Hyponatraemia Nursing Guide

Hyponatraemia Overview

Hyponatraemia is defined as serum sodium <135 mmol/L. It is the most common electrolyte disorder in hospitalised patients — present in 15–20% of admissions. Severe hyponatraemia (<120 mmol/L) is a medical emergency.

Severity Classification

Level	Serum Na⁺	Symptoms
Mild	130–134 mmol/L	Usually asymptomatic; nausea, fatigue
Moderate	125–129 mmol/L	Headache, vomiting, confusion, muscle cramps
Severe	<125 mmol/L	Seizures, reduced consciousness, respiratory arrest, coma

Acute vs chronic: Acute hyponatraemia (<48 hours) causes more severe symptoms at higher sodium levels. Chronic hyponatraemia (>48 hours) — brain has adapted; symptoms may be absent at Na⁺ 115–120 mmol/L.

Symptoms and Signs

Mild: nausea, headache, fatigue, dizziness
Moderate: cognitive impairment, drowsiness, vomiting
Severe: seizures (often refractory), respiratory failure, brain herniation
Gait instability and falls in elderly — even mild chronic hyponatraemia doubles fall risk

Classification Approach

Step 1: Check serum osmolality. Step 2: Assess volume status (clinical + urine sodium).

Step 1 — Serum Osmolality

Osmolality	Type	Causes
Low (<280 mOsm/kg)	True hypotonic hyponatraemia	Most clinical cases — see volume assessment below
Normal (280–295)	Pseudohyponatraemia	Severe hyperlipidaemia or hyperproteinaemia — lab artefact; no treatment needed
High (>295)	Translocational/hypertonic	Severe hyperglycaemia, mannitol, sorbitol — sodium diluted by shift of water from cells

Step 2 — Volume Status (for hypotonic hyponatraemia)

Volume Status	Clinical Signs	Urine Na⁺	Causes
Hypovolaemic (low volume)	Dry mucous membranes, tachycardia, hypotension, reduced skin turgor	<20 (extrarenal) or >20 (renal)	Diarrhoea/vomiting, burns, diuretics (thiazides > loop), adrenal insufficiency
Euvolaemic (normal volume)	No oedema, no signs of dehydration	>20	SIADH (most common), hypothyroidism, glucocorticoid deficiency, water intoxication
Hypervolaemic (excess volume)	Oedema, ascites, raised JVP, pleural effusion	<20	Heart failure, liver cirrhosis, nephrotic syndrome

Corrected Sodium in Hyperglycaemia

For every 5.5 mmol/L rise in glucose above normal → sodium falls by approximately 1.6 mmol/L (dilutional). Corrected Na⁺ = Measured Na⁺ + 1.6 × [(Glucose − 5.5) ÷ 5.5]

GCC relevance: DKA and hyperosmolar hyperglycaemic state (HHS) cause apparent hyponatraemia — always calculate corrected sodium.

SIADH — Syndrome of Inappropriate ADH

Diagnostic Criteria (Bartter-Schwartz)

Serum Na⁺ <135 mmol/L + serum osmolality <280 mOsm/kg
Urine osmolality >100 mOsm/kg (inappropriately concentrated — urine should be dilute if Na⁺ is low)
Urine sodium >20 mmol/L (kidney excreting Na⁺ despite low serum level)
Euvolaemic — no oedema, no signs of dehydration
Normal adrenal, thyroid and renal function (exclude other causes)

Causes of SIADH — SIADH Mnemonic

Category	Examples
CNS disorders	Head injury, stroke, meningitis, encephalitis, brain tumour, SAH
Pulmonary	Pneumonia, TB, COPD, mechanical ventilation (positive pressure)
Drugs	SSRIs, TCAs, carbamazepine, cyclophosphamide, desmopressin, opioids, thiazides, omeprazole, chlorpropamide
Malignancy	Small cell lung cancer (ectopic ADH), pancreatic, duodenal carcinoma
Endocrine	Hypothyroidism, glucocorticoid deficiency
Post-surgical	Major surgery (pain, nausea stimulate ADH release)

Treatment of Hyponatraemia

NEVER OVERCORRECT. Rapid correction of chronic hyponatraemia → Osmotic Demyelination Syndrome (ODS) — irreversible brainstem damage (central pontine myelinolysis). Maximum safe correction: ≤10–12 mmol/L per 24 hours; ≤8 mmol/L per 24 hours in high-risk patients (alcoholism, malnutrition, hypokalaemia).

Treatment by Cause and Severity

Scenario	Treatment
Symptomatic (seizures/reduced consciousness) — EMERGENCY	Hypertonic saline 3% NaCl 150 mL IV over 20 min; repeat if ongoing symptoms; aim for 5 mmol/L rise in first hour to stop seizures
Acute symptomatic (moderate symptoms)	3% NaCl at 0.5–1 mL/kg/hr; target 5–8 mmol/L improvement in first 24 hrs
Hypovolaemic hyponatraemia	0.9% NaCl IV to restore volume; as volume restores, sodium corrects naturally — monitor closely to prevent over-correction
SIADH (euvolaemic)	Fluid restriction 500–1000 mL/day (primary treatment); treat underlying cause; vaptans (tolvaptan) if severe/persistent
Hypervolaemic (HF, cirrhosis)	Fluid restriction + treat underlying cause; loop diuretics for oedema; avoid hypertonic saline
Chronic, asymptomatic	Slow correction; oral sodium supplements ± fluid restriction; NO rapid IV saline

Osmotic Demyelination Syndrome (ODS)

Also called: central pontine myelinolysis (CPM) when affects pons; extrapontine myelinolysis elsewhere
Risk factors: Correction rate >12 mmol/L per 24 hrs; alcoholism; severe malnutrition; hypokalaemia; liver disease
Timing: Symptoms appear 2–6 days AFTER overly rapid correction
Symptoms: Dysarthria, dysphagia, spastic quadriplegia, locked-in syndrome, coma — often irreversible
Prevention: Strict monitoring hourly then 4-hourly sodium levels during correction; stop or reverse correction if rising too fast (infuse 5% dextrose if over-correcting)

Nursing Monitoring Protocol

Parameter	Frequency
Serum sodium	Every 2–4 hrs during acute correction; every 6–12 hrs once stable
Neurological status (GCS, seizure watch)	Every 1–2 hrs during acute treatment
Fluid balance (intake vs output)	Hourly; IDC for accurate urine output
Urine osmolality and sodium	Spot test at baseline; repeat to guide treatment
Daily weight	Daily — reflects fluid shifts in hypervolaemic states

GCC-Specific Context

Hyponatraemia in GCC

Heat-related hyponatraemia: Excessive sweating in GCC summer heat (45°C+) followed by replacement with hypotonic fluids (plain water, diluted drinks) → hypervolaemic hyponatraemia. Seen particularly in outdoor workers, athletes and Hajj pilgrims
Exercise-associated hyponatraemia: Common in endurance events (desert marathons, cycling events in Dubai/Abu Dhabi) — occurs when participants over-drink plain water. Can be fatal. Treatment: hypertonic saline, NOT more fluids
SIADH from medications: High SSRI prescribing in GCC (depression, anxiety) — SSRIs are a leading drug cause of SIADH across GCC outpatient populations
Thiazide diuretics: Widely used for hypertension in GCC — thiazides specifically cause SIADH-like hyponatraemia (unlike loop diuretics). Common in elderly GCC patients on hydrochlorothiazide or indapamide
Diabetic ketoacidosis / HHS: Pseudohyponatraemia from severe hyperglycaemia common in GCC DKA presentations. Corrected sodium must be calculated before treating apparent hyponatraemia

Exam Tips

Normal Na⁺: 135–145 mmol/L. Hyponatraemia: <135
First step: serum osmolality → then volume status
SIADH: euvolaemic + urine osmolality >100 + urine Na >20
Correction max: 10–12 mmol/L per 24 hrs (8 in high-risk)
Rapid over-correction → osmotic demyelination syndrome
Symptomatic (seizures): 3% NaCl 150 mL over 20 min
Fluid restriction = primary treatment for SIADH

Exam MCQs — DHA / SCFHS / QCHP

Q1. A patient has serum Na⁺ 119 mmol/L with seizures. This is an acute presentation confirmed within 24 hours. What is the IMMEDIATE treatment?

A) Fluid restriction 1 L/day — SIADH management B) 0.9% NaCl IV at 150 mL/hr C) 3% hypertonic NaCl 150 mL IV over 20 minutes D) Dextrose 5% IV to dilute remaining sodium further

✅ C — Symptomatic severe hyponatraemia with seizures requires immediate treatment with 3% hypertonic saline 150 mL IV over 20 minutes. Target: raise Na⁺ by 5 mmol/L in first hour to stop seizures. Normal saline (0.9%) is insufficient in this emergency. Dextrose would worsen hyponatraemia.

Q2. A patient with SIADH has Na⁺ 125 mmol/L with mild headache and nausea but no seizures. What is the FIRST-LINE treatment?

A) 3% hypertonic saline infusion B) Fluid restriction to 500–1000 mL/day and treat underlying cause C) 0.9% NaCl 1 L IV over 4 hrs D) Furosemide 40 mg IV to increase free water excretion

✅ B — Mild-moderate SIADH with mild symptoms → fluid restriction (500–1000 mL/day) is first-line treatment. This creates a negative water balance, allowing sodium to correct gradually. Hypertonic saline is for severe/symptomatic cases. Normal saline in SIADH can paradoxically worsen hyponatraemia.

Q3. A patient with chronic hyponatraemia (Na⁺ 108 mmol/L for 5 days) is started on 3% saline. After 12 hours, Na⁺ has risen to 120 mmol/L (+12 mmol/L). What is the CORRECT action?

A) Continue 3% saline at the same rate — 12 mmol/L in 12 hrs is excellent B) Stop or slow hypertonic saline; consider infusing 5% dextrose to prevent further rapid correction and reduce ODS risk C) Administer frusemide to increase urine output D) Increase saline rate — the higher the sodium, the better the outcome

✅ B — In chronic hyponatraemia, maximum safe correction is 10–12 mmol/L per 24 hours total. At 12 mmol/L in only 12 hours, the rate is dangerously fast. Stop or slow hypertonic saline. Infuse 5% dextrose to slow further correction. Consider desmopressin to reduce urinary free water excretion. Overly rapid correction causes irreversible osmotic demyelination syndrome.

Q4. A marathon runner in Dubai collapses at the finish line. GCS is 12. Serum Na⁺ is 118 mmol/L. The runner reports drinking large amounts of water during the race. What type of hyponatraemia is this?

A) Hypovolaemic hyponatraemia from excessive sweating B) Exercise-associated hyponatraemia — hypervolaemic dilutional from excessive plain water intake C) SIADH from physical exertion-induced ADH release D) Pseudohyponatraemia from exercise-induced hyperlipidaemia

✅ B — Exercise-associated hyponatraemia (EAH): athlete over-drinks plain water during exercise → dilutional hyponatraemia. This is the most dangerous cause of collapse in distance runners. Treatment is hypertonic saline (NOT more fluids). Prevention: drink to thirst only; electrolyte sports drinks preferred over plain water in prolonged exercise in heat.

🧪 Hyponatraemia