Sodium & Water Disorders (Hypo/Hypernatremia)
A Step 2 CK high-yield lesson on sodium and water disorders that frames dysnatremias as water problems and drives every case through serum osmolality, then volume status plus urine osmolality and urine Na — covering SIADH, diabetes insipidus, and the correction-rate rules that prevent osmotic demyelination and cerebral edema.
Framework: Sodium Is a Water Problem
Serum sodium reflects water balance, not total-body sodium. Hyponatremia = too much water relative to solute; hypernatremia = too little. ADH (vasopressin) drives free-water reabsorption, so the kidney's ability to dilute or concentrate urine sets the outcome.
Approach every low sodium in two steps: (1) confirm true hypotonic hyponatremia by checking serum osmolality (excludes pseudo- and hypertonic causes), then (2) use volume status + urine osmolality + urine Na to localize the cause.
Hypernatremia is almost always a free-water deficit in someone who cannot access water (elderly, intubated, infants) or has renal water loss (DI).
The brain adapts to chronic dysnatremia by shifting intracellular osmoles, so the rate of correction — not just the target — drives iatrogenic harm (osmotic demyelination vs cerebral edema).
- Step 1 = serum osm. Normal/high osm excludes true hyponatremia: pseudohyponatremia (severe hyperlipidemia/paraproteinemia, isotonic) or hypertonic (hyperglycemia, mannitol).
- Correct Na for glucose: add ~1.6 mEq/L (≈2.4 when glucose is markedly high) per 100 mg/dL glucose above 100.
- Urine osm <100 = ADH appropriately suppressed → primary polydipsia, beer potomania, tea-and-toast (low solute intake).
- Urine osm >100 = ADH acting → SIADH, hypovolemia, HF/cirrhosis, endocrine causes.
- SIADH labs: euvolemic, urine osm >100, urine Na >30, low uric acid, low BUN; normal thyroid + cortisol.
- Urine Na splits volume-depleted states: <20 = extrarenal loss / avid retention (diarrhea, HF, cirrhosis); >20 = renal loss (diuretics, adrenal insufficiency, salt wasting).
- Chronic correction limit: hyponatremia ≤6–8 mEq/L/24h (prevents osmotic demyelination); hypernatremia ≤10 mEq/L/24h (prevents cerebral edema).
- Severe symptomatic hyponatremia (seizure/coma): 3% saline 100–150 mL bolus, raise Na 4–6 mEq/L, then stop and reassess.
Hypotonic Hyponatremia by Volume Status
| Volume | Key causes | Urine Na | Urine osm |
|---|---|---|---|
| Hypovolemic | Extrarenal: vomiting, diarrhea, third-spacing | <20 | >100 (conc.) |
| Hypovolemic | Renal: thiazides, adrenal insufficiency, salt wasting | >20 | variable |
| Euvolemic | SIADH, hypothyroid, glucocorticoid deficiency | >30 | >100 |
| Euvolemic | Primary polydipsia, beer potomania | <20 | <100 (dilute) |
| Hypervolemic | HF, cirrhosis (avid Na retention) | <20 | >100 |
| Hypervolemic | Renal failure | >20 | ~isotonic |
A 64-year-old smoker (40 pack-years) presents with confusion. Exam is euvolemic — no edema, no orthostasis, moist mucosa. Labs: Na 118, serum osm 248, urine osm 470, urine Na 55, uric acid 2.0; TSH and morning cortisol normal. Chest CT shows a central hilar mass.
Diagnosis: SIADH due to small cell lung cancer (ectopic ADH). The euvolemic, concentrated urine with high urine Na, low uric acid, and normal endocrine axes is the classic pattern.
Best next step: Confusion at Na 118 is a moderately-severe symptom → give cautious 3% hypertonic saline targeting a rise of only 6–8 mEq/L over 24h to avoid osmotic demyelination, alongside fluid restriction. Add salt tablets ± loop diuretic, or a vaptan/urea if refractory. Treat the underlying tumor definitively.
"Low to high, the pons will die; high to low, the brain will blow."
- Correcting hyponatremia too fast (Na low → high) → osmotic demyelination syndrome (central pontine myelinolysis). Symptoms appear 2–6 days later: dysarthria, dysphagia, spastic quadriparesis, "locked-in" state. Highest risk: chronic hyponatremia, alcoholism, malnutrition, hypokalemia, liver disease.
- Correcting hypernatremia too fast (Na high → low) → cerebral edema, seizures, herniation.
- Rescue for overcorrection of hyponatremia: re-lower Na with DDAVP + free water (D5W).
A 30-year-old woman on chronic lithium reports polyuria (>4 L/day) and polydipsia. Na 149, serum osm 302, urine osm 150 (inappropriately dilute); urine output stays high after overnight water deprivation. After desmopressin (DDAVP), urine osm rises only to 160 (<10%).
Diagnosis: Nephrogenic diabetes insipidus from lithium (renal ADH resistance). Failure to concentrate despite dehydration and no response to DDAVP localizes the defect to the kidney.
Best next step: Ensure water access and correct hypernatremia slowly (≤10 mEq/L/24h) to avoid cerebral edema; stop/limit lithium if feasible. Manage with low-salt, low-protein diet + a thiazide (paradoxically cuts urine volume) or amiloride for lithium-induced DI. Central DI, by contrast, shows a robust >50% urine-osm rise after DDAVP and is treated with desmopressin.
Central vs Nephrogenic DI
| Feature | Central DI | Nephrogenic DI |
|---|---|---|
| Defect | ↓ ADH secretion | Renal ADH resistance |
| Causes | Pituitary/hypothalamic tumor, trauma, surgery, idiopathic | Lithium, hypercalcemia, hypokalemia, genetic |
| Urine osm after water deprivation | Stays low | Stays low |
| Response to DDAVP | Urine osm ↑ >50% | Little/no rise (<10%) |
| Treatment | Desmopressin | Thiazide, low-salt/protein, amiloride, NSAIDs |
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