Postoperative hyponatraemic encephalopathy following elective surgery in children.

Introduction Effects of hyponatraemia on the paediatric central nervous system In the United States, there are an estimated 15 000 deaths per year as a consequence of postoperative Nattie & Edwards (15) studied the effects of acute hyponatraemia (1) (Figure 1). There have been a hyponatraemia on the brain of puppies. They found number of recent studies which have described that acute lowering of plasma sodium from 140 to postoperative hyponatraemic encephalopathy with 120 mmol·l resulted in severe hypoxaemia (arterial death or permanent brain damage (2–6). From these PO2 fell from 11.4–6.9 kPa (88 to 53 mmHg)) and studies, it appears that brain damage associated with cerebral oedema. In contrast to adults, the brains postoperative hyponatraemic encephalopathy of paediatric animals (three day old puppies and primarily affects menstruant women (1) and neonatal rats) were unable to adapt to hypo-osmotic prepubertal children (6). stress by extrusion of cation (15,16). Adaptation of the brain to hyponatraemia occurs as a consequence of the following sequence of events. Postoperative hyponatraemic encephalopathy First, hyponatraemia leads to a movement of water in prepubertal children into brain cells as a result of osmotic forces. In addition, vasopressin which is usually elevated in There are multiple reports of prepubertal children the plasma of hyponatraemic patients (17) may lead suffering brain damage from postoperative to a direct movement of water into brain cells hyponatraemic encephalopathy (6–9). The aetiology independent of the effects of hyponatraemia (18). of the hyponatraemia usually involves a combination The early response of the brain to this hyponatraemiaof: a) intravenous hyponatraemic fluids; b) elevated mediated oedema is the loss of blood and plasma antidiuretic hormone (ADH); c) respiratory cerebrospinal fluid, followed by extrusion of sodium insufficiency secondary to hyponatraemic from brain cells by several pathways (19). Loss of encephalopathy. It has been demonstrated in several potassium and possibly organic osmolytes follows series that plasma levels of ADH (vasopressin, later, in an attempt to decrease brain cell osmolality antidiuretic hormone) are elevated in virtually every without a gain of water (20). postoperative child (7,10–13). If such patients are given intravenous free water (any solution with a sodium concentration below 140 mmol·l), there will Effects of hormones and physical factors on always be a tendency towards postoperative brain adaptation to hyponatraemia hyponatraemia (14). When compared with other groups, prepubertal children are far more susceptible There is a significantly higher intracellular brain to brain damage from hyponatraemia than are adults water content in prepubertal rats in comparison with (6), and recent experimental evidence demonstrates adult rats, suggesting that the brain occupies a greater why this may be the case. percent of the available intracranial volume in young rats (16). Such physical factors may be important determinants of outcome in hyponatraemic rats. As individuals age, there is a progressive decline in the volume of brain, while skull size remains constant Correspondence to: Allen I. Arieff, 299 South Street, Sausalito, CA 94965, USA. in adult life (21). Thus, elderly individuals of both