HYPERNATRAEMIA DEFINITION A serum sodium concentration greater than 145 mmol/L (mEq/L). TOXIC CAUSES Secondary to insufficient water intake CNS depression from toxic cause Toxic delirium Secondary to excessive water loss Cholinergic syndrome with severe sweating Drug-induced nephrogenic diabetes insipidus Lithium Demeclocycline Lactulose Laxatives Mannitol Severe gastroenteritis from toxic cause Secondary to excessive sodium ingestion Penicillins (some) Sodium Chloride Sodium Valproate NON-TOXIC CAUSES Diabetes insipidus Environmental exposure with dehydration Hyperglycaemia leading to osmotic diuresis Iatrogenic (hypertonic fluid administration, inadequate free water) Interstitial nephritis Polyuric phase of renal failure (eg, after relief of prolonged urinary obstruction) CLINICAL FEATURES Delirium and decreased level of consciousness may occur with severe hypernatraemia. Associated illness or circumstances of exposure may result in hypovolaemia and hypotension. Patients with heat exposure may also be hyperpyrexic. DIFFERENTIAL DIAGNOSIS None RELEVANT INVESTIGATIONS Serum sodium Serum potassium, chloride, and bicarbonate Renal function tests (urea, creatinine) Blood glucose (to exclude hyperglycaemia as a cause of free water loss) Serum calcium and magnesium Urine sodium Urine osmolality (This is the most useful test to determine the cause of hypernatraemia. Patients who are dehydrated but with normal renal function usually have an elevated urine osmolality [greater than 400 mOsm/kg]. Patients with impaired ADH secretion or reduced responsiveness of the kidney to ADH, will usually have a urine osmolality of less than 250 mOsm/kg.) TREATMENT Use caution, as overly rapid correction of serum sodium can lead to cerebral oedema. The goal of treatment should be to correct the serum sodium at a rate no faster than 1 mmol/L/hour or 25 mEq/L/day. In asymptomatic patients, a rate of 0.5 mmol/L/hour is acceptable. Obtain frequent measurements of the serum sodium and adjust treatment accordingly. Patients with hypovolaemia should be initially treated with intravenous isotonic saline. Once volume is restored, this should be changed to half-normal saline with dextrose. Patients with normovolaemic hypernatraemia may be treated with oral water administration or intravenous 5% dextrose solution. Patients who are hypervolaemic may need a loop diuretic such as furosemide to remove excess volume. Patients with lithium-induced nephrogenic diabetic insipidus who do not improve after discontinuation of lithium may be treated with indomethacin, 50 mg every 8 hours, and hydrochlorothiazide 50 to 100 mg/day. CLINICAL COURSE AND MONITORING Follow volume status and electrolytes carefully, and avoid overly rapid correction of the serum sodium. Patients should be monitored for altered mental status and coma. LONG-TERM COMPLICATIONS Overly rapid correction of hypernatraemia may cause cerebral oedema and permanent brain damage. AUTHOR(S)/REVIEWERS Author: Dr Kent R. Olson, University of California, San Francisco, USA (February 1999). Reviewers: Birmingham 3/99: B Groszek, H Kupferschmidt, N Langford, K Olson, J Pronczuk.