Hyponatremia.
The full stepwise approach: confirm true hypotonicity (and the acute vs chronic distinction), read urine osmolality (ADH on/off) then urine sodium (30 mmol/L or less = low effective volume; over 30 = SIAD, diuretics or a renal cause), separate SIAD from its mimics with the FE indices, and correct safely — goals vs limits, ODS risk, the DDAVP brake, and the desalination and potassium-repletion traps.
Reviewed October 2026 · verify against current guidelines
Diagnosis & Workup
Step 1: Confirm tonicity and timing.
Corrected October 2026 — urine sodium is now read at a single cutoff of 30 mmol/L, per the European guideline (ESE 2014), matching the hyponatremia tool. The slides show the older 20/40 split.
Is it truly hypotonic?
- Serum osm <275 mOsm/kg = true hypotonic hyponatremia.
- Isotonic = pseudohyponatremia (high lipids or protein); a lab artifact.
- Hypertonic = hyperglycemia or mannitol; correct Na by ~1.6 to 2.4 mEq per 100 mg/dL of glucose over 100.
- Measured osm can mislead: urea and ethanol raise it but cross cells freely, so true hypotonicity can still hide.
Acute or chronic sets the danger
- Acute (under 48 h): the brain is swollen; cerebral edema is the threat.
- Chronic (over 48 h): the brain has adapted; fast correction risks demyelination.
- Unknown duration: treat as chronic and correct slowly.
Ask two things first: is it truly hypotonic, and how long has it been? Duration decides how fast you may go.
Diagnosis & Workup
Step 2: Urine osmolality.
Is ADH on or off?
- Under 100 mOsm/kg = ADH is off. The kidney dilutes well, so the problem is intake: primary polydipsia or low solute (beer potomania, tea and toast).
- Over 100 = ADH is on, or free-water excretion is impaired. Move to urine sodium.
Watch the ADH-off group
- Once the stimulus is removed, these patients dilute and autocorrect fast.
- High overcorrection risk: reintroduce solute slowly and monitor closely.
A maximally dilute urine (under 100) means the kidney is doing its job; the problem is water intake or low solute.
ADH antidiuretic hormone
Diagnosis & Workup
Step 3: Urine sodium.
Urine Na splits the cause (when ADH is on)
| Na avid (UNa 30 or less) | Low effective arterial volume. Then look: dry = true hypovolemia (GI or skin loss); edematous = heart failure, cirrhosis, nephrotic. |
|---|---|
| Na wasting (UNa over 30) | Euvolemic SIAD; also diuretics, salt wasting, adrenal insufficiency, advanced kidney disease. |
Read it with the volume exam
- Urine Na of 30 mmol/L or less (with urine osm over 100) means the kidney is holding sodium: effective volume is low, whether the patient is dry or edematous (ESE 2014).
- Recent diuretics make urine Na unreliable; lean on FE urea and FE uric acid instead.
Sodium avid (urine Na 30 or less) is the low-volume signature; over 30 points to SIAD, diuretics or a renal cause (ESE 2014).
UNa urine sodiumSIAD syndrome of inappropriate antidiuresisFE fractional excretionGI gastrointestinal
Diagnosis & Workup
SIAD and its mimics.
SIAD is a diagnosis of exclusion
- Euvolemic and hypotonic; urine osm >100; urine Na >30 with normal salt and water intake (ESE 2014).
- Check TSH and a morning cortisol; rule out diuretics and kidney failure.
- Low uric acid (<4 mg/dL) and a low BUN support it.
SIAD vs low effective volume
| FE urea | <35% favors low volume; >55% favors SIAD. Use when FENa is unreliable on diuretics. |
|---|---|
| FE uric acid | ≥12% supports SIAD; <8% favors low effective volume. |
Do not confuse these
- Cerebral salt wasting (a contested entity): hypovolemic, usually neurosurgical. Salt and volume, not restriction.
- Reset osmostat: mild, stable, regulated around a low set point.
FE indices help on diuretics, but they cannot separate SIAD from cerebral salt wasting; only volume status does.
SIAD syndrome of inappropriate antidiuresisFE fractional excretionFENa fractional excretion of sodiumBUN blood urea nitrogenTSH thyroid-stimulating hormone
Acute Management
Severe symptoms and safe correction.
When to reach for 3% saline
- Severe symptoms (seizure, coma): 3% saline 100 to 150 mL IV bolus; repeat to a rise of 4 to 6 mEq, then stop. Treat the brain first.
- Severe but asymptomatic (Na under 120): a controlled 3% saline infusion to target, not a bolus.
Goals and limits
| Goal (symptomatic) | Raise 4 to 6 mEq, then hold. |
|---|---|
| Limit per 24 h | ≤8 mEq/L; ≤6 if high ODS risk. |
| Limit per 48 h | ≤18 mEq/L. |
| High ODS risk | Alcohol, malnutrition, low K, liver disease, Na <105. ODS is unlikely if starting Na is over 120. |
Brakes on correction
- Proactive DDAVP clamp or reactive desmopressin to control the rate.
- A brisk water diuresis (urine output over 100 mL/h) warns of impending overcorrection.
- Overcorrected? Relower with D5W; recheck Na every 2 to 4 h; involve nephrology early.
Overcorrecting chronic hyponatremia causes osmotic demyelination, often irreversible. Guideline limits stay the safe default, though faster correction is under active reappraisal.
ODS osmotic demyelination syndromeDDAVP desmopressin
Pitfalls & Disposition
Treatment by type. What gets missed.
Treatment by volume
| Hypovolemic | Isotonic 0.9% saline; treat the loss. Na often autocorrects, so anticipate overcorrection. |
|---|---|
| Euvolemic / SIAD | Fluid restrict; salt tabs, urea, an SGLT2 inhibitor, or a vaptan. Treat the cause. |
| Hypervolemic | Fluid restrict and diurese; treat the heart, liver, or kidney. |
Pitfalls
- Saline worsens SIAD when urine Na plus K exceeds serum Na (desalination); restrict water instead.
- Sodium tracks exchangeable Na plus K over total body water (the Edelman relationship), so replacing potassium also raises sodium and counts toward the daily limit.
- Thiazides and drugs (SSRIs, carbamazepine, NSAIDs) are common culprits; review the med list.
In SIAD, isotonic saline can paradoxically lower the sodium. Restrict water and treat the trigger.
SIAD syndrome of inappropriate antidiuresisSGLT2 sodium-glucose cotransporter-2 inhibitorSSRIs selective serotonin reuptake inhibitorsNSAIDs nonsteroidal anti-inflammatory drugs
Sources
Verify against current guidelines and local protocol before acting.
- Verbalis JG et al. Diagnosis, evaluation & treatment of hyponatremia: expert panel recommendations. Am J Med 2013;126(10 Suppl 1):S1-42.
- Spasovski G et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol 2014;170:G1-47.
- Spasovski G. Hyponatraemia: treatment standard 2024. Nephrol Dial Transplant 2024;39(10):1583-92.
- Katz MA. Hyperglycemia-induced hyponatremia: expected serum sodium depression (the 1.6 mEq/L factor). N Engl J Med 1973;289(16):843-4.
- Hillier TA, Abbott RD, Barrett EJ. Evaluating the correction factor for hyperglycemia (the 2.4 mEq/L factor). Am J Med 1999;106(4):399-403.
- Fenske W et al. Value of fractional uric acid excretion in hyponatremic patients on diuretics. JCEM 2008;93(8):2991-7.
- Refardt J et al. Empagliflozin (SGLT2 inhibitor) in chronic SIAD: randomized crossover trial. J Am Soc Nephrol 2023;34(2):322-32.
- Mark DG et al. Sodium correction rates & outcomes in severe hyponatremia: retrospective cohort. Ann Intern Med 2026;179(3):330-9.
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