume expansion from water retention triggers natriuresis, so patients appear euvolemic, not edematous.
  • Treatment: fluid restriction; salt tablets (with a loop diuretic in some cases); V2 antagonists (tolvaptan, conivaptan); demeclocycline is a historical option.
  • Infusing normal saline can worsen SIADH if urine osmolality is high, because the salt is excreted and the water retained.

Treatment and osmotic demyelination

Speed of correction matters as much as direction.

SituationApproach
Severe symptoms (seizure, coma)Bolus 3% saline to raise Na by about 4–6 mEq/L quickly
HypovolemicIsotonic saline; ADH falls once volume is restored, so watch for rapid correction
SIADHFluid restriction, salt tablets, vaptans
HypervolemicFluid and sodium restriction, loop diuretics, treat the underlying disease
Correction limitAbout 8–10 mEq/L per 24 hours (lower in high-risk patients)

High-risk patients for osmotic demyelination: alcohol use disorder, malnutrition, hypokalemia, liver disease, and sodium ≤ 105 mEq/L.

Worked example

Use the stepwise approach.

functions Worked example — lung mass

A 64-year-old smoker has confusion and a central lung mass. Serum Na 122 mEq/L, serum osm 255 mOsm/kg, urine osm 520 mOsm/kg, urine Na 58 mEq/L. He appears euvolemic. Diagnosis and the risk of rapid correction?

  1. Low serum osmolality: true hypotonic hyponatremia.
  2. Urine osmolality > 100: ADH is active.
  3. Euvolemic with high urine sodium points to SIADH; a central lung mass suggests small cell carcinoma producing ADH.
  4. Raising sodium faster than about 8–10 mEq/L in 24 hours risks osmotic demyelination of the pons.

Answer. SIADH from small cell lung cancer. Correct slowly to avoid osmotic demyelination syndrome.