Key Facts

Hypernatraemia reflects a deficit of total body water relative to sodium. It is almost always associated with impaired thirst mechanism or restricted access to water, as an intact thirst mechanism will normally drive adequate water intake.

Epidemiology

• Present in ~1-2% of hospitalised patients on admission; develops in up to 7% during admission
• More common in elderly, institutionalised, and critically ill patients
• Hospital-acquired hypernatraemia is an independent predictor of mortality

Aetiology

Unreplaced water losses:

• Inadequate intake: elderly, dementia, reduced consciousness, nil by mouth
• Renal losses: diabetes insipidus (cranial or nephrogenic), osmotic diuresis (hyperglycaemia, mannitol)
• GI losses: diarrhoea (especially osmotic), vomiting
• Insensible losses: fever, burns, excessive sweating

Excess sodium:

• IV hypertonic saline or sodium bicarbonate administration (iatrogenic)
• Mineralocorticoid excess (Conn syndrome) – rare cause
• Salt poisoning (rare)

Pathophysiology

• Rising serum osmolality draws water out of cells (cellular dehydration)
• Brain cells compensate over 24-48 hours by generating intracellular osmolytes (idiogenic osmoles)
• Rapid correction of chronic hypernatraemia causes water to move into brain cells → cerebral oedema
• Therefore, chronic hypernatraemia must be corrected gradually

Mild (146-149 mmol/L)

• Thirst (if thirst mechanism intact)
• Dry mucous membranes
• Mild confusion, irritability

Moderate (150-159 mmol/L)

• Lethargy, weakness
• Nausea
• Muscle twitching, hyperreflexia

Severe (≥160 mmol/L)

• Seizures
• Reduced consciousness, coma
• Intracranial haemorrhage (in infants – cerebral venous sinus thrombosis)

Signs of Underlying Cause

• Polyuria, polydipsia → diabetes insipidus
• Reduced skin turgor, tachycardia, hypotension → hypovolaemia
• Fever → increased insensible losses

Red Flags

• Na >160 mmol/L → significant mortality risk
• Seizures or reduced consciousness → urgent correction needed
• Polyuria + hypernatraemia → consider diabetes insipidus
• Hospital-acquired → iatrogenic cause likely

Bedside

• Volume status assessment: mucous membranes, skin turgor, JVP, postural BP
• Fluid balance chart: input and output
• Urine output monitoring

Bloods

• Serum sodium: confirm and grade severity
• Serum osmolality: elevated (>295 mOsm/kg)
• U&Es: assess renal function
• Serum glucose: exclude osmotic diuresis from hyperglycaemia
• Calcium: hypercalcaemia can cause nephrogenic DI

Urine

• Urine osmolality: key discriminator

  • 800 mOsm/kg: appropriate renal response (extrarenal water loss or inadequate intake)

  • <300 mOsm/kg: diabetes insipidus or primary polydipsia
  • 300-800 mOsm/kg: partial DI or osmotic diuresis
• Urine sodium: helps differentiate causes

Special Tests

• Water deprivation test: if diabetes insipidus suspected (measure urine osmolality before and after desmopressin)
• MRI pituitary: if cranial DI confirmed
• Calculate free water deficit: (Na - 140)/140 × total body water (0.6 × weight in kg for men, 0.5 for women)

General Principles

• Treat underlying cause (e.g., stop offending drug, treat infection, control hyperglycaemia)
• Replace free water to correct sodium deficit
• Rate of correction: ≤10-12 mmol/L per 24 hours for chronic hypernatraemia (>48h)
• Acute hypernatraemia (<48h) can be corrected more rapidly (1-2 mmol/L/hour)
• Monitor serum sodium every 4-6 hours during correction

Fluid Replacement

• Oral water is preferred if patient can drink safely
• IV 5% dextrose (free water) if unable to take oral
• IV 0.45% NaCl (half-normal saline) if also hypovolaemic
• IV 0.9% NaCl if severely hypovolaemic/shocked (prioritise haemodynamic stability)

Specific Management

• Cranial diabetes insipidus: desmopressin (DDAVP) 1-4 mcg SC/IV or 10-40 mcg intranasal
• Nephrogenic diabetes insipidus: treat underlying cause; thiazide diuretics (paradoxically reduce urine volume), NSAIDs (indomethacin), low-salt diet
• Osmotic diuresis: correct hyperglycaemia with insulin

Referral Criteria

• Severe hypernatraemia (Na >160) → critical care
• Diabetes insipidus → endocrinology
• Recurrent or unexplained hypernatraemia → endocrinology

• Hospital-acquired hypernatraemia: mortality rate 40-60% (often reflects severity of underlying illness)
• Acute severe hypernatraemia (Na >160): mortality up to 75% in some studies
• Community-acquired hypernatraemia: mortality 20-30%
• Osmotic demyelination does NOT occur with hypernatraemia; the risk is cerebral oedema from overly rapid correction
• Mild hypernatraemia has good prognosis with appropriate fluid replacement
• Chronic diabetes insipidus is well managed with desmopressin in cranial DI

Free Water Deficit Calculation

Free water deficit (L) = TBW × [(Serum Na / 140) - 1]

• TBW = 0.6 × body weight (kg) for men, 0.5 for women
• Example: 70kg man with Na 160 mmol/L: 0.6 × 70 × [(160/140) - 1] = 6L deficit

Diabetes Insipidus Comparison