Hypoxemia is a major factor contributing to brain damage in patients with hyponatremia (AyyS.,.§D.d.,.AIief!,1.995.; AyyS.,aDd.,Arie.fL1996). From a clinical standpoint, a hypoxic episode (such as respiratory arrest) frequently complicates hyponatremic encephalopathy and is the critical event which determines the likelihood of survival without permanent brain damage. If the patient has intact cognitive responses to verbal stimuli and does not have respiratory insufficiency, complete recovery is possible following appropriate active therapy (AIyS,M...§L 1992). Hypoxia impairs several pathways for homeostatic brain ion transport, decreasing the effectiveness of the brain's compensatory adaptation to hyponatremia. Respiratory arrest often occurs abruptly in patients with hyponatremic encephalopathy, and such patients infrequently survive without permanent brain damage (Ayus., „and.. ..Arieff. .1995). The most frequent prelude to respiratory arrest is delayed initiation of therapy in a symptomatic patient. Since the possibility of hypoxia complicating symptomatic hyponatremia far exceeds that of brain injury due to inappropriate therapy ( Fig 1), there is essentially no modern medical rationale for failure to treat patients with symptomatic hyponatremia actively.
Fig. 1 The major risk factors associated with permanent brain damage among 958 hospital in-patients with hyponatremia (serum sodium below 128 mmol/l). Most patients (96 per cent) suffered a hypoxic episode because of failure to initiate active therapy in a timely manner. In only 4 per cent of patients suffering permanent brain damage could improper therapy for hyponatremia be implicated in the outcome. The incidence of hyponatremic encephalopathy in 11 published series from our laboratory comprising the 958 hospital in-patients with hyponatremia was 23 per cent (220/958). The overall morbidity among patients with hyponatremic encephalopathy was 15 per cent.
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