• Michael N Diringer, Michael T Scalfani, Allyson R Zazulia, Tom O Videen, Rajat Dhar, and William J Powers.
• Department of Neurology, Neurology/Neurosurgery Intensive Care Unit, Washington University School of Medicine, St. Louis, Missouri 63110, USA. diringerm@wustl.edu
• Neurosurgery. 2012 May 1;70(5):1215-8; discussion 1219.

BackgroundMannitol has traditionally been the mainstay of medical therapy for intracranial hypertension in patients with head injury. We previously demonstrated that mannitol reduces brain volume in patients with cerebral edema, although whether this occurs because of a reduction in brain water, blood volume, or both remains poorly understood.ObjectiveTo test the hypothesis that mannitol acts by lowering blood viscosity leading to reflex vasoconstriction and a fall in cerebral blood volume (CBV).MethodsWe used O positron emission tomography to study 6 patients with traumatic brain injuries requiring treatment for intracranial hypertension. Cerebral blood flow (CBF), CBV, and cerebral metabolic rate for oxygen (CMRO2) were measured before and 1 hour after administration of 1.0 g/kg 20% mannitol.ResultsCBV rose from 4.1 ± 0.4 to 4.2 ± 0.2 mL/100 g (P = .3), while intracranial pressure fell from 21.5 ± 4.9 to 13.7 ± 5.1 mm Hg (P < .003) after mannitol. Blood pressure, PaCO2, oxygen content, CBF, and CMRO2 did not change.ConclusionA single bolus of 1 g/kg of 20% mannitol does not acutely lower CBV. Another mechanism, such as a reduction in brain water, may better explain mannitol's ability to lower intracranial pressure and reduce mass effect.

23 keywords...

hide…