Hyponatraemia and hypernatraemia: the AU general practice management guide

Sodium disorders sit at the intersection of the most common and most dangerous electrolyte problems in clinical practice. Hyponatraemia — serum sodium below 135 mmol/L — affects 15–25% of Australian hospital admissions and approximately 7% of community-dwelling older adults. Hypernatraemia — sodium above 145 mmol/L — is less common in the community but carries a hospital mortality of 15–60% in older patients, reflecting the severity of the underlying illness, impaired access to water, and the neurological consequences of cerebral cell dehydration.

Both disorders share a treatment paradox: correcting them too quickly causes a different, equally devastating neurological injury. For hyponatraemia, rapid correction causes osmotic demyelination syndrome (ODS) — destruction of myelin sheaths, particularly in the pons, causing irreversible quadriplegia or death. For hypernatraemia, rapid correction causes cerebral oedema. The correction rate ceilings govern management, not the urgency of the biochemistry.

The practical rule for Australian general practice: a maximum sodium rise of 10 mmol/L per 24 hours for hyponatraemia and a maximum sodium fall of 10 mmol/L per 24 hours for hypernatraemia. These numbers, referenced by eTG nephrology and the ESE 2014 hyponatraemia guideline, must be known before any correction is started.

A. Core clinical — the AU general-practice framework

Step 1: confirm true hyponatraemia — exclude pseudo-hyponatraemia

Before treating any apparent hyponatraemia, measure serum osmolality and serum glucose alongside UEC.

• Pseudo-hyponatraemia (iso-osmolar): severe hyperlipidaemia or paraproteinaemia (multiple myeloma, Waldenström’s) artefactually lowers sodium on older indirect ion-selective electrode analysers. Serum osmolality is normal (285–295 mOsm/kg); no treatment is needed. Direct-ISE analysers (as in blood gas machines) give the true result. The Hillier correction (Am J Med 1999) provides guidance for paraproteinaemia adjustments.
• Hyperosmolar hyponatraemia: severe hyperglycaemia in DKA or HHS depresses measured sodium — each 5.5 mmol/L rise in glucose above normal drops apparent sodium by approximately 1.6 mmol/L. Treat the hyperglycaemia; sodium corrects.
• True hypotonic hyponatraemia (serum osmolality below 275 mOsm/kg): proceed to volume and urine assessment.

Step 2: assess volume status

Examine JVP height, mucous membrane moisture, skin turgor, postural BP change, peripheral oedema, and weight trend. Volume status guides both cause and treatment:

• Hypovolaemic — total body sodium and water both reduced; water loss proportionally less. Causes: GI losses, diuretics, skin losses (burns, sweating), third-space losses (pancreatitis, peritonitis).
• Euvolaemic — clinically normal volume; the most common category in hospital hyponatraemia; dominated by SIADH, hypothyroidism, and glucocorticoid deficiency.
• Hypervolaemic — excess total body sodium and water with oedema; chronic heart failure, cirrhosis, nephrotic syndrome, advanced CKD.

Step 3: urine sodium and urine osmolality

Spot urine sodium (mmol/L) and urine osmolality (mOsm/kg) are the key discriminators:

• Urine osmolality below 100 mOsm/kg → maximally dilute → primary polydipsia (psychiatric, MDMA + water, marathon over-hydration), beer potomania (excess alcohol with low protein), or tea-and-toast low-solute diet (frail elderly).
• Urine osmolality above 100 + urine sodium below 30 → hypovolaemic extra-renal loss OR hypervolaemic (heart failure/cirrhosis/nephrotic) — ADH appropriately elevated.
• Urine osmolality above 100 + urine sodium above 30 → SIADH, current diuretic, cerebral or renal salt wasting, adrenal insufficiency, or severe hypothyroidism.

Step 4: exclude endocrine causes in all euvolaemic hyponatraemia

Per ESE 2014 and eTG: always check a 9 am cortisol (± Synacthen test if low) and TSH + free T4 before labelling any euvolaemic hyponatraemia as SIADH. Missing adrenal insufficiency (Addison’s disease or secondary from pituitary disease or corticosteroid withdrawal) is dangerous — these patients require emergency hydrocortisone. Missing severe hypothyroidism (myxoedema) is similarly dangerous. Normal cortisol and TSH are required to diagnose SIADH.

Drug-induced hyponatraemia — the most reversible community cause

NPS MedicineWise and eTG emphasise that drug-induced hyponatraemia is the most common, and most reversible, cause in Australian community practice. Key drugs: thiazide diuretics (cluster in older women, first 2–4 weeks of therapy — permanently cease and switch to amlodipine or ACEi after a symptomatic event; never re-challenge), SSRIs and SNRIs (SIADH mechanism; agomelatine and mirtazapine carry lower hyponatraemia risk — switch if sodium falls below 130 mmol/L), carbamazepine, oxcarbazepine, opioids, tricyclic antidepressants, and antipsychotics. Check sodium at 2–4 weeks after commencing a thiazide in older adults.

B. Hyponatraemia — severity-based management

Severe symptomatic hyponatraemia — emergency

Seizure, coma, Glasgow Coma Scale drop, or rapidly progressive neurological deterioration in the context of hyponatraemia is a medical emergency. Acute brain swelling can progress to transtentorial herniation.

Treatment per ESE 2014, Verbalis et al. Am J Med 2013, and eTG:

1. Hypertonic 3% saline 100–150 mL IV bolus over 10–20 minutes.
2. Repeat the bolus up to twice if symptoms do not improve; maximum three boluses total.
3. Target a 4–6 mmol/L sodium rise within the first 6 hours — sufficient to reduce cerebral oedema.
4. Absolute ceiling: 10 mmol/L rise in 24 hours; 18 mmol/L in 48 hours. Exceeding these causes ODS (Sterns, NEJM 2015).
5. Check sodium hourly for the first 6 hours, then 2–4 hourly.
6. If sodium over-corrects, re-lower with 5% dextrose ± desmopressin 2 mcg IV — this is an active intervention with case-series evidence.

This is hospital-only management. From general practice: call 000, arrange emergency transfer.

Moderate asymptomatic hyponatraemia (sodium 125–129 mmol/L)

• Hypovolaemic: IV 0.9% saline restores volume → ADH suppresses → sodium rises. Monitor closely — over-correction risk is real as ADH suppresses rapidly.
• Euvolaemic (SIADH): fluid restriction below 800–1,000 mL/day is first-line; treat the underlying cause (cease offending drug, treat pneumonia, investigate lung or CNS for malignancy). If the Furst index (urine [Na+K] ÷ serum Na) exceeds 1, fluid restriction is unlikely to work — escalate to oral urea (compounding pharmacy) or specialist-initiated tolvaptan (PBS Authority Required; specialist initiation only).
• Hypervolaemic: fluid restriction, loop diuretic (furosemide), and treatment of the underlying cardiac, hepatic, or renal cause.

Mild asymptomatic hyponatraemia (sodium 130–134 mmol/L)

Often discovered incidentally. Do not dismiss it — even “mild” chronic hyponatraemia associates with impaired gait stability, falls, and fractures in older adults (Renneboog, Am J Med 2006). Investigate the cause, conduct a thorough medication review, and recheck within 1–2 weeks. Outpatient management is usually appropriate if the patient is stable and truly asymptomatic.

C. Hypernatraemia — diagnosis and management

Hypernatraemia (sodium above 145 mmol/L) almost universally represents water deficit, not excess sodium. If a patient cannot access water or is not thirsty, they are vulnerable. Frail older adults in residential aged care, people with cognitive impairment or reduced consciousness, infants, and Aboriginal and Torres Strait Islander Australians in remote communities during heatwaves are the highest-risk groups. Hospital mortality is 15–60%, largely reflecting the underlying severity of illness (eTG nephrology).

Causes

• Reduced water intake: impaired thirst (age, cognitive impairment, hypothalamic dysfunction), impaired access to water (RACF, post-stroke, dependent on carers), extreme heat events.
• Increased insensible loss: fever, sweating, mechanical ventilation without adequate humidification, burns.
• Renal water loss: diabetes insipidus (central — pituitary pathology, surgery, trauma; nephrogenic — lithium, hypercalcaemia, hypokalaemia, post-obstructive), osmotic diuresis (hyperglycaemia in DKA/HHS, mannitol, high-protein enteral feeds).
• Excess sodium intake (rare): accidental salt ingestion (paediatric — mandatory child protection notification), iatrogenic hypertonic saline or sodium bicarbonate.

Workup

Urine osmolality discriminates the aetiology:

• Above 700 mOsm/kg → appropriate ADH response → extra-renal water loss or reduced intake.
• 300–700 mOsm/kg → partial diabetes insipidus or osmotic diuresis.
• Below 300 mOsm/kg in the context of polyuria and hypernatraemia → diabetes insipidus (central or nephrogenic — specialist assessment required; water deprivation test with desmopressin differentiates).

Management (eTG; Adrogué and Madias, NEJM 2000)

1. Calculate the free water deficit: 0.6 × body weight (kg) × (serum sodium ÷ 140 − 1) in men; use 0.5 in women and older adults. Add estimated ongoing losses.
2. Correction rate: maximum 10 mmol/L sodium fall per 24 hours for chronic hypernatraemia (above 48 hours). Faster correction (~1 mmol/L/hour) is acceptable for acute hypernatraemia under 48 hours.
3. Replacement fluid: oral or nasogastric free water preferred when alert. IV 5% dextrose (D5W) or 0.45% saline when volume-depleted.
4. Monitor sodium 4–6 hourly initially until stable.
5. Treat the underlying cause: manage central DI with desmopressin (PBS Authority Required); nephrogenic DI with thiazide ± amiloride (plus address lithium toxicity or hypercalcaemia); improve water access in residential care; correct hyperglycaemia.

D. Australian operations

MBS items: Level B (item 23), Level C (item 36), and Level D (item 44) GP consultations — the Level D item is appropriate for the complex hyponatraemia workup combining drug review, volume assessment, endocrine testing, and management planning.

Relevant pathology item groups:

• FBC, UEC, LFT panel: item 65070.
• Serum chemistry panel + osmolality: item 66536.
• Urine sodium, potassium, osmolality: item 73529.
• TSH (item 66716), free T4 (item 66717), serum cortisol (item 66825), ACTH (item 66845).
• 75+ Health Assessment (item 707) and ATSI Health Check (item 715) — both include electrolyte screening review.

PBS considerations:

• Tolvaptan (Samsca) for SIADH: PBS Authority Required, specialist initiation, in-hospital monitoring for initial doses.
• Demeclocycline: NOT PBS-listed in Australia per AMH; access via compounding pharmacy private prescription only — impractical in most Australian settings.
• Oral urea: NOT PBS-listed; compounding pharmacy, private prescription; useful in chronic SIADH when fluid restriction fails but palatability is poor.
• Hydrocortisone and fludrocortisone: General Schedule for adrenal insufficiency-related hyponatraemia.
• Desmopressin: Authority Required for central diabetes insipidus.

Kidney Health Australia (KHA-CARI) provides guidance on electrolyte disorders in CKD applicable to Australian general practice. ACAT assessment (item 92024) is appropriate for frail older adults with recurrent hyponatraemia, polypharmacy, and falls.

Referral thresholds for emergency:

• Sodium below 125 mmol/L with neurological symptoms; sodium below 120 mmol/L regardless of symptoms.
• Acute hypernatraemia above 155 mmol/L with neurological features.
• Suspected adrenal crisis (hyponatraemia + hyperkalaemia + hypotension + context of steroid withdrawal or autoimmune disease).
• Seizure or GCS drop attributable to a sodium disorder.

E. Special populations

Older adults in residential aged care: Hypernatraemia from inadequate hydration and reduced thirst is a recurrent, preventable crisis — particularly during heatwaves. Ensure every RACF patient has a documented hydration plan. Identify high-risk individuals (dementia, reduced mobility, reduced oral intake) and implement proactive UEC monitoring during prolonged heat. Chronic mild hyponatraemia in this group most commonly results from SSRI, thiazide, or opioid prescriptions — medication review is often curative.

Postoperative patients: Post-surgical hyponatraemia from non-osmotic ADH release (pain, nausea, opioids, isotonic IV fluid overload) is the most common cause of iatrogenic hyponatraemia in Australian hospitals. Avoid hypotonic IV fluids in adults postoperatively.

People with alcohol use disorder: Highest ODS risk — alcohol, malnutrition, and hypokalaemia all independently elevate risk. Apply the tighter correction ceiling of 6–8 mmol/L per 24 hours. Concurrently replace thiamine (300 mg IV or IM daily for 3 days, then oral 100 mg daily), B12, folate, and magnesium.

Endurance athletes: Exercise-associated hyponatraemia results from excessive plain water intake during prolonged events. The key message: drink to thirst; use electrolyte-containing sports drinks for events lasting more than 90 minutes; weight gain during exercise indicates over-hydration, not good preparation.

ATSI communities in remote areas: Hypernatraemic dehydration from heat events and limited water access is a preventable cause of hospitalisation. The 715 ATSI Health Check should include fluid access review. Aboriginal Health Worker support for hydration monitoring during extreme heat is integral to preventive care.

Children: Hypernatraemic dehydration in infants (excessive formula concentration, gastroenteritis with inadequate fluid replacement, extreme heat) is a paediatric emergency. Salt poisoning in children requires mandatory child protection notification.

When to escalate

Emergency (call 000):

• Sodium below 125 mmol/L with seizure, coma, vomiting, or GCS below 12.
• Sodium below 120 mmol/L at any level.
• Hypernatraemia above 155 mmol/L with reduced consciousness or acute neurological change.
• Suspected adrenal crisis (hyponatraemia + hyperkalaemia + hypotension + corticosteroid context).
• Seizure or acute neurological deterioration attributable to a sodium disorder.

Urgent specialist referral:

• Euvolaemic hyponatraemia with normal cortisol and TSH — SIADH workup required (small cell lung cancer and CNS pathology must be excluded).
• Suspected diabetes insipidus — central versus nephrogenic differentiation requires specialist assessment and formal water deprivation testing.
• Tolvaptan initiation — specialist and hospital-based.

Routine monitoring:

• Mild asymptomatic hyponatraemia (sodium 130–134 mmol/L) — investigate, review medications, recheck in 1–2 weeks.
• Recurrent hyponatraemia — systematic medication review and specialist input.

What this article is and is not

This is general health information drawn from Australian and international guidelines — Therapeutic Guidelines (eTG), AMH, KHA-CARI, NPS MedicineWise, the ESE 2014 Hyponatraemia Guideline, Sterns NEJM 2015, and Verbalis et al. 2013. It is not personal medical advice and does not create a doctor–patient relationship. All sodium disorder management, correction rate calculations, and medication choices for moderate-to-severe presentations are made by treating clinicians, typically in a hospital setting.

For patient-facing resources: HealthDirect — Dehydration, Better Health Channel — Body fluids, Kidney Health Australia.

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Sources cited

1. Therapeutic Guidelines (eTG) — Nephrology (fluid and electrolyte disorders)
2. Australian Medicines Handbook (AMH)
3. RACGP
4. NPS MedicineWise
5. Kidney Health Australia / KHA-CARI
6. ESE 2014 — Clinical Practice Guideline on Hyponatraemia
7. Sterns — Disorders of Plasma Sodium (NEJM 2015)
8. Verbalis et al. — Diagnosis, Evaluation, and Treatment of Hyponatraemia (Am J Med 2013)
9. Adrogué and Madias — Hypernatraemia (NEJM 2000)
10. Hillier — Hyperglycaemia correction factor for sodium (Am J Med 1999)
11. Renneboog et al. — Mild hyponatraemia and falls (Am J Med 2006)
12. HealthDirect — Dehydration
13. Better Health Channel — Body fluids
14. Kidney Health Australia — patient resources