• Jeffrey E Catrambone, Wenzhuan He, Charles J Prestigiacomo, Tracy K McIntosh, Peter W Carmel, and Allen Maniker.
• Department of Neurological Surgery, UMDNJ, Newark, USA. NJKidsNeurosurg@aol.com.
• Eur J Trauma Emerg S. 2008 Aug 1;34(4):397-409.

AbstractEffective methods for treating cerebral edema have recently become a matter of both extensive research and significant debate within the neurosurgery and trauma surgery communities. The pathophysiologic progression and outcome of different forms of cerebral edema associated with traumatic brain injury have yet to be fully elucidated. There are heterogeneous factors influencing the onset and progress of post-traumatic cerebral edema, including the magnitude and type of head injury, age, co-morbid conditions of the patient, the critical window for therapeutic intervention and the presence of secondary insults including hypoxia, hypotension, hypo/hyperthermia, degree of raised intracranial pressure (ICP), and disruption of blood brain barrier (BBB) integrity. Although numerous studies have been designed to improve our understanding of the etiology of post-traumatic cerebral edema, therapeutic interventions have traditionally been focused on minimizing secondary insults especially raised ICP and improving cerebral perfusion pressure. More recently, fluid resuscitation strategies using hyperosmolar agents such as pentastarch and hypertonic saline (HS) have achieved some success. HS treatment is of particular interest due to its apparent advantageous action over other types of hyper-osmotic solutions in both clinical and laboratory studies. In this review, we provide a summary of recent literature concerning the pathogenesis and mechanisms involved in the various types of cerebral edema, and the possible mechanisms of action of HS for the treatment cerebral edema.

4 keywords...

hide…