Hyponatremia: Evaluation and Management
Definition
- Hyponatraemia: serum sodium concentration < 135 mmol/L.
- Classified by severity (mild 130‑134, moderate 125‑129, severe < 125 mmol/L) and duration (acute < 48 h, chronic ≥ 48 h).
- Also classified by volume status: hypovolaemic, euvolaemic (most common), or hypervolaemic.
Epidemiology
- One of the most common electrolyte disorders; prevalence ≈ 20‑30 % in hospitalized patients and ≈ 5‑10 % in the community.
- In Indian tertiary centres, hyponatraemia is reported in 15‑25 % of medical admissions, higher in elderly, heart failure, cirrhosis, and SIADH.
- Mortality rises with serum Na < 125 mmol/L (up to 30 % in ICU).
Aetiology
| Volume status | Common causes (Indian context) |
|---|---|
| Hypovolaemic | GI losses (vomiting, diarrhoea, dysentery), renal losses (diuretics, osmotic diuresis, adrenal insufficiency), third‑spacing (pancreatitis, burns) |
| Euvolaemic | SIADH (lung carcinoma, TB, pneumonia, CNS infections, drugs – carbamazepine, SSRIs, carboplatin), hypothyroidism, glucocorticoid deficiency, primary polydipsia |
| Hypervolaemic | Congestive heart failure, cirrhosis with ascites, nephrotic syndrome, chronic kidney disease (CKD) with impaired free water excretion |
Pathophysiology
- Water‑sodium imbalance: hyponatraemia results when total body water exceeds total body sodium.
- ADH (vasopressin) dysregulation:
- Inappropriate ADH secretion → water reabsorption despite low plasma osmolality.
- Non‑osmotic stimuli (hypovolaemia, pain, nausea, drugs) also trigger ADH.
- Renal handling: impaired free water clearance (low urine osmolality < 100 mOsm/kg in primary polydipsia; > 100 mOsm/kg in SIADH).
- Cellular adaptation: in chronic hyponatraemia, brain cells extrude osmolytes (taurine, glutamate) to prevent cerebral oedema; rapid correction overwhelms this, causing osmotic demyelination.
Clinical Features
| Severity | Typical signs/symptoms |
|---|---|
| Mild | Asymptomatic, nausea, headache, mild lethargy |
| Moderate | Confusion, vomiting, muscle cramps, gait disturbance |
| Severe (acute) | Seizures, coma, respiratory arrest, brain herniation |
| Chronic | Subtle neurocognitive deficits, gait instability, falls, hyponatraemic encephalopathy (rare) |
- Volume assessment: dry mucous membranes & tachycardia (hypovolaemia); oedema, JVD (hypervolaemia); normal skin turgor, no oedema (euvolaemia).
- Associated findings: low serum uric acid in SIADH, high urine sodium (> 30 mmol/L) in most euvolaemic causes.
Investigations
- Serum electrolytes (Na, K, Cl, bicarbonate) – repeat to confirm.
- Serum osmolality – low (< 275 mOsm/kg) confirms hypotonic hyponatraemia.
- Urine osmolality – > 100 mOsm/kg suggests ADH activity; < 100 mOsm/kg points to primary polydipsia or low solute intake.
- Urine sodium – > 30 mmol/L in SIADH, diuretic use, renal losses; < 20 mmol/L in extrarenal losses.
- Thyroid function tests (TSH, free T4) – rule out hypothyroidism.
- Morning cortisol – assess adrenal insufficiency.
- Chest X‑ray / CT thorax – look for lung malignancy, TB, pneumonia.
- Brain MRI (if neurological deterioration) – to detect osmotic demyelination syndrome (ODS) after rapid correction.
- Additional: serum uric acid, BNP (heart failure), liver function tests (cirrhosis).
Management (2023 European Society of Endocrinology (ESE) & Indian Consensus Guidelines)
General Principles
- Identify and treat the underlying cause (e.g., stop offending drug, treat infection, replace cortisol).
- Determine chronicity – acute (< 48 h) may tolerate faster correction; chronic requires slower correction.
- Target correction:
- Acute severe: raise Na by 4‑6 mmol/L in the first 6 h, not exceeding 8‑10 mmol/L in 24 h.
- Chronic: limit to ≤ 8 mmol/L/24 h and ≤ 18 mmol/L/48 h.
- Frequent monitoring: serum Na every 2‑4 h during active correction; urine output and fluid balance hourly in ICU.
Specific Therapeutic Strategies
| Volume status | First‑line therapy | Additional measures |
|---|---|---|
| Hypovolaemic | Isotonic saline (0.9 % NaCl) 1‑2 L bolus, then 0.5‑1 L/24 h until Na rises 4‑6 mmol/L | Replace ongoing losses, correct underlying GI/renal cause |
| Euvolaemic (SIADH) | Fluid restriction 800‑1000 mL/day (or < ½ urine output) | If Na < 125 mmol/L or symptomatic: Vaptans (tolvaptan 15 mg PO, titrate) or Urea 30 g PO daily; Demeclocycline 300 mg BID (avoid in liver disease) |
| Hypervolaemic | Loop diuretics (furosemide 40‑80 mg IV/PO) + fluid restriction | Add hypertonic saline (3 % NaCl) if severe neuro symptoms; consider albumin in cirrhosis with ascites; treat underlying heart failure or CKD |
Hypertonic Saline (3 % NaCl) – Indications
- Severe symptoms (seizures, coma) irrespective of chronicity.
- Dose: 100 mL bolus over 10 min → re‑measure Na after 30 min; repeat up to 2 boluses if needed, aiming for Na rise 4‑6 mmol/L.
- Monitoring: serum Na, serum glucose, osmolar gap, and neurological status.
Pharmacologic ADH Antagonists (Vaptans)
- Tolvaptan: start 15 mg PO once daily; can increase to 30‑60 mg if needed.
- Conivaptan (IV) – limited availability in India.
- Monitoring: serum Na every 6‑8 h for first 24 h; watch for over‑correction and hepatotoxicity (baseline LFTs).
Urea Therapy
- 30 g oral urea dissolved in water, given 2‑3 times daily.
- Effective, inexpensive, especially in resource‑limited settings.
Over‑correction Management
- If Na rise exceeds 10 mmol/L/24 h, give desmopressin (DDAVP) 1‑2 µg IV/SC and free water (D5W) to re‑lower Na to safe range.
- Re‑check Na after 1 h; repeat as needed.
Complications
- Cerebral oedema (acute severe hyponatraemia) → seizures, brain herniation.
- Osmotic demyelination syndrome (ODS) – central pontine and extrapontine demyelination after rapid correction; presents 2‑6 days later with dysarthria, dysphagia, quadriparesis, “locked‑in” syndrome.
- Hypokalaemia and hypocalcaemia secondary to aggressive saline therapy.
- Volume overload in heart failure or cirrhosis if fluid restriction is ignored.
High‑Yield Exam Points
- Hyponatraemia is hypotonic when serum osmolality < 275 mOsm/kg; always rule out hypertonic (e.g., hyperglycaemia) and isotonic (pseudohyponatraemia) causes first.
- Urine Na > 30 mmol/L + urine osmolality > 100 mOsm/kg → SIADH or renal salt loss; Urine Na < 20 mmol/L → extrarenal loss (vomiting, diarrhoea).
- SIADH diagnostic criteria (2023 ESE): hypotonic hyponatraemia, euvolaemia, urine osmolality > 100 mOsm/kg, urine Na > 30 mmol/L, normal thyroid/adrenal function, no diuretics.
- Acute severe hyponatraemia: treat with 3 % NaCl bolus; do not wait for labs.
- Correction limits: ≤ 8 mmol/L/24 h (chronic); ≤ 10‑12 mmol/L/24 h (acute).
- Desmopressin + D5W is the rescue strategy for over‑correction.
- Urea is a cost‑effective alternative to vaptans in Indian settings.
- Drug‑induced SIADH: carbamazepine, SSRIs, cyclophosphamide, vincristine – always review medication list.
- Cerebral ODS risk factors: chronic hyponatraemia, alcoholism, malnutrition, liver disease, rapid correction > 12 mmol/L/24 h.
Practice questions
A 68‑year‑old man with COPD presents with confusion, serum Na = 118 mmol/L, serum osmolality 260 mOsm/kg, urine Na = 45 mmol/L, urine osmolality 550 mOsm/kg. He is euvolaemic and on sertraline. What is the most appropriate next step?
Answer: B – Initiate fluid restriction and stop sertraline (SIADH management).A patient with severe symptomatic hyponatraemia (Na = 112 mmol/L) receives 100 mL of 3 % NaCl over 10 minutes. After 30 minutes the serum Na is 118 mmol/L. What is the recommended further action?
Answer: C – No further hypertonic saline; monitor and consider desmopressin if Na rises > 10 mmol/L/24 h.Which of the following statements about osmotic demyelination syndrome (ODS) is FALSE?
A) It typically presents 2‑6 days after rapid correction of chronic hyponatraemia.
B) MRI shows hyperintensity in the central pons on T2‑weighted images.
C) Administration of high‑dose steroids prevents ODS.
D) Risk is higher in patients with alcoholism and malnutrition.
Answer: C — Steroids have not been proven to prevent ODS.
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