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CC BY-NC-ND 4.0 · J Neuroanaesth Crit Care 2016; 03(04): S22-S28
DOI: 10.4103/2348-0548.174731
Conference Proceeding
Thieme Medical and Scientific Publishers Private Ltd.

Cerebral oedema: Pathophysiological mechanisms and experimental therapies

Shalvi Mahajan
1   Department of Anaesthesia and Intensive Care, Division of Neuroanaesthesia, PGIMER, Chandigarh, India
,
Hemant Bhagat
1   Department of Anaesthesia and Intensive Care, Division of Neuroanaesthesia, PGIMER, Chandigarh, India
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Publikationsdatum:
05. Mai 2018 (online)

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INTRODUCTION

Cerebral oedema per se is not a disease entity. It is a clinico-pathological state that is characterised by an increase in brain water content (above the normal brain water content of approximately 80%). It usually occurs in response to brain insult which is seen in a variety of neurological and non-neurological conditions. Cerebral oedema increases brain volume. Because brain is confined within rigid skull, increase in brain water content ultimately results in raised intracranial pressure (ICP). Raised ICP decreases cerebral perfusion pressure leading to cerebral ischemia. In addition, cerebral oedema may result in brain herniation due to the associated mass effect. Management of cerebral oedema is a great challenge for both the neurosurgeons and neuroanaesthetists as current treatment modalities are largely symptomatic. They range from general measures to osmotherapy, barbiturate coma, steroids and decompressive craniectomy. Though oedema-targeted therapies are being specifically designed, they remain more or less as experimental models.

 

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