Serum sodium concentration and osmolality are normally under tight physiological control.

Causes¹

• Associated with hypovolaemia and dehydration
  • Dermal losses - for example, burns & excessive sweating
    (Endurance sportsmen and women, particularly under heat stress, are vulnerable. One study suggested that 25% of collapsed marathon runners were hypernatraemic, compared to 9% asymptomatic marathon runners.²)
  • GI losses - for example, diarrhoea and vomiting, fistulas
  • Diuretics
  • Post-obstruction
  • Acute and chronic renal failure
  • Hyperosmolar non-ketotic coma (sodium is often raised, even after correction for glucose)
• Associated with hypervolaemia
  • Iatrogenic - for example:
    • Use of hypertonic saline
    • Tube feeding
    • Intravenous antibiotics containing sodium
    • Hypertonic dialysis
  • Hyperaldosteronism (usually only a mildly elevated sodium).
  • Excess salt ingestion
    • Inadvertent - for example, infant formula error
    • Poisoning
    Salt poisoning in children has a recent controversial history: the diagnosis is difficult to make and evidence from clinical history, acute changes in weight, paired serial blood and urine samples to establish sodium and water excretions and estimates of net sodium and water balances should be collected where suspected.³
• Associated with euvolaemia
  • Diabetes insipidus
  • Hypodipsia
  • Fever
  • Hyperventilation
  • Mechanical ventilation.

Epidemiology

Incidence

Hypernatraemia is found in approximately1% hospital patients⁴ but is relatively rare in primary care.

Risk factors

Sustained hypernatraemia can occur only when thirst or independent access to water is impaired. Consequently those most at risk include:

• Elderly patients - usually associated with infirmity or febrile illness.⁵
• Infants - at risk with diarrhoea and inadequate breastfeeding where poor milk supply or inexperienced mother. 2% hospitalised neonates were found to have hypernatraemic dehydration secondary to exclusive breastfeeding.⁶
• Patients with altered mental status.
• Those with hypothalamic lesions affecting sense of thirst (adipsia).

Presentation⁷

Signs and symptoms are largely related to CNS dysfunction and are most prominent where the increase in sodium concentration is rapid and large.

Symptoms in infants

• Muscle weakness
• Restlessness
• High-pitched crying
• Poor sleeping
• Lethargy & coma
• Convulsions (unusual unless sodium loading or aggressive rehydration has taken place)

Symptoms & signs in the elderly

Generally, there are few symptoms until serum sodium >160 mmol/l and clinical manifestations may be nonspecific and subtle in the early stages.

• Intense thirst initially but dissipating with prolonged disturbance
• Decreased level of consciousness - lethargy, irritability, stupor, coma
• Seizures and twitching
• Hyper-reflexia
• Ataxia
• Tremor
• With hypovolaemia: hypotension, tachycardia.

Studies in the elderly have shown abnormal subclavicular and thigh skin turgor, dry oral mucosa and recent change in consciousness to be most significantly associated with hypernatraemia.⁸

Investigation

In primary care:⁹

• Repeat to confirm a single high serum sodium concentration. Try to establish: is this acute/changing or chronic and stable?
  

  Note: Variation of up to 5 mmol/l may be non-significant. Persistent serum Na+ of 146-148 mmol/l without clinical features of hypovolaemia may simply reflect the patient being a statistical outlier.

• Fluid charts to establish intake and losses.
• Blood glucose to exclude diabetes mellitus.
• Where serum Na⁺ is between 149-154 mmol/l:
  • Check serum potassium, urea, creatinine, calcium and plasma glucose and review these in context of the hypernatraemia.
  • Request urine and serum osmolality if diabetes insipidus is suspected.
  • Seek advice if a clinical cause is not apparent and oral rehydration is not possible in a dehydrated patient.
• Where serum Na⁺ is 154 mmol/l or more, seek specialist advice regarding further investigation and management.

Management

Management aims should be:

1. Diagnose and treat underlying cause (for example, stop GI fluid losses, control pyrexia, hyperglycaemia, withhold lactulose and diuretics, correct feeding preparation).
2. Correct hypertonicity.

Initial assessment

• Hydration status - skin turgor, mucous membranes, change in BP on standing, fontanelles in children.
• Consider causes of hypernatraemia (as above) - often cause is evident from history.
• Where cause is unclear, measure urine osmolality in relation to plasma osmolality and urine sodium concentration.

Correction of hypernatraemia⁷

• Where hypernatraemia has developed very rapidly over a few hours, rapid correction improves prognosis without risk of cerebral oedema. In such patients, it is appropriate to reduce serum sodium concentration by 1 mmol/l per hour using 5% dextrose.
• Where hypernatraemia is of longer or unknown duration, a slower reduction is prudent and a targeted fall of 10mmol/l per day is suggested.
• Preferred route for administering fluids is oral or via a feeding tube. Only where neither is possible should intravenous therapy be used.
• Only hypotonic fluids should be used (pure water, 5% dextrose, 0.2% sodium chloride referred to as 'one-quarter isotonic saline', 0.45% sodium chloride or 'one-half isotonic saline'). The more hypotonic the infusate, the lower the infusion rate required.
• Except where the patient is frankly shocked, 0.9% sodium chloride (isotonic saline) is unsuitable. In these instances, correct free water deficit with isotonic saline switching to hypotonic infusions when stable, normally in a high dependency unit with close monitoring.
• Where there has been hypertonic sodium gain, diuretics and 5% dextrose are required to offload fluid and reduce serum sodium. Where there is concurrent renal failure, haemodialysis or filtration may be required.
• Determine:
  • Fluid requirement (allowing for any water deficit and insensible losses)
  • Required serum sodium concentration fall
  • Appropriate infusate
  • Rate of infusion
• Recheck electrolytes frequently over the correction period.

Complications

Brain shrinkage induced by hypernatraemia can cause vascular rupture with cerebral bleeding, subarachnoid haemorrhage, permanent brain damage and death.
Avoid agressive treatment rehydration with hypotonic fluids in those with prolonged hyperosmolality states as this will lead to cerebral oedema. In prolonged situations, adaptive physiological responses exist whereby the brain gains solutes and restores lost water, normalizing brain volume without correcting hyperosmolality.

Prognosis

Mortality rate depends on the severity of the condition and rapidity of its onset.

• Severe hypernatraemia carries a mortality rate of approximately 40-70% in elderly patients. In practice, it is often difficult to separate contribution of hypernatraemia to mortality from that of underlying illness. The level of consciousness is the single best prognostic indicator associated with mortality in the elderly.⁸
• A retrospective study on critically ill patients in ICU suggests that hypernatraemia is an independent risk factor for mortality. Most cases appear to arise after admission to ICU and, therefore, may be at least partially iatrogenic in origin.¹⁰

Prevention⁵

Health professionals need to be alert to the risk of medical care itself precipitating disorders of sodium and water balance in frail elderly or critically unwell patients. The safest assumption is that disruption is very likely to occur during hospitalisation or in long-term care, making it essential for the medical and nursing teams to pay meticulous attention to fluid balance and to have a low threshold for suspecting and screening for the development of these problems.

To prevent hypernatraemic dehydration in breastfed infants, early weighing and lactation support are suggested in order to detect correctable problems swiftly.¹¹

Document references

1. Reynolds RM, Padfield PL, Seckl JR; Disorders of sodium balance. BMJ. 2006 Mar 25;332(7543):702-5.
2. Kratz A, Siegel AJ, Verbalis JG, et al; Sodium status of collapsed marathon runners. Arch Pathol Lab Med. 2005 Feb;129(2):227-30. [abstract]
3. Coulthard MG, Haycock GB; Distinguishing between salt poisoning and hypernatraemic dehydration in children.; BMJ. 2003 Jan 18;326(7381):157-60.
4. Erasmus RT, Matsua TE; Frequency, aetiology and outcome of hypernatraemia in hospitalised patients in Umtata, Transkei, South Africa.; East Afr Med J. 1999 Feb;76(2):85-8. [abstract]
5. Kugler JP, Hustead T; Hyponatremia and hypernatremia in the elderly.; Am Fam Physician. 2000 Jun 15;61(12):3623-30. [abstract]
6. Moritz ML, Manole MD, Bogen DL, et al; Breastfeeding-associated hypernatremia: are we missing the diagnosis?; Pediatrics. 2005 Sep;116(3):e343-7. [abstract]
7. Adrogue HJ, Madias NE; Hypernatremia.; N Engl J Med. 2000 May 18;342(20):1493-9.
8. Chassagne P, Druesne L, Capet C, et al; Clinical presentation of hypernatremia in elderly patients: a case control study.; J Am Geriatr Soc. 2006 Aug;54(8):1225-30. [abstract]
9. Smellie WS, Heald A; Hyponatraemia and hypernatraemia: pitfalls in testing. BMJ. 2007 Mar 3;334(7591):473-6.
10. Lindner G, Funk GC, Schwarz C, et al; Hypernatremia in the critically ill is an independent risk factor for mortality. Am J Kidney Dis. 2007 Dec;50(6):952-7. [abstract]
11. Iyer NP, Srinivasan R, Evans K, et al; Impact of an early weighing policy on neonatal hypernatraemic dehydration and breast feeding. Arch Dis Child. 2008 Apr;93(4):297-9. Epub 2007 May 2. [abstract]

Internet and further reading

• Pham TQ; Hypernatraemia. eMedicine, Feb 2007.

Acknowledgements