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.
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]
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. Hypernatraemic dehydration secondary to exclusive breast-feeding is an increasingly recognised problem. Estimates of prevalence range from 1 in 200 to 1 in 1,400 babies.
- Patients with altered mental status.
- Those with hypothalamic lesions affecting sense of thirst (adipsia).
- Those with critical illness causing acute kidney injury and consequent inability to concentrate urine, or dependency on intravenous fluids.
- Pure free water loss (dehydration):
- Inadequate water intake.
- Diabetes insipidus (DI) - either cranial or nephrogenic in origin.
- Thirst impairment:
- Hypothalamic lesions can impair osmoreceptor function or the thirst response.
- Hypotonic fluid loss (dehydration + hypovolaemia):
- Dermal losses:
- 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.
- Gastrointestinal losses:
- In stool - non-secretory diarrhoea, laxative abuse.
- Nasogastric drains.
- Urinary losses:
- Loop diuretics.
- Osmotic diuresis - eg, hyperglycaemic states.
- Acute tubular necrosis (polyuric early stage).
- Dermal losses:
- Hypertonic sodium gain (may cause hypervolaemia):
- 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, and a type of non-accidental injury. This is thought to be very rare in the UK. The minimum amount of salt that could be fatal to an infant or child is likely to be in the range of 0.75 to 3 g/kg (approximately 13 to 51 mmol) body weight.
- 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).
In older people, symptoms and signs may not always be classical. 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.
- Check serum sodium, potassium, urea, creatinine, calcium and plasma glucose.
- Request lithium levels where appropriate. Hypernatraemia reduces lithium elimination and increases the risk of toxicity.
- Request urine and serum osmolality if DI is suspected; in this case there would be a high serum osmolality (>300 mOsm/kg) combined with an inappropriately dilute urine (less than serum osmolality).
- Neuroimaging where indicated clinically.
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.
- 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
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.
- 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.
- 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 loss of renal function 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.
- 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. Also convulsions and permanent brain injury may occur.
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.
- Studies on critically ill patients in ICU suggest 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, 13]
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. 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.
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