EFFECTS OF SUFENTANIL ON CEREBRAL HEMODYNAMICS AND INTRACRANIAL-PRESSURE IN PATIENTS WITH BRAIN INJURY

Background: The current study investigates the effects of sufentanil o n cerebral blood flow velocity and intracranial pressure (ICP) in 30 p atients with intracranial hypertension after severe brain trauma (Glas gow coma scale <6). Methods: Mechanical ventilation (FIo2) 0.25 - 0.4) was adjusted to maintain arterial carbon dioxide tensions of 28-30 mm Hg. Continuous infusion of midazolam (200 mu g/kg/h intravenous) and f entanyl (2 mu g/kg/h intravenous) was used for sedation. Mean arterial blood pressure (MAP, mmHg) was adjusted using norepinephrine infusion (1-5 mu g/min). Mean blood flow velocity (V-mean, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonog raphy system. ICP (mmHg) was measured using an epidural probe. After b aseline measurements, a bolus of 3 mu g/kg sufentanil was injected, an d all parameters were continuously recorded for 30 min. The patients w ere assigned retrospectively to the following groups according to thei r blood pressure responses to sufentanil: group 1, MAP decrease of les s than 10 mmHg, and group 2, MAP decrease of more than 10 mmHg. Result s: Heart rate, arterial blood gases, and esophageal temperature did no t change over time in all patients. In 18 patients, MAP did not decrea se after sufentanil (group 1). In 12 patients, sufentanil decreased MA P >10 mmHg from baseline despite norepinephrine infusion (group 2). IC P was constant in patients with maintained MAP (group 1) but was signi ficantly increased in patients with decreased MAP. V mean did not chan ge with sufentanil injection regardless of changes in MAP. Conclusions : The current data show that sufentanil (3 mu g/kg intravenous) has no significant effect on middle cerebral artery blood flow velocity and ICP in patients with brain injury, intracranial hypertension, and cont rolled MAP. However, transient increases in ICP without changes in mid dle cerebral artery blood how velocity may occur concomitant with decr eases in MAP. This suggests that increases in ICP seen with sufentanil may be due to autoregulatory decreases in cerebral vascular resistanc e secondary to systemic hypotension.