HYPERNATRAEMIA: A PREVENTABLE CAUSE OF ACQUIRED BRAIN DAMAGE?

HYPERNA-rRAEMlA (defined as a plasma sodium level greater than 150meq/l) has been shown to be the most common electrolyte abnormality in dehydrated infants with gastroenteritis'. It has been found in 47 (63 per cent) of 75 dehydrated babies whose illness was severe enough to warrant electrolyte measurement. 16 of the 75 infants (20 per cent) had plasma sodium values greater than 160meq/l.l FINBERG and HARRISON', in a review of seven years experience i n the management of infantile diarrhoea, reported a 25 per cent incidence of hypernatraemia. MACAULAY and BLACKHALL3 found hypernatraemia in 30 of 100 patients with gastroenteritis. They also reviewed the literature and found the incidence to vary between 1 1 and 34 per cent in I I reports (it was 71 per cent in a single paper). Hypernatraemia is most commonly observed in gastroenteritis, but it may also complicate infections of the respiratory and urinary tracts. These illnesses are often accompanied by gastrointestinal symptoms and they may be more common causes of hypernatraemia than has been recognised hitherto. If this were only a common biochemical disorder needing correction, little interest might be excited. However, R A P O P O K T ~ first recorded the association between high plasma sodium levels and neurological symptoms in the absence of gross central nervous system pathology. Other workers23, 5* confirmed these observations and FINBERG et published supporting experimental work. Clinical features of the acute stage include irritability. sleeplessness, increased muscle tone and a high-pitched 'cerebral' cry. Convulsions also occur, often during the period of therapy rather than at presentation. The cerebrospinal fluid has no characteristic abnormal features at this time. MORRIS-JONES et a/.N found neurological symptoms in 18 (36 per cent) of 50 hypernatraemic children, of whom 39 were aged less than one year. They also found that the likelihood of convulsions occurring was related to the degree of hypernatraemia. At plasma sodium levels less than 158meq/l, the risk was 10 per cent: at or above this concentration the risk was 71 per cent. Ten children (20 per cent) died and autopsy revealed cerebral oedema and haemorrhage in five; three of these children also had cerebral venous or sinus thrombosis. One further patient had extensive cerebral infarction. MACAULAY and WA.I-SON~ found neurological signs in 22 per cent of patients with plasma sodium 160meq/l or more, but only in 14 per cent of those whose sodium values were below this.