cerebral resuscitation


Brain edema is an excess accumulation of water in the intracellular and/or extracellular spaces of the brain and can be divided into vasogenic and cytotoxic

Vasogenic brain edema is caused by disruption of the blood brain barrier

Meanwhile, Cytotoxic edema is characterized by accumulation of water inside the neurons, microglia and astrocytes

Goal of medical management for cerebral edema is to maintain regional and global cerebral blood flow to meet the metabolic requirement and prevent secondary neuronal injury from cerebral ischemia

1) Elevation of head end of bed 15-30 degrees promote cerebral venous drainage. Head is kept in midline to limit neck vein compression. Bed is not tilted in acute carotid or basilar artery occlusion to avoid hypo perfusion distal to occlusion

2) Close monitoring of BP is important sign for increase in ICP (Cushing effect). Keep cMAP more than 65 (MAP - ICP)

3) Surgical decompression and use of osmotherapy to reduce brain edema and its deleterious effect remain the mainstay of treatment even today

4) Mannitol remains as the best choice osmotic agent for osmotherapy. it decrease brain volume by decreasing overall water content, reduce blood volume by vasoconstriction, reduce CSF volume, improve cerebral perfusion by decreasing viscosity or altering red blood cell rheology and exert a protective effect against biochemical injury

5) Loop diuretic, IV Furosemide 0.7 mg/kg can be add to prolong osmotic effect

6) Hypertonic saline is about as effective as mannitol (certainly not more) and is safe and effective alternative to mannitol.

7) Prophylactic and prolonged hyperventilation maneuvers are not recommended during the first 24 hours because CBF is reduced at this time after trauma

8) Prolonged pulmonary hyperventilation must be avoided in the absence of high ICP as sustains vasoconstriction reduces CBF to deleterious levels and could generate brain ischemia

9) There is worse prognosis in severe TBI, routinely treated with hyperventilation

10) Hyperventilation becomes appropriate in the treatment of difficult to control ICH, CBF at normal level or high at onset of ICH and when brain deterioration with suspicion of intracranial mass lesion has occurred

11) Fluid restriction minimally affects cerebral edema and, if pursued to excess, may result in episodes of hypotension, which may increase ICP and is associated with worse neurologic outcome

12) Glucose containing solutions should be avoided

13) Glycerol can be given 30 ml every 4-6 hour or daily IV 50g in 500 ml of 2.5% saline solution

14) Corticosteroid is less effective in cytotoxic edema, and is not recommended in treatment of edema secondary to stroke or hemorrhage. Besides, systemic complications of steroids can worsen the patient’s condition

15) Inj. Dexamethasone 4-6 mg IM every 4-6 hours may be used if there is documented evidence of cerebral vasculitis, acute bacterial meningitis and chronic meningitis

16) Glucocorticoid are used for the management of malignant brain tumors exert their influence on brain tumors mainly by reducing tumor-associated vasogenic edema, probably by decreasing the increased capillary permeability of blood brain barrier

17) Randomized clinical trials are in progress to establish the safety and efficacy of prolonged cerebral hypothermia.

18) Barbiturates, Procaine derivatives, Indomethacin, Propofol and THAM (Thrometamine) are not being used routinely in present practice

19) EEG is not very helpful in the management of cerebral edema


1) Abhishek Patro & Sureswar Mohanty, "Pathophysiology and treatment of traumatic brain edema, Indian Journal of Neurotrauma", Vol 6, No 1,2009.
2) Bhavneet Bharti, "Hypertonic Saline Treatment in Cerebral Edema –Is the Evidence Sufficient?", Indian Pediatrics, Vol 45, June 17, 2008
3) Matheus Oliveira-Abreu & Lajana de Almeida, 'Management of mechanical ventilation in brain injury: hyperventilation and positive end-expiratory pressure", Rev Bras Ter Intensiva, 21(1):72-79, 2009
4) SK Jha Lt Col (Retd), "Cerebral Edema and its Management", MJAFI 2003; 59 : 326-331

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