The actual brain tissue (1300 mL in a 'typical' adult) is subject to swelling due both to the accumulation of intracellular (1100 ml) and extracellular (200 mL) water, i.e., brain edema. Brain injury is classically associated with predominantly intracellular, or 'cytotoxic,' edema, as opposed to the extracellular, or 'vasogenic,' edema associated with brain tumors.
1. Osmotic diuretics such as mannitol (1 gm/kg body weight as first dose in the face of impending herniation; 0.25 gm/kg every 2 hours as needed to reduce elevated ICP) are the principal therapy for cytotoxic brain edema in severe head injury. Due to the relatively intact blood-brain barrier in head injury, mannitol is retained in the intravascular space and creates an osmotic gradient-shifting extracellular water back into the vascular system. However, mannitol may contribute to local brain swelling in
severely contused regions with a defective blood-brain barrier, may exacerbate neurogenic pulmonary edema, and may cause hypotension secondary to diuresis and thereby actually worsen rather than improve cerebral blood flow. Serum sodium, potassium and osmolarity should be checked every 6 hours when using mannitol. Mannitol may be discontinued if serum osmolarity reaches 320, to avoid renal damage.
2. Loop diuretics such as Lasix (1 mg/kg) enhance the effects of mannitol. Urine output should be replaced with isotonic crystalloid or colloid solutions to avoid dehydration and hypotension. Systemic euvolemia is the goal.
3. Use of isotonic fluids. Free water in hypotonic IV fluids may exacerbate brain edema.
4. Maintenance of normoglycemia. Although the scientific evidence is mixed, hyperglycemia in severely head-injured patients may exacerbate brain injury through osmotic and/or metabolic mechanisms. Evidence for this effect is strongest in the developing nervous system.
5. Maintenance of normotension (see above) using appropriate fluid resuscitation with supplemental pressors if necessary. Systemic arterial hypotension exacerbates cerebral ischemia, worsens cerebral edema, may cause secondary increases in ICP, and significantly worsens outcome.
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