Depth of anaesthesia monitoring: time to reject the index?

Depth of anaesthesia monitors can fail to detect consciousness under anaesthesia, primarily because they rely on the frontal EEG, which does not arise from a neural correlate of consciousness. A study published in a previous issue of the British Journal of Anaesthesia showed that indices produced by the different commercial monitors can give highly discordant results when analysing changes in the frontal EEG. Anaesthetists could benefit from routinely assessing the raw EEG and its spectrogram, rather than relying solely on an index produced by a depth of anaesthesia monitor.

Effects of sevoflurane versus propofol on cerebral autoregulation during anaesthesia for robot-assisted laparoscopic prostatectomy.

Robot-assisted laparoscopic prostatectomy requires a pneumoperitoneum combined with steep Trendelenburg positioning, and these conditions can be associated with impairment of cerebral autoregulation. The objective of this study was to determine if choice of anaesthetic agent affects the preservation of cerebral autoregulation during robot-assisted laparoscopic prostatectomy. We randomly assigned 30 patients to maintenance of general anaesthesia with either propofol or sevoflurane. Cerebral autoregulation was tested by administration of intravenous phenylephrine to increase mean arterial pressure from approximately 80 mmHg to 100 mmHg while assessing cerebral blood flow using transcranial Doppler ultrasonography. Autoregulation was first tested in the supine position and then approximately once every hour after Trendelenburg positioning. The main outcome measure was the result of the final autoregulation test prior to completion of surgery. At that time, we found cerebral autoregulation to be significantly impaired in six of the 15 patients receiving sevoflurane and none of the 15 patients receiving propofol (P = 0.02). However, it should be noted that some patients in the propofol group had impaired autoregulation on earlier tests. In conclusion, we found that autoregulation during robot-assisted laparoscopic prostatectomy is less likely to be impaired with propofol compared to sevoflurane anaesthesia, particularly towards the end of the surgery.

Correlation and agreement between the TEG® 5000 and the TEG® 6s during liver transplant surgery.

The TEG® 5000 and novel TEG® 6s measure the viscoelasticity of whole blood during in vitro clot formation. The two devices measure similar coagulation variables but utilize distinctly different technologies. This study aimed to determine the correlation and agreement between the thrombelastographic parameters obtained by the two devices during liver transplant surgery. We obtained blood samples at six predefined intervals during the surgery of 10 consecutive patients. Two operators proficient in the use of the TEG® 6s and TEG® 5000 systems performed thrombelastographic measurements on each sample: non-citrated TEG® 5000, citrated TEG® 5000 and citrated TEG® 6s. Agreement and correlation were assessed using Bland Altman plots and Lin's concordance correlation. There was considerable inter-device variability for the different parameters measured by the TEG® 5000 and TEG® 6s devices. Acceptable agreement was observed when results were within the normal reference ranges. However, with increasing coagulopathy, agreement was poor and results could not be considered interchangeable. Although each of the three tests appeared reliable for qualitative detection of abnormalities of clot formation during liver transplant surgery, we found their quantitative results were not interchangeable.

The evidence supporting WHO recommendations on the promotion of hand hygiene: a critique.

OBJECTIVE: To examine the quality of the evidence relied upon by the World Health Organisation (WHO) in promoting hand hygiene with campaigns such as "Save Lives: Clean Your Hands". RESULTS: The quality of evidence in the studies quoted by the WHO evidence document is highly variable and the methods used limited. In some of the quoted studies, hand hygiene was the primary outcome, rather than the clinically significant outcome of hospital acquired infection (HAI). When HAI was the primary outcome, it was often poorly defined and reported with scant detail. There was wide variation in the hand hygiene compliance achieved in the intervention studies. The majority of studies where the intervention was a campaign to promote hand hygiene used historical control data with variable attempts to account for the fact that HAI rates may have been declining prior to the hand hygiene intervention. The results from trials with a contemporaneous control were conflicting.

Posttraumatic stress disorder in aware patients from the B-aware trial.

BACKGROUND: The long-term consequences of an awareness episode vary. Some patients do not have any long-term disability, whereas others develop psychological problems that may be severe and persistent. In this study, we compared the incidence of posttraumatic stress disorder (PTSD) in patients with and without confirmed awareness who were randomized in the B-Aware Trial. METHODS: We used a matched cohort design, aiming to follow up the 13 patients with confirmed awareness. Each surviving awareness patient was matched with 4 controls for age, sex, surgery type, date of surgery, and hospital. A face-to-face interview was conducted with each awareness patient and matched controls using the Clinician Administered Posttraumatic Stress Disorder Scale. RESULTS: Data collection for this study occurred between June 2006 and March 2007, with a median follow-up time of 5.3 yr (range, 4.3-5.7 yr). Six of the 13 confirmed awareness patients had died. Five of the 7 confirmed awareness patients (71%) and 3 of the 25 controls (12%) fulfilled the criteria for PTSD at the time of the interview (adjusted odds ratio = 13.3 [95% confidence interval: 1.4-650]; P = 0.02). The median onset time of symptoms was 14 days (range, 7-243 days) after surgery, and the median duration of symptoms was 4.7 yr (range, 4.4-5.6 yr). CONCLUSIONS: PTSD was common and persistent in the confirmed awareness patients of the B-Aware Trial. Strategies to prevent awareness in patients under general anesthesia are justified.

The effects of hypocapnia and the cerebral autoregulatory response on cerebrovascular resistance and apparent zero flow pressure during isoflurane anesthesia.

BACKGROUND: Simultaneous recordings of arterial blood pressure (ABP) and middle cerebral artery blood velocity can be used to calculate the apparent zero flow pressure (aZFP). The inverse of the slope of the pressure-velocity relationship is known as resistance area product (RAP) and is an index of cerebrovascular resistance. There is little information available regarding the effects of vasoactive drugs, arterial carbon dioxide (Paco(2)), and impaired cerebral autoregulation on aZFP and RAP during general anesthesia. During isoflurane anesthesia, we investigated the effects of hypocapnia and the effects of a phenylephrine infusion, on aZFP and RAP. METHODS: Radial ABP and transcranial Doppler middle cerebral artery blood velocity signals were recorded in 11 adults undergoing isoflurane anesthesia. A phenylephrine infusion was used to increase ABP and ventilation was adjusted to control Paco(2). Cerebral hemodynamic variables were compared at two levels of mean ABP (approximately 80 and 100 mm Hg) and at two levels of Paco(2): normocapnia (Paco(2) 38-43 mm Hg) and hypocapnia (Paco(2) 27-34 mm Hg). Two aZFP analysis methods were compared: one based on linear regression and one based on Fourier analysis of the waveforms. RESULTS: At the lower ABP, aZFP was 23 +/- 11 mm Hg and 30 +/- 13 mm Hg (mean +/- sd) with normocapnia and hypocapnia, respectively (P < 0.001) and RAP was 0.76 +/- 0.97 mm Hg x s x cm(-1) and 1.16 +/- 0.16 mm Hg x s x cm(-1) with normocapnia and hypocapnia, respectively (P < 0.001). Similar effects of hypocapnia were seen at the higher ABP. With normocapnia, isoflurane impaired cerebral autoregulation and aZFP did not change with the increase in ABP. With hypocapnia, cerebral autoregulation was not significantly impaired and increasing ABP was associated with increased aZFP (from 30 +/- 13 to 35 +/- 13 mm Hg, P < 0.01) and increased RAP (from 1.16 +/- 0.16 to 1.52 +/- 0.20 mm Hg x s x cm(-1), P < 0.001). Calculation of the relative contributions of aZFP and RAP to the cerebral hemodynamic responses indicated that changes in RAP appeared to have a greater influence than changes in aZFP. The mean difference between the two methods of determining aZFP (Fourier-regression) was 0.5 +/- 3.6 mm Hg (mean +/- 2sd). CONCLUSIONS: During isoflurane anesthesia, two interventions that increase cerebral arteriolar tone, hypocapnia and the autoregulatory response to increasing ABP, were associated with increased RAP and increased aZFP. The effect of changes in RAP appeared to be quantitatively greater than the effects of changes in aZFP. These results imply that arteriolar tone influences cerebral blood flow by controlling both resistance and effective downstream pressure.

A randomized crossover comparison of the effects of propofol and sevoflurane on cerebral hemodynamics during carotid endarterectomy.

BACKGROUND: Intravenous and inhalational anesthetic agents have differing effects on cerebral hemodynamics: Sevoflurane causes some vasodilation, whereas propofol does not. The authors hypothesized that these differences affect internal carotid artery pressure (ICAP) and the apparent zero flow pressure (critical closing pressure) during carotid endarterectomy. Vasodilation is expected to increase blood flow, reduce ICAP, and reduce apparent zero flow pressure. METHODS: In a randomized crossover study, the gradient between systemic arterial pressure and ICAP during carotid clamping was measured while changing between sevoflurane and propofol in 32 patients. Middle cerebral artery blood velocity, recorded by transcranial Doppler, and ICAP waveforms were analyzed to determine the apparent zero flow pressure. RESULTS: ICAP increased when changing from sevoflurane to propofol, causing the mean gradient between arterial pressure and ICAP to decrease by 10 mmHg (95% confidence interval, 6-14 mmHg; P<0.0001). Changing from propofol to sevoflurane had the opposite effect: The pressure gradient increased by 5 mmHg (95% confidence interval, 2-7 mmHg; P=0.002). Ipsilateral middle cerebral artery blood velocity decreased when changing from sevoflurane to propofol. Cerebral steal was detected in one patient after changing from propofol to sevoflurane. The apparent zero flow pressure (mean+/-SD) was 22+/-10 mmHg with sevoflurane and 30+/-14 mmHg with propofol (P<0.01). There was incomplete drug crossover due to the limited duration of carotid clamping. CONCLUSIONS: Compared with sevoflurane, ipsilateral ICAP and apparent zero flow pressure are both higher with propofol. Vasodilatation associated with sevoflurane can cause cerebral steal.

The effect of hypocapnia on the autoregulation of cerebral blood flow during administration of isoflurane.

Isoflurane impairs autoregulation of cerebral blood flow in a dose-related manner. Previous investigations in several other conditions have demonstrated that impaired autoregulation can be restored by hyperventilation. We hypothesized that hypocapnia may restore cerebral autoregulation impaired by isoflurane anesthesia. We administered isoflurane in 100% oxygen to 12 healthy patients aged 21-59 yr scheduled for elective nonneurological surgery. Isoflurane end-tidal concentration was individualized at 0.1% to 0.2% less than that required to induce short periods of isoelectric electroencephalogram. This resulted in an end-tidal isoflurane concentration of 1.6% +/- 0.2% (mean +/- sd) corresponding to an age-adjusted minimum alveolar anesthetic concentration multiple of 1.4. Mean arterial blood pressure was reduced to <80 mm Hg, by infusion of remifentanil if required. Cerebral autoregulation was assessed by infusing phenylephrine to increase mean arterial blood pressure to 100 mm Hg while monitoring middle cerebral artery blood flow velocity with transcranial Doppler ultrasonography. The change in flow velocity was used to calculate the autoregulation index (ARI). The ARI ranges between 0 and 1 and an ARI < or =0.4 indicates significantly impaired autoregulation. Autoregulation was tested twice in randomized order: once during normocapnia (Paco(2) 38-43 mm Hg) and once during hypocapnia (Paco(2) 27-34 mm Hg). The median (interquartile range) ARI was 0.29 (0.23-0.64) during normocapnia and 0.77 (0.70-0.78) during hypocapnia (P < 0.005). Of the 12 subjects, autoregulation was significantly impaired in 8 subjects during normocapnia and none during hypocapnia (P = 0.001). Hypocapnia restored cerebral autoregulation in normal subjects during isoflurane-induced impairment of autoregulation.

Cerebral hemodynamics immediately following carotid occlusion.

During carotid endarterectomy, we routinely monitor internal carotid artery pressure (P(ICA)) and middle cerebral artery flow velocity (V(MCA)). P(ICA) has been previously shown to accurately reflect pressure at the origin of the middle cerebral artery, even during times of rapidly changing pressure such as occurs with sudden occlusion of the common carotid artery. We retrospectively analyzed pressure recordings around the time of carotid cross clamping in 29 consecutive carotid endarterectomy operations. Suitable transcranial Doppler recordings of V(MCA) were available from eight of the operations. Comparing the cardiac cycle prior to cross clamping with the first complete cardiac cycle after cross clamping, the mean P(ICA) fell from 93 mm Hg to 62 mm Hg and the mean V(MCA) fell from 41 cm x sec-1 to 25 cm x sec-1. Over the subsequent 10 seconds, there was a further decrease in P(ICA) to 51 mm Hg (P <.0001), while V(MCA) changed in the opposite direction, increasing to 32 cm x sec-1 (P <.01). The patients with the greatest decrease in P(ICA) immediately on cross clamping also had the greatest additional decrease over the following 10 seconds (r = 0.74). The increase in V(MCA) during the first 10 seconds after carotid occlusion is well recognized and is presumed to be due to autoregulatory vasodilatation. The simultaneous decrease that we observed in P(ICA) indicates an increase in the pressure gradient along the collateral vessels, which is to be expected during a period of increasing flow along those vessels.