OBJECTIVE: We have employed bedside multimodality methods to assess the influence of a slow (20 min) bolus of hypertonic mannitol on cerebral hemodynamics in comatose patients with head injuries. METHODS: Middle cerebral artery flow velocities (FV) and cortical microcirculatory flows were measured in comatose patients with head injuries after the administration of 200 ml of 20% mannitol. A comparison was made with the effects of an identical bolus of isotonic saline. Fourteen patients with diffuse head injuries and with raised intracranial pressure were selected, and mannitol infusion studies were conducted when clinically indicated (n = 23). Using transcranial doppler and laser doppler flowmetry (LDF), indices of estimated cerebrovascular resistance (eCVR) were calculated for the macro- (eCVR-FV) and micro- (eCVR-LDF) circulation. RESULTS: During mannitol infusion, a significant rise in cerebral perfusion pressure was detected (+10%, P = 0.03) as a result of a fall in intracranial pressure (-21%, P = 0.001). Increases in both FV (+13%, P < 0.001) and LDF (+14%, P = 0.002) occurred only after the administration of mannitol and persisted beyond completion of infusion. The effect on FV and LDF decayed exponentially, with a time constant of 34.0 and 38.0 minutes, respectively, and was independent of the pressure autoregulatory status. There was a tendency for eCVR-FV and eCVR-LDF to decrease. No significant effects resulted from the administration of saline. CONCLUSION: Bedside multimodality monitoring may provide a useful means for assessing the effects of therapy in the comatose patient. The mechanisms by which mannitol reduces intracranial pressure in patients with head injuries are discussed.
OBJECTIVE: We have employed bedside multimodality methods to assess the influence of a slow (20 min) bolus of hypertonic mannitol on cerebral hemodynamics in comatose patients with head injuries. METHODS: Middle cerebral artery flow velocities (FV) and cortical microcirculatory flows were measured in comatose patients with head injuries after the administration of 200 ml of 20% mannitol. A comparison was made with the effects of an identical bolus of isotonic saline. Fourteen patients with diffuse head injuries and with raised intracranial pressure were selected, and mannitol infusion studies were conducted when clinically indicated (n = 23). Using transcranial doppler and laser doppler flowmetry (LDF), indices of estimated cerebrovascular resistance (eCVR) were calculated for the macro- (eCVR-FV) and micro- (eCVR-LDF) circulation. RESULTS: During mannitol infusion, a significant rise in cerebral perfusion pressure was detected (+10%, P = 0.03) as a result of a fall in intracranial pressure (-21%, P = 0.001). Increases in both FV (+13%, P < 0.001) and LDF (+14%, P = 0.002) occurred only after the administration of mannitol and persisted beyond completion of infusion. The effect on FV and LDF decayed exponentially, with a time constant of 34.0 and 38.0 minutes, respectively, and was independent of the pressure autoregulatory status. There was a tendency for eCVR-FV and eCVR-LDF to decrease. No significant effects resulted from the administration of saline. CONCLUSION: Bedside multimodality monitoring may provide a useful means for assessing the effects of therapy in the comatose patient. The mechanisms by which mannitol reduces intracranial pressure in patients with head injuries are discussed.