Early postoperative cognitive recovery and gas exchange patterns after balanced anesthesia with sevoflurane or desflurane in overweight and obese patients undergoing craniotomy: a prospective randomized trial.

Overweight and obese patients are at especially high risk for delayed awakening after general surgery. Whether this risk also applies to cerebral neurosurgical procedures remains unclear. This study evaluated early postoperative cognitive recovery and gas exchange patterns, after balanced anesthesia with sevoflurane or desflurane, in overweight and obese patients undergoing craniotomy for supratentorial expanding lesions. Fifty-six patients were consecutively enrolled, and randomly assigned to 1 of 2 study groups to receive balanced anesthesia with sevoflurane or desflurane. Cognitive function was evaluated with the Short Orientation Memory Concentration Test and the Rancho Los Amigos Scale and gas exchange patterns (pH, PaO2, and PaCO2) were recorded in all patients at 5 time-points: preoperatively and postoperatively, after patients reached an Aldrete score >or=9, at 15, 30, 45, and 60 minutes. Preoperative cognitive status was similar in the 2 treatment groups. Early postoperative cognitive recovery was more delayed and Short Orientation Memory Concentration Test scores at 15 and 30 minutes postanesthesia were lower in patients receiving sevoflurane-based anesthesia than in those receiving desflurane-based anesthesia (21.5+/-3.5 vs. 14.9+/-3.5) (P<0.005) and (26.9+/-0.7 vs. 21.5+/-1.4) (P<0.005), and the postoperative Rancho Los Amigos Scalegrade 8 showed a similar trend (25/28 patients 89% vs. 8/28 patients 28% (P<0.005) and 28/28 patients (100% vs. 13/28 patients 46%) (P<0.005). Similarly, gas-exchange analysis showed higher PaCO2 at 15 and 30 minutes and lower pH up to 45 minutes postextubation in patients receiving sevoflurane-based anesthesia. In overweight and obese patients undergoing craniotomy desflurane-based anesthesia allows earlier postoperative cognitive recovery and reversal to normocapnia and normal pH.

Esmolol blunts postoperative hemodynamic changes after propofol-remifentanil total intravenous fast-track neuroanesthesia for intracranial surgery.

STUDY OBJECTIVE: To investigate whether esmolol is effective in attenuating postoperative hemodynamic changes related to sympathetic overdrive. DESIGN: Clinical study. SETTING: Operating room of a university hospital. PATIENTS: 60 ASA physical status I, II, and III patients, age 18 to 65 years, scheduled for elective craniotomy for supratentorial neurosurgery. INTERVENTIONS: Patients were given total intravenous anesthesia (TIVA) during emergence from anesthesia and up to 60 minutes after extubation. Those patients who had hypertension (defined as an increase in systolic blood pressure >20% from baseline values) and tachycardia (defined as an increase >20% in heart rate from baseline) received a loading dose of 500 microg/kg esmolol in one minute, followed by an infusion titrated stepwise (50, 100, 200, and 300 microg/kg per min) every two minutes. MEASUREMENTS: The mean dose and duration of esmolol therapy were measured. MAIN RESULTS: Of 60 patients, 49 (82%) who received propofol-remifentanil TIVA developed significant tachycardia and hypertension soon after extubation. Treatment with esmolol (500 microg/kg in bolus maintained at a mean rate of 200 +/- 50 microg/kg per min) effectively controlled hypertension and tachycardia in 45 of 49 patients (92%; P < 0.05) within a mean 4.30 +/- 2.20 minutes. After extubation, mean esmolol infusion time was 29 +/- 8 minutes. CONCLUSION: In patients undergoing elective neurosurgery with propofol-remifentanil TIVA, a relatively small esmolol dose and short infusion time effectively blunts early postoperative arterial hypertension and tachycardia.

Intensive insulin therapy after severe traumatic brain injury: a randomized clinical trial.

INTRODUCTION: To investigate the risks and possible benefits of routine versus intensive insulin therapy, assessed by the frequency of hypoglycemic events defined as a glucose concentration less than 80 mg/dl (<4.44 mmol/l) in patients admitted to the intensive care unit (ICU) after severe traumatic brain injury (TBI). METHODS AND RESULTS: Ninety-seven patients admitted after severe TBI, were enrolled and randomly assigned to two groups of target glycemia. Insulin was infused at conventional rates when blood glucose levels exceeded 220 mg/dl (12.22 mmol/l) or at intensive rates, to maintain glycemia at 80-120 mg/dl (4.44-6.66 mmol/l). The following primary and outcome variables were measured during follow-up: hypoglycemic episodes, duration of ICU stay, infection rate, and 6-month mortality and neurologic outcome measured using the Glasgow Outcome Scale (GOS). Episodes of hypoglycemia (defined as blood glucose <80 mg/dl or 4.44 mmol/l) were significantly higher in patients receiving intensive insulin therapy: median (min-max) conventional insulin therapy 7 (range 0-11) vs. intensive insulin therapy 15 (range 6-33); P<0.0001. Duration of ICU stay was shorter in patients receiving intensive insulin therapy (7.3 vs. 10.0 days; P < 0.05); while infection rates during ICU stay (25.0% vs. 38.8%, P = 0.15), and GOS scores and mortality at 6 months were similar in the two groups. CONCLUSIONS: Intensive insulin therapy significantly increases the risk of hypoglycemic episodes. Even though patients receiving intensive insulin therapy have shorter ICU stays and infection rates similar to those receiving conventional insulin therapy, both groups have similar follow-up mortality and neurologic outcome. Hence if intensive insulin therapy is to be used, great effort must be taken to avoid hypoglycemia.

Endotracheal lidocaine in preventing endotracheal suctioning-induced changes in cerebral hemodynamics in patients with severe head trauma.

INTRODUCTION: In patients with severe head trauma, endotracheal suctioning can result in adverse reactions including cough, systemic hypertension, increased intracranial pressure, and reduced cerebral perfusion pressure. The aim of this prospective, blinded clinical trial in mechanically ventilated patients with severe head trauma whose cough reflexes were still intact was to assess the effectiveness of endotracheally instilled lidocaine in preventing endotracheal suctioning-induced changes in cerebral hemodynamics (increase in intracranial pressure and reduced cerebral perfusion pressure) after a single endotracheal suctioning. METHODS AND RESULTS: Ten minutes after lidocaine instillation into the endotracheal tube, secretions were suctioned for <30 s through a standard closed endotracheal suctioning circuit. Heart rate, arterial pressure, intracranial pressure, and cerebral perfusion pressure were continuously monitored. The first patient studied received an endotracheal lidocaine dose of 2.0 mg/kg. The dose for the next study patient was titrated upwards or downwards in 0.5 mg/kg steps according to, whether the intracranial pressure reached the predefined threshold of > or =20 mmHg. A total of 41 patients were studied. Lidocaine instillation into the endotracheal tube had no effect on hemodynamic and ventilatory variables. In 21 patients lidocaine dose instilled into the endotracheal tube effectively prevented the endotracheal suctioning-induced intracranial pressure increase behind the predefined threshold of > or =20 mmHg and cerebral perfusion pressure remained unchanged. In the remaining 20, although intracranial pressure rose significantly cerebral perfusion pressure remained constant. CONCLUSIONS: In mechanically ventilated patients with severe head trauma endotracheal lidocaine instillation effectively and dose-dependently prevents the endotracheal suctioning-induced intracranial pressure increase and cerebral perfusion pressure reduction.