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Background Opioids are known to stimulate surface electroencephalographic activity in patients with temporal lobe epilepsy. The objective of the current study was to compare the electrocorticographic activation effects of the newer short-acting opioid remifentanil with those of alfentanil during epilepsy surgery under general anaesthesia. Methods Thirteen patients undergoing temporal lobe epilepsy surgery under general anaesthesia received alfentanil 30 μg kg−1 and remifentanil 1 μg kg−1 as i.v. boluses in sequence. The design was a randomized double-blind cross-over study. After opening the dura, electrocorticogram (ECoG) electrode contact strips were placed over the temporal and supratemporal neocortex and depth electrodes were inserted in the amygdala and hippocampus. Alfentanil 30 μg kg−1 or remifentanil 1 μg kg−1 were administered randomly in a blinded fashion. The ECoG was recorded continuously before and after the injection of each drug. The interictal epileptiform activity (spikes and sharp waves) above baseline was analysed. Results Both drugs increased epileptiform activity especially that recorded from depth electrodes in the temporal limbic structures. No epileptiform activity was recorded from the electrodes overlying the supratemporal neocortex before or after drug administration. The more potent activator was alfentanil, which caused an increase in activation from baseline of 99.8% compared with 67.4% for remifentanil. In addition, alfentanil activated the epileptiform activity in 3 patients in which remifentanil had no effect. There were no changes in heart rate after the opioid boluses. Both remifentanil and alfentanil caused significant reductions in blood pressure at 3 and 5 min after administration. Conclusion We conclude that at the doses used in this study, alfentanil is the better opioid for intraoperative activation of the ECoG in neurosurgical patients undergoing resection of a temporal lobe epileptic focus. This pharmacological activation of epileptiform activity assists in localizing and confirming the site of surgical excision. Neither alfentanil nor remifentanil activated epileptiform activity in non-epileptic brain tissue.

To describe loss of the airway during tracheostomy and suggest a method for re-establishment of the airway and providing rescue oxygenation.A 22-yr-old female diagnosed with encephalomyelopathy was admitted to the intensive care unit with a progressively deteriorating level of consciousness and respiratory failure requiring intubation and ventilation. Several weeks later, an elective tracheostomy was performed under anesthesia. The surgeon made an anterior tracheal wall incision and inserted a cuffed #6 Shiley tracheostomy tube. No end-tidal CO(2) was detected and the patient could not be ventilated. After another failed attempt at insertion of a second tracheostomy tube, the diagnosis was made of a false passage within the trachea. The Shiley tracheostomy tube was removed and a #6 regular endotracheal tube was introduced in the trachea through the tracheostomy incision. The patient now could be ventilated with difficulty and low readings of end-tidal CO(2) were noted. Despite all efforts to further ventilate the patient, the arterial oxygen saturation never recovered, resulting in cardiac arrest.To restore a lost airway during tracheostomy, we recommend that a jet ventilation airway exchange catheter (JVAE) be inserted in the endotracheal tube through a bronchoscope port attachment prior to surgical entry into the trachea. The JVAE will also ensure continued ability to oxygenate the patient.

To present a case of preoperative subcutaneous emphysema (SCE) as a complication of trans-cricothyroid membrane (TCM) injection of lidocaine for awake intubation.A 48-yr-old man with cervical myelopathy was scheduled for elective cervical discectomy. Airway topical anesthesia consisted of lidocaine pledgets and TCM injection. After successful awake fibreoptic intubation was performed, SCE was noted in the neck region. The main differential diagnosis of preoperative SCE included air leak via the anterior needle track from TCM injection or disruption of mucosal membrane in the aerodigestive tract. The latter was excluded by panendoscopy and an upper GI swallow study. The most likely explanation for SCE was air leak from the anterior needle tract. The subcutaneous emphysema resolved spontaneously without sequella.Subcutaneous emphysema is a rare but potentially serious complication of TCM injection of lidocaine. Anesthesiologists should be familiar with the differential diagnosis, investigations and management of SCE.

Objectives: To investigate the response of CO 2 -retaining chronic obstructive pulmonary disease (COPD) patients to an increase in Fio 2 following a period of mechanical ventilation with Pao 2 in the normal range.The administration of a high Fio 2 to chronic obstructive pulmonary disease (COPD) patients may result in hypercapnia. Recent evidence indicates that the hypercapnia may be due to reversal of preexisting regional hypoxic pulmonary vasoconstriction resulting in a greater deadspace. This effect would be more pronounced in patients whose initial Pao 2 was

To determine the influence of positive end-expiratory pressure (PEEP) on intracranial pressure and cerebral perfusion pressure.Neurosurgical intensive care patients requiring intracranial pressure monitoring and mechanical ventilation were studied in a randomized, controlled study.Tertiary care, neurosurgical intensive care unit.Eighteen patients were enrolled in the study. Patients had posttraumatic head injuries (n = 9), subarachnoid hemorrhage (n = 7), obstructive hydrocephalus (n = 1), and intracerebral hemorrhage of unknown cause (n = 1).Patients had PEEP levels of 5, 10, and 15 cm H2O applied to their lungs.Changes in intracranial pressure, mean arterial pressure, and cerebral perfusion pressure were measured. The results were analyzed separately for patients with normal and increased intracranial pressure (15 mm Hg). PEEP at 5 cm H2O had no effect on intracranial pressure in the group with normal intracranial pressure. However, PEEP at 10 and 15 cm H2O produced a significant (p.05) increase in intracranial pressure (1.9 and 1.5 mm Hg, respectively). In the group with increased intracranial pressure, no significant change in intracranial pressure occurred at any of the PEEP levels used. In both groups, cerebral perfusion pressure was unchanged throughout.In patients with normal intracranial pressure, PEEP at 5 cm H2O did not significantly alter intracranial pressure. The clinical relevance of the intracranial pressure increase at PEEP levels of 10 and 15 cm H2O is questionable because cerebral perfusion pressure did not change and remained60 mm Hg. In patients with increased intracranial pressure, higher levels of PEEP did not significantly change intracranial pressure or cerebral perfusion pressure.

OBJECTIVE: To assess the ability of the Acute Physiology and Chronic Health Evaluation (APACHE II) system and Trauma-Injury Severity Scoring (TRISS) system in predicting group mortality in intensive care unit (ICU) trauma patients. DESIGN: Prospective study. SETTING: A Canadian adult trauma tertiary referral hospital. PATIENTS: Consecutive trauma patients admitted to the medical-surgical ICU or the neurosurgical ICU. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: For each patient, demographic data, mechanism of injury, and surgical status were collected. Revised Trauma Scores and Injury Severity Scores were calculated from emergency room and operative data. The APACHE II score was calculated based on the data from the first 24 hrs of ICU admission. The probability of death was calculated for each patient based on the APACHE II and TRISS equations. The ability to predict group mortality for APACHE II and TRISS was assessed by receiver operating characteristic curve analysis, two by two decision matrices, and calibration curve analysis. Four hundred seventy trauma patients were admitted to the ICU. Sixty-three (13%) patients died and 407 (87%) survived. There were significant differences between survivors and nonsurvivors in age, Glasgow Coma Scale, Revised Trauma Score, Injury Severity Score, and APACHE II score. By receiver operating characteristic curve analysis, the areas under the curves (+/- SEM) of APACHE II and TRISS were 0.92 +/- 0.02 and 0.89 +/- 0.02, respectively. Using two by two decision matrices with a decision criterion of 0.5, the sensitivities, specificities, and percentages correctly classified were 50.8%, 97.3%, and 91.1%, respectively, for APACHE II, and 50.8%, 97.1%, and 90.9%, respectively, for TRISS. From the calibration curves, the r2 value was .93 (p = .0001) for APACHE II and .67 (p = .004) for TRISS. CONCLUSIONS: Both APACHE II and TRISS scores were shown to accurately predict group mortality in ICU trauma patients. APACHE II and TRISS may be utilized for quality assurance in ICU trauma patients. However, neither APACHE II nor TRISS provides sufficient confidence for prediction of outcome of individual patients. Language: en

Perfusate composition may alter pulmonary hemodynamics and edema formation in perfused lungs. Perfusion for 3 h with Krebs-Henseleit solution with 3% bovine serum albumin did not produce pulmonary hypertension, pulmonary edema (assessed by lung wet-to-dry wt ratio), or increased macromolecular permeability (assessed by 125I-albumin uptake). Addition of blood to hematocrit levels of 10 or 20% resulted in pulmonary hypertension during the final hour of perfusion but not pulmonary edema or increased macromolecular permeability. Pulmonary hypertension during blood perfusion was primarily due to increased precapillary resistance. Perfusion with buffer solution without albumin produced edema and increased macromolecular permeability but not pulmonary hypertension. In lungs perfused with blood (20% hematocrit), thromboxane B2 levels increased in parallel with the pulmonary hypertension, and inhibition of cyclooxygenase or thromboxane synthase with indomethacin or dazmegrel prevented pulmonary hypertension. Perfusion with leukopenic blood (from prior nitrogen mustard administration or from filtration) also prevented pulmonary hypertension. We conclude that blood perfusion produces pulmonary hypertension via thromboxane A2 generation, which depends on leukocyte activation, and that perfusion with buffer solutions without albumin produces edema and increased permeability without pulmonary hypertension.

Increased vascular permeability in the adult respiratory distress syndrome is due in part to toxic oxygen metabolites. In the present study, we produced lung injury in the isolated rabbit lung with hydrogen peroxide (H2O2) and examined its prevention with isoproterenol. Pulmonary arterial pressure (Ppa) and the fluid filtration coefficient (Kf) were measured as indices of lung injury. Rabbits were divided into two groups, and 7 mmol/l H2O2 was administered in both groups. In one group, isoproterenol (2 micrograms/ml) was administered 10 min before H2O2 injury. Ppa increased transiently after H2O2 administration in the control group but was unchanged in the isoproterenol group. Kf was significantly increased by H2O2 administration in the control group but not in the isoproterenol group. We conclude that H2O2 increases pulmonary vascular permeability and that isoproterenol may protect against H2O2-induced pulmonary injury.

To compare patient controlled inhalational induction (PCI) with the most commonly used sevoflurane induction technique, vital capacity inhalational induction (VCI).Following approval of the Research Ethics Board, 124 outpatients undergoing knee arthroscopy were randomly assigned to receive either PCI or VCI sevoflurane followed by laryngeal mask airway (LMA) insertion and sevoflurane maintenance. In the PCI group, the circle circuit was not primed. The patients were asked to hold the facemask themselves and breathe normally with sevoflurane 8% in oxygen at a flow rate of 4 L x min(-1). In the VCI group, the circle circuit was primed and patients were asked to take vital capacity breaths with sevoflurane 8% at an oxygen flow rate of 8 L x min(-1). The LMA was inserted as soon as the patient's jaw was relaxed. Time from induction to LMA insertion was recorded and insertion conditions rated. The amount of sevoflurane used for LMA insertion was calculated. Vital signs were monitored at one-minute intervals until ten minutes after LMA insertion.Demographic data were comparable. There were no differences with respect to LMA insertion time (PCI - 3.4 min vs VCI - 3.3 min), laryngospasm (PCI - 7% vs VCI - 5%), mean arterial pressure, heart rate, SaO(2) as well as patient's overall satisfaction.PCI was comparable to VCI in sevoflurane induction with respect to the speed of induction, side effects during induction and patient satisfaction. However, PCI requires no special training and is widely applicable to all patient populations.

To report a non-fatal case of intraoperative venous air embolism (VAE) during an awake craniotomy. VAE presented with unusual clinical features. VAE during an awake craniotomy has not been reported frequently. The patient we describe presented with persistent coughing followed by tachypnea, hypoxia and reduction in end-tidal CO2 during dural opening while undergoing an awake craniotomy in the supine position. Cardiovascular variables were stable during the episode except for transient hypertension. Having ruled out airway obstruction and low cardiac output, we concluded that air embolism was the cause. The patient responded immediately to the standard treatment of air embolism and recovered without any complication. This case illustrates a VAE during an awake craniotomy and emphasizes the importance of early diagnosis in the management.

To the Editor: In a 65-yr-old man undergoing elective cystolithopaxy anesthesia was induced and a size 4 LMA (Intavent, Oxon, UK) inserted. At emergence, the patient bit on the LMA shaft, shearing it into two pieces (Figure). The proximal shaft outside his clenched teeth was severed. The distal shaft and the inflated LMA remaining inside the patient’s mouth. A facemask with oxygen was applied. He maintained spontaneous breathing but did not open his mouth. One minute later, his mouth opened and the LMA was removed using McGill forceps after cuff deflation. Examination of the LMA showed a spiral fracture of the distal shaft and marked yellowish discoloration of the shaft. The manufacturing date was the second quarter of 1991. Autoclaving (steam, 134°C) at our hospital conforms to the manufacturer’s recommendations.1 We estimate that this LMA had been autoclaved over 400 times. The Canadian supplier (Vitaid, Toronto) recommended the following to ensure safety:1,2 first, record each autoclaving and discard after 40 uses; second, before each use, check colour of shaft, aperture bars, competency of pilot balloon valve, competency of LMA cuff, 15 mm connector fit; third, flex the shaft 180° and observe for kinking; fourth, use a bite block. This case illustrates the potential risk of a fractured LMA due to excessive re-use. Although dramatic in presentation, the patient had no sequlae. It is important to retrieve all pieces of the fractured LMA and that none is aspirated into the lungs.

D ESPITE our extensive clinical experience, anesthesiologists still encounter unexpected difficult intubations. We need to be prepared with an organized plan such as the ASA algorithm ~s for management of the difficult airway. In a "can't intubate/can't ventilate" situation, emergency methods of oxygenation and ventilation must be rapidly available. There are many anecdotal reports of intubating 'tricks'. The ASA task force 2 and a recent review 4 recommend the general types of equipment that should be stocked on a difficult intubation kit. There are commercially available trays specifically designed for certain aspects of airway management. In a university teaching hospital department, we found it necessary to organize a comprehensive difficult intubation cart due to the preferences of different anesthesiologists. Since we do not practice pediatric anesthesia, our intubation cart is designed for adult patients. There is one clearly labeled difficult intubation cart in the operating room area and two portable kit bags. Adult and pediatric fiberoptic bronchoscopes and the BuUard laryngoscope are stored on a separate portable cart. Our purpose is not to mention all possible airway management equipment. We hope this listing will help others formulate and organize their own difficult intubation cart. It is important that anesthesiologists and trainees be familiar with the indications and limitations of these devices. Having previously thought through the steps of emergency airway management and with the equipment readily available, the anesthesiologist will be better prepared to deal efficiently with difficult airway situations. Equipment for airway management and intubation

The aim of our study was to compare the complication rate of convenional surgical and percutaneous dilational tracheostomies performed under general anaesthesia in critically ill patients. Fifty-three consecutive patients whose lungs were mechanically ventilated and who required tracheostomy were randomised to undergo either conventional surgical tracheostomy (n = 28) in the operating room or percutaneous dilational tracheostomy (n = 25) in the intensive care unit under general anaesthesia. All of the procedures were successfully completed. No deaths were related to the performance of either tracheostomy technique. Three patients in each group required a dressing change for minor bleeding at the tracheostomy site. There was no major bleeding requiring blood transfusion. One patient in each group developed atelectasis detected on chest x-ray post-operatively. In the surgical tracheostomy group, there were two patients with cuff leaks, one with a stomal infection and one with a pneumothorax. None of these complications occurred after percutaneous, dilational tracheostomy. We conclude that the low incidence of complications in both groups indicates that percutaneous dilational tracheostomy can be performed as safely in the intensive care unit with general anaesthesia as surgical tracheostomy can be performed in the operating room.