This selection applies only if active IV correction is clinically indicated. The engine will gate this decision.
ODS (formerly "central pontine myelinolysis") occurs when chronic hyponatraemia is corrected too rapidly. In chronic hyponatraemia, brain cells adapt by losing organic osmolytes. If extracellular Na rises too fast, water is pulled out of adapted neurons, causing demyelination. Symptoms appear 2 to 6 days after overcorrection: dysarthria, dysphagia, quadriparesis, "locked-in syndrome," and potentially death. ODS is irreversible. Prevention is the only strategy.
Not every patient with Na⁺ < 135 needs IV correction. This tool gates its output based on severity and clinical context:
| Na⁺ Range | Severity | Default Management |
|---|---|---|
| 130 to 134 | Mild | No IV correction. Fluid restriction (eu/hyper) or NS volume resuscitation (hypo). Investigate cause. |
| 125 to 129 | Moderate | Fluid restriction primary (eu/hyper). Active IV correction only if severely symptomatic or trending down. |
| 120 to 124 | Severe | Active correction indicated. ICU/HDU admission. Calculated infusion. |
| 110 to 119 | Profound | Urgent active correction. ICU mandatory. Consider DDAVP clamping. |
| < 110 | Critical | Life-threatening emergency. ICU, bolus protocol if symptomatic, strict monitoring. |
| Chronicity | ODS Risk | Correction Approach |
|---|---|---|
| Acute (<48h) | Very Low | More aggressive correction permitted (up to 10 mEq/L/24h). Brain has not adapted. |
| Chronic (>48h) | HIGH | Strict slow correction (8 mEq/L/24h max, 6 for high-risk). Brain has adapted by expelling osmolytes. |
| Unknown Duration | Treat as Chronic | If you cannot prove onset was <48h with prior normal labs, assume chronic. |
| Scenario | Max 24h Rise | Notes |
|---|---|---|
| Standard Risk, Chronic/Unknown | 8 mEq/L | European (2014) and API (2019) consensus |
| High Risk (SHAM), Chronic/Unknown | 6 mEq/L | Sterns 2015 |
| Documented Acute, Standard Risk | 10 mEq/L | ODS risk very low |
| Documented Acute, High Risk | 8 mEq/L | Still apply caution despite acuity |
| Volume Status | Clinical Script & Traps | Primary Action |
|---|---|---|
| Hypovolaemic | Dry mucosa, flat JVP, tachycardia. Trap: Once volume is restored with NS, ADH shuts off, kidneys dump free water, Na⁺ skyrockets past the safe limit. | NS to restore volume. Monitor closely for auto-correction. Consider prophylactic DDAVP clamping. |
| Euvolaemic | Normal exam. Think SIADH, hypothyroidism, adrenal insufficiency. Trap: NS can paradoxically worsen SIADH. Always check TSH and morning cortisol first. | Fluid restriction (800-1000 mL/day). HTS only if severely symptomatic. |
| Hypervolaemic | Oedema, raised JVP, ascites. Total body Na⁺ is high but water is massively higher. | Fluid restriction + Loop Diuretics. NEVER give continuous saline. |
Patients at highest risk for ODS require the strict 6 mEq/L/24hr limit. Remember SHAM:
3% NaCl contains 513 mEq/L of Na. It is used for symptomatic hyponatraemia (seizures, coma) to rapidly raise Na by 1 to 2 mEq/L per hour for the first 2 to 3 hours.
Fixed bolus (preferred for emergencies): 150 mL of 3% NaCl IV over 20 minutes. Recheck Na after 20 minutes. Repeat up to 2 more times if symptoms persist (maximum 3 boluses). Each 150 mL bolus raises Na by approximately 1.5 to 2 mEq/L in a 70 kg patient.
Correcting hypokalaemia simultaneously raises serum Na⁺. K⁺ enters cells and displaces Na⁺ outward. Every 1 mEq of K⁺ replaced has the same osmotic effect as 1 mEq of Na⁺ infused. K⁺ correction must be counted against the 24h Na⁺ correction limit.
⚠ The Normal Saline Trap in SIADHIn SIADH, kidneys maximally concentrate urine. If you infuse 1 litre of 0.9% NS (154 mEq Na⁺ in 1000 mL), the kidneys may excrete those 154 mEq in only 500 mL of concentrated urine, retaining 500 mL of electrolyte-free water. Net effect: you have worsened the hyponatraemia despite giving sodium.
Proactive DDAVP Clamping StrategyModern best practice advocates proactive DDAVP clamping rather than reactive rescue. Give DDAVP 1 to 2 mcg IV at the start of therapy, then administer HTS at a calculated rate. This converts the patient into a "closed system" that behaves as the Adrogue-Madias formula predicts. Especially important for hypovolaemic patients at highest risk of auto-correction overshoot.
Pseudohyponatraemia & Dilutional HyponatraemiaHypertonic hyponatraemia: Hyperglycaemia pulls water out of cells, diluting sodium. For every 100 mg/dL rise in glucose above 100, Na drops by 1.6 mEq/L. Corrected Na = Measured Na + 1.6 × ((Glucose - 100) / 100). If corrected Na is normal, treat the hyperglycaemia, not the sodium.
Isotonic hyponatraemia: Severe hyperlipidaemia or hyperproteinaemia (myeloma). Serum osmolality will be normal. Not true hyponatraemia.
Diagnostic criteria: (1) Serum Na < 135, (2) Serum osmolality < 275, (3) Urine osmolality > 100, (4) Urine Na > 40, (5) Euvolaemic, (6) Normal thyroid and adrenal function. Common causes in India: CNS infections (TB meningitis, encephalitis), lung disease (TB, pneumonia, lung cancer), drugs (SSRIs, Carbamazepine, Cyclophosphamide).
Management: (1) Fluid restriction (800 to 1000 mL/day). (2) Salt tablets (NaCl 3g TDS with meals). (3) Tolvaptan 15 mg PO daily if fluid restriction fails (Indian brands: Tolva, Natrise). Start in hospital with Na monitoring every 6 hours. (4) Treat the underlying cause.
ΔNa⁺ = (Infusate Na⁺ - Serum Na⁺) / (Total Body Water + 1)
Limitation: Assumes zero renal water handling. Systematically underestimates correction in hypovolaemic patients and may overestimate in SIADH.
| IV Fluid | Na⁺ (mEq/L) | Typical Use |
|---|---|---|
| 3% HTS | 513 | ICU bolus and infusion for symptomatic hyponatraemia |
| 1.6% HTS | 274 | Peripheral line option |
| 0.9% NS | 154 | Volume resuscitation in hypovolaemic hyponatraemia |
| Ringer's Lactate | 130 | Mild hypovolaemia |
AMA Style:
Umakanth S. Acute Hyponatraemia Protocol. MEDiscuss. Published 2026. Accessed .
Vancouver Style:
Umakanth S. Acute Hyponatraemia Protocol [Internet]. MEDiscuss.org; 2026 [cited ]. Available from: