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Nephrol Dial Transplant (2003) 18: 2486-2491
© 2003 European Renal Association-European Dialysis and Transplant Association


Invited Comment

The pathophysiology and treatment of hyponatraemic encephalopathy: an update

Michael L. Moritz1 and J. Carlos Ayus2

1Division of Nephrology, Department of Pediatrics, Children’s Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA and 2Division of Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA

Correspondence and offprint requests to: Juan C. Ayus, MD, Mail code 7882, Floyd Curl Drive, San Antonio, TX 78229-3900, USA. Email: ayus@uthscsa.edu

Keywords: brain damage; demyelination; encephalopathy; hyponatraemia; hyposmolaity

The first 150 words of the full text of this article appear below.



   Introduction
 
Hyponatraemia is a common disorder that occurs in both the out-patient and in-patient setting. Hyponatraemic encephalopathy can be difficult to recognize, as the most frequent symptoms are non-specific and can easily be incorrectly attributed to other causes. The patient usually presents with headache, nausea, vomiting and confusion, but can present with seizures, respiratory arrest and non-cardiogenic pulmonary oedema [1]. Over the past two decades, risk factors other than changes in the serum sodium level have been found to play a major role in the development of hyponatraemic encephalopathy, such as age, gender and hypoxia.



   Pathogenesis of hyponatraemia
 
Hyponatraemia is defined as a serum sodium <135 mEq/l. Under normal circumstances, the human body is able to maintain the plasma sodium within the normal range (135–145 mEq/l) despite wide fluctuations in fluid intake. The body’s primary defence against developing hyponatraemia is the kidney’s ability to generate a dilute urine and excrete free water. . . . [Full Text of this Article]

Hospital-acquired hyponatraemic encephalopathy
Prophylaxis against hospital-acquired hyponatraemic encaphalopathy
Hyponatraemic encephalopathy in the out-patient setting


   Risk factors for developing hyponatraemic encephalopathy
 
Age (Figure 1) [13]
Gender
Hypoxia (Figure 2) [13]


   Does rapid correction of hyponatraemia lead to brain damage?
 


   Treatment of hyponatraemic encephalopathy
 


   Special problems in the treatment of hyponatraemia
 
Future trends in the treatment of hyponatraemic encephalopathy

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