Pathogenesis of Hyponatremic Encephalopathy Current Concepts Allen I. Arieff, M.D., J. Carlos Ayus, M.D.  CHEST  Volume 103, Issue 2, Pages 607-610 (February 1993) DOI: 10.1378/chest.103.2.607 Copyright © 1993 The American College of Chest Physicians Terms and Conditions

Figure 1 Types of brain damage associated with hyponatremia. The first type, hyponatremic encephalopathy, results from the combined effects of brain swelling with pressure of the brain on the rigid skull, increased intracranial pressure leading to a decline in cerebral blood flow, and systemic hypoxemia leading to cerebral hypoxia, and often cerebral herniation. Hyponatremic encephalopathy accounts for almost all brain damage in patients with hyponatremia. The second entity is brain damage associated with therapy for hyponatremia. Treatment with hypertonic NaCl to elevate serum sodium, either to hypernatremic levels or by more than 25 mmol in the initial 2 days of therapy, can lead to brain damage. This mechanism for brain damage is very rare and is separate from that for hyponatremic encephalopathy. CHEST 1993 103, 607-610DOI: (10.1378/chest.103.2.607) Copyright © 1993 The American College of Chest Physicians Terms and Conditions

Figure 2 Results of prospective therapy in 164 adult and pediatric patients from three countries who underwent rapid correction (rate above 0.6 mmol/L per hour) of severe symptomatic hyponatremia. None had respiratory insufficiency prior to the start of therapy. All were treated with either hypertonic NaCl, isotonic NaCl, or isotonic NaCl plus furosemide. The serum sodium was increased from an initial value of 112 mmol/L to a final value after 24 to 48 h of 132 mmol/L. The absolute change after 24 to 48 h was 20 mmol/L. All patients survived without evidence of morbidity, regardless of whether the hyponatremia was acute or chronic. CHEST 1993 103, 607-610DOI: (10.1378/chest.103.2.607) Copyright © 1993 The American College of Chest Physicians Terms and Conditions