Hypernatraemia

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Hypernatraemia is defined as a serum sodium concentration exceeding 145 mmol/L. Serum sodium concentration, and hence osmolality, is normally kept from rising significantly by the release of antidiuretic hormone (ADH) or vasopressin which limits water losses, and the stimulation of thirst which increases water intake. Hypernatraemia from free water loss causes dehydration as intracellular water is drawn out of cells into the extracellular fluid (ECF) preserving the latter to a large extent; however, if sodium is lost as well as water then significant hypovolaemia (reduction in ECF volume) can also occur. Severe symptoms are usually only found with acute and large rises in sodium plasma concentration above 160 mmol/L.

Incidence

Hypernatraemia is relatively rare in primary care, and more common in hospital where the homeostatic mechanisms are more likely to be impaired or subverted by intravenous fluids. This is particularly true in critically ill patients as shown by two large studies where 9% and 26% of patients had or developed hypernatraemia during an ICU admission.[1][2]

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Risk factors

Sustained hypernatraemia generally occurs when thirst or independent access to water is impaired. Consequently, those most at risk include:

  • Elderly patients - usually associated with infirmity or febrile illness.
  • Infants - at risk with diarrhoea and inadequate breast-feeding, where there is a poor milk supply or an inexperienced mother. 2% of hospitalised neonates were found to have hypernatraemic dehydration secondary to exclusive breast-feeding.[3]
  • Patients with altered mental status.
  • Those with hypothalamic lesions affecting sense of thirst (adipsia).
  • Pure free water loss (dehydration):
    • Inadequate water intake.
    • Diabetes insipidus (DI) - either cranial or nephrogenic in origin.
    • Thirst impairment:
      • Geriatric hypodipsia.
      • Hypothalamic lesions can impair osmoreceptor function or the thirst response.
  • Hypotonic fluid loss (dehydration + hypovolaemia):
    • Dermal losses.
      • 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 with 9% asymptomatic marathon runners.[6]
    • Gastrointestinal losses.
      • In stool - non-secretory diarrhoea, laxative abuse.
      • Vomiting.
      • Nasogastric drains.
      • Fistulas.
    • Urinary losses.
      • Diuretic abuse.
      • Osmotic diuresis, eg hyperglycaemic states.
  • Hypertonic sodium gain (may cause hypervolaemia):
    • Iatrogenic:
      • Use of hypertonic saline.
      • Tube feeding.
      • Intravenous antibiotics containing sodium.
      • Intravenous sodium bicarbonate.
      • Hypertonic dialysis.
      • Use of isotonic saline to replace losses in osmotic diuresis.
    • Excess salt ingestion:
      • Inadvertent - for example, infant formula error.
      • Poisoning - more common in children. A single a teaspoon of table salt (~100 mmol sodium could raise an infant's serum sodium by 15-30 mmol/L).
    • Hyperaldosteronism (usually only a mildly elevated sodium).
  • Intracellular shift of water (rare):
    • Very strenuous exercise or electroshock-induced seizure causes a transient rise in cell osmolality and thus water moves into cells.

In DI there is typically thirst, polydipsia and polyuria. Other signs and symptoms in hypernatraemic states relate mainly to CNS dysfunction (lethargy, weakness, confusion, irritability, myoclonic jerks and seizures) or to dehydration and hypovolaemia (dry mouth, abnormal skin turgor, oliguria, tachycardia, orthostatic hypotension). Studies in the elderly have shown abnormal subclavicular and thigh skin turgor, dry oral mucosa and recent change in consciousness to be significantly associated with hypernatraemia.[8]

  • Check serum sodium, potassium, urea, creatinine, calcium and plasma glucose.
  • Request lithium levels where appropriate.
  • Request urine and serum osmolality if DI is suspected; there should be a high serum osmolality (>300 mOsm/kg) combined with an inappropriately dilute urine (less than serum osmolality). Aims are to:
    • Treat any underlying disorder if possible.
    • Correct dehydration by replacing free water losses.
    • Correct hypovolaemia, if present, by giving electrolytes in addition to free water.

    Assess severity[9][10]

    • Repeat the blood test to confirm the true result, and exclude pseudohypernatraemia which may occur with hypoproteinaemic states and some methods of serum sodium measurement.
    • Try to establish whether this is an acute and rapidly changing or chronic and stable picture; this and the patient's clinical condition are generally more important than the absolute serum sodium value in determining action.
    • Seek specialist advice if a clinical cause is not apparent, oral rehydration is not possible, or where serum sodium is 155 mmol/l or more.

    Correction of hypernatraemia[5][7]

    • Address the underlying cause where possible - for example, stop gastrointestinal fluid losses, control pyrexia, correct hyperglycaemia, withhold lactulose and diuretics. This may be sufficient to reverse the hypernatraemia.
    • Where active correction of hypernatraemia is to be undertaken, fluids should be administered orally or enterally and intravenous therapy used only as a last resort.
    • The keys to hypernatraemia management are regular monitoring of the patient and the serum sodium, and then adjusting the hypotonic (relative to the patient's serum sodium) infusion accordingly.
    • Determine:
      • Fluid requirements:
        • Water deficit.
          This is the amount of free water required to return the serum sodium to normal and can be estimated by the formula:
          Water deficit (L) = TBW x ((serum [Na+] (mmol/L)/145) - 1)

          Where TBW is the total body water which depends on the fat content of the body and varies with age and sex. Hence, to calculate the TBW, multiply the lean body weight (kg) by:
          • 0.6 for children, adult men.
          • 0.5 for adult women and elderly men.
          • 0.45 for elderly women.
          However, if sodium is lost in addition to free water (as in hypotonic fluid loss) then the total water deficit will be more than this.
        • Ongoing measured and insensible fluid losses.
          It can be useful in some cases to calculate the ongoing free water loss in the urine from the electrolyte-free water clearance (EFWC):
          EFWC = volume of urine (1 - ((urinary [Na+] + urinary [K+] + urinary glucose/2)/ serum [Na+])) Where volumes are in L and concentrations in mmol/L.
      • Rate of correction:
        • Where hypernatraemia is known to be chronic (>24 hours) or of unknown duration, avoid correction faster than 0.5 mmol/L/hour or 10-12 mmol/L/day. For example:
          Initial free water replacement rate = water deficit x desired daily [Na+] reduction/desired total [Na+] reduction
        • Where hypernatraemia has developed very rapidly over a few hours, rapid correction decreases the risk of osmotic demyelination and improves prognosis without risk of cerebral oedema. In these patients it is appropriate to reduce serum sodium concentration to near normal values within 24 hours.
      • Appropriate fluids:
        • If significantly hypovolaemic (eg shocked), use isotonic fluid (0.9% saline) to restore circulating volume.
        • If hypervolaemic from hypertonic sodium gain, give diuretics and 5% dextrose to offload fluid and provide free water.
        • Where there is concurrent renal failure and/or the serum sodium is extremely elevated (>170 mmol/L) consider haemodialysis or filtration.
        • Otherwise, give hypotonic fluids (0.45% saline, 5% dextrose, oral water), but note that any sodium- or potassium-containing fluid will only provide a proportion of its volume as free water. For example, 0.45% saline is 50% free water, and 0.45% saline + 40 mmol/L KCl is just 25% free water.
      • Progress:
        • Monitor the patient and recheck electrolytes frequently over the correction period, altering the rate or hypotonic fluid used in order to maintain the desired correction rate.
  • Cerebral bleeding, subarachnoid haemorrhage, permanent brain damage and death secondary to brain shrinkage with acute hypernatraemia.
  • Cerebral oedema with overfast correction of chronic hypernatraemia.

The mortality rate depends on the severity of the condition and the 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.[1]

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 breast-fed infants, early weighing and lactation support are suggested in order to detect correctable problems swiftly.[11] Daily weights and a 'rule of thumb' of referring infants that lose more than 10% of body weight in the first postnatal week are widely used, although some argue that the use of charts for relative weight change is a better screening strategy.[12]

Further reading & references

  1. 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.
  2. Stelfox HT, Ahmed SB, Khandwala F, et al; The epidemiology of intensive care unit-acquired hyponatraemia and hypernatraemia Crit Care. 2008;12(6):R162. Epub 2008 Dec 18.
  3. Moritz ML, Manole MD, Bogen DL, et al; Breastfeeding-associated hypernatremia: are we missing the diagnosis?; Pediatrics. 2005 Sep;116(3):e343-7.
  4. Reynolds RM, Padfield PL, Seckl JR; Disorders of sodium balance. BMJ. 2006 Mar 25;332(7543):702-5.
  5. Wakil A, Atkin SL; Serum sodium disorders: safe management. Clin Med. 2010 Feb;10(1):79-82.
  6. Kratz A, Siegel AJ, Verbalis JG, et al; Sodium status of collapsed marathon runners. Arch Pathol Lab Med. 2005 Feb;129(2):227-30.
  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.
  9. Smellie WS, Heald A; Hyponatraemia and hypernatraemia: pitfalls in testing. BMJ. 2007 Mar 3;334(7591):473-6.
  10. Smellie WS, Hampton KK, Bowley R, et al; Best practice in primary care pathology: review 8. J Clin Pathol. 2007 Jul;60(7):740-8. Epub 2006 Dec 15.
  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.
  12. van Dommelen P, van Wouwe JP, Breuning-Boers JM, et al; Reference chart for relative weight change to detect hypernatraemic dehydration. Arch Dis Child. 2007 Jun;92(6):490-4. Epub 2006 Jul 31.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Adrian Bonsall
Current Version:
Peer Reviewer:
Dr Laurence Knott
Last Checked:
20/02/2012
Document ID:
1364 (v23)
© EMIS