Haemodynamic response at double lumen bronchial tube placement - Airtraq vs. MacIntosh laryngoscope, a randomised controlled trial.

INTRODUCTION: Tracheal intubation causes a haemodynamic response that might be harmful for patients. The Airtraq® laryngoscope has been shown to decrease the haemodynamic response to single-lumen tube intubation. We hypothesised that double-lumen bronchial tube placement with the Double-lumen Airtraq® laryngoscope would cause a reduced haemodynamic response and decreased catecholamine release compared with the MacIntosh laryngoscope. METHODS: Forty adult patients were randomly assigned to the Airtraq® group or to the MacIntosh group. Intubation with either the Airtraq® or the MacIntosh laryngoscope was performed two minutes after standardised induction of anaesthesia. Arterial blood pressure, heart rate, catecholamine levels, bispectral index and duration of the intubation procedure were measured. RESULTS: Mean (standard deviation [95% confidence interval]) systolic arterial blood pressure at laryngoscopy with the Airtraq® laryngoscope was 124 (34 [106 to 141]) mmHg and, with the MacIntosh laryngoscope, it was 110 (25 [99 to 122]) mmHg (p=1.0). Heart rate at laryngoscopy with the Airtraq® laryngoscope was 75 beats·min-1 (16 [67 to 83]) and, with the MacIntosh laryngoscope, it was 64 beats·min-1 (14 [58 to 71]) (p=0.71). Adrenaline levels post-intubation were 54.3 ng·l-1 (41.5) [29.3 to 79.4] in the Airtraq® group and 30.5 ng·l-1 (25.6) [15.1 to 46.0] in the MacIntosh group (p=0.016). The duration of intubation with the Airtraq® laryngoscope was 88 s (31 [72-104]) while, with the MacIntosh laryngoscope, the duration was 75 s (35 [59-92]) (p=0.26). CONCLUSIONS: The use of the Double-lumen Airtraq® laryngoscope provides no benefit regarding stress response compared to the MacIntosh laryngoscope.

Contralateral stroke during carotid endarterectomy due to abnormalities in the circle of Willis.

Approximately 10-20% of patients will not tolerate cross-clamping of the common carotid artery for carotid endarterectomy procedures. The most frequent causes of neurological deficits are either embolization of particulate matter or cerebral hypoperfusion. Insufficient blood flow through primary collaterals of the circle of Willis is the main reason for hypoperfusion that requires immediate shunt placement. Although excessive preoperative imaging is not indicated in many patients undergoing disobliteration of a stenosed internal carotid artery, there are some patients with particular anatomic constellations who would benefit from a more detailed preoperative work-up. In these cases, the specific risk should be evaluated prior to surgery in order to make plans for appropriate intraoperative management regarding neurologic monitoring and shunt insertion. As regional anesthesia permits early detection of ischemic symptoms, it is advantageous in these patients. We report a case where regional anesthesia allowed early detection of rapidly progressing signs of bi-hemispheric brain ischemia in a patient with diabetes and with at that time unknown severe abnormalities of the circle of Willis. Lack of adequate collateralization was detected only after surgery, in a combined perfusion-magnetic resonance imaging study. In symptomatic diabetics with low-grade stenosis of the internal carotid artery, preoperative assessment of the function of the circle of Willis may therefore be helpful in predicting any increased risk for intraoperative cerebral ischemia.

Postoperative analgesia with remifentanil in patients undergoing cardiac surgery.

Remifentanil, a short-acting opioid, is commonly used in cardiac anesthesia. In this study we sought to demonstrate the feasibility of pain treatment and to determine the remifentanil dose necessary for adequate analgesia in tracheally extubated patients after cardiac surgery. Thirty patients undergoing elective cardiac surgery were included in this study. After surgery, the intraoperatively administered remifentanil was initially continued at 0.05 microg . kg(-1) . min(-1). Before tracheal extubation, a nonsteroidal antiinflammatory drug was administered and remifentanil was reduced to 0.035 microg . kg(-1) . min(-1). Pain assessment using a visual analog scale (VAS) was performed after tracheal extubation, in 2-min intervals for 10 min, every 10 min until the end of the first hour and every 30 min during the ensuing 5 h. A VAS score > or =30 or a respiratory rate <10 breaths/min was followed by an increase or decrease in the remifentanil dose by 0.005 microg . kg(-1) . min(-1), respectively. For rapid dose adaptation during the first 10 min, remifentanil was increased twice by 0.005 microg. kg(-1) . min(-1) and then 3 times by 0.01 microg . kg(-1) . min(-1). With a mean remifentanil dose of 0.051 microg . kg(-1) . min(-1) VAS decreased to 26 +/- 14 after 30 min. Sufficient analgesia was achieved with remifentanil doses ranging from 0.03 to 0.09 microg. kg(-1) . min(-1). A maximum mean remifentanil dose of 0.057microg. kg(-1) . min(-1) was reached after 4 h. The combination of remifentanil with a nonsteroidal antiinflammatory drug provided adequate analgesia in 73% of patients 30 min after tracheal extubation. Rapid dose titration was necessary during the first 10 min in 50% of patients. Increasing the initial remifentanil dose could shorten the titration period but may be associated with respiratory complications.

Release of neuron-specific enolase and S100 after implantation of cardioverters/defibrillators.

OBJECTIVE: Repeated induction of ventricular fibrillation with ensuing alterations in electroencephalogram and jugular venous oxygen saturation is common practice during insertion of transvenous implantable cardioverters/defibrillators. We investigated whether these functional changes are also associated with cerebral injury. DESIGN: Prospective study. SETTING: University hospital. PATIENTS: We studied 45 patients undergoing implantable cardioverter/defibrillator insertion. Eleven patients with cardiac pacemaker implantation, which was performed in the same manner yet without the necessity to induce ventricular fibrillation, served as controls. MEASUREMENTS AND MAIN RESULTS: Serum neuron-specific enolase and S100 were determined before, immediately postoperatively, and 2 hrs postoperatively. In a randomly composed subgroup, neuron-specific enolase was also determined 6 and 24 hrs after surgery. Implantable cardioverter/defibrillator patients only showed an increase of both markers postoperatively. Median neuron-specific enolase values climbed from a preoperative 9.9 to 12.3 and 14.4 microg/L at 2 and 24 hrs after surgery, respectively. This increase was associated with the number of shocks and the cumulative time in circulatory arrest. The highest median S100 level (0.075 microg/L) was reached 2 hrs after the procedure. Neuron-specific enolase and S100 were extremely elevated (13.7 and 0.970 microg/L, respectively) in one patient after an extended episode of ventricular fibrillation. Plasma hemoglobin levels were in the normal range in implantable cardioverter/defibrillator patients throughout the observation period. CONCLUSIONS: Apparently, even brief successive periods of global cerebral ischemia cause neuronal damage without obvious severe neurologic deficits. However, they may be related to subtle postoperative neurologic or cognitive dysfunctions that a number of implantable cardioverter/defibrillator patients exhibit after implantation.

The impact of asymptomatic carotid artery disease on the intraoperative course of coronary artery bypass surgery.

Asymptomatic carotid artery stenosis (CAS) may result in neurological injury after coronary artery bypass surgery, but routine preoperative carotid screening is not undisputed. We studied whether routinely determined carotid duplex results, beyond detecting high-risk patients, additionally influence intraoperative course. One hundred and eight patients without new signs of impaired cerebral circulation were investigated. Anesthesiology, perfusionist records, and patient files were reviewed for patient characteristics, intraoperative variables and postoperative neurological sequelae. There was a higher incidence of prior cerebrovascular events and peripheral artery disease in CAS patients (p < 0.05). Pulsatile flow was employed more frequently in this group (p < 0.05). Severe hyperventilation, hyperglycemia, hemodilution, hyperthermia, and lactacidosis were avoided in both groups. However, labile hemodynamics of CAS patients required more corrective interventions (p < 0.05). There was also a tendency toward greater mortality. Stroke and transient ischemic attack (TIA) occurred in two patients without CAS. Since CAS was associated with a greater degree of cardiovascular instability requiring frequent measures to control hemodynamics, positive duplex results should heighten vigilance. Although CAS does not appear to be the major source of cerebral ischemia, it involves significant comorbidity.

Surgical treatment of acute type A dissection: is rupture a risk factor?

BACKGROUND: The purpose of this study was to evaluate the significance of aortic rupture on clinical outcome in patients after aortic repair for acute type A dissection. METHODS: One hundred and twenty patients underwent aortic operations with resection of the intimal tear and open distal anastomosis. Median age was 60 years (range 16 to 87); 78 were male. Thirty-six patients had only ascending aortic replacement, 82 had hemiarch repair, and 2 had the entire arch replaced. Retrograde cerebral perfusion was utilized in 66 patients (53%). Rupture defined as free blood in the pericardial space was present in 60 patients (50%). Univariate and multivariate analyses were performed to assess the risk factors for mortality and neurologic dysfunction. RESULTS: Overall hospital mortality rate was 24.2% +/- 4.0% (+/- 70% confidence level) but did not differ between patients with aortic rupture or without (p = 0.83). The incidence of permanent neurologic dysfunction was 9.4% overall, 10.5% with rupture and 8.3% without rupture (p = 0.75). Multivariate analysis revealed absence of retrograde cerebral perfusion and any postoperative complication as statistically significant indicators for in-hospital mortality (p < 0.05). Overall 1- and 5-year survival was 85.3% and 33.7%; among discharged patients, survival in the nonruptured group was 89% and 37%, versus 81% and 31% in the ruptured group (p = 0.01). CONCLUSIONS: Aortic rupture at the time of surgery does not increase the risk of hospital mortality or permanent neurologic complications in patients with acute type A dissections. However, aortic rupture at the time of surgery does influence long-term survival.

Lack of renoprotective effects of dopamine and furosemide during cardiac surgery.

Because development of acute renal failure is one of the most potent predictors of outcome in cardiac surgery patients, the prevention of renal dysfunction is of utmost importance in perioperative care. In a double-blind randomized controlled trial, the effectiveness of dopamine or furosemide in prevention of renal impairment after cardiac surgery was evaluated. A total of 126 patients with preoperatively normal renal function undergoing elective cardiac surgery received a continuous infusion of either "renal-dose" dopamine (2 microg/kg per min) (group D), furosemide (0.5 microg/kg per min) (group F), or isotonic sodium chloride as placebo (group P), starting at the beginning of surgery and continuing for 48 h or until discharge from the intensive care unit, whichever came first. Renal function parameters and the maximal increase of serum creatinine above baseline value within 48 h (deltaCrea(max)) were determined. The increase in plasma creatinine was twice as high in group F as in groups D and P (P < 0.01). Acute renal injury (defined as deltaCreamax) >0.5 mg/dl) occurred more frequently in group F (six of 41 patients) than in group D (one of 42) and group P (zero of 40) (P < 0.01). (The difference between group D and group P was not significant.) Creatinine clearance was lower in group F (P < 0.05). Two patients in group F required renal replacement therapy. The mean volume of infused fluids, blood urea nitrogen, serum sodium, serum potassium, and osmolar- and free-water clearance was similar in all groups. It was shown that continuous infusion of dopamine for renal protection was ineffective and was not superior to placebo in preventing postoperative dysfunction after cardiac surgery. In contrast, continuous infusion of furosemide was associated with the highest rate of renal impairment. Thus, renaldose dopamine is ineffective and furosemide is even detrimental in the protection of renal dysfunction after cardiac surgery.